Clinical Psychiatry News

Tackling the COVID-19 crisis will require psychiatrists to muster the courage to lead, establish trust, and ultimately provide psychiatric care with competence, honesty, and compassion, said Patrice A. Harris, MD, an Atlanta-based psychiatrist who is president of the American Medical Association.

Leaders in psychiatry are uniquely positioned to combat a wave of disease misinformation, address inequities in care, and meet the logistical challenges of safely meeting patient needs as the outbreak continues, Dr. Harris said at the American Psychiatric Association annual meeting, which was held as a virtual live event.

“I believe you, we, are more than a match for this moment – a moment that requires our leadership and requires us to hold other leaders accountable as we fight this pandemic,” she said in remarks to online attendees.
 

Using trust to fight myths

Misinformation about COVID-19 has been “spreading rapidly, even intentionally, due to fear or political agendas,” said Dr. Harris, who became the 174th president of the AMA in June 2019.

“I spent the first 2 weeks in this pandemic dispelling the myth that African Americans could not become infected with COVID-19,” she said. Others believe the coronavirus crisis is a new way to force vaccinations on people who don’t want them, added Dr. Harris.

Myths, rumors, and conspiracy theories lead to “more illness and death,” she said, at a time when most Americans say they’ve lost trust in the federal government and even in other American citizens.

“Fortunately, people still trust us – their doctors,” she added. “We fight for science, we call out quackery and snake oil when we see it, [and] we are willing to counter the propaganda of the antiscience voice.”

Physicians are ranked among the most trusted professions because they are committed to seeing, acknowledging, and sharing patients’ human experience, “and of course, I believe we do that as psychiatrists more than most,” Dr. Harris said.
 

Fighting COVID-19 at the AMA level

During the pandemic, the AMA has advocated for adequate testing and supplies, adequate insurance coverage, and changes to current procedural technology (CPT) codes to streamline novel coronavirus testing. The AMA has also developed a free COVID-19 resource center on the JAMA Network website, Dr. Harris said, as well as guidance on protecting medical students responding to the pandemic.

The safety of health care clinicians remains a central issue for the AMA at a time when masks and other personal protective equipment (PPE) remain in short supply.

In a recent letter to Vice President Mike Pence, who is leading the White House’s coronavirus task force, AMA Executive Vice President and CEO James L. Madara, MD, urged the Trump administration to undertake a Manhattan Project–like effort to expand capacity for needed supplies.

“We will continue to call on the White House, and APA has as well, to make sure these needs are met,” Dr. Harris said.
 

COVID-19 and inequities in care

Because the pandemic has had dramatic effects on African American communities across the United States, AMA Chief Health Equity Officer Aletha Maybank, MD, has made recent media appearances to highlight care inequities and what can be done about them.

Meanwhile, the AMA and other physician associations have urged the Trump Administration to collect, analyze, and make available COVID-19 data by race and ethnicity: “We can’t fix a problem until we identify a problem,” Dr. Harris said in her address to the APA.
 

Relying on science

In a virtual address hosted by the National Press Club earlier in April, Dr. Harris made an appeal for “relying on the science and evidence” to inform COVID-19–related decisions.

Elected officials need to “affirm science, evidence, and fact in their words and actions,” while media need to be vigilant in citing credible sources and challenging those who “chose to trade in misinformation,” she said in that address.

Speaking at the APA virtual meeting, Dr. Harris spoke of an “assault on science for several years” that inspired the National Press Club address. “We wanted to remind the public of its responsibility to focus on science and the evidence, for us to turn the tide against COVID-19,” she explained.
 

Physician care and self-care

While the AMA urges social distancing, Dr. Harris used the term “physical distancing” in her APA address. Physical distancing emphasizes the need for stay-at-home and shelter-in-place restrictions, while recognizing the need for maintaining meaningful social interactions, she explained.

Social media use represents one “opportunity” to bridge that gap when physical proximity is not an option, she added.

Dr. Harris also stressed the need for physicians to “take time out and practice self-care” to ensure that they are recharged and able to provide optimal patient care.

“We need to be there for others, but we have to put our own masks on first,” she said.

Dr. Harris reported no financial relationships with commercial interests.

SOURCE: Harris PA. APA 2020 Virtual Meeting.

Tackling the COVID-19 crisis will require psychiatrists to muster the courage to lead, establish trust, and ultimately provide psychiatric care with competence, honesty, and compassion, said Patrice A. Harris, MD, an Atlanta-based psychiatrist who is president of the American Medical Association.

Leaders in psychiatry are uniquely positioned to combat a wave of disease misinformation, address inequities in care, and meet the logistical challenges of safely meeting patient needs as the outbreak continues, Dr. Harris said at the American Psychiatric Association annual meeting, which was held as a virtual live event.

“I believe you, we, are more than a match for this moment – a moment that requires our leadership and requires us to hold other leaders accountable as we fight this pandemic,” she said in remarks to online attendees.
 

Using trust to fight myths

Misinformation about COVID-19 has been “spreading rapidly, even intentionally, due to fear or political agendas,” said Dr. Harris, who became the 174th president of the AMA in June 2019.

“I spent the first 2 weeks in this pandemic dispelling the myth that African Americans could not become infected with COVID-19,” she said. Others believe the coronavirus crisis is a new way to force vaccinations on people who don’t want them, added Dr. Harris.

Myths, rumors, and conspiracy theories lead to “more illness and death,” she said, at a time when most Americans say they’ve lost trust in the federal government and even in other American citizens.

“Fortunately, people still trust us – their doctors,” she added. “We fight for science, we call out quackery and snake oil when we see it, [and] we are willing to counter the propaganda of the antiscience voice.”

Physicians are ranked among the most trusted professions because they are committed to seeing, acknowledging, and sharing patients’ human experience, “and of course, I believe we do that as psychiatrists more than most,” Dr. Harris said.
 

Fighting COVID-19 at the AMA level

During the pandemic, the AMA has advocated for adequate testing and supplies, adequate insurance coverage, and changes to current procedural technology (CPT) codes to streamline novel coronavirus testing. The AMA has also developed a free COVID-19 resource center on the JAMA Network website, Dr. Harris said, as well as guidance on protecting medical students responding to the pandemic.

The safety of health care clinicians remains a central issue for the AMA at a time when masks and other personal protective equipment (PPE) remain in short supply.

In a recent letter to Vice President Mike Pence, who is leading the White House’s coronavirus task force, AMA Executive Vice President and CEO James L. Madara, MD, urged the Trump administration to undertake a Manhattan Project–like effort to expand capacity for needed supplies.

“We will continue to call on the White House, and APA has as well, to make sure these needs are met,” Dr. Harris said.
 

COVID-19 and inequities in care

Because the pandemic has had dramatic effects on African American communities across the United States, AMA Chief Health Equity Officer Aletha Maybank, MD, has made recent media appearances to highlight care inequities and what can be done about them.

Meanwhile, the AMA and other physician associations have urged the Trump Administration to collect, analyze, and make available COVID-19 data by race and ethnicity: “We can’t fix a problem until we identify a problem,” Dr. Harris said in her address to the APA.
 

Relying on science

In a virtual address hosted by the National Press Club earlier in April, Dr. Harris made an appeal for “relying on the science and evidence” to inform COVID-19–related decisions.

Elected officials need to “affirm science, evidence, and fact in their words and actions,” while media need to be vigilant in citing credible sources and challenging those who “chose to trade in misinformation,” she said in that address.

Speaking at the APA virtual meeting, Dr. Harris spoke of an “assault on science for several years” that inspired the National Press Club address. “We wanted to remind the public of its responsibility to focus on science and the evidence, for us to turn the tide against COVID-19,” she explained.
 

Physician care and self-care

While the AMA urges social distancing, Dr. Harris used the term “physical distancing” in her APA address. Physical distancing emphasizes the need for stay-at-home and shelter-in-place restrictions, while recognizing the need for maintaining meaningful social interactions, she explained.

Social media use represents one “opportunity” to bridge that gap when physical proximity is not an option, she added.

Dr. Harris also stressed the need for physicians to “take time out and practice self-care” to ensure that they are recharged and able to provide optimal patient care.

“We need to be there for others, but we have to put our own masks on first,” she said.

Dr. Harris reported no financial relationships with commercial interests.

SOURCE: Harris PA. APA 2020 Virtual Meeting.

Tackling the COVID-19 crisis will require psychiatrists to muster the courage to lead, establish trust, and ultimately provide psychiatric care with competence, honesty, and compassion, said Patrice A. Harris, MD, an Atlanta-based psychiatrist who is president of the American Medical Association.

Leaders in psychiatry are uniquely positioned to combat a wave of disease misinformation, address inequities in care, and meet the logistical challenges of safely meeting patient needs as the outbreak continues, Dr. Harris said at the American Psychiatric Association annual meeting, which was held as a virtual live event.

“I believe you, we, are more than a match for this moment – a moment that requires our leadership and requires us to hold other leaders accountable as we fight this pandemic,” she said in remarks to online attendees.
 

Using trust to fight myths

Misinformation about COVID-19 has been “spreading rapidly, even intentionally, due to fear or political agendas,” said Dr. Harris, who became the 174th president of the AMA in June 2019.

“I spent the first 2 weeks in this pandemic dispelling the myth that African Americans could not become infected with COVID-19,” she said. Others believe the coronavirus crisis is a new way to force vaccinations on people who don’t want them, added Dr. Harris.

Myths, rumors, and conspiracy theories lead to “more illness and death,” she said, at a time when most Americans say they’ve lost trust in the federal government and even in other American citizens.

“Fortunately, people still trust us – their doctors,” she added. “We fight for science, we call out quackery and snake oil when we see it, [and] we are willing to counter the propaganda of the antiscience voice.”

Physicians are ranked among the most trusted professions because they are committed to seeing, acknowledging, and sharing patients’ human experience, “and of course, I believe we do that as psychiatrists more than most,” Dr. Harris said.
 

Fighting COVID-19 at the AMA level

During the pandemic, the AMA has advocated for adequate testing and supplies, adequate insurance coverage, and changes to current procedural technology (CPT) codes to streamline novel coronavirus testing. The AMA has also developed a free COVID-19 resource center on the JAMA Network website, Dr. Harris said, as well as guidance on protecting medical students responding to the pandemic.

The safety of health care clinicians remains a central issue for the AMA at a time when masks and other personal protective equipment (PPE) remain in short supply.

In a recent letter to Vice President Mike Pence, who is leading the White House’s coronavirus task force, AMA Executive Vice President and CEO James L. Madara, MD, urged the Trump administration to undertake a Manhattan Project–like effort to expand capacity for needed supplies.

“We will continue to call on the White House, and APA has as well, to make sure these needs are met,” Dr. Harris said.
 

COVID-19 and inequities in care

Because the pandemic has had dramatic effects on African American communities across the United States, AMA Chief Health Equity Officer Aletha Maybank, MD, has made recent media appearances to highlight care inequities and what can be done about them.

Meanwhile, the AMA and other physician associations have urged the Trump Administration to collect, analyze, and make available COVID-19 data by race and ethnicity: “We can’t fix a problem until we identify a problem,” Dr. Harris said in her address to the APA.
 

Relying on science

In a virtual address hosted by the National Press Club earlier in April, Dr. Harris made an appeal for “relying on the science and evidence” to inform COVID-19–related decisions.

Elected officials need to “affirm science, evidence, and fact in their words and actions,” while media need to be vigilant in citing credible sources and challenging those who “chose to trade in misinformation,” she said in that address.

Speaking at the APA virtual meeting, Dr. Harris spoke of an “assault on science for several years” that inspired the National Press Club address. “We wanted to remind the public of its responsibility to focus on science and the evidence, for us to turn the tide against COVID-19,” she explained.
 

Physician care and self-care

While the AMA urges social distancing, Dr. Harris used the term “physical distancing” in her APA address. Physical distancing emphasizes the need for stay-at-home and shelter-in-place restrictions, while recognizing the need for maintaining meaningful social interactions, she explained.

Social media use represents one “opportunity” to bridge that gap when physical proximity is not an option, she added.

Dr. Harris also stressed the need for physicians to “take time out and practice self-care” to ensure that they are recharged and able to provide optimal patient care.

“We need to be there for others, but we have to put our own masks on first,” she said.

Dr. Harris reported no financial relationships with commercial interests.

SOURCE: Harris PA. APA 2020 Virtual Meeting.

There has been a massive decline in outpatient office visits as patients have stayed home – likely deferring needed care – because of COVID-19, new research shows.

The number of visits to ambulatory practices dropped by a whopping 60% in mid-March, and continues to be down by at least 50% since early February, according to new data compiled and analyzed by Harvard University and Phreesia, a health care technology company.

Phreesia – which helps medical practices with patient registration, insurance verification, and payments – has data on 50,000 providers in all 50 states; in a typical year, Phreesia tracks 50 million outpatient visits.

The report was published online April 23 by the Commonwealth Fund.

The company captured data on visits from February 1 through April 16. The decline was greatest in New England and the Mid-Atlantic states, where, at the steepest end of the decline in late March, visits were down 66%.

They have rebounded slightly since then but are still down 64%. Practices in the mountain states had the smallest decline, but visits were down by 45% as of April 16.

Many practices have attempted to reach out to patients through telemedicine. As of April 16, about 30% of all visits tracked by Phreesia were provided via telemedicine – by phone or through video. That’s a monumental increase from mid-February, when zero visits were conducted virtually.

However, the Harvard researchers found that telemedicine visits barely made up for the huge decline in office visits.
 

Decline by specialty

Not surprisingly, declining visits have been steeper in procedure-oriented specialties.

Overall visits – including telemedicine – to ophthalmologists and otolaryngologists had declined by 79% and 75%, respectively, as of the week of April 5. Dermatology saw a 73% decline. Surgery, pulmonology, urology, orthopedics, cardiology, and gastroenterology all experienced declines ranging from 61% to 66%.

Primary care offices, oncology, endocrinology, and obstetrics/gynecology all fared slightly better, with visits down by half. Behavioral health experienced the lowest rate of decline (30%).

School-aged children were skipping care most often. The study showed a 71% drop in visits in 7- to 17-year-olds, and a 59% decline in visits by neonates, infants, and toddlers (up to age 6). Overall, pediatric practices experienced a 62% drop-off in visits.

Nearly two-thirds of Americans over age 65 also stayed away from their doctors. Only half of those aged 18 to 64 reduced their physician visits.

This article first appeared on Medscape.com.

There has been a massive decline in outpatient office visits as patients have stayed home – likely deferring needed care – because of COVID-19, new research shows.

The number of visits to ambulatory practices dropped by a whopping 60% in mid-March, and continues to be down by at least 50% since early February, according to new data compiled and analyzed by Harvard University and Phreesia, a health care technology company.

Phreesia – which helps medical practices with patient registration, insurance verification, and payments – has data on 50,000 providers in all 50 states; in a typical year, Phreesia tracks 50 million outpatient visits.

The report was published online April 23 by the Commonwealth Fund.

The company captured data on visits from February 1 through April 16. The decline was greatest in New England and the Mid-Atlantic states, where, at the steepest end of the decline in late March, visits were down 66%.

They have rebounded slightly since then but are still down 64%. Practices in the mountain states had the smallest decline, but visits were down by 45% as of April 16.

Many practices have attempted to reach out to patients through telemedicine. As of April 16, about 30% of all visits tracked by Phreesia were provided via telemedicine – by phone or through video. That’s a monumental increase from mid-February, when zero visits were conducted virtually.

However, the Harvard researchers found that telemedicine visits barely made up for the huge decline in office visits.
 

Decline by specialty

Not surprisingly, declining visits have been steeper in procedure-oriented specialties.

Overall visits – including telemedicine – to ophthalmologists and otolaryngologists had declined by 79% and 75%, respectively, as of the week of April 5. Dermatology saw a 73% decline. Surgery, pulmonology, urology, orthopedics, cardiology, and gastroenterology all experienced declines ranging from 61% to 66%.

Primary care offices, oncology, endocrinology, and obstetrics/gynecology all fared slightly better, with visits down by half. Behavioral health experienced the lowest rate of decline (30%).

School-aged children were skipping care most often. The study showed a 71% drop in visits in 7- to 17-year-olds, and a 59% decline in visits by neonates, infants, and toddlers (up to age 6). Overall, pediatric practices experienced a 62% drop-off in visits.

Nearly two-thirds of Americans over age 65 also stayed away from their doctors. Only half of those aged 18 to 64 reduced their physician visits.

This article first appeared on Medscape.com.

There has been a massive decline in outpatient office visits as patients have stayed home – likely deferring needed care – because of COVID-19, new research shows.

The number of visits to ambulatory practices dropped by a whopping 60% in mid-March, and continues to be down by at least 50% since early February, according to new data compiled and analyzed by Harvard University and Phreesia, a health care technology company.

Phreesia – which helps medical practices with patient registration, insurance verification, and payments – has data on 50,000 providers in all 50 states; in a typical year, Phreesia tracks 50 million outpatient visits.

The report was published online April 23 by the Commonwealth Fund.

The company captured data on visits from February 1 through April 16. The decline was greatest in New England and the Mid-Atlantic states, where, at the steepest end of the decline in late March, visits were down 66%.

They have rebounded slightly since then but are still down 64%. Practices in the mountain states had the smallest decline, but visits were down by 45% as of April 16.

Many practices have attempted to reach out to patients through telemedicine. As of April 16, about 30% of all visits tracked by Phreesia were provided via telemedicine – by phone or through video. That’s a monumental increase from mid-February, when zero visits were conducted virtually.

However, the Harvard researchers found that telemedicine visits barely made up for the huge decline in office visits.
 

Decline by specialty

Not surprisingly, declining visits have been steeper in procedure-oriented specialties.

Overall visits – including telemedicine – to ophthalmologists and otolaryngologists had declined by 79% and 75%, respectively, as of the week of April 5. Dermatology saw a 73% decline. Surgery, pulmonology, urology, orthopedics, cardiology, and gastroenterology all experienced declines ranging from 61% to 66%.

Primary care offices, oncology, endocrinology, and obstetrics/gynecology all fared slightly better, with visits down by half. Behavioral health experienced the lowest rate of decline (30%).

School-aged children were skipping care most often. The study showed a 71% drop in visits in 7- to 17-year-olds, and a 59% decline in visits by neonates, infants, and toddlers (up to age 6). Overall, pediatric practices experienced a 62% drop-off in visits.

Nearly two-thirds of Americans over age 65 also stayed away from their doctors. Only half of those aged 18 to 64 reduced their physician visits.

This article first appeared on Medscape.com.

We are all experiencing collective loss and grief because of COVID-19, but that doesn’t mean that we are experiencing the same loss or grieving the same way.

PeopleImages/E+/Getty Images

Losses can be unique to individuals, such as the death of a loved one or divorce from a spouse. They can also be more universal, such as the tragedy of Sept. 11, 2001. However, both of these types of losses are generally associated with a distinct event that has a known beginning and endpoint. What makes the losses related to the coronavirus so different is that there is not a known expiration date. This lack of certainty about when the losses caused by the pandemic will end makes it difficult to process and mourn appropriately.

The multitude of potential losses includes, of course, the death of thousands of people. Many of us have personally lost loved ones or know people who have had loss because of COVID-19-related illnesses. There have also been numerous illnesses caused by delayed medical care tied to fears of going to a hospital during the pandemic. Unfortunately, there is an anticipatory loss because of the invariable diseases that will be diagnosed because of the halt of routine and preventive medical care during this current restricted phase of social distancing. There has been a loss of how people can mourn the deceased, having to go without funerals, memorials, and shivas.

There are also losses that are not related to health. These more intangible losses may include the loss of employment and stable income; loss of our children’s completion of their academic year; loss of socialization; loss of travel and visits to friends and family; loss of normal childbirth where a pregnant mother is accompanied by her partner; loss of visiting sick relatives and newborns; loss of dating, weddings, graduations, and milestone birthday celebrations; loss of visits to nursing homes of your loved ones; loss of the needed services and support to help with your young child’s disabilities; and loss of intimacy, connection and touch.

Such losses may seem inconsequential, compared with the death of an acquaintance or loved one. But we do not know the back story behind these other losses. For example, could a family member who is unable to meet the newest addition to the family have a terminal disease and his or her own expiration date? Could the lack of dating exacerbate a new divorcée’s feeling of loneliness and despair?

When we know the details associated with the individual’s loss due to COVID-19, we can understand and better empathize. Continued collective loss without an expiration date will lead to collective grief without an endpoint.
 

Stages of grief

The five distinct stages of grief experienced after a loss were initially developed by psychiatrist Elisabeth Kübler-Ross, in her 1969 book “On Death and Dying” and again explored in her book “On Grief and Grieving” in 2005. The stages of grief are denial, anger, bargaining, depression, and acceptance.

