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extacy
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Will you have cardiac arrest? New tech may predict if and when
Deaths from COVID-19 may have caught more attention lately, but heart disease remains the leading cause of death in the United States.
More than 300,000 Americans will die this year of sudden cardiac arrest (also called sudden cardiac death, or SCD), when the heart abruptly stops working.
These events happen suddenly and often without warning, making them nearly impossible to predict. But that may be changing, thanks to 3D imaging and artificial intelligence (AI) technology under study at Johns Hopkins University, Baltimore.
There, researchers are working to create more accurate and personalized models of the heart – and not just any heart, your heart, if you have heart disease.
“Right now, a clinician can only say whether a patient is at risk or not at risk for sudden death,” says Dan Popescu, PhD, a Johns Hopkins research scientist and first author of a new study on AI’s ability to predict sudden cardiac arrest. “With this new technology, you can have much more nuanced predictions of probability of an event over time.”
Put another way: With AI, clinicians may be able not only to predict if someone is at risk for sudden cardiac arrest, but also when it is most likely to happen. They can do this using a much clearer and more personalized look at the electrical “wiring” of your heart.
Your heart, the conductor
Your heart isn’t just a metronome responsible for keeping a steady stream of blood pumping to tissues with every beat. It’s also a conductor through which vital energy flows.
To make the heart beat, electrical impulses flow from the top to the bottom of the organ. Healthy heart cells relay this electricity seamlessly. But in a heart damaged by inflammation or a past heart attack, scar tissue will block the energy flow.
When an electrical impulse encounters a scarred area, the signal can become erratic, disrupting the set top-to-bottom path and causing irregular heartbeats (arrhythmias), which increase someone’s danger of sudden cardiac death.
Seeing the heart in 3D
Today’s tests offer some insights into the heart’s makeup. For example, MRI scans can reveal damaged areas. PET scans can show inflammation. And EKGs can record the heart’s electrical signals from beat to beat.
But all these technologies offer only a snapshot, showing heart health at a moment in time. They can’t predict the future. That’s why scientists at Johns Hopkins are going further to develop 3D digital replicas of a person’s heart, known as computational heart models.
Computational models are computer-simulated replicas that combine mathematics, physics, and computer science. These models have been around for a long time and are used in many fields, ranging from manufacturing to economics.
In heart medicine, these models are populated with digital “cells,” which imitate living cells and can be programmed with different electrical properties, depending on whether they are healthy or diseased.
“Currently available imaging and testing (MRIs, PETs, EKGs) give some representation of the scarring, but you cannot translate that to what is going to happen over time,” says Natalia Trayanova, PhD, of the Johns Hopkins department of biomedical engineering.
“With computational heart models, we create a dynamic digital image of the heart. We can then give the digital image an electrical stimulus and assess how the heart is able to respond. Then you can better predict what is going to happen.”
The computerized 3D models also mean better, more accurate treatment for heart conditions.
For example, a common treatment for a type of arrhythmia known as atrial fibrillation is ablation, or burning some heart tissue. Ablation stops the erratic electrical impulses causing the arrhythmia, but it can also damage otherwise healthy heart cells.
A personalized computational heart model could allow doctors to see more accurately what areas should and shouldn’t be treated for a specific patient.
Using deep learning AI to predict health outcomes
Dr. Trayanova’s colleague Dr. Popescu is applying deep learning and AI to do more with computerized heart models to predict the future.
In a recent paper in Nature Cardiovascular Research, the research team showed their algorithm assessed the health of 269 patients and was able to predict the chance of sudden cardiac arrest up to 10 years in advance.
“This is really the first time ever, as far as we know, where deep learning technology has been proven to analyze scarring of the heart in a successful way,” Dr. Popescu says.
Dr. Popescu and Dr. Trayanova say the AI algorithm gathers information from the 3D computational heart models with patient data like MRIs, ethnicity, age, lifestyle, and other clinical information. Analyzing all these data can produce accurate and consistent estimates about how long patients might live if they are at risk for sudden death.
“You can’t afford to be wrong. If you are wrong, you can actually impact a patient’s quality of life dramatically,” Dr. Popescu says. “Having clinicians use this technology in the decision-making process will provide confidence in a better diagnosis and prognosis.”
While the current study was specifically about patients with a particular type of heart disease, Dr. Popescu says his algorithm can also be trained to assess other health conditions.
So when might you see this being used outside of a research study? Dr. Trayanova predicts 3D imaging of heart models could be available in 2 years, but first the technique must be tested in more clinical trials – some of which are happening right now.
Adding AI to the heart models will require more studies and Food and Drug Administration approval, so the timeline is less clear. But perhaps the biggest hurdle is that after approval the technologies would need to be adopted and used by clinicians and caregivers.
“The much harder question to answer is, ‘When will doctors be perfectly comfortable with AI tools?’ And I don’t know the answer,” Dr. Popescu says. “How to use AI as an aid in the decision-making process is something that’s not currently taught.”
A version of this article first appeared on WebMD.com.
Deaths from COVID-19 may have caught more attention lately, but heart disease remains the leading cause of death in the United States.
More than 300,000 Americans will die this year of sudden cardiac arrest (also called sudden cardiac death, or SCD), when the heart abruptly stops working.
These events happen suddenly and often without warning, making them nearly impossible to predict. But that may be changing, thanks to 3D imaging and artificial intelligence (AI) technology under study at Johns Hopkins University, Baltimore.
There, researchers are working to create more accurate and personalized models of the heart – and not just any heart, your heart, if you have heart disease.
“Right now, a clinician can only say whether a patient is at risk or not at risk for sudden death,” says Dan Popescu, PhD, a Johns Hopkins research scientist and first author of a new study on AI’s ability to predict sudden cardiac arrest. “With this new technology, you can have much more nuanced predictions of probability of an event over time.”
Put another way: With AI, clinicians may be able not only to predict if someone is at risk for sudden cardiac arrest, but also when it is most likely to happen. They can do this using a much clearer and more personalized look at the electrical “wiring” of your heart.
Your heart, the conductor
Your heart isn’t just a metronome responsible for keeping a steady stream of blood pumping to tissues with every beat. It’s also a conductor through which vital energy flows.
To make the heart beat, electrical impulses flow from the top to the bottom of the organ. Healthy heart cells relay this electricity seamlessly. But in a heart damaged by inflammation or a past heart attack, scar tissue will block the energy flow.
When an electrical impulse encounters a scarred area, the signal can become erratic, disrupting the set top-to-bottom path and causing irregular heartbeats (arrhythmias), which increase someone’s danger of sudden cardiac death.
Seeing the heart in 3D
Today’s tests offer some insights into the heart’s makeup. For example, MRI scans can reveal damaged areas. PET scans can show inflammation. And EKGs can record the heart’s electrical signals from beat to beat.
But all these technologies offer only a snapshot, showing heart health at a moment in time. They can’t predict the future. That’s why scientists at Johns Hopkins are going further to develop 3D digital replicas of a person’s heart, known as computational heart models.
Computational models are computer-simulated replicas that combine mathematics, physics, and computer science. These models have been around for a long time and are used in many fields, ranging from manufacturing to economics.
In heart medicine, these models are populated with digital “cells,” which imitate living cells and can be programmed with different electrical properties, depending on whether they are healthy or diseased.
“Currently available imaging and testing (MRIs, PETs, EKGs) give some representation of the scarring, but you cannot translate that to what is going to happen over time,” says Natalia Trayanova, PhD, of the Johns Hopkins department of biomedical engineering.
“With computational heart models, we create a dynamic digital image of the heart. We can then give the digital image an electrical stimulus and assess how the heart is able to respond. Then you can better predict what is going to happen.”
The computerized 3D models also mean better, more accurate treatment for heart conditions.
For example, a common treatment for a type of arrhythmia known as atrial fibrillation is ablation, or burning some heart tissue. Ablation stops the erratic electrical impulses causing the arrhythmia, but it can also damage otherwise healthy heart cells.
A personalized computational heart model could allow doctors to see more accurately what areas should and shouldn’t be treated for a specific patient.
Using deep learning AI to predict health outcomes
Dr. Trayanova’s colleague Dr. Popescu is applying deep learning and AI to do more with computerized heart models to predict the future.
In a recent paper in Nature Cardiovascular Research, the research team showed their algorithm assessed the health of 269 patients and was able to predict the chance of sudden cardiac arrest up to 10 years in advance.
“This is really the first time ever, as far as we know, where deep learning technology has been proven to analyze scarring of the heart in a successful way,” Dr. Popescu says.
Dr. Popescu and Dr. Trayanova say the AI algorithm gathers information from the 3D computational heart models with patient data like MRIs, ethnicity, age, lifestyle, and other clinical information. Analyzing all these data can produce accurate and consistent estimates about how long patients might live if they are at risk for sudden death.
“You can’t afford to be wrong. If you are wrong, you can actually impact a patient’s quality of life dramatically,” Dr. Popescu says. “Having clinicians use this technology in the decision-making process will provide confidence in a better diagnosis and prognosis.”
While the current study was specifically about patients with a particular type of heart disease, Dr. Popescu says his algorithm can also be trained to assess other health conditions.
So when might you see this being used outside of a research study? Dr. Trayanova predicts 3D imaging of heart models could be available in 2 years, but first the technique must be tested in more clinical trials – some of which are happening right now.
Adding AI to the heart models will require more studies and Food and Drug Administration approval, so the timeline is less clear. But perhaps the biggest hurdle is that after approval the technologies would need to be adopted and used by clinicians and caregivers.
“The much harder question to answer is, ‘When will doctors be perfectly comfortable with AI tools?’ And I don’t know the answer,” Dr. Popescu says. “How to use AI as an aid in the decision-making process is something that’s not currently taught.”
A version of this article first appeared on WebMD.com.
Deaths from COVID-19 may have caught more attention lately, but heart disease remains the leading cause of death in the United States.
More than 300,000 Americans will die this year of sudden cardiac arrest (also called sudden cardiac death, or SCD), when the heart abruptly stops working.
These events happen suddenly and often without warning, making them nearly impossible to predict. But that may be changing, thanks to 3D imaging and artificial intelligence (AI) technology under study at Johns Hopkins University, Baltimore.
There, researchers are working to create more accurate and personalized models of the heart – and not just any heart, your heart, if you have heart disease.
“Right now, a clinician can only say whether a patient is at risk or not at risk for sudden death,” says Dan Popescu, PhD, a Johns Hopkins research scientist and first author of a new study on AI’s ability to predict sudden cardiac arrest. “With this new technology, you can have much more nuanced predictions of probability of an event over time.”
Put another way: With AI, clinicians may be able not only to predict if someone is at risk for sudden cardiac arrest, but also when it is most likely to happen. They can do this using a much clearer and more personalized look at the electrical “wiring” of your heart.
Your heart, the conductor
Your heart isn’t just a metronome responsible for keeping a steady stream of blood pumping to tissues with every beat. It’s also a conductor through which vital energy flows.
To make the heart beat, electrical impulses flow from the top to the bottom of the organ. Healthy heart cells relay this electricity seamlessly. But in a heart damaged by inflammation or a past heart attack, scar tissue will block the energy flow.
When an electrical impulse encounters a scarred area, the signal can become erratic, disrupting the set top-to-bottom path and causing irregular heartbeats (arrhythmias), which increase someone’s danger of sudden cardiac death.
Seeing the heart in 3D
Today’s tests offer some insights into the heart’s makeup. For example, MRI scans can reveal damaged areas. PET scans can show inflammation. And EKGs can record the heart’s electrical signals from beat to beat.
But all these technologies offer only a snapshot, showing heart health at a moment in time. They can’t predict the future. That’s why scientists at Johns Hopkins are going further to develop 3D digital replicas of a person’s heart, known as computational heart models.
Computational models are computer-simulated replicas that combine mathematics, physics, and computer science. These models have been around for a long time and are used in many fields, ranging from manufacturing to economics.
In heart medicine, these models are populated with digital “cells,” which imitate living cells and can be programmed with different electrical properties, depending on whether they are healthy or diseased.
“Currently available imaging and testing (MRIs, PETs, EKGs) give some representation of the scarring, but you cannot translate that to what is going to happen over time,” says Natalia Trayanova, PhD, of the Johns Hopkins department of biomedical engineering.
“With computational heart models, we create a dynamic digital image of the heart. We can then give the digital image an electrical stimulus and assess how the heart is able to respond. Then you can better predict what is going to happen.”
The computerized 3D models also mean better, more accurate treatment for heart conditions.
For example, a common treatment for a type of arrhythmia known as atrial fibrillation is ablation, or burning some heart tissue. Ablation stops the erratic electrical impulses causing the arrhythmia, but it can also damage otherwise healthy heart cells.
A personalized computational heart model could allow doctors to see more accurately what areas should and shouldn’t be treated for a specific patient.
Using deep learning AI to predict health outcomes
Dr. Trayanova’s colleague Dr. Popescu is applying deep learning and AI to do more with computerized heart models to predict the future.
In a recent paper in Nature Cardiovascular Research, the research team showed their algorithm assessed the health of 269 patients and was able to predict the chance of sudden cardiac arrest up to 10 years in advance.
“This is really the first time ever, as far as we know, where deep learning technology has been proven to analyze scarring of the heart in a successful way,” Dr. Popescu says.
Dr. Popescu and Dr. Trayanova say the AI algorithm gathers information from the 3D computational heart models with patient data like MRIs, ethnicity, age, lifestyle, and other clinical information. Analyzing all these data can produce accurate and consistent estimates about how long patients might live if they are at risk for sudden death.
“You can’t afford to be wrong. If you are wrong, you can actually impact a patient’s quality of life dramatically,” Dr. Popescu says. “Having clinicians use this technology in the decision-making process will provide confidence in a better diagnosis and prognosis.”
While the current study was specifically about patients with a particular type of heart disease, Dr. Popescu says his algorithm can also be trained to assess other health conditions.
So when might you see this being used outside of a research study? Dr. Trayanova predicts 3D imaging of heart models could be available in 2 years, but first the technique must be tested in more clinical trials – some of which are happening right now.
Adding AI to the heart models will require more studies and Food and Drug Administration approval, so the timeline is less clear. But perhaps the biggest hurdle is that after approval the technologies would need to be adopted and used by clinicians and caregivers.
“The much harder question to answer is, ‘When will doctors be perfectly comfortable with AI tools?’ And I don’t know the answer,” Dr. Popescu says. “How to use AI as an aid in the decision-making process is something that’s not currently taught.”
A version of this article first appeared on WebMD.com.
Almost 60% of U.S. population has been infected by COVID-19: CDC
The percentage of Americans who have been infected with COVID-19 jumped from 34% in December 2021 to 58% in February 2022, a new study from the Centers for Disease Control and Prevention reveals.
This is the first time the seroprevalence of prior infection is more than 50% in the American population.
“I definitely expected that we were going to see an increase continue ... but I didn’t expect it to increase quite this much. But we follow the data ... and this is what the evidence is showing us,” lead study researcher Kristie E. N. Clarke, MD, said during a CDC media briefing April 26.
Researchers found that presence of antinucleocapsid (anti-N) antibodies from prior infection varied by age. The rate varied from as high as 75% in children and teenagers 17 years and younger to 33% in those 65 and older, for example.
The study showed that the anti-N antibodies were more common in age groups with the lowest vaccination numbers.
Combined with up-to-date CDC data on deaths, hospitalizations, and cases, the study provides a clearer picture of where we are now and where we might be headed in terms of the pandemic.
Vaccination still valuable
The fact that nearly 60% of Americans have antibodies from prior infection is not a reason to think people with a history of COVID-19 should skip vaccination, said CDC director Rochelle P. Walensky, MD.
“I can’t underscore enough that those with detectable antibodies from previous infection, we encourage them to still get vaccinated,” Dr. Walensky said.
“We do know that reinfections happen,” she said, “so that’s important in terms of thinking forward.”
The CDC continues to encourage all Americans to stay up to date with their COVID-19 vaccinations, said Dr. Clarke, colead for the CDC’s COVID-19 Epidemiology and Surveillance Taskforce Seroprevalence Team. “Having infection-induced antibodies does not necessarily mean you are protected against future infections.”
The study, published in the CDC’s Morbidity and Mortality Weekly Report (MMWR), did not evaluate antibody protection from COVID-19 vaccination.
It should also be noted that the study looked at presence or absence of anti-N antibodies, and not whether certain levels were linked to less or more protection.
Where are we now?
Dr. Walensky used the media briefing as an opportunity to share current COVID-19 numbers.
“Overall, we can continue to have some mixed trends. Deaths, fortunately, are continuing to trend downward with a 7-day average of about 300 per day, which represents an estimated 18% decline from the prior week,” she said.
Hospital admissions also remain low, at about 1,500 per day. “But we should note that for the second week in a row, they are slowly trending upwards,” Dr. Walensky said. There was an increase of about 9% at press time compared with the prior week.
Cases remain “comparatively low” to even where we were a month ago, at 44,000 per day,” Dr. Walensky said. “Although this too represents an increase of about 25% in the past week.”
Dr. Walensky noted that positive test numbers are not as reliable a metric as they were before the growth in use of rapid home tests. But it’s not the only measure. “We continue to believe that our PCR testing data, especially when we corroborate it with information from our other surveillance systems – like wastewater surveillance and emergency department surveillance – provide us a reliable picture of the trajectory of COVID-19 across our country.”
She recommended that people continue to consult the CDC’s COVID-19 county tracker to monitor local levels of COVID-19.
Dr. Walensky also shared recent findings from genomic sequencing that continue to show the predominance of the Omicron variant. “Essentially a hundred percent of what we’re finding now is Omicron,” she said. In terms of individual variants, the Omicron BA.1 variant is about 3% of circulating virus, the BA.2 variant is about 68%, and BA.2.12.1 makes up about 35%.
“We’re just starting to learn about the impact of BA2.121,” Dr. Walensky said. “It appears it might have a transmission advantage of about 25% over the BA2 subvariant.”
A version of this article first appeared on Medscape.com.
The percentage of Americans who have been infected with COVID-19 jumped from 34% in December 2021 to 58% in February 2022, a new study from the Centers for Disease Control and Prevention reveals.
This is the first time the seroprevalence of prior infection is more than 50% in the American population.
“I definitely expected that we were going to see an increase continue ... but I didn’t expect it to increase quite this much. But we follow the data ... and this is what the evidence is showing us,” lead study researcher Kristie E. N. Clarke, MD, said during a CDC media briefing April 26.
Researchers found that presence of antinucleocapsid (anti-N) antibodies from prior infection varied by age. The rate varied from as high as 75% in children and teenagers 17 years and younger to 33% in those 65 and older, for example.
The study showed that the anti-N antibodies were more common in age groups with the lowest vaccination numbers.
Combined with up-to-date CDC data on deaths, hospitalizations, and cases, the study provides a clearer picture of where we are now and where we might be headed in terms of the pandemic.
Vaccination still valuable
The fact that nearly 60% of Americans have antibodies from prior infection is not a reason to think people with a history of COVID-19 should skip vaccination, said CDC director Rochelle P. Walensky, MD.
“I can’t underscore enough that those with detectable antibodies from previous infection, we encourage them to still get vaccinated,” Dr. Walensky said.
“We do know that reinfections happen,” she said, “so that’s important in terms of thinking forward.”
The CDC continues to encourage all Americans to stay up to date with their COVID-19 vaccinations, said Dr. Clarke, colead for the CDC’s COVID-19 Epidemiology and Surveillance Taskforce Seroprevalence Team. “Having infection-induced antibodies does not necessarily mean you are protected against future infections.”
The study, published in the CDC’s Morbidity and Mortality Weekly Report (MMWR), did not evaluate antibody protection from COVID-19 vaccination.
It should also be noted that the study looked at presence or absence of anti-N antibodies, and not whether certain levels were linked to less or more protection.
Where are we now?
Dr. Walensky used the media briefing as an opportunity to share current COVID-19 numbers.
“Overall, we can continue to have some mixed trends. Deaths, fortunately, are continuing to trend downward with a 7-day average of about 300 per day, which represents an estimated 18% decline from the prior week,” she said.
Hospital admissions also remain low, at about 1,500 per day. “But we should note that for the second week in a row, they are slowly trending upwards,” Dr. Walensky said. There was an increase of about 9% at press time compared with the prior week.
Cases remain “comparatively low” to even where we were a month ago, at 44,000 per day,” Dr. Walensky said. “Although this too represents an increase of about 25% in the past week.”
Dr. Walensky noted that positive test numbers are not as reliable a metric as they were before the growth in use of rapid home tests. But it’s not the only measure. “We continue to believe that our PCR testing data, especially when we corroborate it with information from our other surveillance systems – like wastewater surveillance and emergency department surveillance – provide us a reliable picture of the trajectory of COVID-19 across our country.”
She recommended that people continue to consult the CDC’s COVID-19 county tracker to monitor local levels of COVID-19.
Dr. Walensky also shared recent findings from genomic sequencing that continue to show the predominance of the Omicron variant. “Essentially a hundred percent of what we’re finding now is Omicron,” she said. In terms of individual variants, the Omicron BA.1 variant is about 3% of circulating virus, the BA.2 variant is about 68%, and BA.2.12.1 makes up about 35%.
“We’re just starting to learn about the impact of BA2.121,” Dr. Walensky said. “It appears it might have a transmission advantage of about 25% over the BA2 subvariant.”
A version of this article first appeared on Medscape.com.
The percentage of Americans who have been infected with COVID-19 jumped from 34% in December 2021 to 58% in February 2022, a new study from the Centers for Disease Control and Prevention reveals.
This is the first time the seroprevalence of prior infection is more than 50% in the American population.
“I definitely expected that we were going to see an increase continue ... but I didn’t expect it to increase quite this much. But we follow the data ... and this is what the evidence is showing us,” lead study researcher Kristie E. N. Clarke, MD, said during a CDC media briefing April 26.
Researchers found that presence of antinucleocapsid (anti-N) antibodies from prior infection varied by age. The rate varied from as high as 75% in children and teenagers 17 years and younger to 33% in those 65 and older, for example.
The study showed that the anti-N antibodies were more common in age groups with the lowest vaccination numbers.
Combined with up-to-date CDC data on deaths, hospitalizations, and cases, the study provides a clearer picture of where we are now and where we might be headed in terms of the pandemic.
Vaccination still valuable
The fact that nearly 60% of Americans have antibodies from prior infection is not a reason to think people with a history of COVID-19 should skip vaccination, said CDC director Rochelle P. Walensky, MD.
“I can’t underscore enough that those with detectable antibodies from previous infection, we encourage them to still get vaccinated,” Dr. Walensky said.
“We do know that reinfections happen,” she said, “so that’s important in terms of thinking forward.”
The CDC continues to encourage all Americans to stay up to date with their COVID-19 vaccinations, said Dr. Clarke, colead for the CDC’s COVID-19 Epidemiology and Surveillance Taskforce Seroprevalence Team. “Having infection-induced antibodies does not necessarily mean you are protected against future infections.”
The study, published in the CDC’s Morbidity and Mortality Weekly Report (MMWR), did not evaluate antibody protection from COVID-19 vaccination.
It should also be noted that the study looked at presence or absence of anti-N antibodies, and not whether certain levels were linked to less or more protection.
Where are we now?
Dr. Walensky used the media briefing as an opportunity to share current COVID-19 numbers.
“Overall, we can continue to have some mixed trends. Deaths, fortunately, are continuing to trend downward with a 7-day average of about 300 per day, which represents an estimated 18% decline from the prior week,” she said.
Hospital admissions also remain low, at about 1,500 per day. “But we should note that for the second week in a row, they are slowly trending upwards,” Dr. Walensky said. There was an increase of about 9% at press time compared with the prior week.
Cases remain “comparatively low” to even where we were a month ago, at 44,000 per day,” Dr. Walensky said. “Although this too represents an increase of about 25% in the past week.”
Dr. Walensky noted that positive test numbers are not as reliable a metric as they were before the growth in use of rapid home tests. But it’s not the only measure. “We continue to believe that our PCR testing data, especially when we corroborate it with information from our other surveillance systems – like wastewater surveillance and emergency department surveillance – provide us a reliable picture of the trajectory of COVID-19 across our country.”
She recommended that people continue to consult the CDC’s COVID-19 county tracker to monitor local levels of COVID-19.
Dr. Walensky also shared recent findings from genomic sequencing that continue to show the predominance of the Omicron variant. “Essentially a hundred percent of what we’re finding now is Omicron,” she said. In terms of individual variants, the Omicron BA.1 variant is about 3% of circulating virus, the BA.2 variant is about 68%, and BA.2.12.1 makes up about 35%.
“We’re just starting to learn about the impact of BA2.121,” Dr. Walensky said. “It appears it might have a transmission advantage of about 25% over the BA2 subvariant.”
A version of this article first appeared on Medscape.com.
FROM MMWR
How do we distinguish between viral and bacterial meningitis?
Bacteria and viruses are the leading causes of community-acquired meningitis. Bacterial meningitis is associated with high morbidity and mortality, and prompt treatment with appropriate antibiotics is essential to optimize outcomes. Early diagnosis is therefore crucial for selecting patients who need antibiotics. On the other hand, the course of viral meningitis is generally benign, and there is usually no specific antimicrobial treatment required. Distinguishing between viral and bacterial causes of meningitis can be challenging; therefore, many patients receive empiric antibiotic treatment.
Etiology
Among the etiologic agents of viral meningitis, the nonpolio enteroviruses (Echovirus 30, 11, 9, 6, 7, 18, 16, 71, 25; Coxsackie B2, A9, B1, B3, B4) are the most common, responsible for more than 85% of cases. Other viruses potentially responsible for meningitis include the herpes simplex virus (HSV), primarily type 2, and flavivirus (such as the Dengue virus).
Clinical presentation
The clinical presentation of bacterial meningitis is more severe than that of viral meningitis. The classic clinical triad of bacterial meningitis consists of fever, neck stiffness, and altered mental status. Only 41% of cases present with these three symptoms, however. Other clinical characteristics include severe headaches, decreased level of consciousness, nausea, vomiting, seizures, focal neurologic signs, and skin rash.
Viral meningitis is usually not associated with a decreased level of consciousness or significant decline in overall health status. The most frequently reported symptoms are unusual headaches, fever, nausea, vomiting, sensitivity to light, and neck stiffness. Patients may also present with skin changes and lymphadenopathy, and, depending on etiology, genital ulcers.
Diagnosis
The diagnosis of bacterial meningitis is based on clinical symptoms, blood panels (blood count, inflammation markers, cultures), and cerebrospinal fluid (CSF) cultures. Gram staining and latex agglutination may lead to false-negative results, and cultures may take a few days to provide a definitive result. Therefore, empiric antibiotic treatment is often started until the etiology can be determined.
A spinal tap must always be performed, preferably after a scan is taken, to rule out the risk of herniation. After CSF samples have been collected, they must undergo complete analysis, including cytological, biochemical, and microbiological evaluation, using conventional and molecular testing methods, when available.
Cytological and biochemical analyses of CSF may be helpful, as findings may indicate a higher probability of either bacterial or viral etiology.
CSF samples collected from patients with acute bacterial meningitis present characteristic neutrophilic pleocytosis (cell count usually ranging from hundreds to a few thousand, with >80% polymorphonuclear cells). In some cases of L. monocytogenes meningitis (from 25% to 30%), a lymphocytic predominance may occur. Normally, glucose is low (CSF glucose-to-blood-glucose ratio of ≤0.4 or <40 mg/dL), protein is very high (>200 mg/dL), and the CSF lactate level is high (≥31.53 mg/dL).
In viral meningitis, the white blood cell count is generally 10-300 cells/mm3. Although glucose levels are normal in most cases, they may be below normal limits in lymphocytic choriomeningitis virus (LCMV), HSV, mumps virus, and poliovirus meningitis. Protein levels tend to be slightly elevated, but they may still be within the reference range.
A recent study investigated which of the cytological or biochemical markers best correlate with the definite etiologic diagnosis. This study, in which CSF samples were collected and analyzed from 2013 to 2017, considered cases of bacterial or viral meningitis confirmed via microbiological evaluation or polymerase chain reaction (PCR). CSF lactate was the best single CSF parameter, and CSF lactate above 30 mg/dL virtually excludes the possibility of a viral etiology.
Etiologic determination
Despite the major contribution of globally analyzing CSF and secondary parameters, particularly CSF lactate, the precise etiologic definition is of great importance in cases of acute meningitis. Such precise definition is not simple, as identification of the causative microorganism is often difficult. Moreover, there are limits to conventional microbiological methods. Bacterioscopy is poorly sensitive, and although bacterial cultures are more sensitive, they can delay diagnosis because of the time it takes for the bacteria to grow in culture media.