The grief process is unique to each individual and not necessarily a predictable process, with some moving through the stages at a slower pace while others can get stuck in one or more of the stages. This non-linear pattern of grief is evident in our grief response to the COVID-19 pandemic.

Some of us had experiences of denial back in early March, when initial thoughts crept up, such as “this can’t be as bad as what the medical officials are proposing” and “how is this any different from the flu?” Denial is used as a protective defense against feeling an abundance of emotions all at once, while allowing us time to adjust to the new situation.

Most of us have also had experiences with anger directed at our leaders for not adequately preparing us and intense rage at health care administrators for lack of proper protective gear for our first-line health care workers.

Bargaining tactics were noticeable with common thoughts such as “if we stay home and risk the demise of our economy, we will have the chance to protect our most vulnerable populations and therefore save lives.” Unfortunately, many of us have also experienced thoughts of despair and depression. Feelings of hopelessness and helplessness set in with many parents, who, overnight, were given dual roles as a parent and teacher. Many parents are attempting to simultaneously juggle a full-time workload.

Some of us already have begun to move to the last stage of grief, which is acceptance. Although most of us will experience all five of the stages of grief, we are not necessarily in the same stage at the same time. This can lead to contentious conversations among colleagues, friends, and family members. We might not necessarily be in the same mourning stage as our spouse, child, mother, father, sister, brother, aunt, uncle, cousins, or friend. The differences in how we mourn can result in your spouse remaining in the denial phase of grief and refusing to wear a mask to the grocery store. At the same time, you may have already entered the bargaining phase and are willing to forgo the niceties of grocery shopping to protect and promote the common good.

With loss inevitably comes change

This difference in these stages of loss can affect how we all return to a new sense of routine when we begin to reopen our communities.

Unfortunately, we will not have defined guidelines or cookbook steps and rules to abide by. The one thing we will have is our ability to accept each other’s differences, especially when it comes to grief.

Remember, we all will grieve in our way, and this isn’t a race to the finish line. What we do know is that none of us are coming out of this unscathed. This global loss will forever change us. Our new standard will take time for acclimation, but we will get there. With loss inevitably comes change, and this experience will allow us to redefine who we are and what we choose to prioritize and focus on post pandemic. There will be a post-pandemic period, whether it is 6 months, 1 year, or 2 years from now; we will eventually start to shake hands again, even hug and kiss hello. What we need to make sure of is that we don’t forget this time. Whatever meaning you find, and change for the better, will hopefully transcend to your post-pandemic life.
 

Dr. Abraham is a psychiatrist in private practice in Philadelphia. She has no disclosures.

We are all experiencing collective loss and grief because of COVID-19, but that doesn’t mean that we are experiencing the same loss or grieving the same way.

PeopleImages/E+/Getty Images

Losses can be unique to individuals, such as the death of a loved one or divorce from a spouse. They can also be more universal, such as the tragedy of Sept. 11, 2001. However, both of these types of losses are generally associated with a distinct event that has a known beginning and endpoint. What makes the losses related to the coronavirus so different is that there is not a known expiration date. This lack of certainty about when the losses caused by the pandemic will end makes it difficult to process and mourn appropriately.

The multitude of potential losses includes, of course, the death of thousands of people. Many of us have personally lost loved ones or know people who have had loss because of COVID-19-related illnesses. There have also been numerous illnesses caused by delayed medical care tied to fears of going to a hospital during the pandemic. Unfortunately, there is an anticipatory loss because of the invariable diseases that will be diagnosed because of the halt of routine and preventive medical care during this current restricted phase of social distancing. There has been a loss of how people can mourn the deceased, having to go without funerals, memorials, and shivas.

There are also losses that are not related to health. These more intangible losses may include the loss of employment and stable income; loss of our children’s completion of their academic year; loss of socialization; loss of travel and visits to friends and family; loss of normal childbirth where a pregnant mother is accompanied by her partner; loss of visiting sick relatives and newborns; loss of dating, weddings, graduations, and milestone birthday celebrations; loss of visits to nursing homes of your loved ones; loss of the needed services and support to help with your young child’s disabilities; and loss of intimacy, connection and touch.

Such losses may seem inconsequential, compared with the death of an acquaintance or loved one. But we do not know the back story behind these other losses. For example, could a family member who is unable to meet the newest addition to the family have a terminal disease and his or her own expiration date? Could the lack of dating exacerbate a new divorcée’s feeling of loneliness and despair?

When we know the details associated with the individual’s loss due to COVID-19, we can understand and better empathize. Continued collective loss without an expiration date will lead to collective grief without an endpoint.
 

Stages of grief

The five distinct stages of grief experienced after a loss were initially developed by psychiatrist Elisabeth Kübler-Ross, in her 1969 book “On Death and Dying” and again explored in her book “On Grief and Grieving” in 2005. The stages of grief are denial, anger, bargaining, depression, and acceptance.

The grief process is unique to each individual and not necessarily a predictable process, with some moving through the stages at a slower pace while others can get stuck in one or more of the stages. This non-linear pattern of grief is evident in our grief response to the COVID-19 pandemic.

Some of us had experiences of denial back in early March, when initial thoughts crept up, such as “this can’t be as bad as what the medical officials are proposing” and “how is this any different from the flu?” Denial is used as a protective defense against feeling an abundance of emotions all at once, while allowing us time to adjust to the new situation.

Most of us have also had experiences with anger directed at our leaders for not adequately preparing us and intense rage at health care administrators for lack of proper protective gear for our first-line health care workers.

Bargaining tactics were noticeable with common thoughts such as “if we stay home and risk the demise of our economy, we will have the chance to protect our most vulnerable populations and therefore save lives.” Unfortunately, many of us have also experienced thoughts of despair and depression. Feelings of hopelessness and helplessness set in with many parents, who, overnight, were given dual roles as a parent and teacher. Many parents are attempting to simultaneously juggle a full-time workload.

Some of us already have begun to move to the last stage of grief, which is acceptance. Although most of us will experience all five of the stages of grief, we are not necessarily in the same stage at the same time. This can lead to contentious conversations among colleagues, friends, and family members. We might not necessarily be in the same mourning stage as our spouse, child, mother, father, sister, brother, aunt, uncle, cousins, or friend. The differences in how we mourn can result in your spouse remaining in the denial phase of grief and refusing to wear a mask to the grocery store. At the same time, you may have already entered the bargaining phase and are willing to forgo the niceties of grocery shopping to protect and promote the common good.

With loss inevitably comes change

This difference in these stages of loss can affect how we all return to a new sense of routine when we begin to reopen our communities.

Unfortunately, we will not have defined guidelines or cookbook steps and rules to abide by. The one thing we will have is our ability to accept each other’s differences, especially when it comes to grief.

Remember, we all will grieve in our way, and this isn’t a race to the finish line. What we do know is that none of us are coming out of this unscathed. This global loss will forever change us. Our new standard will take time for acclimation, but we will get there. With loss inevitably comes change, and this experience will allow us to redefine who we are and what we choose to prioritize and focus on post pandemic. There will be a post-pandemic period, whether it is 6 months, 1 year, or 2 years from now; we will eventually start to shake hands again, even hug and kiss hello. What we need to make sure of is that we don’t forget this time. Whatever meaning you find, and change for the better, will hopefully transcend to your post-pandemic life.
 

Dr. Abraham is a psychiatrist in private practice in Philadelphia. She has no disclosures.

We are all experiencing collective loss and grief because of COVID-19, but that doesn’t mean that we are experiencing the same loss or grieving the same way.

PeopleImages/E+/Getty Images

Losses can be unique to individuals, such as the death of a loved one or divorce from a spouse. They can also be more universal, such as the tragedy of Sept. 11, 2001. However, both of these types of losses are generally associated with a distinct event that has a known beginning and endpoint. What makes the losses related to the coronavirus so different is that there is not a known expiration date. This lack of certainty about when the losses caused by the pandemic will end makes it difficult to process and mourn appropriately.

The multitude of potential losses includes, of course, the death of thousands of people. Many of us have personally lost loved ones or know people who have had loss because of COVID-19-related illnesses. There have also been numerous illnesses caused by delayed medical care tied to fears of going to a hospital during the pandemic. Unfortunately, there is an anticipatory loss because of the invariable diseases that will be diagnosed because of the halt of routine and preventive medical care during this current restricted phase of social distancing. There has been a loss of how people can mourn the deceased, having to go without funerals, memorials, and shivas.

There are also losses that are not related to health. These more intangible losses may include the loss of employment and stable income; loss of our children’s completion of their academic year; loss of socialization; loss of travel and visits to friends and family; loss of normal childbirth where a pregnant mother is accompanied by her partner; loss of visiting sick relatives and newborns; loss of dating, weddings, graduations, and milestone birthday celebrations; loss of visits to nursing homes of your loved ones; loss of the needed services and support to help with your young child’s disabilities; and loss of intimacy, connection and touch.

Such losses may seem inconsequential, compared with the death of an acquaintance or loved one. But we do not know the back story behind these other losses. For example, could a family member who is unable to meet the newest addition to the family have a terminal disease and his or her own expiration date? Could the lack of dating exacerbate a new divorcée’s feeling of loneliness and despair?

When we know the details associated with the individual’s loss due to COVID-19, we can understand and better empathize. Continued collective loss without an expiration date will lead to collective grief without an endpoint.
 

Stages of grief

The five distinct stages of grief experienced after a loss were initially developed by psychiatrist Elisabeth Kübler-Ross, in her 1969 book “On Death and Dying” and again explored in her book “On Grief and Grieving” in 2005. The stages of grief are denial, anger, bargaining, depression, and acceptance.

The grief process is unique to each individual and not necessarily a predictable process, with some moving through the stages at a slower pace while others can get stuck in one or more of the stages. This non-linear pattern of grief is evident in our grief response to the COVID-19 pandemic.

Some of us had experiences of denial back in early March, when initial thoughts crept up, such as “this can’t be as bad as what the medical officials are proposing” and “how is this any different from the flu?” Denial is used as a protective defense against feeling an abundance of emotions all at once, while allowing us time to adjust to the new situation.

Most of us have also had experiences with anger directed at our leaders for not adequately preparing us and intense rage at health care administrators for lack of proper protective gear for our first-line health care workers.

Bargaining tactics were noticeable with common thoughts such as “if we stay home and risk the demise of our economy, we will have the chance to protect our most vulnerable populations and therefore save lives.” Unfortunately, many of us have also experienced thoughts of despair and depression. Feelings of hopelessness and helplessness set in with many parents, who, overnight, were given dual roles as a parent and teacher. Many parents are attempting to simultaneously juggle a full-time workload.

Some of us already have begun to move to the last stage of grief, which is acceptance. Although most of us will experience all five of the stages of grief, we are not necessarily in the same stage at the same time. This can lead to contentious conversations among colleagues, friends, and family members. We might not necessarily be in the same mourning stage as our spouse, child, mother, father, sister, brother, aunt, uncle, cousins, or friend. The differences in how we mourn can result in your spouse remaining in the denial phase of grief and refusing to wear a mask to the grocery store. At the same time, you may have already entered the bargaining phase and are willing to forgo the niceties of grocery shopping to protect and promote the common good.

With loss inevitably comes change

This difference in these stages of loss can affect how we all return to a new sense of routine when we begin to reopen our communities.

Unfortunately, we will not have defined guidelines or cookbook steps and rules to abide by. The one thing we will have is our ability to accept each other’s differences, especially when it comes to grief.

Remember, we all will grieve in our way, and this isn’t a race to the finish line. What we do know is that none of us are coming out of this unscathed. This global loss will forever change us. Our new standard will take time for acclimation, but we will get there. With loss inevitably comes change, and this experience will allow us to redefine who we are and what we choose to prioritize and focus on post pandemic. There will be a post-pandemic period, whether it is 6 months, 1 year, or 2 years from now; we will eventually start to shake hands again, even hug and kiss hello. What we need to make sure of is that we don’t forget this time. Whatever meaning you find, and change for the better, will hopefully transcend to your post-pandemic life.
 

Dr. Abraham is a psychiatrist in private practice in Philadelphia. She has no disclosures.

Many questions on the care of patients with regard to COVID-19 have been coming up in clinic lately. We periodically try to answer some of the most common and important ones, including the following:

Courtesy NIAID-RML

Question

How should patients on immunosuppressive therapy be advised during the COVID-19 pandemic?

Answer

In general, those patients who have not tested positive, have not been exposed, and are asymptomatic should continue their medications as prescribed.

The American College of Rheumatology issued a statement on April 14, recommending that stable patients continue their medications. Those with known exposure but without confirmed infection may continue hydroxychloroquine, sulfasalazine, and NSAIDs.

Immunosuppressants, non–IL-6 biologics, and JAK inhibitors should be stopped temporarily, pending a negative test or after two weeks without symptoms. In patients with confirmed positive COVID-19 infection, sulfasalazine, methotrexate, leflunomide, immunosuppressants, non-IL-6 biologics, and JAK inhibitors should be stopped temporarily, pending a negative test or after two weeks without symptoms. In patients with confirmed positive COVID-19 infection, sulfasalazine, methotrexate, leflunomide, immunosuppressants, non-IL-6 biologics, and JAK inhibitors should be stopped temporarily. Anti-malarial therapies (hydroxycholoroquine and chloroquine) may be continued and IL-6 inhibitors may be continued in select circumstances.¹

The American Academy of Dermatology recommends that the discussion of continuation of biologics be based on a case-by-case basis, citing insufficient evidence to recommend against discontinuation at this time in those patients who have not tested positive. In patients who have tested positive for COVID-19 it is recommended that biologic therapy be suspended until symptoms have resolved.²

Question

Should I continue preventive services during peak COVID-19?

Answer

The Centers for Disease Control and Prevention recommends delaying all elective ambulatory provider visits. In general, preventative services, such as adult immunizations, lipid screening, and cancer screenings, should be delayed. Additionally, the CDC recommends reaching out to patients who are at high risk for complications from respiratory diseases to ensure medication adherence and provide resources if these patients become ill. Facilities can reduce transmission of COVID-19 by triaging and assessing patients through virtual visits through phone calls, video conferences, text-monitoring systems, and other telemedicine tools. Physicians should try to provide routine and chronic care through virtual visits when possible over in-person visits.³

Question

Should I continue to vaccinate my pediatric population during peak COVID-19?

Answer

Practices that schedule separate well visits and sick visits in different sessions or locations can continue to provide well child visits. A practice could, for example, schedule well visits in the morning and sick visits in the afternoon if a single facility is used. These practices should prioritize newborn care and vaccinations of children, especially for those under the age of 24 months.⁴

Question

Can physicians use telehealth (phone only or audiovisual) to conduct visits with Medicare patients even if they are new patients?

Answer

Effective March 1 through the duration of the pandemic, Medicare will pay physicians for telehealth services at the same rate as an in-office visit. On March 30th, the Centers for Medicare & Medcaid Services announced new policies for physicians and hospitals during the COVID-19 pandemic. These guidelines were updated on April 9.

Audio-only visits are now permitted and the limit on the number of these kinds of visits allowed per month has been waived. Controlled substances can be prescribed via telehealth; however, complying with each state’s individual laws is still required.

Use of any two-way, audiovisual device is permitted. The level of service billed for visits with both audio and visual components is the same as an in-office visit. Telemedicine can be used for both new and existing patients.⁵

A list of services that may be rendered via telehealth are available on the CMS website.⁶


It will be important to regularly check the references given, as information on some of these topics is updated frequently.
 

Dr. Chuong is a second-year resident in the family medicine residency, Dr. Flanagan is a third-year resident, and Dr. Matthews is an intern, all at Abington (Pa.) Jefferson Health. Dr. Skolnik is professor of family and community medicine at the Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.

References

1. ACR issues COVID-19 treatment guidance for rheumatic disease patients.

2. American Academy of Dermatology: Guidance on the use of biologic agents during COVID-19 outbreak.

3. Centers for Disease Control and Prevention. Actions to take in response to community transmission of COVID-19.

4. Centers for Disease Control and Prevention. Maintaining childhood immunizations during COVID19 pandemic.

5. Centers for Medicare & Medcaid Services. COVID-19 frequently asked questions (FAQs) on Medicare Fee-for-Service (FFS) billing.

6. Centers for Medicare & Medcaid Services. List of telehealth services.
 

Many questions on the care of patients with regard to COVID-19 have been coming up in clinic lately. We periodically try to answer some of the most common and important ones, including the following:

Courtesy NIAID-RML

Question

How should patients on immunosuppressive therapy be advised during the COVID-19 pandemic?

Answer

In general, those patients who have not tested positive, have not been exposed, and are asymptomatic should continue their medications as prescribed.

The American College of Rheumatology issued a statement on April 14, recommending that stable patients continue their medications. Those with known exposure but without confirmed infection may continue hydroxychloroquine, sulfasalazine, and NSAIDs.

Immunosuppressants, non–IL-6 biologics, and JAK inhibitors should be stopped temporarily, pending a negative test or after two weeks without symptoms. In patients with confirmed positive COVID-19 infection, sulfasalazine, methotrexate, leflunomide, immunosuppressants, non-IL-6 biologics, and JAK inhibitors should be stopped temporarily, pending a negative test or after two weeks without symptoms. In patients with confirmed positive COVID-19 infection, sulfasalazine, methotrexate, leflunomide, immunosuppressants, non-IL-6 biologics, and JAK inhibitors should be stopped temporarily. Anti-malarial therapies (hydroxycholoroquine and chloroquine) may be continued and IL-6 inhibitors may be continued in select circumstances.¹

The American Academy of Dermatology recommends that the discussion of continuation of biologics be based on a case-by-case basis, citing insufficient evidence to recommend against discontinuation at this time in those patients who have not tested positive. In patients who have tested positive for COVID-19 it is recommended that biologic therapy be suspended until symptoms have resolved.²

Question

Should I continue preventive services during peak COVID-19?

Answer

The Centers for Disease Control and Prevention recommends delaying all elective ambulatory provider visits. In general, preventative services, such as adult immunizations, lipid screening, and cancer screenings, should be delayed. Additionally, the CDC recommends reaching out to patients who are at high risk for complications from respiratory diseases to ensure medication adherence and provide resources if these patients become ill. Facilities can reduce transmission of COVID-19 by triaging and assessing patients through virtual visits through phone calls, video conferences, text-monitoring systems, and other telemedicine tools. Physicians should try to provide routine and chronic care through virtual visits when possible over in-person visits.³

Question

Should I continue to vaccinate my pediatric population during peak COVID-19?

Answer

Practices that schedule separate well visits and sick visits in different sessions or locations can continue to provide well child visits. A practice could, for example, schedule well visits in the morning and sick visits in the afternoon if a single facility is used. These practices should prioritize newborn care and vaccinations of children, especially for those under the age of 24 months.⁴

Question

Can physicians use telehealth (phone only or audiovisual) to conduct visits with Medicare patients even if they are new patients?

Answer

Effective March 1 through the duration of the pandemic, Medicare will pay physicians for telehealth services at the same rate as an in-office visit. On March 30th, the Centers for Medicare & Medcaid Services announced new policies for physicians and hospitals during the COVID-19 pandemic. These guidelines were updated on April 9.

Audio-only visits are now permitted and the limit on the number of these kinds of visits allowed per month has been waived. Controlled substances can be prescribed via telehealth; however, complying with each state’s individual laws is still required.

Use of any two-way, audiovisual device is permitted. The level of service billed for visits with both audio and visual components is the same as an in-office visit. Telemedicine can be used for both new and existing patients.⁵

A list of services that may be rendered via telehealth are available on the CMS website.⁶


It will be important to regularly check the references given, as information on some of these topics is updated frequently.
 

Dr. Chuong is a second-year resident in the family medicine residency, Dr. Flanagan is a third-year resident, and Dr. Matthews is an intern, all at Abington (Pa.) Jefferson Health. Dr. Skolnik is professor of family and community medicine at the Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.

References

1. ACR issues COVID-19 treatment guidance for rheumatic disease patients.

2. American Academy of Dermatology: Guidance on the use of biologic agents during COVID-19 outbreak.

3. Centers for Disease Control and Prevention. Actions to take in response to community transmission of COVID-19.

4. Centers for Disease Control and Prevention. Maintaining childhood immunizations during COVID19 pandemic.

5. Centers for Medicare & Medcaid Services. COVID-19 frequently asked questions (FAQs) on Medicare Fee-for-Service (FFS) billing.

6. Centers for Medicare & Medcaid Services. List of telehealth services.
 

Many questions on the care of patients with regard to COVID-19 have been coming up in clinic lately. We periodically try to answer some of the most common and important ones, including the following:

Courtesy NIAID-RML

Question

How should patients on immunosuppressive therapy be advised during the COVID-19 pandemic?

Answer

In general, those patients who have not tested positive, have not been exposed, and are asymptomatic should continue their medications as prescribed.