Targeted molecular detection methods are usually more sensitive than conventional microbiological methods. Panel-based molecular tests identify multiple pathogens in a single test. In 2015, the U.S. Food and Drug Administration authorized the first commercial multiplex detection system for infectious causes of community-acquired meningitis and encephalitis. This test, the BioFire FilmArray system, detects 14 bacterial, viral, and fungal pathogens in a turnaround time of about 1 hour, including S. pneumoniae, N. meningitidis, H. influenzae, S. agalactiae (i.e., group B Streptococcus), E. coli (serotype K1), L. monocytogenes, HSV-1, HSV-2, varicella-zoster virus (VZV), cytomegalovirus (CMV), human herpesvirus 6 (HHV-6), human parechovirus (HPeV), and Cryptococcus neoformans/gattii.
A meta-analysis of eight precise diagnostic studies evaluating the BioFire FilmArray system showed a high sensitivity of 90% (95% confidence interval, 86%-93%) and specificity of 97% (95% CI, 94%-99%). The FilmArray ME panel can halve the time to microbiological result, allowing for earlier discontinuation of antimicrobial agents and hospital discharge in cases of viral meningitis.
Conclusion
Acute community-acquired meningitis is usually the result of viral or bacterial infections. Given the low specificity of clinical symptoms and, very often, of the general laboratory panel findings, many patients are empirically treated with antibiotics. High-sensitivity and -specificity molecular techniques allow for rapid identification of the bacterial etiology (which requires antibiotic therapy) or the viral etiology of meningitis. The latter can be managed only with symptom-specific medications and does not usually require extended hospitalization. Therefore, these new techniques can improve the quality of care for these patients with viral meningitis.
A version of this article first appeared on Medscape.com.
Bacteria and viruses are the leading causes of community-acquired meningitis. Bacterial meningitis is associated with high morbidity and mortality, and prompt treatment with appropriate antibiotics is essential to optimize outcomes. Early diagnosis is therefore crucial for selecting patients who need antibiotics. On the other hand, the course of viral meningitis is generally benign, and there is usually no specific antimicrobial treatment required. Distinguishing between viral and bacterial causes of meningitis can be challenging; therefore, many patients receive empiric antibiotic treatment.
Etiology
Among the etiologic agents of viral meningitis, the nonpolio enteroviruses (Echovirus 30, 11, 9, 6, 7, 18, 16, 71, 25; Coxsackie B2, A9, B1, B3, B4) are the most common, responsible for more than 85% of cases. Other viruses potentially responsible for meningitis include the herpes simplex virus (HSV), primarily type 2, and flavivirus (such as the Dengue virus).
Clinical presentation
The clinical presentation of bacterial meningitis is more severe than that of viral meningitis. The classic clinical triad of bacterial meningitis consists of fever, neck stiffness, and altered mental status. Only 41% of cases present with these three symptoms, however. Other clinical characteristics include severe headaches, decreased level of consciousness, nausea, vomiting, seizures, focal neurologic signs, and skin rash.
Viral meningitis is usually not associated with a decreased level of consciousness or significant decline in overall health status. The most frequently reported symptoms are unusual headaches, fever, nausea, vomiting, sensitivity to light, and neck stiffness. Patients may also present with skin changes and lymphadenopathy, and, depending on etiology, genital ulcers.
Diagnosis
The diagnosis of bacterial meningitis is based on clinical symptoms, blood panels (blood count, inflammation markers, cultures), and cerebrospinal fluid (CSF) cultures. Gram staining and latex agglutination may lead to false-negative results, and cultures may take a few days to provide a definitive result. Therefore, empiric antibiotic treatment is often started until the etiology can be determined.
A spinal tap must always be performed, preferably after a scan is taken, to rule out the risk of herniation. After CSF samples have been collected, they must undergo complete analysis, including cytological, biochemical, and microbiological evaluation, using conventional and molecular testing methods, when available.
Cytological and biochemical analyses of CSF may be helpful, as findings may indicate a higher probability of either bacterial or viral etiology.
CSF samples collected from patients with acute bacterial meningitis present characteristic neutrophilic pleocytosis (cell count usually ranging from hundreds to a few thousand, with >80% polymorphonuclear cells). In some cases of L. monocytogenes meningitis (from 25% to 30%), a lymphocytic predominance may occur. Normally, glucose is low (CSF glucose-to-blood-glucose ratio of ≤0.4 or <40 mg/dL), protein is very high (>200 mg/dL), and the CSF lactate level is high (≥31.53 mg/dL).
In viral meningitis, the white blood cell count is generally 10-300 cells/mm3. Although glucose levels are normal in most cases, they may be below normal limits in lymphocytic choriomeningitis virus (LCMV), HSV, mumps virus, and poliovirus meningitis. Protein levels tend to be slightly elevated, but they may still be within the reference range.
A recent study investigated which of the cytological or biochemical markers best correlate with the definite etiologic diagnosis. This study, in which CSF samples were collected and analyzed from 2013 to 2017, considered cases of bacterial or viral meningitis confirmed via microbiological evaluation or polymerase chain reaction (PCR). CSF lactate was the best single CSF parameter, and CSF lactate above 30 mg/dL virtually excludes the possibility of a viral etiology.
Etiologic determination
Despite the major contribution of globally analyzing CSF and secondary parameters, particularly CSF lactate, the precise etiologic definition is of great importance in cases of acute meningitis. Such precise definition is not simple, as identification of the causative microorganism is often difficult. Moreover, there are limits to conventional microbiological methods. Bacterioscopy is poorly sensitive, and although bacterial cultures are more sensitive, they can delay diagnosis because of the time it takes for the bacteria to grow in culture media.
Targeted molecular detection methods are usually more sensitive than conventional microbiological methods. Panel-based molecular tests identify multiple pathogens in a single test. In 2015, the U.S. Food and Drug Administration authorized the first commercial multiplex detection system for infectious causes of community-acquired meningitis and encephalitis. This test, the BioFire FilmArray system, detects 14 bacterial, viral, and fungal pathogens in a turnaround time of about 1 hour, including S. pneumoniae, N. meningitidis, H. influenzae, S. agalactiae (i.e., group B Streptococcus), E. coli (serotype K1), L. monocytogenes, HSV-1, HSV-2, varicella-zoster virus (VZV), cytomegalovirus (CMV), human herpesvirus 6 (HHV-6), human parechovirus (HPeV), and Cryptococcus neoformans/gattii.
A meta-analysis of eight precise diagnostic studies evaluating the BioFire FilmArray system showed a high sensitivity of 90% (95% confidence interval, 86%-93%) and specificity of 97% (95% CI, 94%-99%). The FilmArray ME panel can halve the time to microbiological result, allowing for earlier discontinuation of antimicrobial agents and hospital discharge in cases of viral meningitis.
Conclusion
Acute community-acquired meningitis is usually the result of viral or bacterial infections. Given the low specificity of clinical symptoms and, very often, of the general laboratory panel findings, many patients are empirically treated with antibiotics. High-sensitivity and -specificity molecular techniques allow for rapid identification of the bacterial etiology (which requires antibiotic therapy) or the viral etiology of meningitis. The latter can be managed only with symptom-specific medications and does not usually require extended hospitalization. Therefore, these new techniques can improve the quality of care for these patients with viral meningitis.
A version of this article first appeared on Medscape.com.
Bacteria and viruses are the leading causes of community-acquired meningitis. Bacterial meningitis is associated with high morbidity and mortality, and prompt treatment with appropriate antibiotics is essential to optimize outcomes. Early diagnosis is therefore crucial for selecting patients who need antibiotics. On the other hand, the course of viral meningitis is generally benign, and there is usually no specific antimicrobial treatment required. Distinguishing between viral and bacterial causes of meningitis can be challenging; therefore, many patients receive empiric antibiotic treatment.
Etiology
Among the etiologic agents of viral meningitis, the nonpolio enteroviruses (Echovirus 30, 11, 9, 6, 7, 18, 16, 71, 25; Coxsackie B2, A9, B1, B3, B4) are the most common, responsible for more than 85% of cases. Other viruses potentially responsible for meningitis include the herpes simplex virus (HSV), primarily type 2, and flavivirus (such as the Dengue virus).
Clinical presentation
The clinical presentation of bacterial meningitis is more severe than that of viral meningitis. The classic clinical triad of bacterial meningitis consists of fever, neck stiffness, and altered mental status. Only 41% of cases present with these three symptoms, however. Other clinical characteristics include severe headaches, decreased level of consciousness, nausea, vomiting, seizures, focal neurologic signs, and skin rash.
Viral meningitis is usually not associated with a decreased level of consciousness or significant decline in overall health status. The most frequently reported symptoms are unusual headaches, fever, nausea, vomiting, sensitivity to light, and neck stiffness. Patients may also present with skin changes and lymphadenopathy, and, depending on etiology, genital ulcers.
Diagnosis
The diagnosis of bacterial meningitis is based on clinical symptoms, blood panels (blood count, inflammation markers, cultures), and cerebrospinal fluid (CSF) cultures. Gram staining and latex agglutination may lead to false-negative results, and cultures may take a few days to provide a definitive result. Therefore, empiric antibiotic treatment is often started until the etiology can be determined.
A spinal tap must always be performed, preferably after a scan is taken, to rule out the risk of herniation. After CSF samples have been collected, they must undergo complete analysis, including cytological, biochemical, and microbiological evaluation, using conventional and molecular testing methods, when available.
Cytological and biochemical analyses of CSF may be helpful, as findings may indicate a higher probability of either bacterial or viral etiology.
CSF samples collected from patients with acute bacterial meningitis present characteristic neutrophilic pleocytosis (cell count usually ranging from hundreds to a few thousand, with >80% polymorphonuclear cells). In some cases of L. monocytogenes meningitis (from 25% to 30%), a lymphocytic predominance may occur. Normally, glucose is low (CSF glucose-to-blood-glucose ratio of ≤0.4 or <40 mg/dL), protein is very high (>200 mg/dL), and the CSF lactate level is high (≥31.53 mg/dL).
In viral meningitis, the white blood cell count is generally 10-300 cells/mm3. Although glucose levels are normal in most cases, they may be below normal limits in lymphocytic choriomeningitis virus (LCMV), HSV, mumps virus, and poliovirus meningitis. Protein levels tend to be slightly elevated, but they may still be within the reference range.
A recent study investigated which of the cytological or biochemical markers best correlate with the definite etiologic diagnosis. This study, in which CSF samples were collected and analyzed from 2013 to 2017, considered cases of bacterial or viral meningitis confirmed via microbiological evaluation or polymerase chain reaction (PCR). CSF lactate was the best single CSF parameter, and CSF lactate above 30 mg/dL virtually excludes the possibility of a viral etiology.
Etiologic determination
Despite the major contribution of globally analyzing CSF and secondary parameters, particularly CSF lactate, the precise etiologic definition is of great importance in cases of acute meningitis. Such precise definition is not simple, as identification of the causative microorganism is often difficult. Moreover, there are limits to conventional microbiological methods. Bacterioscopy is poorly sensitive, and although bacterial cultures are more sensitive, they can delay diagnosis because of the time it takes for the bacteria to grow in culture media.
Targeted molecular detection methods are usually more sensitive than conventional microbiological methods. Panel-based molecular tests identify multiple pathogens in a single test. In 2015, the U.S. Food and Drug Administration authorized the first commercial multiplex detection system for infectious causes of community-acquired meningitis and encephalitis. This test, the BioFire FilmArray system, detects 14 bacterial, viral, and fungal pathogens in a turnaround time of about 1 hour, including S. pneumoniae, N. meningitidis, H. influenzae, S. agalactiae (i.e., group B Streptococcus), E. coli (serotype K1), L. monocytogenes, HSV-1, HSV-2, varicella-zoster virus (VZV), cytomegalovirus (CMV), human herpesvirus 6 (HHV-6), human parechovirus (HPeV), and Cryptococcus neoformans/gattii.
A meta-analysis of eight precise diagnostic studies evaluating the BioFire FilmArray system showed a high sensitivity of 90% (95% confidence interval, 86%-93%) and specificity of 97% (95% CI, 94%-99%). The FilmArray ME panel can halve the time to microbiological result, allowing for earlier discontinuation of antimicrobial agents and hospital discharge in cases of viral meningitis.
Conclusion
Acute community-acquired meningitis is usually the result of viral or bacterial infections. Given the low specificity of clinical symptoms and, very often, of the general laboratory panel findings, many patients are empirically treated with antibiotics. High-sensitivity and -specificity molecular techniques allow for rapid identification of the bacterial etiology (which requires antibiotic therapy) or the viral etiology of meningitis. The latter can be managed only with symptom-specific medications and does not usually require extended hospitalization. Therefore, these new techniques can improve the quality of care for these patients with viral meningitis.
A version of this article first appeared on Medscape.com.
USPSTF final recommendation on aspirin for primary CV prevention
The U.S. Preventive Services Task Force has published a final recommendation statement on aspirin use to prevent cardiovascular disease.
For people aged 40-59 years, the USPSTF suggests that aspirin could be considered in those at increased risk of cardiovascular disease (10-year risk of 10% or greater) but that the decision should be individualized.
It notes that in the 40-59 age group, evidence indicates that the net benefit of aspirin use is small, and that persons who are not at increased risk for bleeding are more likely to benefit.
It adds that these recommendations apply only to people who do not have a history of cardiovascular disease and are not already taking daily aspirin.
The USPSTF statement was published online in the Journal of the American Medical Association. It is accompanied by an evidence review, a modeling study, a patient page, and an editorial.
A draft version of the recommendation statement, evidence review, and modeling report were previously available for public comment. The final recommendation statement is consistent with the draft version.
The task force concludes that there is adequate evidence that low-dose aspirin has a small benefit to reduce risk for cardiovascular events (nonfatal myocardial infarction and stroke) in adults 40 years or older who have no history of cardiovascular disease but are at increased cardiovascular risk.
Evidence shows that the absolute magnitude of benefit increases with increasing 10-year cardiovascular risk and that the magnitude of the lifetime benefits is greater when aspirin is initiated at a younger age.
But it adds that there is also adequate evidence that aspirin use in adults increases the risk for gastrointestinal bleeding, intracranial bleeding, and hemorrhagic stroke. The USPSTF determined that the magnitude of the harms is small overall but increases in older age groups, particularly in adults older than 60 years.
For patients who are eligible and choose to start taking aspirin, the benefits become smaller with advancing age, and data suggest that clinicians and patients should consider stopping aspirin use around age 75 years, the statement advises.
It also says that evidence is unclear whether aspirin use reduces the risk of colorectal cancer incidence or mortality.
USPSTF vice chair Michael Barry, MD, director of the Informed Medical Decisions Program in the Health Decision Sciences Center at Massachusetts General Hospital, Boston, told this news organization that these recommendations apply only to patients not taking aspirin already and who have no evidence of existing cardiovascular disease.
“In adults aged 60 or over we do not recommend starting aspirin for primary prevention. That is because in this age group the risk of bleeding outweighs the cardiovascular benefit,” he said.
“For adults aged 40-59 years with a greater than 10% predicted risk of cardiovascular disease, there appears to be a net benefit from taking aspirin, but this net benefit is relatively small and will vary with other factors such as magnitude of cardiovascular and bleeding risk. People should talk to their physician about these factors and whether to take aspirin or not,” he added.
Dr. Barry noted that these recommendations do not apply to people who are already taking aspirin for primary prevention. “These people need to talk to their physicians about whether they should continue. They need to review the reasons why they started aspirin in the first place, and they need to have their bleeding risk evaluated. Someone who has taken aspirin long term without any bleeding complications has a lower risk of future bleeding complications,” he said.
The task force recommends an aspirin dose of 81 mg daily for those people deciding to take aspirin for primary prevention.
“There is an abundance of evidence that less than 100 mg a day is enough. The lower the dose the lower the bleeding risk. So, the most convenient dose is the widely available 81-mg baby aspirin tablet,” Dr. Barry noted. “While enteric coated products are meant to reduce gastric irritation, the data do not show any difference in bleeding risk between various aspirin formulations,” he added.
Dr. Barry pointed out that aspirin is just one tool for reducing cardiovascular risk.
“People can reduce their risk significantly in many other ways including taking regular exercise, eating a healthy diet, controlling blood pressure and diabetes, and taking statins if they are at increased cardiovascular risk.”
He noted that recent trials have suggested that aspirin has only a marginal value over and above all these other factors. And the risk reduction with aspirin is smaller than with some other interventions.
“For example, aspirin is associated with a 12% reduction in MI whereas statins are associated with a 25%-30% reduction. Statins are a more powerful tool in reducing cardiovascular risk than aspirin, so perhaps people should consider taking statins first. The benefit of aspirin may be smaller in individuals already taking a statin, and clinicians need to think about the big picture,” Dr. Barry said.
He explained that physicians need to evaluate the cardiovascular and bleeding risk in each individual patient. “While there are widely available tools to estimate cardiovascular risk, there are no easy tools yet available to evaluate bleeding risk, so physicians need to consider clinical factors such as history of peptic ulcers.”
He suggests for the many people who have an average bleeding risk, then personal preference may come into play. “In the 40-59 age group, the benefits and harms of aspirin are pretty well-balanced. For the average person we think there may be a small net benefit, but this is small enough for personal preference to be considered as well.”
Pendulum swinging away from aspirin use
In an editorial accompanying publication of the task force statement in JAMA, Allan S. Brett, MD, clinical professor of internal medicine at the University of Colorado at Denver, Aurora, explains that the USPSTF recommendations on aspirin use for primary prevention of cardiovascular disease have changed numerous times over the past 30 years, with the last update in 2016 narrowing the eligible population.
In the new recommendation statement, “the pendulum has swung further away from aspirin prophylaxis for primary prevention: The guideline does not recommend routine preventive aspirin for anyone,” Dr. Brett notes.
He points out that an important development between the 2016 and current version was the publication in 2018 of three large placebo-controlled randomized clinical trials of primary prevention with aspirin – ARRIVE, ASPREE and ASCEND – which taken together “cast doubt about net benefit for aspirin prophylaxis in current practice.”
Asked how physicians should go about “individualizing” the decision on the use of aspirin in the 40-59 age group at increased cardiovascular risk, Dr. Brett suggests that some patents will have a general philosophy of medical care of “don’t prescribe medication for me unless there is strong evidence to support it,” while others may favor preventive interventions even in borderline cases.
But he notes that many patients have no strong general preferences and often ask a trusted clinician to decide for them. “For such patients, the best approach is for clinicians to be knowledgeable about the data on primary prevention with aspirin. Close reading of the new USPSTF guideline and its companion evidence review, and becoming familiar with the three more recent aspirin trials, is a good way to prepare for these clinical encounters,” he concludes.
A cardiologist’s view
Commenting on the task force statement for this news organization, Andrew Freeman, MD, a cardiologist at National Jewish Health, Denver, noted that cardiology societies are already making similar recommendations on aspirin use in primary prevention. “The American College of Cardiology prevention guidelines have been giving similar advice for a couple of years now. It takes a few years for professional societies to catch up with each other,” he said.
“Over the last few years, it has become obvious that the benefit of aspirin is not really very positive until a patient has had a cardiovascular event. In primary prevention, it doesn’t become beneficial unless they are at quite a high risk of having an event,” Dr. Freeman noted.
“In general, most cardiologists are now telling people that, despite what they may have been told in the past, they don’t need to be on aspirin unless they have had a cardiovascular event,” he added. “Our understanding has changed over the years and the weight of evidence has now become clear that the risk of bleeding is not insignificant.”
Dr. Freeman agreed with the shared decision-making advocated for patients in the 40-59 age group. “If a patient is particularly worried about a family history of heart disease, taking aspirin may make some sense, but for most people who have not had a cardiovascular event, the net benefit is very low and gets lower with age as the bleeding risk increases,” he said.
The USPSTF is an independent, voluntary body. The U.S. Congress mandates that the Agency for Healthcare Research and Quality support the operations of the USPSTF.
A version of this article first appeared on Medscape.com.
The U.S. Preventive Services Task Force has published a final recommendation statement on aspirin use to prevent cardiovascular disease.
For people aged 40-59 years, the USPSTF suggests that aspirin could be considered in those at increased risk of cardiovascular disease (10-year risk of 10% or greater) but that the decision should be individualized.
It notes that in the 40-59 age group, evidence indicates that the net benefit of aspirin use is small, and that persons who are not at increased risk for bleeding are more likely to benefit.
It adds that these recommendations apply only to people who do not have a history of cardiovascular disease and are not already taking daily aspirin.
The USPSTF statement was published online in the Journal of the American Medical Association. It is accompanied by an evidence review, a modeling study, a patient page, and an editorial.
A draft version of the recommendation statement, evidence review, and modeling report were previously available for public comment. The final recommendation statement is consistent with the draft version.
The task force concludes that there is adequate evidence that low-dose aspirin has a small benefit to reduce risk for cardiovascular events (nonfatal myocardial infarction and stroke) in adults 40 years or older who have no history of cardiovascular disease but are at increased cardiovascular risk.
Evidence shows that the absolute magnitude of benefit increases with increasing 10-year cardiovascular risk and that the magnitude of the lifetime benefits is greater when aspirin is initiated at a younger age.
But it adds that there is also adequate evidence that aspirin use in adults increases the risk for gastrointestinal bleeding, intracranial bleeding, and hemorrhagic stroke. The USPSTF determined that the magnitude of the harms is small overall but increases in older age groups, particularly in adults older than 60 years.
For patients who are eligible and choose to start taking aspirin, the benefits become smaller with advancing age, and data suggest that clinicians and patients should consider stopping aspirin use around age 75 years, the statement advises.
It also says that evidence is unclear whether aspirin use reduces the risk of colorectal cancer incidence or mortality.
USPSTF vice chair Michael Barry, MD, director of the Informed Medical Decisions Program in the Health Decision Sciences Center at Massachusetts General Hospital, Boston, told this news organization that these recommendations apply only to patients not taking aspirin already and who have no evidence of existing cardiovascular disease.
“In adults aged 60 or over we do not recommend starting aspirin for primary prevention. That is because in this age group the risk of bleeding outweighs the cardiovascular benefit,” he said.
“For adults aged 40-59 years with a greater than 10% predicted risk of cardiovascular disease, there appears to be a net benefit from taking aspirin, but this net benefit is relatively small and will vary with other factors such as magnitude of cardiovascular and bleeding risk. People should talk to their physician about these factors and whether to take aspirin or not,” he added.
Dr. Barry noted that these recommendations do not apply to people who are already taking aspirin for primary prevention. “These people need to talk to their physicians about whether they should continue. They need to review the reasons why they started aspirin in the first place, and they need to have their bleeding risk evaluated. Someone who has taken aspirin long term without any bleeding complications has a lower risk of future bleeding complications,” he said.
The task force recommends an aspirin dose of 81 mg daily for those people deciding to take aspirin for primary prevention.
“There is an abundance of evidence that less than 100 mg a day is enough. The lower the dose the lower the bleeding risk. So, the most convenient dose is the widely available 81-mg baby aspirin tablet,” Dr. Barry noted. “While enteric coated products are meant to reduce gastric irritation, the data do not show any difference in bleeding risk between various aspirin formulations,” he added.
Dr. Barry pointed out that aspirin is just one tool for reducing cardiovascular risk.
“People can reduce their risk significantly in many other ways including taking regular exercise, eating a healthy diet, controlling blood pressure and diabetes, and taking statins if they are at increased cardiovascular risk.”
He noted that recent trials have suggested that aspirin has only a marginal value over and above all these other factors. And the risk reduction with aspirin is smaller than with some other interventions.
“For example, aspirin is associated with a 12% reduction in MI whereas statins are associated with a 25%-30% reduction. Statins are a more powerful tool in reducing cardiovascular risk than aspirin, so perhaps people should consider taking statins first. The benefit of aspirin may be smaller in individuals already taking a statin, and clinicians need to think about the big picture,” Dr. Barry said.
He explained that physicians need to evaluate the cardiovascular and bleeding risk in each individual patient. “While there are widely available tools to estimate cardiovascular risk, there are no easy tools yet available to evaluate bleeding risk, so physicians need to consider clinical factors such as history of peptic ulcers.”
He suggests for the many people who have an average bleeding risk, then personal preference may come into play. “In the 40-59 age group, the benefits and harms of aspirin are pretty well-balanced. For the average person we think there may be a small net benefit, but this is small enough for personal preference to be considered as well.”
Pendulum swinging away from aspirin use
In an editorial accompanying publication of the task force statement in JAMA, Allan S. Brett, MD, clinical professor of internal medicine at the University of Colorado at Denver, Aurora, explains that the USPSTF recommendations on aspirin use for primary prevention of cardiovascular disease have changed numerous times over the past 30 years, with the last update in 2016 narrowing the eligible population.
In the new recommendation statement, “the pendulum has swung further away from aspirin prophylaxis for primary prevention: The guideline does not recommend routine preventive aspirin for anyone,” Dr. Brett notes.
He points out that an important development between the 2016 and current version was the publication in 2018 of three large placebo-controlled randomized clinical trials of primary prevention with aspirin – ARRIVE, ASPREE and ASCEND – which taken together “cast doubt about net benefit for aspirin prophylaxis in current practice.”
Asked how physicians should go about “individualizing” the decision on the use of aspirin in the 40-59 age group at increased cardiovascular risk, Dr. Brett suggests that some patents will have a general philosophy of medical care of “don’t prescribe medication for me unless there is strong evidence to support it,” while others may favor preventive interventions even in borderline cases.
But he notes that many patients have no strong general preferences and often ask a trusted clinician to decide for them. “For such patients, the best approach is for clinicians to be knowledgeable about the data on primary prevention with aspirin. Close reading of the new USPSTF guideline and its companion evidence review, and becoming familiar with the three more recent aspirin trials, is a good way to prepare for these clinical encounters,” he concludes.
A cardiologist’s view
Commenting on the task force statement for this news organization, Andrew Freeman, MD, a cardiologist at National Jewish Health, Denver, noted that cardiology societies are already making similar recommendations on aspirin use in primary prevention. “The American College of Cardiology prevention guidelines have been giving similar advice for a couple of years now. It takes a few years for professional societies to catch up with each other,” he said.
“Over the last few years, it has become obvious that the benefit of aspirin is not really very positive until a patient has had a cardiovascular event. In primary prevention, it doesn’t become beneficial unless they are at quite a high risk of having an event,” Dr. Freeman noted.
“In general, most cardiologists are now telling people that, despite what they may have been told in the past, they don’t need to be on aspirin unless they have had a cardiovascular event,” he added. “Our understanding has changed over the years and the weight of evidence has now become clear that the risk of bleeding is not insignificant.”
Dr. Freeman agreed with the shared decision-making advocated for patients in the 40-59 age group. “If a patient is particularly worried about a family history of heart disease, taking aspirin may make some sense, but for most people who have not had a cardiovascular event, the net benefit is very low and gets lower with age as the bleeding risk increases,” he said.
The USPSTF is an independent, voluntary body. The U.S. Congress mandates that the Agency for Healthcare Research and Quality support the operations of the USPSTF.
A version of this article first appeared on Medscape.com.
The U.S. Preventive Services Task Force has published a final recommendation statement on aspirin use to prevent cardiovascular disease.
For people aged 40-59 years, the USPSTF suggests that aspirin could be considered in those at increased risk of cardiovascular disease (10-year risk of 10% or greater) but that the decision should be individualized.
It notes that in the 40-59 age group, evidence indicates that the net benefit of aspirin use is small, and that persons who are not at increased risk for bleeding are more likely to benefit.
It adds that these recommendations apply only to people who do not have a history of cardiovascular disease and are not already taking daily aspirin.
The USPSTF statement was published online in the Journal of the American Medical Association. It is accompanied by an evidence review, a modeling study, a patient page, and an editorial.
A draft version of the recommendation statement, evidence review, and modeling report were previously available for public comment. The final recommendation statement is consistent with the draft version.
The task force concludes that there is adequate evidence that low-dose aspirin has a small benefit to reduce risk for cardiovascular events (nonfatal myocardial infarction and stroke) in adults 40 years or older who have no history of cardiovascular disease but are at increased cardiovascular risk.
Evidence shows that the absolute magnitude of benefit increases with increasing 10-year cardiovascular risk and that the magnitude of the lifetime benefits is greater when aspirin is initiated at a younger age.
But it adds that there is also adequate evidence that aspirin use in adults increases the risk for gastrointestinal bleeding, intracranial bleeding, and hemorrhagic stroke. The USPSTF determined that the magnitude of the harms is small overall but increases in older age groups, particularly in adults older than 60 years.
For patients who are eligible and choose to start taking aspirin, the benefits become smaller with advancing age, and data suggest that clinicians and patients should consider stopping aspirin use around age 75 years, the statement advises.
It also says that evidence is unclear whether aspirin use reduces the risk of colorectal cancer incidence or mortality.
USPSTF vice chair Michael Barry, MD, director of the Informed Medical Decisions Program in the Health Decision Sciences Center at Massachusetts General Hospital, Boston, told this news organization that these recommendations apply only to patients not taking aspirin already and who have no evidence of existing cardiovascular disease.