The American College of Rheumatology issued a statement on April 14, recommending that stable patients continue their medications. Those with known exposure but without confirmed infection may continue hydroxychloroquine, sulfasalazine, and NSAIDs.

Immunosuppressants, non–IL-6 biologics, and JAK inhibitors should be stopped temporarily, pending a negative test or after two weeks without symptoms. In patients with confirmed positive COVID-19 infection, sulfasalazine, methotrexate, leflunomide, immunosuppressants, non-IL-6 biologics, and JAK inhibitors should be stopped temporarily, pending a negative test or after two weeks without symptoms. In patients with confirmed positive COVID-19 infection, sulfasalazine, methotrexate, leflunomide, immunosuppressants, non-IL-6 biologics, and JAK inhibitors should be stopped temporarily. Anti-malarial therapies (hydroxycholoroquine and chloroquine) may be continued and IL-6 inhibitors may be continued in select circumstances.¹

The American Academy of Dermatology recommends that the discussion of continuation of biologics be based on a case-by-case basis, citing insufficient evidence to recommend against discontinuation at this time in those patients who have not tested positive. In patients who have tested positive for COVID-19 it is recommended that biologic therapy be suspended until symptoms have resolved.²

Question

Should I continue preventive services during peak COVID-19?

Answer

The Centers for Disease Control and Prevention recommends delaying all elective ambulatory provider visits. In general, preventative services, such as adult immunizations, lipid screening, and cancer screenings, should be delayed. Additionally, the CDC recommends reaching out to patients who are at high risk for complications from respiratory diseases to ensure medication adherence and provide resources if these patients become ill. Facilities can reduce transmission of COVID-19 by triaging and assessing patients through virtual visits through phone calls, video conferences, text-monitoring systems, and other telemedicine tools. Physicians should try to provide routine and chronic care through virtual visits when possible over in-person visits.³

Question

Should I continue to vaccinate my pediatric population during peak COVID-19?

Answer

Practices that schedule separate well visits and sick visits in different sessions or locations can continue to provide well child visits. A practice could, for example, schedule well visits in the morning and sick visits in the afternoon if a single facility is used. These practices should prioritize newborn care and vaccinations of children, especially for those under the age of 24 months.⁴

Question

Can physicians use telehealth (phone only or audiovisual) to conduct visits with Medicare patients even if they are new patients?

Answer

Effective March 1 through the duration of the pandemic, Medicare will pay physicians for telehealth services at the same rate as an in-office visit. On March 30th, the Centers for Medicare & Medcaid Services announced new policies for physicians and hospitals during the COVID-19 pandemic. These guidelines were updated on April 9.

Audio-only visits are now permitted and the limit on the number of these kinds of visits allowed per month has been waived. Controlled substances can be prescribed via telehealth; however, complying with each state’s individual laws is still required.

Use of any two-way, audiovisual device is permitted. The level of service billed for visits with both audio and visual components is the same as an in-office visit. Telemedicine can be used for both new and existing patients.⁵

A list of services that may be rendered via telehealth are available on the CMS website.⁶


It will be important to regularly check the references given, as information on some of these topics is updated frequently.
 

Dr. Chuong is a second-year resident in the family medicine residency, Dr. Flanagan is a third-year resident, and Dr. Matthews is an intern, all at Abington (Pa.) Jefferson Health. Dr. Skolnik is professor of family and community medicine at the Sidney Kimmel Medical College of Thomas Jefferson University, Philadelphia, and associate director of the family medicine residency program at Abington (Pa.) Jefferson Health.

References

1. ACR issues COVID-19 treatment guidance for rheumatic disease patients.

2. American Academy of Dermatology: Guidance on the use of biologic agents during COVID-19 outbreak.

3. Centers for Disease Control and Prevention. Actions to take in response to community transmission of COVID-19.

4. Centers for Disease Control and Prevention. Maintaining childhood immunizations during COVID19 pandemic.

5. Centers for Medicare & Medcaid Services. COVID-19 frequently asked questions (FAQs) on Medicare Fee-for-Service (FFS) billing.

6. Centers for Medicare & Medcaid Services. List of telehealth services.
 

The U.S. Food and Drug Administration reinforced its March guidance on when it’s permissible to use hydroxychloroquine and chloroquine to treat COVID-19 patients and on the multiple risks these drugs pose in a Safety Communication on April 24.

Wikimedia Commons/FitzColinGerald/ Creative Commons License

The new communication reiterated the agency’s position from the Emergency Use Authorization (EUA) it granted on March 28 to allow hydroxychloroquine and chloroquine treatment of COVID-19 patients only when they are hospitalized and participation in a clinical trial is “not available,” or “not feasible.” The April 24 update to the EUA noted that “the FDA is aware of reports of serious heart rhythm problems in patients with COVID-19 treated with hydroxychloroquine or chloroquine, often in combination with azithromycin and other QT-prolonging medicines. We are also aware of increased use of these medicines through outpatient prescriptions.”

In addition to reiterating the prior limitations on permissible patients for these treatment the agency also said in the new communication that “close supervision is strongly recommended, “ specifying that “we recommend initial evaluation and monitoring when using hydroxychloroquine or chloroquine under the EUA or in clinical trials that investigate these medicines for the treatment or prevention of COVID-19. Monitoring may include baseline ECG, electrolytes, renal function, and hepatic tests.” The communication also highlighted several potential serious adverse effects from hydroxychloroquine or chloroquine that include QT prolongation with increased risk in patients with renal insufficiency or failure, increased insulin levels and insulin action causing increased risk of severe hypoglycemia, hemolysis in selected patients, and interaction with other medicines that cause QT prolongation.

“If a healthcare professional is considering use of hydroxychloroquine or chloroquine to treat or prevent COVID-19, FDA recommends checking www.clinicaltrials.gov for a suitable clinical trial and consider enrolling the patient,” the statement added.

The FDA’s Safety Communication came a day after the European Medicines Agency issued a similar reminder about the risk for serious adverse effects from treatment with hydroxychloroquine and chloroquine, the need for adverse effect monitoring, and the unproven status of purported benefits from these agents.

The statement came after ongoing promotion by the Trump administration of hydroxychloroquine, in particular, for COVID-19 despite a lack of evidence.

The FDA’s communication cited recent case reports sent to the FDA, as well as published findings, and reports to the National Poison Data System that have described serious, heart-related adverse events and death in COVID-19 patients who received hydroxychloroquine and chloroquine, alone or in combination with azithromycin or another QT-prolonging drug. One recent, notable but not peer-reviewed report on 368 patients treated at any of several U.S. VA medical centers showed no apparent benefit to hospitalized COVID-19 patients treated with hydroxychloroquine and a signal for increased mortality among certain patients on this drug (medRxiv. 2020 Apr 23; doi: 10.1101/2020.04.16.20065920). Several cardiology societies have also highlighted the cardiac considerations for using these drugs in patients with COVID-19, including a summary coauthored by the presidents of the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society (Circulation. 2020 Apr 8. doi: 10.1161/CIRCULATIONAHA.120.047521), and in guidance from the European Society of Cardiology.

[email protected]

The U.S. Food and Drug Administration reinforced its March guidance on when it’s permissible to use hydroxychloroquine and chloroquine to treat COVID-19 patients and on the multiple risks these drugs pose in a Safety Communication on April 24.

Wikimedia Commons/FitzColinGerald/ Creative Commons License

The new communication reiterated the agency’s position from the Emergency Use Authorization (EUA) it granted on March 28 to allow hydroxychloroquine and chloroquine treatment of COVID-19 patients only when they are hospitalized and participation in a clinical trial is “not available,” or “not feasible.” The April 24 update to the EUA noted that “the FDA is aware of reports of serious heart rhythm problems in patients with COVID-19 treated with hydroxychloroquine or chloroquine, often in combination with azithromycin and other QT-prolonging medicines. We are also aware of increased use of these medicines through outpatient prescriptions.”

In addition to reiterating the prior limitations on permissible patients for these treatment the agency also said in the new communication that “close supervision is strongly recommended, “ specifying that “we recommend initial evaluation and monitoring when using hydroxychloroquine or chloroquine under the EUA or in clinical trials that investigate these medicines for the treatment or prevention of COVID-19. Monitoring may include baseline ECG, electrolytes, renal function, and hepatic tests.” The communication also highlighted several potential serious adverse effects from hydroxychloroquine or chloroquine that include QT prolongation with increased risk in patients with renal insufficiency or failure, increased insulin levels and insulin action causing increased risk of severe hypoglycemia, hemolysis in selected patients, and interaction with other medicines that cause QT prolongation.

“If a healthcare professional is considering use of hydroxychloroquine or chloroquine to treat or prevent COVID-19, FDA recommends checking www.clinicaltrials.gov for a suitable clinical trial and consider enrolling the patient,” the statement added.

The FDA’s Safety Communication came a day after the European Medicines Agency issued a similar reminder about the risk for serious adverse effects from treatment with hydroxychloroquine and chloroquine, the need for adverse effect monitoring, and the unproven status of purported benefits from these agents.

The statement came after ongoing promotion by the Trump administration of hydroxychloroquine, in particular, for COVID-19 despite a lack of evidence.

The FDA’s communication cited recent case reports sent to the FDA, as well as published findings, and reports to the National Poison Data System that have described serious, heart-related adverse events and death in COVID-19 patients who received hydroxychloroquine and chloroquine, alone or in combination with azithromycin or another QT-prolonging drug. One recent, notable but not peer-reviewed report on 368 patients treated at any of several U.S. VA medical centers showed no apparent benefit to hospitalized COVID-19 patients treated with hydroxychloroquine and a signal for increased mortality among certain patients on this drug (medRxiv. 2020 Apr 23; doi: 10.1101/2020.04.16.20065920). Several cardiology societies have also highlighted the cardiac considerations for using these drugs in patients with COVID-19, including a summary coauthored by the presidents of the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society (Circulation. 2020 Apr 8. doi: 10.1161/CIRCULATIONAHA.120.047521), and in guidance from the European Society of Cardiology.

[email protected]

The U.S. Food and Drug Administration reinforced its March guidance on when it’s permissible to use hydroxychloroquine and chloroquine to treat COVID-19 patients and on the multiple risks these drugs pose in a Safety Communication on April 24.

Wikimedia Commons/FitzColinGerald/ Creative Commons License

The new communication reiterated the agency’s position from the Emergency Use Authorization (EUA) it granted on March 28 to allow hydroxychloroquine and chloroquine treatment of COVID-19 patients only when they are hospitalized and participation in a clinical trial is “not available,” or “not feasible.” The April 24 update to the EUA noted that “the FDA is aware of reports of serious heart rhythm problems in patients with COVID-19 treated with hydroxychloroquine or chloroquine, often in combination with azithromycin and other QT-prolonging medicines. We are also aware of increased use of these medicines through outpatient prescriptions.”

In addition to reiterating the prior limitations on permissible patients for these treatment the agency also said in the new communication that “close supervision is strongly recommended, “ specifying that “we recommend initial evaluation and monitoring when using hydroxychloroquine or chloroquine under the EUA or in clinical trials that investigate these medicines for the treatment or prevention of COVID-19. Monitoring may include baseline ECG, electrolytes, renal function, and hepatic tests.” The communication also highlighted several potential serious adverse effects from hydroxychloroquine or chloroquine that include QT prolongation with increased risk in patients with renal insufficiency or failure, increased insulin levels and insulin action causing increased risk of severe hypoglycemia, hemolysis in selected patients, and interaction with other medicines that cause QT prolongation.

“If a healthcare professional is considering use of hydroxychloroquine or chloroquine to treat or prevent COVID-19, FDA recommends checking www.clinicaltrials.gov for a suitable clinical trial and consider enrolling the patient,” the statement added.

The FDA’s Safety Communication came a day after the European Medicines Agency issued a similar reminder about the risk for serious adverse effects from treatment with hydroxychloroquine and chloroquine, the need for adverse effect monitoring, and the unproven status of purported benefits from these agents.

The statement came after ongoing promotion by the Trump administration of hydroxychloroquine, in particular, for COVID-19 despite a lack of evidence.

The FDA’s communication cited recent case reports sent to the FDA, as well as published findings, and reports to the National Poison Data System that have described serious, heart-related adverse events and death in COVID-19 patients who received hydroxychloroquine and chloroquine, alone or in combination with azithromycin or another QT-prolonging drug. One recent, notable but not peer-reviewed report on 368 patients treated at any of several U.S. VA medical centers showed no apparent benefit to hospitalized COVID-19 patients treated with hydroxychloroquine and a signal for increased mortality among certain patients on this drug (medRxiv. 2020 Apr 23; doi: 10.1101/2020.04.16.20065920). Several cardiology societies have also highlighted the cardiac considerations for using these drugs in patients with COVID-19, including a summary coauthored by the presidents of the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society (Circulation. 2020 Apr 8. doi: 10.1161/CIRCULATIONAHA.120.047521), and in guidance from the European Society of Cardiology.

[email protected]

A global group of suicide experts is urging governments around the world to take action to prevent a possible jump in suicide rates because of the ongoing COVID-19 pandemic.

In a commentary published online April 21 in Lancet Psychiatry, members of the International COVID-19 Suicide Prevention Research Collaboration warned that suicide rates are likely to rise as the pandemic spreads and its ensuing long-term effects on the general population, economy, and vulnerable groups emerge.

“Preventing suicide therefore needs urgent consideration. The response must capitalize on, but extend beyond, general mental health policies and practices,” the experts wrote.

The COVID-19 collaboration was started by David Gunnell, MBChB, PhD, University of Bristol, England, and includes 42 members with suicide expertise from around the world.

“We’re an ad hoc grouping of international suicide prevention researchers, research leaders, and members of larger international suicide prevention organizations. We include specialists in public health, psychiatry, psychology, and other clinical disciplines,” Dr. Gunnell said in an interview.

“Through this comment piece we hope to share our ideas and experiences about best practice, and ask others working in the field of suicide prevention at a regional, national, and international level to share our intervention and surveillance/data collection recommendations with relevant policy makers,” he added.

Lessons from the past

During times of crisis, people with existing mental health disorders may suffer worsening symptoms, whereas others may develop new mental health problems, especially depression, anxiety, and posttraumatic stress disorder (PTSD), the group notes.

There is some evidence that suicide increased in the United States during the Spanish flu pandemic of 1918 and among older people in Hong Kong during the 2003 severe acute respiratory syndrome (SARS) outbreak. 

An increase in suicide related to COVID-19 is not inevitable provided preventive action is prompt, the group notes.

In their article, the group offered several potential public health responses to mitigate suicide risk associated with the COVID-19 pandemic.

These include:

• Clear care pathways for those who are suicidal.
• Remote or digital assessments for patients currently under the care of a mental health professional.
• Staff training to support new ways of working.
• Increased support for mental health helplines.
• Providing easily accessible grief counseling for those who have lost a loved one to the virus.
• Financial safety nets and labor market programs.
• Dissemination of evidence-based online interventions.

Public health responses must also ensure that those facing domestic violence have access to support and a place to go during times of crisis, they suggested.

“These are unprecedented times. The pandemic will cause distress and leave many vulnerable. Mental health consequences are likely to be present for longer and peak later than the actual pandemic. However, research evidence and the experience of national strategies provide a strong basis for suicide prevention,” the group wrote.

Dr. Gunnell said it’s hard to predict what impact the pandemic will have on suicide rates, “but given the range of concerns, it is important to be prepared and take steps to mitigate risk as much as possible.”
 

Concerning spike in gun sales

Eric Fleegler, MD, MPH, and colleagues from Boston Children’s Hospital and Harvard Medical School, Boston, agreed.

“The time to act is now. Both population and individual approaches are needed to reduce the risk for suicide in the coming months,” they wrote in a commentary published online April 22 in Annals of Internal Medicine.

Dr. Fleegler and colleagues are particularly concerned about a potential increase in gun-related suicides, as gun sales in the United States have “skyrocketed” during the COVID-19 pandemic.

In March, more than 2.5 million firearms were sold, including 1.5 million handguns. That’s an 85% increase in gun sales compared with March 2019 and the highest firearm sales ever recorded in the United States, they reported. 

In addition, research has shown that individuals who buy handguns have a 22-fold higher rate of firearm-related suicide within the first year vs. those who don’t purchase a handgun.

“In the best of times, increased gun ownership is associated with a heightened risk for firearm-related suicide. These are not the best of times,” the authors wrote.

Dr. Fleegler and colleagues said it’s also important to realize that firearm-related suicides were mounting well before COVID-19 hit. From 2006 to 2018, firearm-related suicide rates increased by more than 25%, according to the National Center for Injury Prevention and Control. In 2018 alone, there were 24,432 firearm-related suicides in the United States.

“The United States should take policy and clinical action to avoid a potential epidemic of firearm-related suicide in the wake of the COVID-19 pandemic,” they concluded.

This research had no specific funding. Dr. Gunnell and Dr. Fleegler disclosed no relevant financial relationships .
 

A version of this article originally appeared on Medscape.com.

A global group of suicide experts is urging governments around the world to take action to prevent a possible jump in suicide rates because of the ongoing COVID-19 pandemic.

In a commentary published online April 21 in Lancet Psychiatry, members of the International COVID-19 Suicide Prevention Research Collaboration warned that suicide rates are likely to rise as the pandemic spreads and its ensuing long-term effects on the general population, economy, and vulnerable groups emerge.

“Preventing suicide therefore needs urgent consideration. The response must capitalize on, but extend beyond, general mental health policies and practices,” the experts wrote.

The COVID-19 collaboration was started by David Gunnell, MBChB, PhD, University of Bristol, England, and includes 42 members with suicide expertise from around the world.

“We’re an ad hoc grouping of international suicide prevention researchers, research leaders, and members of larger international suicide prevention organizations. We include specialists in public health, psychiatry, psychology, and other clinical disciplines,” Dr. Gunnell said in an interview.

“Through this comment piece we hope to share our ideas and experiences about best practice, and ask others working in the field of suicide prevention at a regional, national, and international level to share our intervention and surveillance/data collection recommendations with relevant policy makers,” he added.

Lessons from the past

During times of crisis, people with existing mental health disorders may suffer worsening symptoms, whereas others may develop new mental health problems, especially depression, anxiety, and posttraumatic stress disorder (PTSD), the group notes.

There is some evidence that suicide increased in the United States during the Spanish flu pandemic of 1918 and among older people in Hong Kong during the 2003 severe acute respiratory syndrome (SARS) outbreak. 

An increase in suicide related to COVID-19 is not inevitable provided preventive action is prompt, the group notes.

In their article, the group offered several potential public health responses to mitigate suicide risk associated with the COVID-19 pandemic.

These include:

• Clear care pathways for those who are suicidal.
• Remote or digital assessments for patients currently under the care of a mental health professional.
• Staff training to support new ways of working.
• Increased support for mental health helplines.
• Providing easily accessible grief counseling for those who have lost a loved one to the virus.
• Financial safety nets and labor market programs.
• Dissemination of evidence-based online interventions.

Public health responses must also ensure that those facing domestic violence have access to support and a place to go during times of crisis, they suggested.

“These are unprecedented times. The pandemic will cause distress and leave many vulnerable. Mental health consequences are likely to be present for longer and peak later than the actual pandemic. However, research evidence and the experience of national strategies provide a strong basis for suicide prevention,” the group wrote.

Dr. Gunnell said it’s hard to predict what impact the pandemic will have on suicide rates, “but given the range of concerns, it is important to be prepared and take steps to mitigate risk as much as possible.”
 

Concerning spike in gun sales

Eric Fleegler, MD, MPH, and colleagues from Boston Children’s Hospital and Harvard Medical School, Boston, agreed.

“The time to act is now. Both population and individual approaches are needed to reduce the risk for suicide in the coming months,” they wrote in a commentary published online April 22 in Annals of Internal Medicine.

Dr. Fleegler and colleagues are particularly concerned about a potential increase in gun-related suicides, as gun sales in the United States have “skyrocketed” during the COVID-19 pandemic.

In March, more than 2.5 million firearms were sold, including 1.5 million handguns. That’s an 85% increase in gun sales compared with March 2019 and the highest firearm sales ever recorded in the United States, they reported. 

In addition, research has shown that individuals who buy handguns have a 22-fold higher rate of firearm-related suicide within the first year vs. those who don’t purchase a handgun.

“In the best of times, increased gun ownership is associated with a heightened risk for firearm-related suicide. These are not the best of times,” the authors wrote.

Dr. Fleegler and colleagues said it’s also important to realize that firearm-related suicides were mounting well before COVID-19 hit. From 2006 to 2018, firearm-related suicide rates increased by more than 25%, according to the National Center for Injury Prevention and Control. In 2018 alone, there were 24,432 firearm-related suicides in the United States.

“The United States should take policy and clinical action to avoid a potential epidemic of firearm-related suicide in the wake of the COVID-19 pandemic,” they concluded.