“In adults aged 60 or over we do not recommend starting aspirin for primary prevention. That is because in this age group the risk of bleeding outweighs the cardiovascular benefit,” he said.
“For adults aged 40-59 years with a greater than 10% predicted risk of cardiovascular disease, there appears to be a net benefit from taking aspirin, but this net benefit is relatively small and will vary with other factors such as magnitude of cardiovascular and bleeding risk. People should talk to their physician about these factors and whether to take aspirin or not,” he added.
Dr. Barry noted that these recommendations do not apply to people who are already taking aspirin for primary prevention. “These people need to talk to their physicians about whether they should continue. They need to review the reasons why they started aspirin in the first place, and they need to have their bleeding risk evaluated. Someone who has taken aspirin long term without any bleeding complications has a lower risk of future bleeding complications,” he said.
The task force recommends an aspirin dose of 81 mg daily for those people deciding to take aspirin for primary prevention.
“There is an abundance of evidence that less than 100 mg a day is enough. The lower the dose the lower the bleeding risk. So, the most convenient dose is the widely available 81-mg baby aspirin tablet,” Dr. Barry noted. “While enteric coated products are meant to reduce gastric irritation, the data do not show any difference in bleeding risk between various aspirin formulations,” he added.
Dr. Barry pointed out that aspirin is just one tool for reducing cardiovascular risk.
“People can reduce their risk significantly in many other ways including taking regular exercise, eating a healthy diet, controlling blood pressure and diabetes, and taking statins if they are at increased cardiovascular risk.”
He noted that recent trials have suggested that aspirin has only a marginal value over and above all these other factors. And the risk reduction with aspirin is smaller than with some other interventions.
“For example, aspirin is associated with a 12% reduction in MI whereas statins are associated with a 25%-30% reduction. Statins are a more powerful tool in reducing cardiovascular risk than aspirin, so perhaps people should consider taking statins first. The benefit of aspirin may be smaller in individuals already taking a statin, and clinicians need to think about the big picture,” Dr. Barry said.
He explained that physicians need to evaluate the cardiovascular and bleeding risk in each individual patient. “While there are widely available tools to estimate cardiovascular risk, there are no easy tools yet available to evaluate bleeding risk, so physicians need to consider clinical factors such as history of peptic ulcers.”
He suggests for the many people who have an average bleeding risk, then personal preference may come into play. “In the 40-59 age group, the benefits and harms of aspirin are pretty well-balanced. For the average person we think there may be a small net benefit, but this is small enough for personal preference to be considered as well.”
Pendulum swinging away from aspirin use
In an editorial accompanying publication of the task force statement in JAMA, Allan S. Brett, MD, clinical professor of internal medicine at the University of Colorado at Denver, Aurora, explains that the USPSTF recommendations on aspirin use for primary prevention of cardiovascular disease have changed numerous times over the past 30 years, with the last update in 2016 narrowing the eligible population.
In the new recommendation statement, “the pendulum has swung further away from aspirin prophylaxis for primary prevention: The guideline does not recommend routine preventive aspirin for anyone,” Dr. Brett notes.
He points out that an important development between the 2016 and current version was the publication in 2018 of three large placebo-controlled randomized clinical trials of primary prevention with aspirin – ARRIVE, ASPREE and ASCEND – which taken together “cast doubt about net benefit for aspirin prophylaxis in current practice.”
Asked how physicians should go about “individualizing” the decision on the use of aspirin in the 40-59 age group at increased cardiovascular risk, Dr. Brett suggests that some patents will have a general philosophy of medical care of “don’t prescribe medication for me unless there is strong evidence to support it,” while others may favor preventive interventions even in borderline cases.
But he notes that many patients have no strong general preferences and often ask a trusted clinician to decide for them. “For such patients, the best approach is for clinicians to be knowledgeable about the data on primary prevention with aspirin. Close reading of the new USPSTF guideline and its companion evidence review, and becoming familiar with the three more recent aspirin trials, is a good way to prepare for these clinical encounters,” he concludes.
A cardiologist’s view
Commenting on the task force statement for this news organization, Andrew Freeman, MD, a cardiologist at National Jewish Health, Denver, noted that cardiology societies are already making similar recommendations on aspirin use in primary prevention. “The American College of Cardiology prevention guidelines have been giving similar advice for a couple of years now. It takes a few years for professional societies to catch up with each other,” he said.
“Over the last few years, it has become obvious that the benefit of aspirin is not really very positive until a patient has had a cardiovascular event. In primary prevention, it doesn’t become beneficial unless they are at quite a high risk of having an event,” Dr. Freeman noted.
“In general, most cardiologists are now telling people that, despite what they may have been told in the past, they don’t need to be on aspirin unless they have had a cardiovascular event,” he added. “Our understanding has changed over the years and the weight of evidence has now become clear that the risk of bleeding is not insignificant.”
Dr. Freeman agreed with the shared decision-making advocated for patients in the 40-59 age group. “If a patient is particularly worried about a family history of heart disease, taking aspirin may make some sense, but for most people who have not had a cardiovascular event, the net benefit is very low and gets lower with age as the bleeding risk increases,” he said.
The USPSTF is an independent, voluntary body. The U.S. Congress mandates that the Agency for Healthcare Research and Quality support the operations of the USPSTF.
A version of this article first appeared on Medscape.com.
FROM JAMA
Shortage of ICU beds did not drive COVID-19 deaths
Contrary to popular belief, no association appeared between the number of intensive care unit beds and COVID-19 deaths, based on a review of data from all 50 states between March 1, 2020, and June 30, 2021.
One of the reasons for poor patient outcomes in the early months of the COVID-19 pandemic was the presumed scarcity of ICU beds, Omar Haider, MD, of Houston Methodist Hospital, and colleagues said. “We hypothesized that the states having a lower number of ICU beds had more COVID-related deaths when compared to the states that had a higher number of ICU beds,” they wrote in an abstract presented at the Critical Care Congress sponsored by the Society of Critical Care Medicine.
According to the researchers, the total number of ICU beds in the United States is approximately 85,000. Hawaii has the highest number of beds per 10,000 persons, and the District of Columbia has the lowest (6.0 vs. 1.6).
The researchers collected data on ICU bed totals from the Kaiser Family Foundation. Statistics on COVID-19 deaths were obtained from The New York Times database, which provided real-time information collected from the Department of Health & Human Services, the Centers for Disease Control and Prevention, and the Census Bureau.
The researchers used the Pearson Correlation Coefficient to compare ICU beds and COVID deaths per 10,000 persons in each state. The R value was 0.29, which indicates no inverse correlation. “Our value of R2, the coefficient of determination, was 0.0858,” they added. They confirmed the results using the Spearman’s Rho, which yielded an rs of 0.3, also a sign of no inverse correlation. No correlation was found between low numbers of ICU beds and high numbers of COVID-19 deaths for any states.
The study findings were limited by several factors, including the lack of standardized reporting timelines across states, differences in state-based vaccination rates, the emergence of the Delta variant during the study period, and time-lag in contemporaneous database updates, the researchers noted.
However, the results suggest that physical ICU beds do not play a role in determining the number of COVID-related deaths. Instead, “other constraints such as less staffing, lack of medical supplies (ventilators and [personal protective equipment]) should be evaluated for potential implications on poor patients’ outcomes,” they concluded.
Pandemic challenges can inform future plans
“As the health care system emerges from the effects of the pandemic, it is important to understand the factors that contributed to adverse outcomes to better prepare for future challenges and improve the delivery of care,” Suman Pal, MBBS, of the University of New Mexico, Albuquerque, said in an interview.
“The findings are not surprising considering what is known about the multitude of factors that determine outcomes for our patients from medical comorbidities, and social determinants of health to upstream structural factors such as systemic inequities and generational trauma,” said Dr. Pal, who was not involved with the study. “Thus, a simple correlation of the number of ICU beds to COVID-19 outcomes is not likely to capture the interplay of all these factors.”
The challenges of the pandemic offer insights to inform future planning, said Dr. Pal.
“In my opinion, a key factor to understand and address would be employee wellness for health care workers,” he said. “The problem of burnout leading to health care workers leaving the workforce has exacerbated the already acute shortages in personnel in recent years.
“In the long term, it may be prudent to reconsider the approach to health by increasing support for preventative and primary care, addressing social factors such as education, nutrition, and housing, to mitigate preventable aspects of diseases.”
Further research is needed to examine the multitude of factors associated with the pandemic, and their interplay, said Dr. Pal. The goals of such research “would be needed to develop a deeper understanding of the factors that contributed to mortality in COVID-19 and the disparities with this across different subpopulations.”
The study received no outside funding. The researchers and Dr. Pal disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Contrary to popular belief, no association appeared between the number of intensive care unit beds and COVID-19 deaths, based on a review of data from all 50 states between March 1, 2020, and June 30, 2021.
One of the reasons for poor patient outcomes in the early months of the COVID-19 pandemic was the presumed scarcity of ICU beds, Omar Haider, MD, of Houston Methodist Hospital, and colleagues said. “We hypothesized that the states having a lower number of ICU beds had more COVID-related deaths when compared to the states that had a higher number of ICU beds,” they wrote in an abstract presented at the Critical Care Congress sponsored by the Society of Critical Care Medicine.
According to the researchers, the total number of ICU beds in the United States is approximately 85,000. Hawaii has the highest number of beds per 10,000 persons, and the District of Columbia has the lowest (6.0 vs. 1.6).
The researchers collected data on ICU bed totals from the Kaiser Family Foundation. Statistics on COVID-19 deaths were obtained from The New York Times database, which provided real-time information collected from the Department of Health & Human Services, the Centers for Disease Control and Prevention, and the Census Bureau.
The researchers used the Pearson Correlation Coefficient to compare ICU beds and COVID deaths per 10,000 persons in each state. The R value was 0.29, which indicates no inverse correlation. “Our value of R2, the coefficient of determination, was 0.0858,” they added. They confirmed the results using the Spearman’s Rho, which yielded an rs of 0.3, also a sign of no inverse correlation. No correlation was found between low numbers of ICU beds and high numbers of COVID-19 deaths for any states.
The study findings were limited by several factors, including the lack of standardized reporting timelines across states, differences in state-based vaccination rates, the emergence of the Delta variant during the study period, and time-lag in contemporaneous database updates, the researchers noted.
However, the results suggest that physical ICU beds do not play a role in determining the number of COVID-related deaths. Instead, “other constraints such as less staffing, lack of medical supplies (ventilators and [personal protective equipment]) should be evaluated for potential implications on poor patients’ outcomes,” they concluded.
Pandemic challenges can inform future plans
“As the health care system emerges from the effects of the pandemic, it is important to understand the factors that contributed to adverse outcomes to better prepare for future challenges and improve the delivery of care,” Suman Pal, MBBS, of the University of New Mexico, Albuquerque, said in an interview.
“The findings are not surprising considering what is known about the multitude of factors that determine outcomes for our patients from medical comorbidities, and social determinants of health to upstream structural factors such as systemic inequities and generational trauma,” said Dr. Pal, who was not involved with the study. “Thus, a simple correlation of the number of ICU beds to COVID-19 outcomes is not likely to capture the interplay of all these factors.”
The challenges of the pandemic offer insights to inform future planning, said Dr. Pal.
“In my opinion, a key factor to understand and address would be employee wellness for health care workers,” he said. “The problem of burnout leading to health care workers leaving the workforce has exacerbated the already acute shortages in personnel in recent years.
“In the long term, it may be prudent to reconsider the approach to health by increasing support for preventative and primary care, addressing social factors such as education, nutrition, and housing, to mitigate preventable aspects of diseases.”
Further research is needed to examine the multitude of factors associated with the pandemic, and their interplay, said Dr. Pal. The goals of such research “would be needed to develop a deeper understanding of the factors that contributed to mortality in COVID-19 and the disparities with this across different subpopulations.”
The study received no outside funding. The researchers and Dr. Pal disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Contrary to popular belief, no association appeared between the number of intensive care unit beds and COVID-19 deaths, based on a review of data from all 50 states between March 1, 2020, and June 30, 2021.
One of the reasons for poor patient outcomes in the early months of the COVID-19 pandemic was the presumed scarcity of ICU beds, Omar Haider, MD, of Houston Methodist Hospital, and colleagues said. “We hypothesized that the states having a lower number of ICU beds had more COVID-related deaths when compared to the states that had a higher number of ICU beds,” they wrote in an abstract presented at the Critical Care Congress sponsored by the Society of Critical Care Medicine.
According to the researchers, the total number of ICU beds in the United States is approximately 85,000. Hawaii has the highest number of beds per 10,000 persons, and the District of Columbia has the lowest (6.0 vs. 1.6).
The researchers collected data on ICU bed totals from the Kaiser Family Foundation. Statistics on COVID-19 deaths were obtained from The New York Times database, which provided real-time information collected from the Department of Health & Human Services, the Centers for Disease Control and Prevention, and the Census Bureau.
The researchers used the Pearson Correlation Coefficient to compare ICU beds and COVID deaths per 10,000 persons in each state. The R value was 0.29, which indicates no inverse correlation. “Our value of R2, the coefficient of determination, was 0.0858,” they added. They confirmed the results using the Spearman’s Rho, which yielded an rs of 0.3, also a sign of no inverse correlation. No correlation was found between low numbers of ICU beds and high numbers of COVID-19 deaths for any states.
The study findings were limited by several factors, including the lack of standardized reporting timelines across states, differences in state-based vaccination rates, the emergence of the Delta variant during the study period, and time-lag in contemporaneous database updates, the researchers noted.
However, the results suggest that physical ICU beds do not play a role in determining the number of COVID-related deaths. Instead, “other constraints such as less staffing, lack of medical supplies (ventilators and [personal protective equipment]) should be evaluated for potential implications on poor patients’ outcomes,” they concluded.
Pandemic challenges can inform future plans
“As the health care system emerges from the effects of the pandemic, it is important to understand the factors that contributed to adverse outcomes to better prepare for future challenges and improve the delivery of care,” Suman Pal, MBBS, of the University of New Mexico, Albuquerque, said in an interview.
“The findings are not surprising considering what is known about the multitude of factors that determine outcomes for our patients from medical comorbidities, and social determinants of health to upstream structural factors such as systemic inequities and generational trauma,” said Dr. Pal, who was not involved with the study. “Thus, a simple correlation of the number of ICU beds to COVID-19 outcomes is not likely to capture the interplay of all these factors.”
The challenges of the pandemic offer insights to inform future planning, said Dr. Pal.
“In my opinion, a key factor to understand and address would be employee wellness for health care workers,” he said. “The problem of burnout leading to health care workers leaving the workforce has exacerbated the already acute shortages in personnel in recent years.
“In the long term, it may be prudent to reconsider the approach to health by increasing support for preventative and primary care, addressing social factors such as education, nutrition, and housing, to mitigate preventable aspects of diseases.”
Further research is needed to examine the multitude of factors associated with the pandemic, and their interplay, said Dr. Pal. The goals of such research “would be needed to develop a deeper understanding of the factors that contributed to mortality in COVID-19 and the disparities with this across different subpopulations.”
The study received no outside funding. The researchers and Dr. Pal disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Antidepressant study yields controversial findings
Researchers who conducted the study admit this finding was unexpected, and outside experts say no firm conclusions can be drawn from the research.
“Of course we were surprised by the results,” first author Omar Almohammed, PharmD, PhD, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia, told this news organization.
“We were expecting to see some positive impact with the use of antidepressant medications on the HRQoL measures when we compared these patients to patients that did not use antidepressant medications,” Dr. Almohammed said.
The study was published online in PLOS ONE.
Controversial impact on quality of life
Depression is known to harm HRQoL. Despite evidence that antidepressants improve depressed mood, their effect on patients’ overall well-being and HRQoL remains controversial.
The researchers examined the effect of antidepressants on HRQoL in adults with depression using 11 years of data from the U.S. Medical Expenditures Panel Survey (MEPS), a large longitudinal survey that tracks health service use in the United States. HRQoL was measured using the 12-item Short Form Health Survey (SF-12).
On average, about 17.5 million adults were diagnosed with depression each year during the study period (2005-2016). More than half (57.6%) of these patients were treated with antidepressants.
Patients with depression had an average age of 48.3 years. Women made up more than two-thirds of the total sample (68%), and more women than men received antidepressants (61% vs. 52%).
Compared with no antidepressant use, antidepressant use was associated with some improvement on the mental, but not physical, component of the SF-12, the researchers report.
However, difference-in-differences (D-I-D) univariate analysis showed no significant difference between adults using and not using antidepressants in the SF-12 physical (-0.35 vs. -0.34; P = .9,595) or mental component (1.28 vs. 1.13; P = .6,405).
“The multivariate D-I-D analyses ensured the robustness of these results,” the researchers note.
The change in HRQoL observed in patients using antidepressants was not significantly different from that seen among peers not using these drugs, the researchers report.
“We are not saying that antidepressant medications are not helpful at all; HRQoL is only one of many measures intended to assess health outcomes,” Dr. Almohammed told this news organization.
“Based on our research design and data, we can only say that patients who used antidepressant medications did not experience better change in terms of HRQoL compared to patients who did not use antidepressant medications,” he said.
“These patients may have had some improvement on other clinical outcome measures, but that clinical improvement did not have a significant positive impact on HRQoL,” he noted.
“We still recommend that patients continue using their antidepressant medications, but they may want to ask their doctors to provide them with other nonpharmacologic interventions as this may have additional impact on their HRQoL,” Dr. Almohammed said.
Further research is needed to address a “gap in knowledge” about the impact of nondrug interventions – alone or in combination with antidepressant medications – on patients’ HRQoL, Dr. Almohammed added.
Experts weigh in
Several experts weighed in on the study in a statement from the British nonprofit Science Media Center.
Gemma Lewis, PhD, with University College London (UCL), noted that “clinical trials with experimental designs have found that antidepressants improve mental health-related quality of life.”
“In this study, the people who received antidepressants had worse quality of life, and are likely to have been more severely depressed, than those who did not. This type of bias is difficult to eliminate in a naturalistic study like this, which does not involve an experimental design,” Dr. Lewis commented.
Eduard Vieta, PhD, with University of Barcelona, noted the “inability to control for severity of depression between the two different groups is a crucial flaw, and therefore, there is little we can learn from this data.”
Echoing Dr. Vieta, David Curtis, MBBS, MD, PhD, with UCL Genetics Institute, said, “One might well assume that the people who were taking antidepressants had been more severely depressed than those who were not.”
“From this point of view, one could argue that it seems that the antidepressants were effective and that with their use people who had presented with more severe depression did not have markedly reduced quality of life,” Dr. Curtis said.
“However, the reality is that this kind of observational study tells us nothing about causation. For that, clinical trials are required, and numerous such trials have demonstrated that, on average, antidepressants are effective in terms of treating depressive illness and in improving the quality of life of patients with significant depression,” he added.
Michael Sharpe, MD, with University of Oxford, said the study highlights the importance of measuring the long-term outcomes of treatments for depression. “However, this study has no clear implication for the care of patients with depression and certainly should not discourage patients who may benefit from taking these drugs.”
Livia de Picker, MD, PhD, with University of Antwerp, Belgium, said, “What these data do point towards is the persistent treatment gap for depression in the United States, with only 57.6% of patients with major depressive disorder receiving treatment with antidepressants over a 2-year follow-up.”
Funding for the study was provided by King Saud University, Riyadh, Saudi Arabia. Dr. Almohammed, Dr. de Picker, Dr. Curtis, Dr. Lewis, and Dr. Sharpe have disclosed no relevant financial relationships. Dr. Vieta has participated in clinical trials of antidepressants and advisory boards for Angelini, Biogen, Janssen, and Lundbeck.
A version of this article first appeared on Medscape.com.
Researchers who conducted the study admit this finding was unexpected, and outside experts say no firm conclusions can be drawn from the research.
“Of course we were surprised by the results,” first author Omar Almohammed, PharmD, PhD, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia, told this news organization.
“We were expecting to see some positive impact with the use of antidepressant medications on the HRQoL measures when we compared these patients to patients that did not use antidepressant medications,” Dr. Almohammed said.
The study was published online in PLOS ONE.
Controversial impact on quality of life
Depression is known to harm HRQoL. Despite evidence that antidepressants improve depressed mood, their effect on patients’ overall well-being and HRQoL remains controversial.
The researchers examined the effect of antidepressants on HRQoL in adults with depression using 11 years of data from the U.S. Medical Expenditures Panel Survey (MEPS), a large longitudinal survey that tracks health service use in the United States. HRQoL was measured using the 12-item Short Form Health Survey (SF-12).
On average, about 17.5 million adults were diagnosed with depression each year during the study period (2005-2016). More than half (57.6%) of these patients were treated with antidepressants.
Patients with depression had an average age of 48.3 years. Women made up more than two-thirds of the total sample (68%), and more women than men received antidepressants (61% vs. 52%).
Compared with no antidepressant use, antidepressant use was associated with some improvement on the mental, but not physical, component of the SF-12, the researchers report.
However, difference-in-differences (D-I-D) univariate analysis showed no significant difference between adults using and not using antidepressants in the SF-12 physical (-0.35 vs. -0.34; P = .9,595) or mental component (1.28 vs. 1.13; P = .6,405).
“The multivariate D-I-D analyses ensured the robustness of these results,” the researchers note.
The change in HRQoL observed in patients using antidepressants was not significantly different from that seen among peers not using these drugs, the researchers report.
“We are not saying that antidepressant medications are not helpful at all; HRQoL is only one of many measures intended to assess health outcomes,” Dr. Almohammed told this news organization.
“Based on our research design and data, we can only say that patients who used antidepressant medications did not experience better change in terms of HRQoL compared to patients who did not use antidepressant medications,” he said.
“These patients may have had some improvement on other clinical outcome measures, but that clinical improvement did not have a significant positive impact on HRQoL,” he noted.
“We still recommend that patients continue using their antidepressant medications, but they may want to ask their doctors to provide them with other nonpharmacologic interventions as this may have additional impact on their HRQoL,” Dr. Almohammed said.
Further research is needed to address a “gap in knowledge” about the impact of nondrug interventions – alone or in combination with antidepressant medications – on patients’ HRQoL, Dr. Almohammed added.
Experts weigh in
Several experts weighed in on the study in a statement from the British nonprofit Science Media Center.
Gemma Lewis, PhD, with University College London (UCL), noted that “clinical trials with experimental designs have found that antidepressants improve mental health-related quality of life.”
“In this study, the people who received antidepressants had worse quality of life, and are likely to have been more severely depressed, than those who did not. This type of bias is difficult to eliminate in a naturalistic study like this, which does not involve an experimental design,” Dr. Lewis commented.
Eduard Vieta, PhD, with University of Barcelona, noted the “inability to control for severity of depression between the two different groups is a crucial flaw, and therefore, there is little we can learn from this data.”
Echoing Dr. Vieta, David Curtis, MBBS, MD, PhD, with UCL Genetics Institute, said, “One might well assume that the people who were taking antidepressants had been more severely depressed than those who were not.”
“From this point of view, one could argue that it seems that the antidepressants were effective and that with their use people who had presented with more severe depression did not have markedly reduced quality of life,” Dr. Curtis said.
“However, the reality is that this kind of observational study tells us nothing about causation. For that, clinical trials are required, and numerous such trials have demonstrated that, on average, antidepressants are effective in terms of treating depressive illness and in improving the quality of life of patients with significant depression,” he added.
Michael Sharpe, MD, with University of Oxford, said the study highlights the importance of measuring the long-term outcomes of treatments for depression. “However, this study has no clear implication for the care of patients with depression and certainly should not discourage patients who may benefit from taking these drugs.”
Livia de Picker, MD, PhD, with University of Antwerp, Belgium, said, “What these data do point towards is the persistent treatment gap for depression in the United States, with only 57.6% of patients with major depressive disorder receiving treatment with antidepressants over a 2-year follow-up.”
Funding for the study was provided by King Saud University, Riyadh, Saudi Arabia. Dr. Almohammed, Dr. de Picker, Dr. Curtis, Dr. Lewis, and Dr. Sharpe have disclosed no relevant financial relationships. Dr. Vieta has participated in clinical trials of antidepressants and advisory boards for Angelini, Biogen, Janssen, and Lundbeck.
A version of this article first appeared on Medscape.com.
Researchers who conducted the study admit this finding was unexpected, and outside experts say no firm conclusions can be drawn from the research.
“Of course we were surprised by the results,” first author Omar Almohammed, PharmD, PhD, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia, told this news organization.
“We were expecting to see some positive impact with the use of antidepressant medications on the HRQoL measures when we compared these patients to patients that did not use antidepressant medications,” Dr. Almohammed said.
The study was published online in PLOS ONE.
Controversial impact on quality of life
Depression is known to harm HRQoL. Despite evidence that antidepressants improve depressed mood, their effect on patients’ overall well-being and HRQoL remains controversial.
The researchers examined the effect of antidepressants on HRQoL in adults with depression using 11 years of data from the U.S. Medical Expenditures Panel Survey (MEPS), a large longitudinal survey that tracks health service use in the United States. HRQoL was measured using the 12-item Short Form Health Survey (SF-12).
On average, about 17.5 million adults were diagnosed with depression each year during the study period (2005-2016). More than half (57.6%) of these patients were treated with antidepressants.
Patients with depression had an average age of 48.3 years. Women made up more than two-thirds of the total sample (68%), and more women than men received antidepressants (61% vs. 52%).
Compared with no antidepressant use, antidepressant use was associated with some improvement on the mental, but not physical, component of the SF-12, the researchers report.
However, difference-in-differences (D-I-D) univariate analysis showed no significant difference between adults using and not using antidepressants in the SF-12 physical (-0.35 vs. -0.34; P = .9,595) or mental component (1.28 vs. 1.13; P = .6,405).
“The multivariate D-I-D analyses ensured the robustness of these results,” the researchers note.
The change in HRQoL observed in patients using antidepressants was not significantly different from that seen among peers not using these drugs, the researchers report.
“We are not saying that antidepressant medications are not helpful at all; HRQoL is only one of many measures intended to assess health outcomes,” Dr. Almohammed told this news organization.
“Based on our research design and data, we can only say that patients who used antidepressant medications did not experience better change in terms of HRQoL compared to patients who did not use antidepressant medications,” he said.
“These patients may have had some improvement on other clinical outcome measures, but that clinical improvement did not have a significant positive impact on HRQoL,” he noted.
“We still recommend that patients continue using their antidepressant medications, but they may want to ask their doctors to provide them with other nonpharmacologic interventions as this may have additional impact on their HRQoL,” Dr. Almohammed said.
Further research is needed to address a “gap in knowledge” about the impact of nondrug interventions – alone or in combination with antidepressant medications – on patients’ HRQoL, Dr. Almohammed added.
Experts weigh in
Several experts weighed in on the study in a statement from the British nonprofit Science Media Center.
Gemma Lewis, PhD, with University College London (UCL), noted that “clinical trials with experimental designs have found that antidepressants improve mental health-related quality of life.”
“In this study, the people who received antidepressants had worse quality of life, and are likely to have been more severely depressed, than those who did not. This type of bias is difficult to eliminate in a naturalistic study like this, which does not involve an experimental design,” Dr. Lewis commented.
Eduard Vieta, PhD, with University of Barcelona, noted the “inability to control for severity of depression between the two different groups is a crucial flaw, and therefore, there is little we can learn from this data.”
Echoing Dr. Vieta, David Curtis, MBBS, MD, PhD, with UCL Genetics Institute, said, “One might well assume that the people who were taking antidepressants had been more severely depressed than those who were not.”
“From this point of view, one could argue that it seems that the antidepressants were effective and that with their use people who had presented with more severe depression did not have markedly reduced quality of life,” Dr. Curtis said.
“However, the reality is that this kind of observational study tells us nothing about causation. For that, clinical trials are required, and numerous such trials have demonstrated that, on average, antidepressants are effective in terms of treating depressive illness and in improving the quality of life of patients with significant depression,” he added.
Michael Sharpe, MD, with University of Oxford, said the study highlights the importance of measuring the long-term outcomes of treatments for depression. “However, this study has no clear implication for the care of patients with depression and certainly should not discourage patients who may benefit from taking these drugs.”
Livia de Picker, MD, PhD, with University of Antwerp, Belgium, said, “What these data do point towards is the persistent treatment gap for depression in the United States, with only 57.6% of patients with major depressive disorder receiving treatment with antidepressants over a 2-year follow-up.”
Funding for the study was provided by King Saud University, Riyadh, Saudi Arabia. Dr. Almohammed, Dr. de Picker, Dr. Curtis, Dr. Lewis, and Dr. Sharpe have disclosed no relevant financial relationships. Dr. Vieta has participated in clinical trials of antidepressants and advisory boards for Angelini, Biogen, Janssen, and Lundbeck.