This research had no specific funding. Dr. Gunnell and Dr. Fleegler disclosed no relevant financial relationships .
 

A version of this article originally appeared on Medscape.com.

A global group of suicide experts is urging governments around the world to take action to prevent a possible jump in suicide rates because of the ongoing COVID-19 pandemic.

In a commentary published online April 21 in Lancet Psychiatry, members of the International COVID-19 Suicide Prevention Research Collaboration warned that suicide rates are likely to rise as the pandemic spreads and its ensuing long-term effects on the general population, economy, and vulnerable groups emerge.

“Preventing suicide therefore needs urgent consideration. The response must capitalize on, but extend beyond, general mental health policies and practices,” the experts wrote.

The COVID-19 collaboration was started by David Gunnell, MBChB, PhD, University of Bristol, England, and includes 42 members with suicide expertise from around the world.

“We’re an ad hoc grouping of international suicide prevention researchers, research leaders, and members of larger international suicide prevention organizations. We include specialists in public health, psychiatry, psychology, and other clinical disciplines,” Dr. Gunnell said in an interview.

“Through this comment piece we hope to share our ideas and experiences about best practice, and ask others working in the field of suicide prevention at a regional, national, and international level to share our intervention and surveillance/data collection recommendations with relevant policy makers,” he added.

Lessons from the past

During times of crisis, people with existing mental health disorders may suffer worsening symptoms, whereas others may develop new mental health problems, especially depression, anxiety, and posttraumatic stress disorder (PTSD), the group notes.

There is some evidence that suicide increased in the United States during the Spanish flu pandemic of 1918 and among older people in Hong Kong during the 2003 severe acute respiratory syndrome (SARS) outbreak. 

An increase in suicide related to COVID-19 is not inevitable provided preventive action is prompt, the group notes.

In their article, the group offered several potential public health responses to mitigate suicide risk associated with the COVID-19 pandemic.

These include:

• Clear care pathways for those who are suicidal.
• Remote or digital assessments for patients currently under the care of a mental health professional.
• Staff training to support new ways of working.
• Increased support for mental health helplines.
• Providing easily accessible grief counseling for those who have lost a loved one to the virus.
• Financial safety nets and labor market programs.
• Dissemination of evidence-based online interventions.

Public health responses must also ensure that those facing domestic violence have access to support and a place to go during times of crisis, they suggested.

“These are unprecedented times. The pandemic will cause distress and leave many vulnerable. Mental health consequences are likely to be present for longer and peak later than the actual pandemic. However, research evidence and the experience of national strategies provide a strong basis for suicide prevention,” the group wrote.

Dr. Gunnell said it’s hard to predict what impact the pandemic will have on suicide rates, “but given the range of concerns, it is important to be prepared and take steps to mitigate risk as much as possible.”
 

Concerning spike in gun sales

Eric Fleegler, MD, MPH, and colleagues from Boston Children’s Hospital and Harvard Medical School, Boston, agreed.

“The time to act is now. Both population and individual approaches are needed to reduce the risk for suicide in the coming months,” they wrote in a commentary published online April 22 in Annals of Internal Medicine.

Dr. Fleegler and colleagues are particularly concerned about a potential increase in gun-related suicides, as gun sales in the United States have “skyrocketed” during the COVID-19 pandemic.

In March, more than 2.5 million firearms were sold, including 1.5 million handguns. That’s an 85% increase in gun sales compared with March 2019 and the highest firearm sales ever recorded in the United States, they reported. 

In addition, research has shown that individuals who buy handguns have a 22-fold higher rate of firearm-related suicide within the first year vs. those who don’t purchase a handgun.

“In the best of times, increased gun ownership is associated with a heightened risk for firearm-related suicide. These are not the best of times,” the authors wrote.

Dr. Fleegler and colleagues said it’s also important to realize that firearm-related suicides were mounting well before COVID-19 hit. From 2006 to 2018, firearm-related suicide rates increased by more than 25%, according to the National Center for Injury Prevention and Control. In 2018 alone, there were 24,432 firearm-related suicides in the United States.

“The United States should take policy and clinical action to avoid a potential epidemic of firearm-related suicide in the wake of the COVID-19 pandemic,” they concluded.

This research had no specific funding. Dr. Gunnell and Dr. Fleegler disclosed no relevant financial relationships .
 

A version of this article originally appeared on Medscape.com.

Frontline health care workers are facing escalating challenges with rapidly spreading coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.¹ Hospitalists will often deal with various manifestations of acute cardiac injury, controversial withholding of ACE inhibitors (ACEI) or angiotensin receptor blockers (ARBs), arrhythmic toxicities from such drug therapies as hydroxychloroquine.

Presentation and cardiac risks from COVID-19

Patients with COVID-19 often have presented with noncardiac symptoms, usually a febrile illness associated with cough or shortness of breath. Recent reports from Italy and New York have suggested patients also can present with isolated cardiac involvement without any other symptoms that can portend a grim prognosis.² Cardiac effects include myocarditis, acute coronary syndrome, malignant arrhythmias ultimately cardiogenic shock and cardiac arrest.³

The mortality rate correlates with older age, preexisting health conditions, and availability of medical resources. A recent meta-analysis including 53,000 COVID-19 patients found the most common comorbidities were hypertension (19%), diabetes (8 %) and cardiovascular disease (CVD) (3%).⁴ Half of the cases died from respiratory failure and one-third have died from concomitant respiratory and heart failure. Acute heart failure alone accounted for about 7% of cases.⁵

Overall mortality rate can be better understood with the largest case series to-date of COVID-19 in mainland China published by the Chinese Center for Disease Control and Prevention. The overall case-fatality rate was 2.3% (1,023 deaths among 44,672 confirmed cases), but the mortality reached 10.5% in patients with underlying CVD.⁶

Acute cardiac injuries in COVID-19

Acute cardiac injury (ACI) is defined as troponin elevation above the 99th percentile of the upper reference limit.⁷ A practical description of ACI in COVID-19 patients should also include broader definition with new abnormalities in ECG since not all patients with acute cardiac effects have developed troponin elevation.³ More recent reports showed up to 28% of hospitalized patients had a myocardial injury.³

It is not uncommon to see a patient with COVID-19 myocarditis as a mimicker of acute ST-elevation myocardial infarction (STEMI). The mechanism of ACI is unknown, though several hypotheses have been proposed based on case series and retrospective reviews. These include direct viral invasion into myocardial cells leading to myocarditis, oxygen demand-supply mismatch, acute coronary syndrome from plaque rupture, stress, or cytokine-mediated cardiomyopathy.³ The exact incidence of true MI from occlusive coronary disease in the COVID-19 population is yet unknown.

In some cases, troponin elevation may be a late manifestation of COVID-19. As coronavirus disease progressed slowly, a rapid rise of troponin was noted when patients developed acute respiratory failure after 10 days of illness. Among nonsurvivors, a steady rise in troponin was observed from day 4 through day 22.⁸

ACI is associated with ICU admission and mortality. Both troponin and BNP levels increased significantly during the course of hospitalization in those who ultimately died, but no such changes were evident in survivors.³ ACI was higher in nonsurvivors (59%) than in survivors (1%).⁸ ACI was higher in ICU patients (22%), compared with non-ICU patients (2%).⁹ Patients with CVD were more likely to exhibit elevation of troponin levels (54%), compared with patients without CVD (13%).³

Higher troponin levels and the presence of CVD are directly proportional to severe disease and death. Patients with elevated troponin developed more frequent complications including acute respiratory distress syndrome, malignant arrhythmias including ventricular tachycardia/ventricular fibrillation, acute coagulopathy, and acute kidney injury.^3,8 Death was markedly higher in patients with elevated troponin, compared with normal levels: 60% versus 9%. Only 8% with no CVD and normal troponin died, whereas 69% of people with underlying CVD and elevated troponin died.³

The median duration from illness onset to death was 23 (8-41) days in the group with elevated troponin. Patients with CVD and escalation of troponin levels had the shortest survival of 1-5 days. The dynamic rise of cardiac biomarkers and increased incidence of malignant arrhythmias during the course of illness shows that myocardial injury played a greater role in the fatal outcome of COVID-19 than the presence of preexisting CVD itself.³

Management of acute cardiac issues in COVID-19

There are no established therapeutic options with randomized, clinical trials specific to the management of COVID-19 patients at this point. Standard supportive care and individualized treatment plan based on existing guidelines is probably the best approach. Disposition of cases and cardiac testing should be tailored, based on local protocols, availability of resources and expertise.¹⁰

There seems to be a consensus that baseline troponin levels should be obtained in all admitted patients. Repeat troponin levels can be obtained based on the severity of illness, for example, daily troponin checks are reasonable in ICU patients and every-other-day troponin testing may be reasonable in general inpatients. Routine troponin testing in minimally symptomatic or asymptomatic patients will likely not change any outcome.^3,11,12

Daily ECG is reasonable in severe COVID-19. However, routine transthoracic ECGs are not reasonable, unless it will change further treatment plans. Transthoracic electrocardiograms (TTE) are reasonable in patients with significant troponin elevation, a decline in central venous oxygen saturation, new heart failure, shock, new persistent arrhythmias, or significant new ECG changes.¹²

Limited TTEs for a focused exam enough to answer the clinical question should be ordered to minimize the risk of viral exposure to the sonographers. Transesophageal echo will rarely be needed, and its use should be minimized to reduce direct contact exposure and because of anesthesia risks.¹³ Routine stress testing should not be ordered in active COVID-19 and should be deferred for outpatient evaluation, if clinically indicated, once the patient recovers from the infection.¹²

Myocarditis and pericarditis are potential manifestations of acute cardiac injury. Recent case reports have suggested evidence of myocarditis confirmed with cardiac MRI.¹¹ Because of high fatality rates with cardiac involvement and no proven therapies yet, the role of routine advanced cardiac imaging such as cardiac CT, cardiac MRI, or cardiac biopsy is unclear.

Myocarditis can likely be caused either by the virus itself, or the body’s immune and inflammatory response (cytokine storm) to the virus.^2,3 The use of anti-inflammatory drugs like colchicine, ibuprofen, steroids, or statins is not yet established.^10,12 Drugs like remdesivir, lopinavir-ritonavir, hydroxychloroquine, chloroquine, and anti-interleukin-6 agents have been invariably used with some anecdotal success and randomized clinical trials for some of these drugs are presently undergoing.

Physicians may encounter situations to call a STEMI code or not in COVID-19 patients.^2,11 Patients may have substernal pain, diffuse or regional ST elevations in ECG and reduced left ventricular dysfunction with regional wall motion abnormalities on ECG. These findings may be casued by myocarditis, acute type 1 MI, or stress-induced cardiomyopathy. Clinicians should make their judgment based on the overall pretest probability for type 1 MI, incorporating risk factor profiles and the presence of typical symptoms.

Treatment practice for questionable STEMI cases will likely vary across the country as we are learning more about the virus. Cath lab operators are at risk for COVID-19 infection through direct contact with patients. Few cardiologists were admitted after COVID-19 infections in the ICU at a New York hospital after they were involved in a acute MI case in a cath lab.¹⁴ Based on the Chinese experience, some have suggested the idea of lytic therapy first with follow-up cardiac CT to assess the recanalization of perfusion status, but at this point, this strategy remains controversial in the United States. In addition, if the patient has myocarditis instead, there will be a risk for pericardial effusion and hemorrhagic complications with lytic therapy.

Case examples

1. A 70-year-old male presents with fevers, chest pain, cough, shortness of breath. He has a history of metabolic syndrome and 30 pack-years of smoking. His ECG showed 1.5 mm ST elevation in inferior leads with reciprocal ST depressions in lateral leads, and his initial troponin is 2. Echocardiogram showed reduced left ventricle ejection fraction of 32% and inferior wall hypokinesis. He is suspected COVID-19 and his PCR result is pending. How would you manage this patient?

This patient presented with febrile illness and, but he had a very high pretest probability for obstructive coronary artery disease based on his age, male sex, and multiple risk factors. He may have a viral syndrome and it is a stressful situation for him. This may have precipitated plaque rupture causing acute MI.

Activating the STEMI pathway for emergent left heart catheterization is likely appropriate in this case. Coronary angiogram in this patient showed a 100% occluded mid-right coronary artery with a fresh thrombus. Delaying cardiac cath would have possibly led to malignant arrhythmias and death from ischemic injury. We need to be cognizant patients can die from non–COVID-related emergencies also.

2. An 18-year-old healthy male presents with cough and chest pain and has bilateral lung infiltrates. ECG showed anterolateral 2 mm ST elevations and no reciprocal ST changes. Stat TTE showed anterior wall hypokinesis and LV function 30% and his initial troponin are 0.6 (normal is < .05). The nasopharyngeal swab is sent out and his COVID result is pending. How would you manage this patient?

A young patient with no cardiovascular risk factors has a very low pretest probability for obstructive coronary disease and the likelihood of having a true ischemic MI is low even though he has significant new ST elevations. Especially with presumed COVID-19 and risk of virus exposure to the cath lab personnel, it will be prudent to manage this patient with supportive therapy including beta-blockers, ACEIs, etc. Repeat echo in 7 days before discharge showed improved LVEF 45%.
 

Controversy on ACEI/ARB

The SARS-CoV-2 virus enters via cell-entry receptor namely angiotensin-converting enzyme 2 (ACE2). SARS-CoV-2 is thought to have a higher affinity for ACE2 than other SARS-viruses.¹⁵

ACE2 is expressed in the heart, lungs, vasculature, and kidneys. ACEI and ARBs in animal models increase the expression of ACE2,¹⁶ though this has not been confirmed in human studies. This has led to the hypothesis that ACEI and ARBs might worsen myocarditis or precipitate the acute coronary syndrome. It has also been hypothesized that the upregulation of ACE2 is therapeutic in COVID-19 and that ARBs might be protective during infection.¹⁷

The increased ACE2 expression induced by ACEI or ARB would aggravate lung injury of patients with COVID-19. However, a previous study showed a beneficial effect of ACEI/ARB in patients admitted with viral pneumonia, as it significantly reduced the pulmonary inflammatory response and cytokine release caused by virus infection.¹⁸

Therefore, this remains an area of investigation and it is unclear how these medications affect patients with COVID-19. In a recent review, with a limited number of patients, the mortality of those treated with or without the use of ACEI/ARB did not show a significant difference in the outcome.³

Both American and European cardiology societies recommend against routine discontinuation of ACEI and ARBs in patients with COVID-19 because of risks of uncontrolled hypertension and heart failure, stroke, or heart attack.¹⁹ However, it will be reasonable to hold off in inpatients in cases of acute kidney injury, hypotension, shock, etc.¹²

Cardiac concern about hydroxychloroquine and chloroquine

Hydroxychloroquine (HCQ) is an antimalarial drug shown to have in vitro (but not yet in vivo) activity against diverse RNA viruses, including SARS-CoV-1.²⁰ An expert consensus group from China suggests that chloroquine improved lung imaging and shortened disease course.²¹ HCQ was found to be more potent than chloroquine in inhibiting SARS-CoV-2 in vitro.²²

Based on limited in vitro and anecdotal clinical data from other countries, the U.S. Food and Drug Administration recently authorized emergency use of chloroquine and HCQ in hopes of slowing the progression of the disease when a clinical trial is not available, or participation is not feasible for use of these drugs in hospitalized patients. However, with no clear benefit, there is a concern for possible risks with cardiac toxicity.

HCQ is known to cause cardiomyopathy in a dose-dependent manner over several years. Given the anticipated short duration in COVID-19, it is not an expected risk. QT-segment prolongation and torsades de pointes, especially if administered in combination with azithromycin, is possible even in short term use.²³

Given above, frequent ECG monitoring is indicated for patients being treated with chloroquine or HCQ. All other QT-prolonging drugs should be discontinued. Continuous telemetry monitoring while under treatment is reasonable. HCQ should not be started if baseline QTc is > 500 msec and it should be stopped if the patient develops ventricular arrhythmias.¹²
 

Dr. Subedi is a noninvasive cardiologist for Wellspan Health System in Franklin and Cumberland counties in south central Pennsylvania. He is a clinical assistant professor of medicine at Penn State College of Medicine, Hershey, Pa. He is an active member of the critical care committee at Wellspan Chambersburg (Pa.) Hospital. Dr. Tirupathi is the medical director of Keystone Infectious Diseases/HIV in Chambersburg and currently chair of infection prevention at Wellspan Chambersburg and Waynesboro Hospitals, all in Pennsylvania. He also is the lead physician for antibiotic stewardship at these hospitals. Dr. Areti is currently working as a hospitalist at Wellspan Chambersburg Hospital and is a member of the Wellspan pharmacy and therapeutics committee. Dr. Palabindala is hospital medicine division chief at the University of Mississippi Medical Center, Jackson.

Key points

• Acute cardiac injury or myocarditis is common among patients infected with COVID-19. Often, COVID myocarditis can mimic acute MI or stress cardiomyopathy and will present diagnostic and therapeutic challenges. On the other hand, isolated cardiac involvement can occur, even without symptoms and signs of interstitial pneumonia.
• A most important indicator of worse prediction is the degree of myocardial injury, regardless of preexisting conditions or underlying cardiovascular disease.
• Early recognition of cardiac involvement will be helpful in targeting more aggressive supportive therapies. Commonly available clinical tools like bloodwork, ECG, or echocardiogram should be adequate to diagnose carditis in most cases.
• Advanced cardiac imaging tests or cardiac biopsy are of uncertain benefits. Meticulous evaluation is needed for possible ischemic changes before taking the patient to the cardiac cath lab in order to reduce unnecessary virus exposure to the operators.
• ACEI/ARB should be continued in most cases in COVID patients based on cardiology societies’ recommendations.
• With the widespread use of antimalarial drugs like chloroquine or hydroxychloroquine, frequent ECG and continuous telemetry monitoring is reasonable to rule out ventricular arrhythmias like torsades.
• There is no specific treatment to date for acute cardiac injuries. Since there are no specific guidelines and information about the virus is rapidly changing, it will be prudent to follow common-sense approaches outlined by institutions like the Brigham and Women’s Hospital COVID-19 Critical Care clinical guidelines, which incorporate new clinical information on a daily basis ().

References

1. Rothan HA and Byrareddy SN. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J Autoimmun. 2020 May;109:102433. doi: 10.1016/j.jaut.2020.102433.

2. Kolata G. A heart attack? No, it was the coronavirus. New York Times 2020 Mar 27.

3. Guo T et al. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020 Mar 27. doi: 10.1001/jamacardio.2020.1017.

4. Zhao X et al. Incidence, clinical characteristics and prognostic factor of patients with COVID-19: a systematic review and meta-analysis. MedRxIV. 2020 Mar 20. doi: 10.1101/2020.03.17.20037572.

5. Ruan Q et al. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020 Mar 3. doi: 10.1007/s00134-020-05991-x.

6. Wu Z and McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72,314 cases from the Chinese Center for Disease Control and Prevention. JAMA. 2020 Feb 24. doi: 10.1001/jama.2020.2648.

7. Thygesen K et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018 Oct;72:2231-64.

8. Zhou F et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020 Mar 28;395(10229):1054-62.

9. Wang D et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020 Feb 7. doi: 10.1001/jama.2020.1585.

10. CDC: Therapeutic options for patients with COVID-19. Updated April 13, 2020.

11. Inciardi RM et al. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020 Mar 27. doi: 10.1001/jamacardio.2020.1096.

12. Brigham and Women’s Hospital COVID-19 Critical Care Clinical Guidelines.

13. American Society of Echocardiography Statement on COVID-19. 2020 Apr 1.

14. A cardiologist in Brooklyn infected with COVID-19. @jigneshpatelMD. 2020 Mar 20.

15. Paules CI et al. Coronavirus infections – more than just the common cold. JAMA. 2020 Jan 23. doi: 10.1001/jama.2020.0757.

16. Zheng YY et al. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020 May;17(5):259-60.

17. Gurwitz D. Angiotensin receptor blockers as tentative SARS-CoV-2 therapeutics. Drug Dev Res. 2020 Mar 4. doi: 10.1002/ddr.21656.

18. Henry C et al. Impact of angiotensin-converting enzyme inhibitors and statins on viral pneumonia. Proc (Bayl Univ Med Cent). 2018 Oct 26;31(4):419-23.

19. HFSA/ACC/AHA statement addresses concerns re: Using RAAS antagonists in COVID-19. 2020 Mar 17.

20. Touret F and de Lamballerie X. Of chloroquine and COVID-19. Antiviral Res. 2020 May;177:104762. doi: 10.1016/j.antiviral.2020.104762.

21. Expert consensus on chloroquine phosphate for the treatment of novel coronavirus pneumonia. Chinese journal of tuberculosis and respiratory diseases. 2020 Mar 12;43(3):185-8.