A version of this article first appeared on Medscape.com.
Polypharmacy common among patients aged 65 or older with HIV
People aged 65 or older with human immunodeficiency virus (HIV) receive significantly more nonantiretroviral therapy (non-ART) medications, compared with patients with HIV who are between ages 50 and 64, according to a new study.
Moreover, in a sample of more than 900 patients with HIV, about 60% were taking at least one potentially inappropriate medication (PIM).
“Clinicians looking after persons living with HIV need to provide medication reconciliation with prioritization of medications based on the patients’ wishes and patients’ goals and life expectancy,” lead author Jacqueline McMillan, MD, clinical assistant professor of geriatric medicine at the University of Calgary (Alt.) told this news organization.
The findings were published online in the Canadian Journal of General Internal Medicine.
Examining the pill burden
A geriatrician by training and a clinical researcher with an interest in aging in patients with HIV, Dr. McMillan said she began to observe that many older adults with HIV were on polypharmacy. “There are many other things that aging people with HIV experience, such as frailty, falls, cognitive impairment, medication nonadherence, and mortality, but in this study, we focused just on the polypharmacy,” said Dr. McMillan.
Her aim was to see if there was a way to improve the pill burden in these older adults.
“Do they need to be on all of these medications? Is there anything that we were overprescribing that they no longer needed, or possibly not prescribing and undertreating people because they were older? I wanted to have a better sense that the medications we were prescribing were appropriate and that we minimized the pill burden for older adults,” Dr. McMillan said.
Persons with HIV are at a particularly increased risk of polypharmacy and potential drug-drug interactions because they need antiretroviral therapy medications and medications to treat comorbidities.
“Certainly, when the ARTs were first discovered, sometimes that regimen required several pills a day, but as time has gone on and our retrovirals have gotten better, some of those requirements have narrowed down to one-pill-a-day regimens. We are now replacing that pill burden with non-HIV drugs,” said Dr. McMillan.
The researchers obtained medication reconciliation data for 951 persons with HIV aged 50 or older as of Feb. 1, 2020. The study population was receiving HIV care through the Southern Alberta HIV Clinic in Calgary. The researchers defined polypharmacy as taking five or more non-ART drugs. They defined PIMs according to the 2019 Beers criteria.
In their analysis, the researchers compared patients aged 65 or older with patients aged 50-64, as well as patients with shorter (< 10 years) and longer (> 10 years) duration of HIV infection.
PIM use common
The population’s mean age was 59 years, and 82% were men. The mean time since HIV diagnosis was 17.8 years, and the median time was 17 years. Most (80%) of the patients were aged 50-64 years, and 20% were 65 and older.
The researchers collected sociodemographic, clinical, medication, and laboratory data for all patients at each clinical visit.
The mean number of non-ART medications was 6.7 for the population. Patients aged 65 years or older were taking significantly more non-ART medications than patients aged 50-64 (8.4 vs. 6.3; P < .001).
Similarly, those living with HIV for more than 10 years were taking significantly more non-ART medications (mean, 6.9) than those living with HIV for 10 or fewer years (mean 6.1; P = .0168).
In all, almost 60% of patients were taking at least one PIM. The mean number of PIMs per patient was 1.6.
Patients living with diagnosed HIV infection for more than 10 years were at greater risk of PIMs (1.6 PIMs) than those with shorter duration of HIV diagnosis (1.4 PIMs; P = .06).
Dr. McMillan says she hopes her study reminds clinicians to review patients’ medications at each visit and ensure they are neither over- nor underprescribing.
“From my perspective as a geriatrician, I hope that we do more dedicated medication reconciliation to actually make sure we know what people are taking,” she said. She asks patients to bring all their medications to the office so that they can review which ones match their diagnoses.
“I want to do more patient-centered personalized care for older adults, with a focus on people who are frail and who may have a limited life expectancy, so that we don’t have someone with a short life expectancy still taking 15 medications a day,” said Dr. McMillan.
‘Carefully document medications’
“This study identifies potentially inappropriate medication use in a group of older people living with HIV who are particularly vulnerable to it at an earlier age because of their medical complexity or frailty than perhaps healthy older adults,” Adrian Wagg, MD, professor of healthy aging in the department of medicine at the University of Alberta, Edmonton, told this news organization.
The study emphasizes the importance of careful documentation of medications that the patient is taking at every clinical visit, he said.
“Make sure you carefully document medications which are taken whenever you see the individual. Also try to limit the number of prescribers, because we know multiple prescribers are associated with greater likelihood of inappropriate prescribing,” Dr. Wagg said.
The move to wean patients from inappropriate medications is gaining momentum, he added.
“There is a huge movement now around actively deprescribing medications which are either no longer indicated or potentially of little benefit, given remaining life expectancy,” said Dr. Wagg. Drugs such as proton pump inhibitors, hypnotics, unrequired antidepressants, and benzodiazepines are the first targets for elimination, he concluded.
The study was funded by the University of Calgary. Dr. McMillan and Dr. Wagg reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
People aged 65 or older with human immunodeficiency virus (HIV) receive significantly more nonantiretroviral therapy (non-ART) medications, compared with patients with HIV who are between ages 50 and 64, according to a new study.
Moreover, in a sample of more than 900 patients with HIV, about 60% were taking at least one potentially inappropriate medication (PIM).
“Clinicians looking after persons living with HIV need to provide medication reconciliation with prioritization of medications based on the patients’ wishes and patients’ goals and life expectancy,” lead author Jacqueline McMillan, MD, clinical assistant professor of geriatric medicine at the University of Calgary (Alt.) told this news organization.
The findings were published online in the Canadian Journal of General Internal Medicine.
Examining the pill burden
A geriatrician by training and a clinical researcher with an interest in aging in patients with HIV, Dr. McMillan said she began to observe that many older adults with HIV were on polypharmacy. “There are many other things that aging people with HIV experience, such as frailty, falls, cognitive impairment, medication nonadherence, and mortality, but in this study, we focused just on the polypharmacy,” said Dr. McMillan.
Her aim was to see if there was a way to improve the pill burden in these older adults.
“Do they need to be on all of these medications? Is there anything that we were overprescribing that they no longer needed, or possibly not prescribing and undertreating people because they were older? I wanted to have a better sense that the medications we were prescribing were appropriate and that we minimized the pill burden for older adults,” Dr. McMillan said.
Persons with HIV are at a particularly increased risk of polypharmacy and potential drug-drug interactions because they need antiretroviral therapy medications and medications to treat comorbidities.
“Certainly, when the ARTs were first discovered, sometimes that regimen required several pills a day, but as time has gone on and our retrovirals have gotten better, some of those requirements have narrowed down to one-pill-a-day regimens. We are now replacing that pill burden with non-HIV drugs,” said Dr. McMillan.
The researchers obtained medication reconciliation data for 951 persons with HIV aged 50 or older as of Feb. 1, 2020. The study population was receiving HIV care through the Southern Alberta HIV Clinic in Calgary. The researchers defined polypharmacy as taking five or more non-ART drugs. They defined PIMs according to the 2019 Beers criteria.
In their analysis, the researchers compared patients aged 65 or older with patients aged 50-64, as well as patients with shorter (< 10 years) and longer (> 10 years) duration of HIV infection.
PIM use common
The population’s mean age was 59 years, and 82% were men. The mean time since HIV diagnosis was 17.8 years, and the median time was 17 years. Most (80%) of the patients were aged 50-64 years, and 20% were 65 and older.
The researchers collected sociodemographic, clinical, medication, and laboratory data for all patients at each clinical visit.
The mean number of non-ART medications was 6.7 for the population. Patients aged 65 years or older were taking significantly more non-ART medications than patients aged 50-64 (8.4 vs. 6.3; P < .001).
Similarly, those living with HIV for more than 10 years were taking significantly more non-ART medications (mean, 6.9) than those living with HIV for 10 or fewer years (mean 6.1; P = .0168).
In all, almost 60% of patients were taking at least one PIM. The mean number of PIMs per patient was 1.6.
Patients living with diagnosed HIV infection for more than 10 years were at greater risk of PIMs (1.6 PIMs) than those with shorter duration of HIV diagnosis (1.4 PIMs; P = .06).
Dr. McMillan says she hopes her study reminds clinicians to review patients’ medications at each visit and ensure they are neither over- nor underprescribing.
“From my perspective as a geriatrician, I hope that we do more dedicated medication reconciliation to actually make sure we know what people are taking,” she said. She asks patients to bring all their medications to the office so that they can review which ones match their diagnoses.
“I want to do more patient-centered personalized care for older adults, with a focus on people who are frail and who may have a limited life expectancy, so that we don’t have someone with a short life expectancy still taking 15 medications a day,” said Dr. McMillan.
‘Carefully document medications’
“This study identifies potentially inappropriate medication use in a group of older people living with HIV who are particularly vulnerable to it at an earlier age because of their medical complexity or frailty than perhaps healthy older adults,” Adrian Wagg, MD, professor of healthy aging in the department of medicine at the University of Alberta, Edmonton, told this news organization.
The study emphasizes the importance of careful documentation of medications that the patient is taking at every clinical visit, he said.
“Make sure you carefully document medications which are taken whenever you see the individual. Also try to limit the number of prescribers, because we know multiple prescribers are associated with greater likelihood of inappropriate prescribing,” Dr. Wagg said.
The move to wean patients from inappropriate medications is gaining momentum, he added.
“There is a huge movement now around actively deprescribing medications which are either no longer indicated or potentially of little benefit, given remaining life expectancy,” said Dr. Wagg. Drugs such as proton pump inhibitors, hypnotics, unrequired antidepressants, and benzodiazepines are the first targets for elimination, he concluded.
The study was funded by the University of Calgary. Dr. McMillan and Dr. Wagg reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
People aged 65 or older with human immunodeficiency virus (HIV) receive significantly more nonantiretroviral therapy (non-ART) medications, compared with patients with HIV who are between ages 50 and 64, according to a new study.
Moreover, in a sample of more than 900 patients with HIV, about 60% were taking at least one potentially inappropriate medication (PIM).
“Clinicians looking after persons living with HIV need to provide medication reconciliation with prioritization of medications based on the patients’ wishes and patients’ goals and life expectancy,” lead author Jacqueline McMillan, MD, clinical assistant professor of geriatric medicine at the University of Calgary (Alt.) told this news organization.
The findings were published online in the Canadian Journal of General Internal Medicine.
Examining the pill burden
A geriatrician by training and a clinical researcher with an interest in aging in patients with HIV, Dr. McMillan said she began to observe that many older adults with HIV were on polypharmacy. “There are many other things that aging people with HIV experience, such as frailty, falls, cognitive impairment, medication nonadherence, and mortality, but in this study, we focused just on the polypharmacy,” said Dr. McMillan.
Her aim was to see if there was a way to improve the pill burden in these older adults.
“Do they need to be on all of these medications? Is there anything that we were overprescribing that they no longer needed, or possibly not prescribing and undertreating people because they were older? I wanted to have a better sense that the medications we were prescribing were appropriate and that we minimized the pill burden for older adults,” Dr. McMillan said.
Persons with HIV are at a particularly increased risk of polypharmacy and potential drug-drug interactions because they need antiretroviral therapy medications and medications to treat comorbidities.
“Certainly, when the ARTs were first discovered, sometimes that regimen required several pills a day, but as time has gone on and our retrovirals have gotten better, some of those requirements have narrowed down to one-pill-a-day regimens. We are now replacing that pill burden with non-HIV drugs,” said Dr. McMillan.
The researchers obtained medication reconciliation data for 951 persons with HIV aged 50 or older as of Feb. 1, 2020. The study population was receiving HIV care through the Southern Alberta HIV Clinic in Calgary. The researchers defined polypharmacy as taking five or more non-ART drugs. They defined PIMs according to the 2019 Beers criteria.
In their analysis, the researchers compared patients aged 65 or older with patients aged 50-64, as well as patients with shorter (< 10 years) and longer (> 10 years) duration of HIV infection.
PIM use common
The population’s mean age was 59 years, and 82% were men. The mean time since HIV diagnosis was 17.8 years, and the median time was 17 years. Most (80%) of the patients were aged 50-64 years, and 20% were 65 and older.
The researchers collected sociodemographic, clinical, medication, and laboratory data for all patients at each clinical visit.
The mean number of non-ART medications was 6.7 for the population. Patients aged 65 years or older were taking significantly more non-ART medications than patients aged 50-64 (8.4 vs. 6.3; P < .001).
Similarly, those living with HIV for more than 10 years were taking significantly more non-ART medications (mean, 6.9) than those living with HIV for 10 or fewer years (mean 6.1; P = .0168).
In all, almost 60% of patients were taking at least one PIM. The mean number of PIMs per patient was 1.6.
Patients living with diagnosed HIV infection for more than 10 years were at greater risk of PIMs (1.6 PIMs) than those with shorter duration of HIV diagnosis (1.4 PIMs; P = .06).
Dr. McMillan says she hopes her study reminds clinicians to review patients’ medications at each visit and ensure they are neither over- nor underprescribing.
“From my perspective as a geriatrician, I hope that we do more dedicated medication reconciliation to actually make sure we know what people are taking,” she said. She asks patients to bring all their medications to the office so that they can review which ones match their diagnoses.
“I want to do more patient-centered personalized care for older adults, with a focus on people who are frail and who may have a limited life expectancy, so that we don’t have someone with a short life expectancy still taking 15 medications a day,” said Dr. McMillan.
‘Carefully document medications’
“This study identifies potentially inappropriate medication use in a group of older people living with HIV who are particularly vulnerable to it at an earlier age because of their medical complexity or frailty than perhaps healthy older adults,” Adrian Wagg, MD, professor of healthy aging in the department of medicine at the University of Alberta, Edmonton, told this news organization.
The study emphasizes the importance of careful documentation of medications that the patient is taking at every clinical visit, he said.
“Make sure you carefully document medications which are taken whenever you see the individual. Also try to limit the number of prescribers, because we know multiple prescribers are associated with greater likelihood of inappropriate prescribing,” Dr. Wagg said.
The move to wean patients from inappropriate medications is gaining momentum, he added.
“There is a huge movement now around actively deprescribing medications which are either no longer indicated or potentially of little benefit, given remaining life expectancy,” said Dr. Wagg. Drugs such as proton pump inhibitors, hypnotics, unrequired antidepressants, and benzodiazepines are the first targets for elimination, he concluded.