22. Yao X et al. In vitro antiviral activity and projection of optimized dosing design of hydroxychloroquine for the treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Clin Infect Dis. 2020 Mar 9. doi: 10.1093/cid/ciaa237.

23. Devaux CA et al. New insights on the antiviral effects of chloroquine against coronavirus: What to expect for COVID-19? Int J Antimicrob Agents. 2020 Mar 12:105938. doi: 10.1016/j.ijantimicag.2020.105938.

Frontline health care workers are facing escalating challenges with rapidly spreading coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.¹ Hospitalists will often deal with various manifestations of acute cardiac injury, controversial withholding of ACE inhibitors (ACEI) or angiotensin receptor blockers (ARBs), arrhythmic toxicities from such drug therapies as hydroxychloroquine.

Presentation and cardiac risks from COVID-19

Patients with COVID-19 often have presented with noncardiac symptoms, usually a febrile illness associated with cough or shortness of breath. Recent reports from Italy and New York have suggested patients also can present with isolated cardiac involvement without any other symptoms that can portend a grim prognosis.² Cardiac effects include myocarditis, acute coronary syndrome, malignant arrhythmias ultimately cardiogenic shock and cardiac arrest.³

The mortality rate correlates with older age, preexisting health conditions, and availability of medical resources. A recent meta-analysis including 53,000 COVID-19 patients found the most common comorbidities were hypertension (19%), diabetes (8 %) and cardiovascular disease (CVD) (3%).⁴ Half of the cases died from respiratory failure and one-third have died from concomitant respiratory and heart failure. Acute heart failure alone accounted for about 7% of cases.⁵

Overall mortality rate can be better understood with the largest case series to-date of COVID-19 in mainland China published by the Chinese Center for Disease Control and Prevention. The overall case-fatality rate was 2.3% (1,023 deaths among 44,672 confirmed cases), but the mortality reached 10.5% in patients with underlying CVD.⁶

Acute cardiac injuries in COVID-19

Acute cardiac injury (ACI) is defined as troponin elevation above the 99th percentile of the upper reference limit.⁷ A practical description of ACI in COVID-19 patients should also include broader definition with new abnormalities in ECG since not all patients with acute cardiac effects have developed troponin elevation.³ More recent reports showed up to 28% of hospitalized patients had a myocardial injury.³

It is not uncommon to see a patient with COVID-19 myocarditis as a mimicker of acute ST-elevation myocardial infarction (STEMI). The mechanism of ACI is unknown, though several hypotheses have been proposed based on case series and retrospective reviews. These include direct viral invasion into myocardial cells leading to myocarditis, oxygen demand-supply mismatch, acute coronary syndrome from plaque rupture, stress, or cytokine-mediated cardiomyopathy.³ The exact incidence of true MI from occlusive coronary disease in the COVID-19 population is yet unknown.

In some cases, troponin elevation may be a late manifestation of COVID-19. As coronavirus disease progressed slowly, a rapid rise of troponin was noted when patients developed acute respiratory failure after 10 days of illness. Among nonsurvivors, a steady rise in troponin was observed from day 4 through day 22.⁸

ACI is associated with ICU admission and mortality. Both troponin and BNP levels increased significantly during the course of hospitalization in those who ultimately died, but no such changes were evident in survivors.³ ACI was higher in nonsurvivors (59%) than in survivors (1%).⁸ ACI was higher in ICU patients (22%), compared with non-ICU patients (2%).⁹ Patients with CVD were more likely to exhibit elevation of troponin levels (54%), compared with patients without CVD (13%).³

Higher troponin levels and the presence of CVD are directly proportional to severe disease and death. Patients with elevated troponin developed more frequent complications including acute respiratory distress syndrome, malignant arrhythmias including ventricular tachycardia/ventricular fibrillation, acute coagulopathy, and acute kidney injury.^3,8 Death was markedly higher in patients with elevated troponin, compared with normal levels: 60% versus 9%. Only 8% with no CVD and normal troponin died, whereas 69% of people with underlying CVD and elevated troponin died.³

The median duration from illness onset to death was 23 (8-41) days in the group with elevated troponin. Patients with CVD and escalation of troponin levels had the shortest survival of 1-5 days. The dynamic rise of cardiac biomarkers and increased incidence of malignant arrhythmias during the course of illness shows that myocardial injury played a greater role in the fatal outcome of COVID-19 than the presence of preexisting CVD itself.³

Management of acute cardiac issues in COVID-19

There are no established therapeutic options with randomized, clinical trials specific to the management of COVID-19 patients at this point. Standard supportive care and individualized treatment plan based on existing guidelines is probably the best approach. Disposition of cases and cardiac testing should be tailored, based on local protocols, availability of resources and expertise.¹⁰

There seems to be a consensus that baseline troponin levels should be obtained in all admitted patients. Repeat troponin levels can be obtained based on the severity of illness, for example, daily troponin checks are reasonable in ICU patients and every-other-day troponin testing may be reasonable in general inpatients. Routine troponin testing in minimally symptomatic or asymptomatic patients will likely not change any outcome.^3,11,12

Daily ECG is reasonable in severe COVID-19. However, routine transthoracic ECGs are not reasonable, unless it will change further treatment plans. Transthoracic electrocardiograms (TTE) are reasonable in patients with significant troponin elevation, a decline in central venous oxygen saturation, new heart failure, shock, new persistent arrhythmias, or significant new ECG changes.¹²

Limited TTEs for a focused exam enough to answer the clinical question should be ordered to minimize the risk of viral exposure to the sonographers. Transesophageal echo will rarely be needed, and its use should be minimized to reduce direct contact exposure and because of anesthesia risks.¹³ Routine stress testing should not be ordered in active COVID-19 and should be deferred for outpatient evaluation, if clinically indicated, once the patient recovers from the infection.¹²

Myocarditis and pericarditis are potential manifestations of acute cardiac injury. Recent case reports have suggested evidence of myocarditis confirmed with cardiac MRI.¹¹ Because of high fatality rates with cardiac involvement and no proven therapies yet, the role of routine advanced cardiac imaging such as cardiac CT, cardiac MRI, or cardiac biopsy is unclear.

Myocarditis can likely be caused either by the virus itself, or the body’s immune and inflammatory response (cytokine storm) to the virus.^2,3 The use of anti-inflammatory drugs like colchicine, ibuprofen, steroids, or statins is not yet established.^10,12 Drugs like remdesivir, lopinavir-ritonavir, hydroxychloroquine, chloroquine, and anti-interleukin-6 agents have been invariably used with some anecdotal success and randomized clinical trials for some of these drugs are presently undergoing.

Physicians may encounter situations to call a STEMI code or not in COVID-19 patients.^2,11 Patients may have substernal pain, diffuse or regional ST elevations in ECG and reduced left ventricular dysfunction with regional wall motion abnormalities on ECG. These findings may be casued by myocarditis, acute type 1 MI, or stress-induced cardiomyopathy. Clinicians should make their judgment based on the overall pretest probability for type 1 MI, incorporating risk factor profiles and the presence of typical symptoms.

Treatment practice for questionable STEMI cases will likely vary across the country as we are learning more about the virus. Cath lab operators are at risk for COVID-19 infection through direct contact with patients. Few cardiologists were admitted after COVID-19 infections in the ICU at a New York hospital after they were involved in a acute MI case in a cath lab.¹⁴ Based on the Chinese experience, some have suggested the idea of lytic therapy first with follow-up cardiac CT to assess the recanalization of perfusion status, but at this point, this strategy remains controversial in the United States. In addition, if the patient has myocarditis instead, there will be a risk for pericardial effusion and hemorrhagic complications with lytic therapy.

Case examples

1. A 70-year-old male presents with fevers, chest pain, cough, shortness of breath. He has a history of metabolic syndrome and 30 pack-years of smoking. His ECG showed 1.5 mm ST elevation in inferior leads with reciprocal ST depressions in lateral leads, and his initial troponin is 2. Echocardiogram showed reduced left ventricle ejection fraction of 32% and inferior wall hypokinesis. He is suspected COVID-19 and his PCR result is pending. How would you manage this patient?

This patient presented with febrile illness and, but he had a very high pretest probability for obstructive coronary artery disease based on his age, male sex, and multiple risk factors. He may have a viral syndrome and it is a stressful situation for him. This may have precipitated plaque rupture causing acute MI.

Activating the STEMI pathway for emergent left heart catheterization is likely appropriate in this case. Coronary angiogram in this patient showed a 100% occluded mid-right coronary artery with a fresh thrombus. Delaying cardiac cath would have possibly led to malignant arrhythmias and death from ischemic injury. We need to be cognizant patients can die from non–COVID-related emergencies also.

2. An 18-year-old healthy male presents with cough and chest pain and has bilateral lung infiltrates. ECG showed anterolateral 2 mm ST elevations and no reciprocal ST changes. Stat TTE showed anterior wall hypokinesis and LV function 30% and his initial troponin are 0.6 (normal is < .05). The nasopharyngeal swab is sent out and his COVID result is pending. How would you manage this patient?

A young patient with no cardiovascular risk factors has a very low pretest probability for obstructive coronary disease and the likelihood of having a true ischemic MI is low even though he has significant new ST elevations. Especially with presumed COVID-19 and risk of virus exposure to the cath lab personnel, it will be prudent to manage this patient with supportive therapy including beta-blockers, ACEIs, etc. Repeat echo in 7 days before discharge showed improved LVEF 45%.
 

Controversy on ACEI/ARB

The SARS-CoV-2 virus enters via cell-entry receptor namely angiotensin-converting enzyme 2 (ACE2). SARS-CoV-2 is thought to have a higher affinity for ACE2 than other SARS-viruses.¹⁵

ACE2 is expressed in the heart, lungs, vasculature, and kidneys. ACEI and ARBs in animal models increase the expression of ACE2,¹⁶ though this has not been confirmed in human studies. This has led to the hypothesis that ACEI and ARBs might worsen myocarditis or precipitate the acute coronary syndrome. It has also been hypothesized that the upregulation of ACE2 is therapeutic in COVID-19 and that ARBs might be protective during infection.¹⁷

The increased ACE2 expression induced by ACEI or ARB would aggravate lung injury of patients with COVID-19. However, a previous study showed a beneficial effect of ACEI/ARB in patients admitted with viral pneumonia, as it significantly reduced the pulmonary inflammatory response and cytokine release caused by virus infection.¹⁸

Therefore, this remains an area of investigation and it is unclear how these medications affect patients with COVID-19. In a recent review, with a limited number of patients, the mortality of those treated with or without the use of ACEI/ARB did not show a significant difference in the outcome.³

Both American and European cardiology societies recommend against routine discontinuation of ACEI and ARBs in patients with COVID-19 because of risks of uncontrolled hypertension and heart failure, stroke, or heart attack.¹⁹ However, it will be reasonable to hold off in inpatients in cases of acute kidney injury, hypotension, shock, etc.¹²

Cardiac concern about hydroxychloroquine and chloroquine

Hydroxychloroquine (HCQ) is an antimalarial drug shown to have in vitro (but not yet in vivo) activity against diverse RNA viruses, including SARS-CoV-1.²⁰ An expert consensus group from China suggests that chloroquine improved lung imaging and shortened disease course.²¹ HCQ was found to be more potent than chloroquine in inhibiting SARS-CoV-2 in vitro.²²

Based on limited in vitro and anecdotal clinical data from other countries, the U.S. Food and Drug Administration recently authorized emergency use of chloroquine and HCQ in hopes of slowing the progression of the disease when a clinical trial is not available, or participation is not feasible for use of these drugs in hospitalized patients. However, with no clear benefit, there is a concern for possible risks with cardiac toxicity.

HCQ is known to cause cardiomyopathy in a dose-dependent manner over several years. Given the anticipated short duration in COVID-19, it is not an expected risk. QT-segment prolongation and torsades de pointes, especially if administered in combination with azithromycin, is possible even in short term use.²³

Given above, frequent ECG monitoring is indicated for patients being treated with chloroquine or HCQ. All other QT-prolonging drugs should be discontinued. Continuous telemetry monitoring while under treatment is reasonable. HCQ should not be started if baseline QTc is > 500 msec and it should be stopped if the patient develops ventricular arrhythmias.¹²
 

Dr. Subedi is a noninvasive cardiologist for Wellspan Health System in Franklin and Cumberland counties in south central Pennsylvania. He is a clinical assistant professor of medicine at Penn State College of Medicine, Hershey, Pa. He is an active member of the critical care committee at Wellspan Chambersburg (Pa.) Hospital. Dr. Tirupathi is the medical director of Keystone Infectious Diseases/HIV in Chambersburg and currently chair of infection prevention at Wellspan Chambersburg and Waynesboro Hospitals, all in Pennsylvania. He also is the lead physician for antibiotic stewardship at these hospitals. Dr. Areti is currently working as a hospitalist at Wellspan Chambersburg Hospital and is a member of the Wellspan pharmacy and therapeutics committee. Dr. Palabindala is hospital medicine division chief at the University of Mississippi Medical Center, Jackson.

Key points

• Acute cardiac injury or myocarditis is common among patients infected with COVID-19. Often, COVID myocarditis can mimic acute MI or stress cardiomyopathy and will present diagnostic and therapeutic challenges. On the other hand, isolated cardiac involvement can occur, even without symptoms and signs of interstitial pneumonia.
• A most important indicator of worse prediction is the degree of myocardial injury, regardless of preexisting conditions or underlying cardiovascular disease.
• Early recognition of cardiac involvement will be helpful in targeting more aggressive supportive therapies. Commonly available clinical tools like bloodwork, ECG, or echocardiogram should be adequate to diagnose carditis in most cases.
• Advanced cardiac imaging tests or cardiac biopsy are of uncertain benefits. Meticulous evaluation is needed for possible ischemic changes before taking the patient to the cardiac cath lab in order to reduce unnecessary virus exposure to the operators.
• ACEI/ARB should be continued in most cases in COVID patients based on cardiology societies’ recommendations.
• With the widespread use of antimalarial drugs like chloroquine or hydroxychloroquine, frequent ECG and continuous telemetry monitoring is reasonable to rule out ventricular arrhythmias like torsades.
• There is no specific treatment to date for acute cardiac injuries. Since there are no specific guidelines and information about the virus is rapidly changing, it will be prudent to follow common-sense approaches outlined by institutions like the Brigham and Women’s Hospital COVID-19 Critical Care clinical guidelines, which incorporate new clinical information on a daily basis ().

References

1. Rothan HA and Byrareddy SN. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J Autoimmun. 2020 May;109:102433. doi: 10.1016/j.jaut.2020.102433.

2. Kolata G. A heart attack? No, it was the coronavirus. New York Times 2020 Mar 27.

3. Guo T et al. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020 Mar 27. doi: 10.1001/jamacardio.2020.1017.

4. Zhao X et al. Incidence, clinical characteristics and prognostic factor of patients with COVID-19: a systematic review and meta-analysis. MedRxIV. 2020 Mar 20. doi: 10.1101/2020.03.17.20037572.

5. Ruan Q et al. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020 Mar 3. doi: 10.1007/s00134-020-05991-x.

6. Wu Z and McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72,314 cases from the Chinese Center for Disease Control and Prevention. JAMA. 2020 Feb 24. doi: 10.1001/jama.2020.2648.

7. Thygesen K et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018 Oct;72:2231-64.

8. Zhou F et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020 Mar 28;395(10229):1054-62.

9. Wang D et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020 Feb 7. doi: 10.1001/jama.2020.1585.

10. CDC: Therapeutic options for patients with COVID-19. Updated April 13, 2020.

11. Inciardi RM et al. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020 Mar 27. doi: 10.1001/jamacardio.2020.1096.

12. Brigham and Women’s Hospital COVID-19 Critical Care Clinical Guidelines.

13. American Society of Echocardiography Statement on COVID-19. 2020 Apr 1.

14. A cardiologist in Brooklyn infected with COVID-19. @jigneshpatelMD. 2020 Mar 20.

15. Paules CI et al. Coronavirus infections – more than just the common cold. JAMA. 2020 Jan 23. doi: 10.1001/jama.2020.0757.

16. Zheng YY et al. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020 May;17(5):259-60.

17. Gurwitz D. Angiotensin receptor blockers as tentative SARS-CoV-2 therapeutics. Drug Dev Res. 2020 Mar 4. doi: 10.1002/ddr.21656.

18. Henry C et al. Impact of angiotensin-converting enzyme inhibitors and statins on viral pneumonia. Proc (Bayl Univ Med Cent). 2018 Oct 26;31(4):419-23.

19. HFSA/ACC/AHA statement addresses concerns re: Using RAAS antagonists in COVID-19. 2020 Mar 17.

20. Touret F and de Lamballerie X. Of chloroquine and COVID-19. Antiviral Res. 2020 May;177:104762. doi: 10.1016/j.antiviral.2020.104762.

21. Expert consensus on chloroquine phosphate for the treatment of novel coronavirus pneumonia. Chinese journal of tuberculosis and respiratory diseases. 2020 Mar 12;43(3):185-8.

22. Yao X et al. In vitro antiviral activity and projection of optimized dosing design of hydroxychloroquine for the treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Clin Infect Dis. 2020 Mar 9. doi: 10.1093/cid/ciaa237.

23. Devaux CA et al. New insights on the antiviral effects of chloroquine against coronavirus: What to expect for COVID-19? Int J Antimicrob Agents. 2020 Mar 12:105938. doi: 10.1016/j.ijantimicag.2020.105938.

Frontline health care workers are facing escalating challenges with rapidly spreading coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.¹ Hospitalists will often deal with various manifestations of acute cardiac injury, controversial withholding of ACE inhibitors (ACEI) or angiotensin receptor blockers (ARBs), arrhythmic toxicities from such drug therapies as hydroxychloroquine.

Presentation and cardiac risks from COVID-19

Patients with COVID-19 often have presented with noncardiac symptoms, usually a febrile illness associated with cough or shortness of breath. Recent reports from Italy and New York have suggested patients also can present with isolated cardiac involvement without any other symptoms that can portend a grim prognosis.² Cardiac effects include myocarditis, acute coronary syndrome, malignant arrhythmias ultimately cardiogenic shock and cardiac arrest.³

The mortality rate correlates with older age, preexisting health conditions, and availability of medical resources. A recent meta-analysis including 53,000 COVID-19 patients found the most common comorbidities were hypertension (19%), diabetes (8 %) and cardiovascular disease (CVD) (3%).⁴ Half of the cases died from respiratory failure and one-third have died from concomitant respiratory and heart failure. Acute heart failure alone accounted for about 7% of cases.⁵

Overall mortality rate can be better understood with the largest case series to-date of COVID-19 in mainland China published by the Chinese Center for Disease Control and Prevention. The overall case-fatality rate was 2.3% (1,023 deaths among 44,672 confirmed cases), but the mortality reached 10.5% in patients with underlying CVD.⁶

Acute cardiac injuries in COVID-19

Acute cardiac injury (ACI) is defined as troponin elevation above the 99th percentile of the upper reference limit.⁷ A practical description of ACI in COVID-19 patients should also include broader definition with new abnormalities in ECG since not all patients with acute cardiac effects have developed troponin elevation.³ More recent reports showed up to 28% of hospitalized patients had a myocardial injury.³

It is not uncommon to see a patient with COVID-19 myocarditis as a mimicker of acute ST-elevation myocardial infarction (STEMI). The mechanism of ACI is unknown, though several hypotheses have been proposed based on case series and retrospective reviews. These include direct viral invasion into myocardial cells leading to myocarditis, oxygen demand-supply mismatch, acute coronary syndrome from plaque rupture, stress, or cytokine-mediated cardiomyopathy.³ The exact incidence of true MI from occlusive coronary disease in the COVID-19 population is yet unknown.

In some cases, troponin elevation may be a late manifestation of COVID-19. As coronavirus disease progressed slowly, a rapid rise of troponin was noted when patients developed acute respiratory failure after 10 days of illness. Among nonsurvivors, a steady rise in troponin was observed from day 4 through day 22.⁸

ACI is associated with ICU admission and mortality. Both troponin and BNP levels increased significantly during the course of hospitalization in those who ultimately died, but no such changes were evident in survivors.³ ACI was higher in nonsurvivors (59%) than in survivors (1%).⁸ ACI was higher in ICU patients (22%), compared with non-ICU patients (2%).⁹ Patients with CVD were more likely to exhibit elevation of troponin levels (54%), compared with patients without CVD (13%).³

Higher troponin levels and the presence of CVD are directly proportional to severe disease and death. Patients with elevated troponin developed more frequent complications including acute respiratory distress syndrome, malignant arrhythmias including ventricular tachycardia/ventricular fibrillation, acute coagulopathy, and acute kidney injury.^3,8 Death was markedly higher in patients with elevated troponin, compared with normal levels: 60% versus 9%. Only 8% with no CVD and normal troponin died, whereas 69% of people with underlying CVD and elevated troponin died.³

The median duration from illness onset to death was 23 (8-41) days in the group with elevated troponin. Patients with CVD and escalation of troponin levels had the shortest survival of 1-5 days. The dynamic rise of cardiac biomarkers and increased incidence of malignant arrhythmias during the course of illness shows that myocardial injury played a greater role in the fatal outcome of COVID-19 than the presence of preexisting CVD itself.³

Management of acute cardiac issues in COVID-19

There are no established therapeutic options with randomized, clinical trials specific to the management of COVID-19 patients at this point. Standard supportive care and individualized treatment plan based on existing guidelines is probably the best approach. Disposition of cases and cardiac testing should be tailored, based on local protocols, availability of resources and expertise.¹⁰

There seems to be a consensus that baseline troponin levels should be obtained in all admitted patients. Repeat troponin levels can be obtained based on the severity of illness, for example, daily troponin checks are reasonable in ICU patients and every-other-day troponin testing may be reasonable in general inpatients. Routine troponin testing in minimally symptomatic or asymptomatic patients will likely not change any outcome.^3,11,12

Daily ECG is reasonable in severe COVID-19. However, routine transthoracic ECGs are not reasonable, unless it will change further treatment plans. Transthoracic electrocardiograms (TTE) are reasonable in patients with significant troponin elevation, a decline in central venous oxygen saturation, new heart failure, shock, new persistent arrhythmias, or significant new ECG changes.¹²

Limited TTEs for a focused exam enough to answer the clinical question should be ordered to minimize the risk of viral exposure to the sonographers. Transesophageal echo will rarely be needed, and its use should be minimized to reduce direct contact exposure and because of anesthesia risks.¹³ Routine stress testing should not be ordered in active COVID-19 and should be deferred for outpatient evaluation, if clinically indicated, once the patient recovers from the infection.¹²

Myocarditis and pericarditis are potential manifestations of acute cardiac injury. Recent case reports have suggested evidence of myocarditis confirmed with cardiac MRI.¹¹ Because of high fatality rates with cardiac involvement and no proven therapies yet, the role of routine advanced cardiac imaging such as cardiac CT, cardiac MRI, or cardiac biopsy is unclear.

Myocarditis can likely be caused either by the virus itself, or the body’s immune and inflammatory response (cytokine storm) to the virus.^2,3 The use of anti-inflammatory drugs like colchicine, ibuprofen, steroids, or statins is not yet established.^10,12 Drugs like remdesivir, lopinavir-ritonavir, hydroxychloroquine, chloroquine, and anti-interleukin-6 agents have been invariably used with some anecdotal success and randomized clinical trials for some of these drugs are presently undergoing.

Physicians may encounter situations to call a STEMI code or not in COVID-19 patients.^2,11 Patients may have substernal pain, diffuse or regional ST elevations in ECG and reduced left ventricular dysfunction with regional wall motion abnormalities on ECG. These findings may be casued by myocarditis, acute type 1 MI, or stress-induced cardiomyopathy. Clinicians should make their judgment based on the overall pretest probability for type 1 MI, incorporating risk factor profiles and the presence of typical symptoms.

Treatment practice for questionable STEMI cases will likely vary across the country as we are learning more about the virus. Cath lab operators are at risk for COVID-19 infection through direct contact with patients. Few cardiologists were admitted after COVID-19 infections in the ICU at a New York hospital after they were involved in a acute MI case in a cath lab.¹⁴ Based on the Chinese experience, some have suggested the idea of lytic therapy first with follow-up cardiac CT to assess the recanalization of perfusion status, but at this point, this strategy remains controversial in the United States. In addition, if the patient has myocarditis instead, there will be a risk for pericardial effusion and hemorrhagic complications with lytic therapy.

Case examples

1. A 70-year-old male presents with fevers, chest pain, cough, shortness of breath. He has a history of metabolic syndrome and 30 pack-years of smoking. His ECG showed 1.5 mm ST elevation in inferior leads with reciprocal ST depressions in lateral leads, and his initial troponin is 2. Echocardiogram showed reduced left ventricle ejection fraction of 32% and inferior wall hypokinesis. He is suspected COVID-19 and his PCR result is pending. How would you manage this patient?

This patient presented with febrile illness and, but he had a very high pretest probability for obstructive coronary artery disease based on his age, male sex, and multiple risk factors. He may have a viral syndrome and it is a stressful situation for him. This may have precipitated plaque rupture causing acute MI.

Activating the STEMI pathway for emergent left heart catheterization is likely appropriate in this case. Coronary angiogram in this patient showed a 100% occluded mid-right coronary artery with a fresh thrombus. Delaying cardiac cath would have possibly led to malignant arrhythmias and death from ischemic injury. We need to be cognizant patients can die from non–COVID-related emergencies also.

2. An 18-year-old healthy male presents with cough and chest pain and has bilateral lung infiltrates. ECG showed anterolateral 2 mm ST elevations and no reciprocal ST changes. Stat TTE showed anterior wall hypokinesis and LV function 30% and his initial troponin are 0.6 (normal is < .05). The nasopharyngeal swab is sent out and his COVID result is pending. How would you manage this patient?

A young patient with no cardiovascular risk factors has a very low pretest probability for obstructive coronary disease and the likelihood of having a true ischemic MI is low even though he has significant new ST elevations. Especially with presumed COVID-19 and risk of virus exposure to the cath lab personnel, it will be prudent to manage this patient with supportive therapy including beta-blockers, ACEIs, etc. Repeat echo in 7 days before discharge showed improved LVEF 45%.
 

Controversy on ACEI/ARB

The SARS-CoV-2 virus enters via cell-entry receptor namely angiotensin-converting enzyme 2 (ACE2). SARS-CoV-2 is thought to have a higher affinity for ACE2 than other SARS-viruses.¹⁵

ACE2 is expressed in the heart, lungs, vasculature, and kidneys. ACEI and ARBs in animal models increase the expression of ACE2,¹⁶ though this has not been confirmed in human studies. This has led to the hypothesis that ACEI and ARBs might worsen myocarditis or precipitate the acute coronary syndrome. It has also been hypothesized that the upregulation of ACE2 is therapeutic in COVID-19 and that ARBs might be protective during infection.¹⁷

The increased ACE2 expression induced by ACEI or ARB would aggravate lung injury of patients with COVID-19. However, a previous study showed a beneficial effect of ACEI/ARB in patients admitted with viral pneumonia, as it significantly reduced the pulmonary inflammatory response and cytokine release caused by virus infection.¹⁸

Therefore, this remains an area of investigation and it is unclear how these medications affect patients with COVID-19. In a recent review, with a limited number of patients, the mortality of those treated with or without the use of ACEI/ARB did not show a significant difference in the outcome.³

Both American and European cardiology societies recommend against routine discontinuation of ACEI and ARBs in patients with COVID-19 because of risks of uncontrolled hypertension and heart failure, stroke, or heart attack.¹⁹ However, it will be reasonable to hold off in inpatients in cases of acute kidney injury, hypotension, shock, etc.¹²

Cardiac concern about hydroxychloroquine and chloroquine

Hydroxychloroquine (HCQ) is an antimalarial drug shown to have in vitro (but not yet in vivo) activity against diverse RNA viruses, including SARS-CoV-1.²⁰ An expert consensus group from China suggests that chloroquine improved lung imaging and shortened disease course.²¹ HCQ was found to be more potent than chloroquine in inhibiting SARS-CoV-2 in vitro.²²

Based on limited in vitro and anecdotal clinical data from other countries, the U.S. Food and Drug Administration recently authorized emergency use of chloroquine and HCQ in hopes of slowing the progression of the disease when a clinical trial is not available, or participation is not feasible for use of these drugs in hospitalized patients. However, with no clear benefit, there is a concern for possible risks with cardiac toxicity.

HCQ is known to cause cardiomyopathy in a dose-dependent manner over several years. Given the anticipated short duration in COVID-19, it is not an expected risk. QT-segment prolongation and torsades de pointes, especially if administered in combination with azithromycin, is possible even in short term use.²³

Given above, frequent ECG monitoring is indicated for patients being treated with chloroquine or HCQ. All other QT-prolonging drugs should be discontinued. Continuous telemetry monitoring while under treatment is reasonable. HCQ should not be started if baseline QTc is > 500 msec and it should be stopped if the patient develops ventricular arrhythmias.¹²
 

Dr. Subedi is a noninvasive cardiologist for Wellspan Health System in Franklin and Cumberland counties in south central Pennsylvania. He is a clinical assistant professor of medicine at Penn State College of Medicine, Hershey, Pa. He is an active member of the critical care committee at Wellspan Chambersburg (Pa.) Hospital. Dr. Tirupathi is the medical director of Keystone Infectious Diseases/HIV in Chambersburg and currently chair of infection prevention at Wellspan Chambersburg and Waynesboro Hospitals, all in Pennsylvania. He also is the lead physician for antibiotic stewardship at these hospitals. Dr. Areti is currently working as a hospitalist at Wellspan Chambersburg Hospital and is a member of the Wellspan pharmacy and therapeutics committee. Dr. Palabindala is hospital medicine division chief at the University of Mississippi Medical Center, Jackson.

Key points

• Acute cardiac injury or myocarditis is common among patients infected with COVID-19. Often, COVID myocarditis can mimic acute MI or stress cardiomyopathy and will present diagnostic and therapeutic challenges. On the other hand, isolated cardiac involvement can occur, even without symptoms and signs of interstitial pneumonia.
• A most important indicator of worse prediction is the degree of myocardial injury, regardless of preexisting conditions or underlying cardiovascular disease.
• Early recognition of cardiac involvement will be helpful in targeting more aggressive supportive therapies. Commonly available clinical tools like bloodwork, ECG, or echocardiogram should be adequate to diagnose carditis in most cases.
• Advanced cardiac imaging tests or cardiac biopsy are of uncertain benefits. Meticulous evaluation is needed for possible ischemic changes before taking the patient to the cardiac cath lab in order to reduce unnecessary virus exposure to the operators.
• ACEI/ARB should be continued in most cases in COVID patients based on cardiology societies’ recommendations.
• With the widespread use of antimalarial drugs like chloroquine or hydroxychloroquine, frequent ECG and continuous telemetry monitoring is reasonable to rule out ventricular arrhythmias like torsades.
• There is no specific treatment to date for acute cardiac injuries. Since there are no specific guidelines and information about the virus is rapidly changing, it will be prudent to follow common-sense approaches outlined by institutions like the Brigham and Women’s Hospital COVID-19 Critical Care clinical guidelines, which incorporate new clinical information on a daily basis ().

References

1. Rothan HA and Byrareddy SN. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J Autoimmun. 2020 May;109:102433. doi: 10.1016/j.jaut.2020.102433.

2. Kolata G. A heart attack? No, it was the coronavirus. New York Times 2020 Mar 27.

3. Guo T et al. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020 Mar 27. doi: 10.1001/jamacardio.2020.1017.

4. Zhao X et al. Incidence, clinical characteristics and prognostic factor of patients with COVID-19: a systematic review and meta-analysis. MedRxIV. 2020 Mar 20. doi: 10.1101/2020.03.17.20037572.

5. Ruan Q et al. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020 Mar 3. doi: 10.1007/s00134-020-05991-x.

6. Wu Z and McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72,314 cases from the Chinese Center for Disease Control and Prevention. JAMA. 2020 Feb 24. doi: 10.1001/jama.2020.2648.

7. Thygesen K et al. Fourth universal definition of myocardial infarction (2018). J Am Coll Cardiol. 2018 Oct;72:2231-64.

8. Zhou F et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020 Mar 28;395(10229):1054-62.

9. Wang D et al. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020 Feb 7. doi: 10.1001/jama.2020.1585.

10. CDC: Therapeutic options for patients with COVID-19. Updated April 13, 2020.

11. Inciardi RM et al. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020 Mar 27. doi: 10.1001/jamacardio.2020.1096.

12. Brigham and Women’s Hospital COVID-19 Critical Care Clinical Guidelines.

13. American Society of Echocardiography Statement on COVID-19. 2020 Apr 1.

14. A cardiologist in Brooklyn infected with COVID-19. @jigneshpatelMD. 2020 Mar 20.

15. Paules CI et al. Coronavirus infections – more than just the common cold. JAMA. 2020 Jan 23. doi: 10.1001/jama.2020.0757.

16. Zheng YY et al. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020 May;17(5):259-60.

17. Gurwitz D. Angiotensin receptor blockers as tentative SARS-CoV-2 therapeutics. Drug Dev Res. 2020 Mar 4. doi: 10.1002/ddr.21656.

18. Henry C et al. Impact of angiotensin-converting enzyme inhibitors and statins on viral pneumonia. Proc (Bayl Univ Med Cent). 2018 Oct 26;31(4):419-23.

19. HFSA/ACC/AHA statement addresses concerns re: Using RAAS antagonists in COVID-19. 2020 Mar 17.

20. Touret F and de Lamballerie X. Of chloroquine and COVID-19. Antiviral Res. 2020 May;177:104762. doi: 10.1016/j.antiviral.2020.104762.

21. Expert consensus on chloroquine phosphate for the treatment of novel coronavirus pneumonia. Chinese journal of tuberculosis and respiratory diseases. 2020 Mar 12;43(3):185-8.

22. Yao X et al. In vitro antiviral activity and projection of optimized dosing design of hydroxychloroquine for the treatment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Clin Infect Dis. 2020 Mar 9. doi: 10.1093/cid/ciaa237.

23. Devaux CA et al. New insights on the antiviral effects of chloroquine against coronavirus: What to expect for COVID-19? Int J Antimicrob Agents. 2020 Mar 12:105938. doi: 10.1016/j.ijantimicag.2020.105938.

The risk for suicide is higher at night than at any other time of day, new research shows.

In findings that may offer an opportunity for suicide prevention, investigators found that the risk of dying by suicide between midnight and 6:00 a.m. was roughly three times higher than at other times of day regardless of month, method of suicide, or a wide range of other factors.

“The take-home message is that helping at-risk patients sleep through the night may be an excellent way to reduce suicide risk,” lead author Andrew Tubbs, an MD/PhD candidate at the Sleep and Health Research Program, department of psychiatry, University of Arizona, Tucson, said in an interview.

The study was published in the March/April issue of the Journal of Clinical Psychiatry.

Time, method of suicide

Previous research suggests that waking at night is linked to a heightened risk for suicidal thoughts and behaviors, the investigators note.

“The motivation for this study was to expand our understanding of factors that increase suicide risk at night. Since night length changes across seasons, we wondered if suicide risk at night would be lower during summer months and higher during winter months,” he said.

“Similarly, we thought the availability of some suicide methods may vary by time of day — for example, perhaps nighttime would involve more ‘silent’ methods, such as poisoning or asphyxiation, over ‘louder methods,’ such as firearms or vehicle suicides,” Mr. Tubbs added.

The investigators also examined whether the risk for nocturnal suicide was influenced by demographic or geographic factors.

They analyzed data on 35,338 suicides from the U.S. National Violent Death Reporting System for the years 2003-2010.

Time of suicide was divided into four categories: night (12:00 a.m.–5:59 a.m.), morning (6:00 a.m.–11:59 a.m.), afternoon (12:00 p.m.–5:59 p.m.), and evening (6:00 p.m.–11:59 p.m.).

Suicide methods included guns, asphyxiation, poisons, falls, vehicles, sharp weapons, drowning, and fire. Demographics included sex, age, race, and ethnicity. Geographic analyses were based on latitude (at or above 40° N or below 35° N) and region (West, Midwest, South, and Northeast).

Raw data revealed that more males than females died by suicide (n = 28,700 vs. 6636), that most suicides occurred in May (n = 3196), and that the most common method of suicide was by firearms (n = 21,937). Most suicides occurred in those aged 45-54 years (n = 7252) and in whites (n = 31,239) and non-Hispanics (33,384).

Interestingly, most suicides occurred during the afternoon (n = 11,381). Mr. Tubbs explained that suicides are more common during the day, typically around midday, when most people are awake, “so the ‘eligible’ population for suicide is highest at noon,” he said. However, this does not translate into level of risk, so the researchers accounted for nocturnal wakefulness in the analyses.

“When reason sleeps”

The incidence rate ratio at night was 3.18, significantly higher than at any other time of day across all months. The highest IRR was in May (3.90), and the lowest was in November (2.74).

An analysis of variance (ANOVA) for month and time of day indicated that the IRR varied significantly only by time of day (P < .001), not across months (P = .33) or by interaction (P = 1.00).

Initially, a two-way ANOVA showed that the risk for suicide varied both by time of day and by suicide method (both Ps < .001), but the interaction between them was not significant (P = .3026). The mean (SD) nocturnal IRR was 3.09 (.472) across all methods.

Although more than half of suicides involved firearms, “no method had a significantly higher risk at a specific time than any other method at that same time,” the authors note. In addition, an analysis of nocturnal risk by method showed no differences on the basis of sex, age, ethnicity, latitude, and region.

“There are probably many overlapping reasons why the risk of suicide is highest at night. Certainly, social and family supports are minimized if you are awake and everyone you know and love is asleep – you’re isolated, no one’s reaching out to you, and there’s no one there to stop you,” said Mr. Tubbs.

On the other hand, “recent evidence indicates nighttime changes in brain function can impair impulse control, decision making, and long-term planning, which can definitely increase suicidal behaviors.

“Whether these changes are due to sleep deprivation or circadian rhythms is unknown, but it is clearly dangerous to be awake when reason sleeps,” he said.

Clinicians who treat suicidal patients, said Mr. Tubbs, should ask about sleep. If a patient has a problem with sleep, cognitive-behavioral therapy for insomnia should be initiated. This first-line treatment, he said, is more effective and much safer than prescribing a hypnotic.
 

Difficult hours

Commenting on the study, Christopher W. Drapeau, PhD, of the department of education, Valparaiso University, Indiana, said that sleep disturbances “may be a modifiable risk factor for suicide, especially when sleep disturbances are cited by patients as a primary reason for wanting to attempt suicide.”

Dr. Drapeau, who was not involved in the study, said that this “presents an area for health professionals to focus on when developing treatment approaches based on patient information collected during suicide-risk screenings and comprehensive risk assessments.”

Also commenting on the study, Michael Nadorff, PhD, of the department of psychology, Mississippi State University, Starkville, who was not involved with the study, said the study findings are clinically relevant.

These data, he said, inform clinicians about when patients are most likely to be struggling with suicide intent and offer an opportunity to develop safety plans to mitigate suicide risk during these “difficult hours” when coping mechanisms are at a low ebb and sources of support are unavailable.

Support for the study was provided by grants from the National Institutes of Health and the Veterans Administration. Mr. Tubbs and Dr. Drapeau, and Dr. Nadorff report no relevant financial relationships.

This article first appeared on Medscape.com.

The risk for suicide is higher at night than at any other time of day, new research shows.

In findings that may offer an opportunity for suicide prevention, investigators found that the risk of dying by suicide between midnight and 6:00 a.m. was roughly three times higher than at other times of day regardless of month, method of suicide, or a wide range of other factors.

“The take-home message is that helping at-risk patients sleep through the night may be an excellent way to reduce suicide risk,” lead author Andrew Tubbs, an MD/PhD candidate at the Sleep and Health Research Program, department of psychiatry, University of Arizona, Tucson, said in an interview.

The study was published in the March/April issue of the Journal of Clinical Psychiatry.

Time, method of suicide

Previous research suggests that waking at night is linked to a heightened risk for suicidal thoughts and behaviors, the investigators note.

“The motivation for this study was to expand our understanding of factors that increase suicide risk at night. Since night length changes across seasons, we wondered if suicide risk at night would be lower during summer months and higher during winter months,” he said.

“Similarly, we thought the availability of some suicide methods may vary by time of day — for example, perhaps nighttime would involve more ‘silent’ methods, such as poisoning or asphyxiation, over ‘louder methods,’ such as firearms or vehicle suicides,” Mr. Tubbs added.

The investigators also examined whether the risk for nocturnal suicide was influenced by demographic or geographic factors.

They analyzed data on 35,338 suicides from the U.S. National Violent Death Reporting System for the years 2003-2010.

Time of suicide was divided into four categories: night (12:00 a.m.–5:59 a.m.), morning (6:00 a.m.–11:59 a.m.), afternoon (12:00 p.m.–5:59 p.m.), and evening (6:00 p.m.–11:59 p.m.).

Suicide methods included guns, asphyxiation, poisons, falls, vehicles, sharp weapons, drowning, and fire. Demographics included sex, age, race, and ethnicity. Geographic analyses were based on latitude (at or above 40° N or below 35° N) and region (West, Midwest, South, and Northeast).

Raw data revealed that more males than females died by suicide (n = 28,700 vs. 6636), that most suicides occurred in May (n = 3196), and that the most common method of suicide was by firearms (n = 21,937). Most suicides occurred in those aged 45-54 years (n = 7252) and in whites (n = 31,239) and non-Hispanics (33,384).

Interestingly, most suicides occurred during the afternoon (n = 11,381). Mr. Tubbs explained that suicides are more common during the day, typically around midday, when most people are awake, “so the ‘eligible’ population for suicide is highest at noon,” he said. However, this does not translate into level of risk, so the researchers accounted for nocturnal wakefulness in the analyses.

“When reason sleeps”

The incidence rate ratio at night was 3.18, significantly higher than at any other time of day across all months. The highest IRR was in May (3.90), and the lowest was in November (2.74).

An analysis of variance (ANOVA) for month and time of day indicated that the IRR varied significantly only by time of day (P < .001), not across months (P = .33) or by interaction (P = 1.00).

Initially, a two-way ANOVA showed that the risk for suicide varied both by time of day and by suicide method (both Ps < .001), but the interaction between them was not significant (P = .3026). The mean (SD) nocturnal IRR was 3.09 (.472) across all methods.

Although more than half of suicides involved firearms, “no method had a significantly higher risk at a specific time than any other method at that same time,” the authors note. In addition, an analysis of nocturnal risk by method showed no differences on the basis of sex, age, ethnicity, latitude, and region.

“There are probably many overlapping reasons why the risk of suicide is highest at night. Certainly, social and family supports are minimized if you are awake and everyone you know and love is asleep – you’re isolated, no one’s reaching out to you, and there’s no one there to stop you,” said Mr. Tubbs.

On the other hand, “recent evidence indicates nighttime changes in brain function can impair impulse control, decision making, and long-term planning, which can definitely increase suicidal behaviors.

“Whether these changes are due to sleep deprivation or circadian rhythms is unknown, but it is clearly dangerous to be awake when reason sleeps,” he said.

Clinicians who treat suicidal patients, said Mr. Tubbs, should ask about sleep. If a patient has a problem with sleep, cognitive-behavioral therapy for insomnia should be initiated. This first-line treatment, he said, is more effective and much safer than prescribing a hypnotic.
 

Difficult hours

Commenting on the study, Christopher W. Drapeau, PhD, of the department of education, Valparaiso University, Indiana, said that sleep disturbances “may be a modifiable risk factor for suicide, especially when sleep disturbances are cited by patients as a primary reason for wanting to attempt suicide.”

Dr. Drapeau, who was not involved in the study, said that this “presents an area for health professionals to focus on when developing treatment approaches based on patient information collected during suicide-risk screenings and comprehensive risk assessments.”

Also commenting on the study, Michael Nadorff, PhD, of the department of psychology, Mississippi State University, Starkville, who was not involved with the study, said the study findings are clinically relevant.

These data, he said, inform clinicians about when patients are most likely to be struggling with suicide intent and offer an opportunity to develop safety plans to mitigate suicide risk during these “difficult hours” when coping mechanisms are at a low ebb and sources of support are unavailable.

Support for the study was provided by grants from the National Institutes of Health and the Veterans Administration. Mr. Tubbs and Dr. Drapeau, and Dr. Nadorff report no relevant financial relationships.

This article first appeared on Medscape.com.

The risk for suicide is higher at night than at any other time of day, new research shows.

In findings that may offer an opportunity for suicide prevention, investigators found that the risk of dying by suicide between midnight and 6:00 a.m. was roughly three times higher than at other times of day regardless of month, method of suicide, or a wide range of other factors.

“The take-home message is that helping at-risk patients sleep through the night may be an excellent way to reduce suicide risk,” lead author Andrew Tubbs, an MD/PhD candidate at the Sleep and Health Research Program, department of psychiatry, University of Arizona, Tucson, said in an interview.

The study was published in the March/April issue of the Journal of Clinical Psychiatry.

Time, method of suicide

Previous research suggests that waking at night is linked to a heightened risk for suicidal thoughts and behaviors, the investigators note.

“The motivation for this study was to expand our understanding of factors that increase suicide risk at night. Since night length changes across seasons, we wondered if suicide risk at night would be lower during summer months and higher during winter months,” he said.

“Similarly, we thought the availability of some suicide methods may vary by time of day — for example, perhaps nighttime would involve more ‘silent’ methods, such as poisoning or asphyxiation, over ‘louder methods,’ such as firearms or vehicle suicides,” Mr. Tubbs added.

The investigators also examined whether the risk for nocturnal suicide was influenced by demographic or geographic factors.

They analyzed data on 35,338 suicides from the U.S. National Violent Death Reporting System for the years 2003-2010.

Time of suicide was divided into four categories: night (12:00 a.m.–5:59 a.m.), morning (6:00 a.m.–11:59 a.m.), afternoon (12:00 p.m.–5:59 p.m.), and evening (6:00 p.m.–11:59 p.m.).

Suicide methods included guns, asphyxiation, poisons, falls, vehicles, sharp weapons, drowning, and fire. Demographics included sex, age, race, and ethnicity. Geographic analyses were based on latitude (at or above 40° N or below 35° N) and region (West, Midwest, South, and Northeast).

Raw data revealed that more males than females died by suicide (n = 28,700 vs. 6636), that most suicides occurred in May (n = 3196), and that the most common method of suicide was by firearms (n = 21,937). Most suicides occurred in those aged 45-54 years (n = 7252) and in whites (n = 31,239) and non-Hispanics (33,384).

Interestingly, most suicides occurred during the afternoon (n = 11,381). Mr. Tubbs explained that suicides are more common during the day, typically around midday, when most people are awake, “so the ‘eligible’ population for suicide is highest at noon,” he said. However, this does not translate into level of risk, so the researchers accounted for nocturnal wakefulness in the analyses.

“When reason sleeps”

The incidence rate ratio at night was 3.18, significantly higher than at any other time of day across all months. The highest IRR was in May (3.90), and the lowest was in November (2.74).

An analysis of variance (ANOVA) for month and time of day indicated that the IRR varied significantly only by time of day (P < .001), not across months (P = .33) or by interaction (P = 1.00).

Initially, a two-way ANOVA showed that the risk for suicide varied both by time of day and by suicide method (both Ps < .001), but the interaction between them was not significant (P = .3026). The mean (SD) nocturnal IRR was 3.09 (.472) across all methods.

Although more than half of suicides involved firearms, “no method had a significantly higher risk at a specific time than any other method at that same time,” the authors note. In addition, an analysis of nocturnal risk by method showed no differences on the basis of sex, age, ethnicity, latitude, and region.

“There are probably many overlapping reasons why the risk of suicide is highest at night. Certainly, social and family supports are minimized if you are awake and everyone you know and love is asleep – you’re isolated, no one’s reaching out to you, and there’s no one there to stop you,” said Mr. Tubbs.

On the other hand, “recent evidence indicates nighttime changes in brain function can impair impulse control, decision making, and long-term planning, which can definitely increase suicidal behaviors.

“Whether these changes are due to sleep deprivation or circadian rhythms is unknown, but it is clearly dangerous to be awake when reason sleeps,” he said.

Clinicians who treat suicidal patients, said Mr. Tubbs, should ask about sleep. If a patient has a problem with sleep, cognitive-behavioral therapy for insomnia should be initiated. This first-line treatment, he said, is more effective and much safer than prescribing a hypnotic.
 

Difficult hours

Commenting on the study, Christopher W. Drapeau, PhD, of the department of education, Valparaiso University, Indiana, said that sleep disturbances “may be a modifiable risk factor for suicide, especially when sleep disturbances are cited by patients as a primary reason for wanting to attempt suicide.”

Dr. Drapeau, who was not involved in the study, said that this “presents an area for health professionals to focus on when developing treatment approaches based on patient information collected during suicide-risk screenings and comprehensive risk assessments.”

Also commenting on the study, Michael Nadorff, PhD, of the department of psychology, Mississippi State University, Starkville, who was not involved with the study, said the study findings are clinically relevant.

These data, he said, inform clinicians about when patients are most likely to be struggling with suicide intent and offer an opportunity to develop safety plans to mitigate suicide risk during these “difficult hours” when coping mechanisms are at a low ebb and sources of support are unavailable.

Support for the study was provided by grants from the National Institutes of Health and the Veterans Administration. Mr. Tubbs and Dr. Drapeau, and Dr. Nadorff report no relevant financial relationships.

This article first appeared on Medscape.com.

In 1966 I was struggling with the decision of whether to become an art historian or go to medical school. I decided corporate ladder climbs and tenure chases were not for me. I wanted to be my own boss. I reckoned that medicine would offer me rock-solid job security and a comfortable income that I could adjust to my needs simply by working harder. In my Norman Rockwell–influenced view of the world, there would always be sick children. There would never be a quiet week or even a day when I would have to worry about not having an income.

Tomacco/iStock/Getty Images

So it was an idyllic existence for decades, tarnished only slightly when corporate entities began gobbling up owner-operator practices. But I never envisioned a pandemic that would turn the world – including its pediatricians – upside down. For the last several weeks as I pedal past my old office, I am dumbstruck by the empty parking lot. For the present I appear to be buffered by my retirement, but know that many of you are under serious financial pressure as a result of the pandemic.

We are all yearning to return to business as usual, but we know that it isn’t going to happen because everything has changed. The usual has yet to be defined. When you finally reopen your offices, you will be walking into a strange and eerie new normal. Initially you may struggle to make it feel like nothing has changed, but very quickly the full force of the postpandemic tsunami will hit us all broadside. In 2 years, the ship may still be rocking but what will clinical pediatrics look like in the late spring of 2022?

Will the patient mix have shifted even more toward behavioral and mental health complaints as a ripple effect of the pandemic’s emotional turmoil? Will more parents have begun to realize that they can manage minor complaints without an office visit? Will your waiting room have become a maze of plexiglass barriers to separate the sick from the well? Has the hospital invested hundreds of thousands of dollars in a ventilation system in hopes of minimizing contagion in your exam rooms? Maybe you will have instituted an appointment schedule with sick visits in the morning and well checks in the afternoon. Or you may no longer have a waiting room because patients are queuing in their cars in the parking lot. Your support staff may be rollerskating around like carhops at a drive-in recording histories and taking vital signs.

Telemedicine will hopefully have gone mainstream with more robust guidelines for billing and quality control. Medical schools may be devoting more attention to teaching student how to assess remotely. Parents may now be equipped with a tool kit of remote sensors so that you can assess their child’s tympanic membranes, pulse rate, oxygen saturation, and blood pressure on your office computer screen.

Will the EHR finally have begun to emerge from its awkward and at times painful adolescence into an easily accessible and transportable nationwide data bank that includes immunization records for all ages? Patients may have been asked or ordered to allow their cell phones to be used as tracking devices for serious communicable diseases. How many vaccine-resistant people will have responded to the pandemic by deciding that immunizations are worth the minimal risks? I fear not many.

How many of your colleagues will have left pediatrics and heeded the call for more epidemiologists? Will you be required to take a CME course in ventilation management? The good news may be that to keep the pediatric workforce robust the government has decided to forgive your student loans.

None of these changes may have come to pass because we have notoriously short memories. But I am sure that we will all still bear the deep scars of this world changing event.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

In 1966 I was struggling with the decision of whether to become an art historian or go to medical school. I decided corporate ladder climbs and tenure chases were not for me. I wanted to be my own boss. I reckoned that medicine would offer me rock-solid job security and a comfortable income that I could adjust to my needs simply by working harder. In my Norman Rockwell–influenced view of the world, there would always be sick children. There would never be a quiet week or even a day when I would have to worry about not having an income.

Tomacco/iStock/Getty Images

So it was an idyllic existence for decades, tarnished only slightly when corporate entities began gobbling up owner-operator practices. But I never envisioned a pandemic that would turn the world – including its pediatricians – upside down. For the last several weeks as I pedal past my old office, I am dumbstruck by the empty parking lot. For the present I appear to be buffered by my retirement, but know that many of you are under serious financial pressure as a result of the pandemic.

We are all yearning to return to business as usual, but we know that it isn’t going to happen because everything has changed. The usual has yet to be defined. When you finally reopen your offices, you will be walking into a strange and eerie new normal. Initially you may struggle to make it feel like nothing has changed, but very quickly the full force of the postpandemic tsunami will hit us all broadside. In 2 years, the ship may still be rocking but what will clinical pediatrics look like in the late spring of 2022?

Will the patient mix have shifted even more toward behavioral and mental health complaints as a ripple effect of the pandemic’s emotional turmoil? Will more parents have begun to realize that they can manage minor complaints without an office visit? Will your waiting room have become a maze of plexiglass barriers to separate the sick from the well? Has the hospital invested hundreds of thousands of dollars in a ventilation system in hopes of minimizing contagion in your exam rooms? Maybe you will have instituted an appointment schedule with sick visits in the morning and well checks in the afternoon. Or you may no longer have a waiting room because patients are queuing in their cars in the parking lot. Your support staff may be rollerskating around like carhops at a drive-in recording histories and taking vital signs.

Telemedicine will hopefully have gone mainstream with more robust guidelines for billing and quality control. Medical schools may be devoting more attention to teaching student how to assess remotely. Parents may now be equipped with a tool kit of remote sensors so that you can assess their child’s tympanic membranes, pulse rate, oxygen saturation, and blood pressure on your office computer screen.

Will the EHR finally have begun to emerge from its awkward and at times painful adolescence into an easily accessible and transportable nationwide data bank that includes immunization records for all ages? Patients may have been asked or ordered to allow their cell phones to be used as tracking devices for serious communicable diseases. How many vaccine-resistant people will have responded to the pandemic by deciding that immunizations are worth the minimal risks? I fear not many.

How many of your colleagues will have left pediatrics and heeded the call for more epidemiologists? Will you be required to take a CME course in ventilation management? The good news may be that to keep the pediatric workforce robust the government has decided to forgive your student loans.

None of these changes may have come to pass because we have notoriously short memories. But I am sure that we will all still bear the deep scars of this world changing event.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

In 1966 I was struggling with the decision of whether to become an art historian or go to medical school. I decided corporate ladder climbs and tenure chases were not for me. I wanted to be my own boss. I reckoned that medicine would offer me rock-solid job security and a comfortable income that I could adjust to my needs simply by working harder. In my Norman Rockwell–influenced view of the world, there would always be sick children. There would never be a quiet week or even a day when I would have to worry about not having an income.

Tomacco/iStock/Getty Images

So it was an idyllic existence for decades, tarnished only slightly when corporate entities began gobbling up owner-operator practices. But I never envisioned a pandemic that would turn the world – including its pediatricians – upside down. For the last several weeks as I pedal past my old office, I am dumbstruck by the empty parking lot. For the present I appear to be buffered by my retirement, but know that many of you are under serious financial pressure as a result of the pandemic.

We are all yearning to return to business as usual, but we know that it isn’t going to happen because everything has changed. The usual has yet to be defined. When you finally reopen your offices, you will be walking into a strange and eerie new normal. Initially you may struggle to make it feel like nothing has changed, but very quickly the full force of the postpandemic tsunami will hit us all broadside. In 2 years, the ship may still be rocking but what will clinical pediatrics look like in the late spring of 2022?

Will the patient mix have shifted even more toward behavioral and mental health complaints as a ripple effect of the pandemic’s emotional turmoil? Will more parents have begun to realize that they can manage minor complaints without an office visit? Will your waiting room have become a maze of plexiglass barriers to separate the sick from the well? Has the hospital invested hundreds of thousands of dollars in a ventilation system in hopes of minimizing contagion in your exam rooms? Maybe you will have instituted an appointment schedule with sick visits in the morning and well checks in the afternoon. Or you may no longer have a waiting room because patients are queuing in their cars in the parking lot. Your support staff may be rollerskating around like carhops at a drive-in recording histories and taking vital signs.

Telemedicine will hopefully have gone mainstream with more robust guidelines for billing and quality control. Medical schools may be devoting more attention to teaching student how to assess remotely. Parents may now be equipped with a tool kit of remote sensors so that you can assess their child’s tympanic membranes, pulse rate, oxygen saturation, and blood pressure on your office computer screen.

Will the EHR finally have begun to emerge from its awkward and at times painful adolescence into an easily accessible and transportable nationwide data bank that includes immunization records for all ages? Patients may have been asked or ordered to allow their cell phones to be used as tracking devices for serious communicable diseases. How many vaccine-resistant people will have responded to the pandemic by deciding that immunizations are worth the minimal risks? I fear not many.

How many of your colleagues will have left pediatrics and heeded the call for more epidemiologists? Will you be required to take a CME course in ventilation management? The good news may be that to keep the pediatric workforce robust the government has decided to forgive your student loans.

None of these changes may have come to pass because we have notoriously short memories. But I am sure that we will all still bear the deep scars of this world changing event.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at [email protected].

Initial data from one Chinese center on the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) in patients hospitalized with COVID-19 appear to give some further reassurance about continued use of these drugs.

The report from one hospital in Wuhan found that among patients with hypertension hospitalized with the COVID-19 virus, there was no difference in disease severity or death rate in patients taking ACE inhibitors or ARBs and those not taking such medications.

The data were published online April 23 in JAMA Cardiology.

The study adds to another recent report in a larger number of COVID-19 patients from nine Chinese hospitals that suggested a beneficial effect of ACE inhibitors or ARBs on mortality.

Additional studies

Two other similar studies have also been recently released. Another study from China, published online March 31 in Emerging Microbes & Infections, included a small sample of 42 hospitalized patients with COVID-19 on antihypertensive therapy. Those on ACE inhibitor/ARB therapy had a lower rate of severe disease and a trend toward a lower level of IL-6 in peripheral blood. In addition, patients on ACE inhibitor/ARB therapy had increased CD3+ and CD8+ T-cell counts in peripheral blood and decreased peak viral load compared with other antihypertensive drugs.

And a preliminary study from the UK, which has not yet been peer reviewed, found that treatment with ACE inhibitors was associated with a reduced risk of rapidly deteriorating severe COVID-19 disease.

The study, available online on MedRxiv, a preprint server for health sciences, reports on 205 acute inpatients with COVID-19 at King’s College Hospital and Princess Royal University Hospital, London.

Of these, 51.2% had hypertension, 30.2% had diabetes, and 14.6% had ischemic heart disease or heart failure. Of the 37 patients on ACE inhibitors, five (14%) died or required critical care support compared with 29% (48/168) of patients not taking an ACE inhibitor.
 

New Wuhan study

The authors of the new article published in JAMA Cardiology, led by Juyi Li, MD, reported on a case series of 1,178 patients hospitalized with COVID-19 at the Central Hospital of Wuhan, Hubei, China, between Jan. 15 and March 15, 2020.

Patients were a median age of 55 years, and 46% were men. They had an overall in-hospital mortality rate of 11%.

Of the 1,178 patients, 362 (30.7%) had a diagnosis of hypertension. These patients were older (median age, 66 years) and had a greater prevalence of chronic diseases. Patients with hypertension also had more severe manifestations of COVID-19 compared to those without hypertension, including higher rates of acute respiratory distress syndrome and in-hospital mortality (21.3% vs. 6.5%).

Of the 362 patients with hypertension, 31.8% were taking ACE inhibitors or ARBs.

Apart from a greater prevalence of coronary artery disease, patients taking ACE inhibitors or ARBs had similar comorbidities to those not taking these medications, and also similar laboratory profile results including blood counts, inflammatory markers, renal and liver function tests, and cardiac biomarkers, although those taking ACE inhibitors/ARBs had higher levels of alkaline phosphatase.

The most commonly used antihypertensive drugs were calcium blockers. The percentage of patients with hypertension taking any drug or drug combination did not differ between those with severe and nonsevere infections and between those who survived and those who died.

Specifically regarding ACE inhibitors/ARBs, there was no difference between those with severe versus nonsevere illness in the use of ACE inhibitors (9.2% vs. 10.1%; P = .80), ARBs (24.9% vs. 21.2%; P = .40), or the composite of ACE inhibitors or ARBs (32.9% vs. 30.7%; P = .65).

Similarly, there were no differences in nonsurvivors and survivors in the use of ACE inhibitors (9.1% vs. 9.8%; P = .85); ARBs (19.5% vs. 23.9%; P = .42), or the composite of ACE inhibitors or ARBs (27.3% vs. 33.0%; P = .34).

The frequency of severe illness and death also did not differ between those treated with and without ACE inhibitors/ARBs in patients with hypertension and other various chronic conditions including coronary heart disease, cerebrovascular disease, diabetes, neurological disease, and chronic renal disease.

The authors noted that these data confirm previous reports showing that patients with hypertension have more severe illness and higher mortality rates associated with COVID-19 than those without hypertension.

But they added: “Our data provide some reassurance that ACE inhibitors/ARBs are not associated with the progression or outcome of COVID-19 hospitalizations in patients with hypertension.”

They also noted that these results support the recommendations from almost all major cardiovascular societies that patients do not discontinue ACE inhibitors or ARBs because of worries about COVID-19.

However, the authors did point out some limitations of their study, which included a small number of patients with hypertension taking ACE inhibitors or ARBs and the fact that a nonsevere disease course was still severe enough to require hospitalization. In addition, it was not clear whether ACE inhibitor/ARB treatment at baseline was maintained throughout hospitalization for all patients.

This was also an observational comparison and may be biased by differences in patients taking versus not taking ACE inhibitors or ARBs at the time of hospitalization, although the measured baseline characteristics were similar in both groups.

But the authors also highlighted the finding that, in this cohort, patients with hypertension had three times the mortality rate of all other patients hospitalized with COVID-19.

“Hypertension combined with cardiovascular and cerebrovascular disease, diabetes, and chronic kidney disease would predispose patients to an increased risk of severity and mortality of COVID-19. Therefore, patients with these underlying conditions who develop COVID-19 require particularly intensive surveillance and care,” they wrote.
 

Experts cautiously optimistic

Some cardiovascular experts were cautiously optimistic about these latest results.

Michael A. Weber, MD, professor of medicine at the State University of New York, Brooklyn, and editor-in-chief of the Journal of Clinical Hypertension, said: “This new report from Wuhan, China, gives modest reassurance that the use of ACE inhibitors or ARBs in hypertensive patients with COVID-19 disease does not increase the risk of clinical deterioration or death.

“Ongoing, more definitive studies should help resolve competing hypotheses regarding the effects of these agents: whether the increased ACE2 enzyme levels they produce can worsen outcomes by increasing access of the COVID virus to lung tissue; or whether there is a benefit linked to a protective effect of increased ACE2 on alveolar cell function,” Dr. Weber noted.

“Though the number of patients included in this new report is small, it is startling that hypertensive patients were three times as likely as nonhypertensives to have a fatal outcome, presumably reflecting vulnerability due to the cardiovascular and metabolic comorbidities associated with hypertension,” he added.

“In any case, for now, clinicians should continue treating hypertensive patients with whichever drugs, including ACE inhibitors and ARBs, best provide protection from adverse outcomes,” Dr. Weber concluded.

John McMurray, MD, professor of medical cardiology, University of Glasgow, Scotland, commented: “This study from Wuhan provides some reassurance about one of the two questions about ACEI/ARBs: Do these drugs increase susceptibility to infection? And if [the patient is] infected, do they increase the severity of infection? This study addresses the latter question and appears to suggest no increased severity.”

However, Dr. McMurray pointed out that the study had many limitations. There were only small patient numbers and the data were unadjusted, “although it looks like the ACE inhibitor/ARB treated patients were higher risk to start with.” It was an observational study, and patients were not randomized and were predominantly treated with ARBs, and not ACE inhibitors, so “we don’t know if the concerns apply equally to these two classes of drug.

“Other data published and unpublished supporting this (even showing better outcomes in patients treated with an ACE inhibitor/ARB), and, to date, any concerns about these drugs remain unsubstantiated and the guidance from medical societies to continue treatment with these agents in patients prescribed them seems wise,” Dr. McMurray added.

Franz H. Messerli, MD, professor of medicine at the University of Bern, Switzerland, commented: “The study from Wuhan is not a great study. They didn’t even do a multivariable analysis. They could have done a bit more with the data, but it still gives some reassurance.”

Dr. Messerli said it was “interesting” that 30% of the patients hospitalized with COVID-19 in the sample had hypertension. “That corresponds to the general population, so does not suggest that having hypertension increases susceptibility to infection – but it does seem to increase the risk of a bad outcome.”

Dr. Messerli noted that there are two more similar studies due to be published soon, both said to suggest either a beneficial or neutral effect of ACE inhibitors/ARBs on COVID-19 outcomes in hospitalized patients.

“This does help with confidence in prescribing these agents and reinforces the recommendations for patients to stay on these drugs,” he said.

“However, none of these studies address the infectivity issue – whether their use upregulates the ACE2 receptor, which the virus uses to gain entry to cells, thereby increasing susceptibility to the infection,” Dr. Messerli cautioned. “But the similar or better outcomes on these drugs are encouraging,” he added.

The Wuhan study was supported by the Health and Family Planning Commission of Wuhan City, China. The authors have reported no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

Initial data from one Chinese center on the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) in patients hospitalized with COVID-19 appear to give some further reassurance about continued use of these drugs.

The report from one hospital in Wuhan found that among patients with hypertension hospitalized with the COVID-19 virus, there was no difference in disease severity or death rate in patients taking ACE inhibitors or ARBs and those not taking such medications.

The data were published online April 23 in JAMA Cardiology.

The study adds to another recent report in a larger number of COVID-19 patients from nine Chinese hospitals that suggested a beneficial effect of ACE inhibitors or ARBs on mortality.

Additional studies

Two other similar studies have also been recently released. Another study from China, published online March 31 in Emerging Microbes & Infections, included a small sample of 42 hospitalized patients with COVID-19 on antihypertensive therapy. Those on ACE inhibitor/ARB therapy had a lower rate of severe disease and a trend toward a lower level of IL-6 in peripheral blood. In addition, patients on ACE inhibitor/ARB therapy had increased CD3+ and CD8+ T-cell counts in peripheral blood and decreased peak viral load compared with other antihypertensive drugs.

And a preliminary study from the UK, which has not yet been peer reviewed, found that treatment with ACE inhibitors was associated with a reduced risk of rapidly deteriorating severe COVID-19 disease.

The study, available online on MedRxiv, a preprint server for health sciences, reports on 205 acute inpatients with COVID-19 at King’s College Hospital and Princess Royal University Hospital, London.

Of these, 51.2% had hypertension, 30.2% had diabetes, and 14.6% had ischemic heart disease or heart failure. Of the 37 patients on ACE inhibitors, five (14%) died or required critical care support compared with 29% (48/168) of patients not taking an ACE inhibitor.
 

New Wuhan study

The authors of the new article published in JAMA Cardiology, led by Juyi Li, MD, reported on a case series of 1,178 patients hospitalized with COVID-19 at the Central Hospital of Wuhan, Hubei, China, between Jan. 15 and March 15, 2020.

Patients were a median age of 55 years, and 46% were men. They had an overall in-hospital mortality rate of 11%.

Of the 1,178 patients, 362 (30.7%) had a diagnosis of hypertension. These patients were older (median age, 66 years) and had a greater prevalence of chronic diseases. Patients with hypertension also had more severe manifestations of COVID-19 compared to those without hypertension, including higher rates of acute respiratory distress syndrome and in-hospital mortality (21.3% vs. 6.5%).

Of the 362 patients with hypertension, 31.8% were taking ACE inhibitors or ARBs.

Apart from a greater prevalence of coronary artery disease, patients taking ACE inhibitors or ARBs had similar comorbidities to those not taking these medications, and also similar laboratory profile results including blood counts, inflammatory markers, renal and liver function tests, and cardiac biomarkers, although those taking ACE inhibitors/ARBs had higher levels of alkaline phosphatase.

The most commonly used antihypertensive drugs were calcium blockers. The percentage of patients with hypertension taking any drug or drug combination did not differ between those with severe and nonsevere infections and between those who survived and those who died.

Specifically regarding ACE inhibitors/ARBs, there was no difference between those with severe versus nonsevere illness in the use of ACE inhibitors (9.2% vs. 10.1%; P = .80), ARBs (24.9% vs. 21.2%; P = .40), or the composite of ACE inhibitors or ARBs (32.9% vs. 30.7%; P = .65).

Similarly, there were no differences in nonsurvivors and survivors in the use of ACE inhibitors (9.1% vs. 9.8%; P = .85); ARBs (19.5% vs. 23.9%; P = .42), or the composite of ACE inhibitors or ARBs (27.3% vs. 33.0%; P = .34).

The frequency of severe illness and death also did not differ between those treated with and without ACE inhibitors/ARBs in patients with hypertension and other various chronic conditions including coronary heart disease, cerebrovascular disease, diabetes, neurological disease, and chronic renal disease.

The authors noted that these data confirm previous reports showing that patients with hypertension have more severe illness and higher mortality rates associated with COVID-19 than those without hypertension.

But they added: “Our data provide some reassurance that ACE inhibitors/ARBs are not associated with the progression or outcome of COVID-19 hospitalizations in patients with hypertension.”

They also noted that these results support the recommendations from almost all major cardiovascular societies that patients do not discontinue ACE inhibitors or ARBs because of worries about COVID-19.

However, the authors did point out some limitations of their study, which included a small number of patients with hypertension taking ACE inhibitors or ARBs and the fact that a nonsevere disease course was still severe enough to require hospitalization. In addition, it was not clear whether ACE inhibitor/ARB treatment at baseline was maintained throughout hospitalization for all patients.

This was also an observational comparison and may be biased by differences in patients taking versus not taking ACE inhibitors or ARBs at the time of hospitalization, although the measured baseline characteristics were similar in both groups.

But the authors also highlighted the finding that, in this cohort, patients with hypertension had three times the mortality rate of all other patients hospitalized with COVID-19.

“Hypertension combined with cardiovascular and cerebrovascular disease, diabetes, and chronic kidney disease would predispose patients to an increased risk of severity and mortality of COVID-19. Therefore, patients with these underlying conditions who develop COVID-19 require particularly intensive surveillance and care,” they wrote.
 

Experts cautiously optimistic

Some cardiovascular experts were cautiously optimistic about these latest results.

Michael A. Weber, MD, professor of medicine at the State University of New York, Brooklyn, and editor-in-chief of the Journal of Clinical Hypertension, said: “This new report from Wuhan, China, gives modest reassurance that the use of ACE inhibitors or ARBs in hypertensive patients with COVID-19 disease does not increase the risk of clinical deterioration or death.

“Ongoing, more definitive studies should help resolve competing hypotheses regarding the effects of these agents: whether the increased ACE2 enzyme levels they produce can worsen outcomes by increasing access of the COVID virus to lung tissue; or whether there is a benefit linked to a protective effect of increased ACE2 on alveolar cell function,” Dr. Weber noted.

“Though the number of patients included in this new report is small, it is startling that hypertensive patients were three times as likely as nonhypertensives to have a fatal outcome, presumably reflecting vulnerability due to the cardiovascular and metabolic comorbidities associated with hypertension,” he added.

“In any case, for now, clinicians should continue treating hypertensive patients with whichever drugs, including ACE inhibitors and ARBs, best provide protection from adverse outcomes,” Dr. Weber concluded.

John McMurray, MD, professor of medical cardiology, University of Glasgow, Scotland, commented: “This study from Wuhan provides some reassurance about one of the two questions about ACEI/ARBs: Do these drugs increase susceptibility to infection? And if [the patient is] infected, do they increase the severity of infection? This study addresses the latter question and appears to suggest no increased severity.”

However, Dr. McMurray pointed out that the study had many limitations. There were only small patient numbers and the data were unadjusted, “although it looks like the ACE inhibitor/ARB treated patients were higher risk to start with.” It was an observational study, and patients were not randomized and were predominantly treated with ARBs, and not ACE inhibitors, so “we don’t know if the concerns apply equally to these two classes of drug.

“Other data published and unpublished supporting this (even showing better outcomes in patients treated with an ACE inhibitor/ARB), and, to date, any concerns about these drugs remain unsubstantiated and the guidance from medical societies to continue treatment with these agents in patients prescribed them seems wise,” Dr. McMurray added.

Franz H. Messerli, MD, professor of medicine at the University of Bern, Switzerland, commented: “The study from Wuhan is not a great study. They didn’t even do a multivariable analysis. They could have done a bit more with the data, but it still gives some reassurance.”

Dr. Messerli said it was “interesting” that 30% of the patients hospitalized with COVID-19 in the sample had hypertension. “That corresponds to the general population, so does not suggest that having hypertension increases susceptibility to infection – but it does seem to increase the risk of a bad outcome.”

Dr. Messerli noted that there are two more similar studies due to be published soon, both said to suggest either a beneficial or neutral effect of ACE inhibitors/ARBs on COVID-19 outcomes in hospitalized patients.

“This does help with confidence in prescribing these agents and reinforces the recommendations for patients to stay on these drugs,” he said.

“However, none of these studies address the infectivity issue – whether their use upregulates the ACE2 receptor, which the virus uses to gain entry to cells, thereby increasing susceptibility to the infection,” Dr. Messerli cautioned. “But the similar or better outcomes on these drugs are encouraging,” he added.

The Wuhan study was supported by the Health and Family Planning Commission of Wuhan City, China. The authors have reported no relevant financial relationships.

A version of this article originally appeared on Medscape.com.

Initial data from one Chinese center on the use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) in patients hospitalized with COVID-19 appear to give some further reassurance about continued use of these drugs.

The report from one hospital in Wuhan found that among patients with hypertension hospitalized with the COVID-19 virus, there was no difference in disease severity or death rate in patients taking ACE inhibitors or ARBs and those not taking such medications.

The data were published online April 23 in JAMA Cardiology.

The study adds to another recent report in a larger number of COVID-19 patients from nine Chinese hospitals that suggested a beneficial effect of ACE inhibitors or ARBs on mortality.

Additional studies

Two other similar studies have also been recently released. Another study from China, published online March 31 in Emerging Microbes & Infections, included a small sample of 42 hospitalized patients with COVID-19 on antihypertensive therapy. Those on ACE inhibitor/ARB therapy had a lower rate of severe disease and a trend toward a lower level of IL-6 in peripheral blood. In addition, patients on ACE inhibitor/ARB therapy had increased CD3+ and CD8+ T-cell counts in peripheral blood and decreased peak viral load compared with other antihypertensive drugs.

And a preliminary study from the UK, which has not yet been peer reviewed, found that treatment with ACE inhibitors was associated with a reduced risk of rapidly deteriorating severe COVID-19 disease.

The study, available online on MedRxiv, a preprint server for health sciences, reports on 205 acute inpatients with COVID-19 at King’s College Hospital and Princess Royal University Hospital, London.

Of these, 51.2% had hypertension, 30.2% had diabetes, and 14.6% had ischemic heart disease or heart failure. Of the 37 patients on ACE inhibitors, five (14%) died or required critical care support compared with 29% (48/168) of patients not taking an ACE inhibitor.
 

New Wuhan study

The authors of the new article published in JAMA Cardiology, led by Juyi Li, MD, reported on a case series of 1,178 patients hospitalized with COVID-19 at the Central Hospital of Wuhan, Hubei, China, between Jan. 15 and March 15, 2020.

Patients were a median age of 55 years, and 46% were men. They had an overall in-hospital mortality rate of 11%.

Of the 1,178 patients, 362 (30.7%) had a diagnosis of hypertension. These patients were older (median age, 66 years) and had a greater prevalence of chronic diseases. Patients with hypertension also had more severe manifestations of COVID-19 compared to those without hypertension, including higher rates of acute respiratory distress syndrome and in-hospital mortality (21.3% vs. 6.5%).

Of the 362 patients with hypertension, 31.8% were taking ACE inhibitors or ARBs.

Apart from a greater prevalence of coronary artery disease, patients taking ACE inhibitors or ARBs had similar comorbidities to those not taking these medications, and also similar laboratory profile results including blood counts, inflammatory markers, renal and liver function tests, and cardiac biomarkers, although those taking ACE inhibitors/ARBs had higher levels of alkaline phosphatase.

The most commonly used antihypertensive drugs were calcium blockers. The percentage of patients with hypertension taking any drug or drug combination did not differ between those with severe and nonsevere infections and between those who survived and those who died.

Specifically regarding ACE inhibitors/ARBs, there was no difference between those with severe versus nonsevere illness in the use of ACE inhibitors (9.2% vs. 10.1%; P = .80), ARBs (24.9% vs. 21.2%; P = .40), or the composite of ACE inhibitors or ARBs (32.9% vs. 30.7%; P = .65).

Similarly, there were no differences in nonsurvivors and survivors in the use of ACE inhibitors (9.1% vs. 9.8%; P = .85); ARBs (19.5% vs. 23.9%; P = .42), or the composite of ACE inhibitors or ARBs (27.3% vs. 33.0%; P = .34).

The frequency of severe illness and death also did not differ between those treated with and without ACE inhibitors/ARBs in patients with hypertension and other various chronic conditions including coronary heart disease, cerebrovascular disease, diabetes, neurological disease, and chronic renal disease.

The authors noted that these data confirm previous reports showing that patients with hypertension have more severe illness and higher mortality rates associated with COVID-19 than those without hypertension.

But they added: “Our data provide some reassurance that ACE inhibitors/ARBs are not associated with the progression or outcome of COVID-19 hospitalizations in patients with hypertension.”

They also noted that these results support the recommendations from almost all major cardiovascular societies that patients do not discontinue ACE inhibitors or ARBs because of worries about COVID-19.

However, the authors did point out some limitations of their study, which included a small number of patients with hypertension taking ACE inhibitors or ARBs and the fact that a nonsevere disease course was still severe enough to require hospitalization. In addition, it was not clear whether ACE inhibitor/ARB treatment at baseline was maintained throughout hospitalization for all patients.

This was also an observational comparison and may be biased by differences in patients taking versus not taking ACE inhibitors or ARBs at the time of hospitalization, although the measured baseline characteristics were similar in both groups.

But the authors also highlighted the finding that, in this cohort, patients with hypertension had three times the mortality rate of all other patients hospitalized with COVID-19.

“Hypertension combined with cardiovascular and cerebrovascular disease, diabetes, and chronic kidney disease would predispose patients to an increased risk of severity and mortality of COVID-19. Therefore, patients with these underlying conditions who develop COVID-19 require particularly intensive surveillance and care,” they wrote.
 

Experts cautiously optimistic

Some cardiovascular experts were cautiously optimistic about these latest results.

Michael A. Weber, MD, professor of medicine at the State University of New York, Brooklyn, and editor-in-chief of the Journal of Clinical Hypertension, said: “This new report from Wuhan, China, gives modest reassurance that the use of ACE inhibitors or ARBs in hypertensive patients with COVID-19 disease does not increase the risk of clinical deterioration or death.

“Ongoing, more definitive studies should help resolve competing hypotheses regarding the effects of these agents: whether the increased ACE2 enzyme levels they produce can worsen outcomes by increasing access of the COVID virus to lung tissue; or whether there is a benefit linked to a protective effect of increased ACE2 on alveolar cell function,” Dr. Weber noted.

“Though the number of patients included in this new report is small, it is startling that hypertensive patients were three times as likely as nonhypertensives to have a fatal outcome, presumably reflecting vulnerability due to the cardiovascular and metabolic comorbidities associated with hypertension,” he added.

“In any case, for now, clinicians should continue treating hypertensive patients with whichever drugs, including ACE inhibitors and ARBs, best provide protection from adverse outcomes,” Dr. Weber concluded.

John McMurray, MD, professor of medical cardiology, University of Glasgow, Scotland, commented: “This study from Wuhan provides some reassurance about one of the two questions about ACEI/ARBs: Do these drugs increase susceptibility to infection? And if [the patient is] infected, do they increase the severity of infection? This study addresses the latter question and appears to suggest no increased severity.”

However, Dr. McMurray pointed out that the study had many limitations. There were only small patient numbers and the data were unadjusted, “although it looks like the ACE inhibitor/ARB treated patients were higher risk to start with.” It was an observational study, and patients were not randomized and were predominantly treated with ARBs, and not ACE inhibitors, so “we don’t know if the concerns apply equally to these two classes of drug.

“Other data published and unpublished supporting this (even showing better outcomes in patients treated with an ACE inhibitor/ARB), and, to date, any concerns about these drugs remain unsubstantiated and the guidance from medical societies to continue treatment with these agents in patients prescribed them seems wise,” Dr. McMurray added.

Franz H. Messerli, MD, professor of medicine at the University of Bern, Switzerland, commented: “The study from Wuhan is not a great study. They didn’t even do a multivariable analysis. They could have done a bit more with the data, but it still gives some reassurance.”

Dr. Messerli said it was “interesting” that 30% of the patients hospitalized with COVID-19 in the sample had hypertension. “That corresponds to the general population, so does not suggest that having hypertension increases susceptibility to infection – but it does seem to increase the risk of a bad outcome.”

Dr. Messerli noted that there are two more similar studies due to be published soon, both said to suggest either a beneficial or neutral effect of ACE inhibitors/ARBs on COVID-19 outcomes in hospitalized patients.

“This does help with confidence in prescribing these agents and reinforces the recommendations for patients to stay on these drugs,” he said.

“However, none of these studies address the infectivity issue – whether their use upregulates the ACE2 receptor, which the virus uses to gain entry to cells, thereby increasing susceptibility to the infection,” Dr. Messerli cautioned. “But the similar or better outcomes on these drugs are encouraging,” he added.

The Wuhan study was supported by the Health and Family Planning Commission of Wuhan City, China. The authors have reported no relevant financial relationships.

A version of this article originally appeared on Medscape.com.