The study was funded by the University of Calgary. Dr. McMillan and Dr. Wagg reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE CANADIAN JOURNAL OF GENERAL INTERNAL MEDICINE
One in four feel fully recovered following COVID-19 hospitalization
One year after hospitalization for COVID-19 only a minority of people feel fully recovered, with being female, obesity, and having had mechanical ventilation in hospital risk factors for not feeling fully recovered.
In the new U.K. study of more than 2,000 patients, presented at this year’s European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022), and published in The Lancet Respiratory Medicine, research showed that one in four patients feel fully well again 1 year after hospitalization for COVID-19.
For their study, researchers from the University of Leicester used data from the post-hospitalization COVID-19 (PHOSP-COVID) prospective, longitudinal cohort study, which assessed adults aged 18 years and over who had been hospitalized with COVID-19 across the United Kingdom and subsequently discharged. The researchers assessed the recovery of 2,320 participants discharged from 39 U.K. hospitals between March 7, 2020, and April 18, 2021, who were assessed via patient-reported outcome measures, physical performance, and organ function at 5 months and at 1 year after hospital discharge. Blood samples were taken at the 5-month visit to be analyzed for the presence of various inflammatory proteins.
All participants were assessed at 5 months after discharge and 807 participants (33%) completed both the 5-month and 1-year visits at the time of the analysis. The study is ongoing. The 807 patients were mean age of 59 years, 36% were women, and 28% received invasive mechanical ventilation. The proportion of patients reporting full recovery was similar between 5 months (26%) and 1 year (29%).
Female sex and obesity major risk factors for not recovering
Being female, obese, and having had mechanical ventilation in hospital makes someone 32%, 50%, and 58%, respectively, less likely to feel fully recovered 1 year after COVID-19 hospitalization, the authors said.
“We found female sex and obesity were major risk factors for not recovering at one year,” said the researchers, led by Rachael Evans, PhD, Louise V. Wain, and Christopher E. Brightling, PhD, National Institute for Health Research, Leicester Biomedical Research Centre, University of Leicester.
The authors said fatigue, muscle pain, physically slowing down, poor sleep, and breathlessness were most common ongoing long COVID symptoms. They noted how the total number and range of ongoing symptoms at 1 year was “striking,” positively associated with the severity of long COVID, and emphasizes the “multisystem nature of long COVID.”
Several inflammatory mediators increased
An earlier publication from this study identified four groups or “clusters” of symptom severity at 5 months, which were confirmed by this new study at 1 year, the authors said. They reported that 20% had very severe physical and mental health impairment, 30% had severe physical and mental health impairment, 11% had moderate physical health impairment with cognitive impairment, and 39% had mild mental and physical health impairment.
They added that having obesity, reduced exercise capacity, a greater number of symptoms, and increased levels of C-reactive protein were associated with the “more severe clusters.” In both the very severe and the moderate with cognitive impairment clusters, levels of interleukin-6 (IL-6) were higher when compared with the mild cluster.
“The limited recovery from 5 months to 1 year after hospitalisation in our study across symptoms, mental health, exercise capacity, organ impairment, and quality-of-life is striking,” the researchers noted.
“In our clusters, female sex and obesity were also associated with more severe ongoing health impairments including reduced exercise performance and health-related quality of life at one year,” and suggested that this potentially highlighted a group that “might need higher intensity interventions such as supervised rehabilitation,” they added.
There are no specific therapeutics for long COVID, the researchers said, noting that “effective interventions are urgently required.” The persistent systemic inflammation identified, particularly in those in the very severe and moderate with cognitive impairment clusters, suggested that these groups “might respond to anti-inflammatory strategies,” the authors wrote.
“We found that a minority of participants felt fully recovered 1 year after hospital discharge, with minimal improvement after a 5-month assessment,” they noted.
They added that the findings suggest the need for complex interventions that target both physical and mental health impairments to alleviate symptoms, and that specific therapeutic approaches to manage posttraumatic stress disorder might also be needed. The authors pointed out how “pharmacological and non-pharmacological interventions are urgently needed,” with a “precision-medicine approach with potential treatable traits of systemic inflammation and obesity.”
They said their study highlighted the “urgent need for health-care services to support the large and rapidly increasing patient population in whom a substantial burden of symptoms exist, including reduced exercise capacity and substantially decreased health-related quality of life one year after hospital discharge.”
They warned that without effective treatments, long COVID could become a “highly prevalent new long-term condition.”
A version of this article first appeared on Medscape UK.
One year after hospitalization for COVID-19 only a minority of people feel fully recovered, with being female, obesity, and having had mechanical ventilation in hospital risk factors for not feeling fully recovered.
In the new U.K. study of more than 2,000 patients, presented at this year’s European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022), and published in The Lancet Respiratory Medicine, research showed that one in four patients feel fully well again 1 year after hospitalization for COVID-19.
For their study, researchers from the University of Leicester used data from the post-hospitalization COVID-19 (PHOSP-COVID) prospective, longitudinal cohort study, which assessed adults aged 18 years and over who had been hospitalized with COVID-19 across the United Kingdom and subsequently discharged. The researchers assessed the recovery of 2,320 participants discharged from 39 U.K. hospitals between March 7, 2020, and April 18, 2021, who were assessed via patient-reported outcome measures, physical performance, and organ function at 5 months and at 1 year after hospital discharge. Blood samples were taken at the 5-month visit to be analyzed for the presence of various inflammatory proteins.
All participants were assessed at 5 months after discharge and 807 participants (33%) completed both the 5-month and 1-year visits at the time of the analysis. The study is ongoing. The 807 patients were mean age of 59 years, 36% were women, and 28% received invasive mechanical ventilation. The proportion of patients reporting full recovery was similar between 5 months (26%) and 1 year (29%).
Female sex and obesity major risk factors for not recovering
Being female, obese, and having had mechanical ventilation in hospital makes someone 32%, 50%, and 58%, respectively, less likely to feel fully recovered 1 year after COVID-19 hospitalization, the authors said.
“We found female sex and obesity were major risk factors for not recovering at one year,” said the researchers, led by Rachael Evans, PhD, Louise V. Wain, and Christopher E. Brightling, PhD, National Institute for Health Research, Leicester Biomedical Research Centre, University of Leicester.
The authors said fatigue, muscle pain, physically slowing down, poor sleep, and breathlessness were most common ongoing long COVID symptoms. They noted how the total number and range of ongoing symptoms at 1 year was “striking,” positively associated with the severity of long COVID, and emphasizes the “multisystem nature of long COVID.”
Several inflammatory mediators increased
An earlier publication from this study identified four groups or “clusters” of symptom severity at 5 months, which were confirmed by this new study at 1 year, the authors said. They reported that 20% had very severe physical and mental health impairment, 30% had severe physical and mental health impairment, 11% had moderate physical health impairment with cognitive impairment, and 39% had mild mental and physical health impairment.
They added that having obesity, reduced exercise capacity, a greater number of symptoms, and increased levels of C-reactive protein were associated with the “more severe clusters.” In both the very severe and the moderate with cognitive impairment clusters, levels of interleukin-6 (IL-6) were higher when compared with the mild cluster.
“The limited recovery from 5 months to 1 year after hospitalisation in our study across symptoms, mental health, exercise capacity, organ impairment, and quality-of-life is striking,” the researchers noted.
“In our clusters, female sex and obesity were also associated with more severe ongoing health impairments including reduced exercise performance and health-related quality of life at one year,” and suggested that this potentially highlighted a group that “might need higher intensity interventions such as supervised rehabilitation,” they added.
There are no specific therapeutics for long COVID, the researchers said, noting that “effective interventions are urgently required.” The persistent systemic inflammation identified, particularly in those in the very severe and moderate with cognitive impairment clusters, suggested that these groups “might respond to anti-inflammatory strategies,” the authors wrote.
“We found that a minority of participants felt fully recovered 1 year after hospital discharge, with minimal improvement after a 5-month assessment,” they noted.
They added that the findings suggest the need for complex interventions that target both physical and mental health impairments to alleviate symptoms, and that specific therapeutic approaches to manage posttraumatic stress disorder might also be needed. The authors pointed out how “pharmacological and non-pharmacological interventions are urgently needed,” with a “precision-medicine approach with potential treatable traits of systemic inflammation and obesity.”
They said their study highlighted the “urgent need for health-care services to support the large and rapidly increasing patient population in whom a substantial burden of symptoms exist, including reduced exercise capacity and substantially decreased health-related quality of life one year after hospital discharge.”
They warned that without effective treatments, long COVID could become a “highly prevalent new long-term condition.”
A version of this article first appeared on Medscape UK.
One year after hospitalization for COVID-19 only a minority of people feel fully recovered, with being female, obesity, and having had mechanical ventilation in hospital risk factors for not feeling fully recovered.
In the new U.K. study of more than 2,000 patients, presented at this year’s European Congress of Clinical Microbiology & Infectious Diseases (ECCMID 2022), and published in The Lancet Respiratory Medicine, research showed that one in four patients feel fully well again 1 year after hospitalization for COVID-19.
For their study, researchers from the University of Leicester used data from the post-hospitalization COVID-19 (PHOSP-COVID) prospective, longitudinal cohort study, which assessed adults aged 18 years and over who had been hospitalized with COVID-19 across the United Kingdom and subsequently discharged. The researchers assessed the recovery of 2,320 participants discharged from 39 U.K. hospitals between March 7, 2020, and April 18, 2021, who were assessed via patient-reported outcome measures, physical performance, and organ function at 5 months and at 1 year after hospital discharge. Blood samples were taken at the 5-month visit to be analyzed for the presence of various inflammatory proteins.
All participants were assessed at 5 months after discharge and 807 participants (33%) completed both the 5-month and 1-year visits at the time of the analysis. The study is ongoing. The 807 patients were mean age of 59 years, 36% were women, and 28% received invasive mechanical ventilation. The proportion of patients reporting full recovery was similar between 5 months (26%) and 1 year (29%).
Female sex and obesity major risk factors for not recovering
Being female, obese, and having had mechanical ventilation in hospital makes someone 32%, 50%, and 58%, respectively, less likely to feel fully recovered 1 year after COVID-19 hospitalization, the authors said.
“We found female sex and obesity were major risk factors for not recovering at one year,” said the researchers, led by Rachael Evans, PhD, Louise V. Wain, and Christopher E. Brightling, PhD, National Institute for Health Research, Leicester Biomedical Research Centre, University of Leicester.
The authors said fatigue, muscle pain, physically slowing down, poor sleep, and breathlessness were most common ongoing long COVID symptoms. They noted how the total number and range of ongoing symptoms at 1 year was “striking,” positively associated with the severity of long COVID, and emphasizes the “multisystem nature of long COVID.”
Several inflammatory mediators increased
An earlier publication from this study identified four groups or “clusters” of symptom severity at 5 months, which were confirmed by this new study at 1 year, the authors said. They reported that 20% had very severe physical and mental health impairment, 30% had severe physical and mental health impairment, 11% had moderate physical health impairment with cognitive impairment, and 39% had mild mental and physical health impairment.
They added that having obesity, reduced exercise capacity, a greater number of symptoms, and increased levels of C-reactive protein were associated with the “more severe clusters.” In both the very severe and the moderate with cognitive impairment clusters, levels of interleukin-6 (IL-6) were higher when compared with the mild cluster.
“The limited recovery from 5 months to 1 year after hospitalisation in our study across symptoms, mental health, exercise capacity, organ impairment, and quality-of-life is striking,” the researchers noted.
“In our clusters, female sex and obesity were also associated with more severe ongoing health impairments including reduced exercise performance and health-related quality of life at one year,” and suggested that this potentially highlighted a group that “might need higher intensity interventions such as supervised rehabilitation,” they added.
There are no specific therapeutics for long COVID, the researchers said, noting that “effective interventions are urgently required.” The persistent systemic inflammation identified, particularly in those in the very severe and moderate with cognitive impairment clusters, suggested that these groups “might respond to anti-inflammatory strategies,” the authors wrote.
“We found that a minority of participants felt fully recovered 1 year after hospital discharge, with minimal improvement after a 5-month assessment,” they noted.
They added that the findings suggest the need for complex interventions that target both physical and mental health impairments to alleviate symptoms, and that specific therapeutic approaches to manage posttraumatic stress disorder might also be needed. The authors pointed out how “pharmacological and non-pharmacological interventions are urgently needed,” with a “precision-medicine approach with potential treatable traits of systemic inflammation and obesity.”
They said their study highlighted the “urgent need for health-care services to support the large and rapidly increasing patient population in whom a substantial burden of symptoms exist, including reduced exercise capacity and substantially decreased health-related quality of life one year after hospital discharge.”
They warned that without effective treatments, long COVID could become a “highly prevalent new long-term condition.”
A version of this article first appeared on Medscape UK.
FROM THE LANCET RESPIRATORY MEDICINE
Malaria: Testing parasite DNA in travelers’ blood may help predict drug resistance
Testing the DNA of antimicrobial-resistant Plasmodium falciparum in the blood of travelers from malaria-endemic regions may help researchers monitor how drug resistance changes over time, a study from Canada reports.
“Malaria remains the deadliest vector-borne infectious disease worldwide. Plasmodium spp., most commonly P. falciparum, are responsible for [approximately] 229 million cases and 500,000 deaths from malaria annually,” the authors write in Emerging Infectious Diseases.
“Our findings demonstrate an absence of genetic markers of resistance to the most powerful antimalarials on the planet – the artemisinins – in potentially deadly malaria imported primarily from sub-Saharan Africa over time. This is good news,” senior study author Andrea K. Boggild, MD, MSc, DTMH, told this news organization.
“We also showed that over 90% of falciparum malaria imports were resistant to the proguanil component of the fixed drug combination atovaquone-proguanil, a popular oral antimalarial that is first-line treatment for uncomplicated malaria in Canada,” Dr. Boggild, an associate professor in the department of medicine at the University of Toronto, Canada, added in an email. “We documented no genetic markers of atovaquone resistance.”
Search for global patterns of emerging drug resistance
Dr. Boggild, the medical director of the tropical disease unit at Toronto General Hospital, and colleagues analyzed 243 whole-blood specimens that contained P. falciparum and no other Plasmodium species from the malaria biobank at the Public Health Ontario Laboratory in Toronto. They analyzed specimens from the years 2008-2009, 2013-2014, and 2017-2018 from patients ranging in age from 3 to 88 years. Of the 186 patients with a documented travel history, 81 had traveled in West Africa, the most common region, and 40 in Nigeria, the most common country. Five specimens came from travelers to Southeast Asia, and one came from a traveler to the Caribbean.
The researchers extracted DNA from whole blood and detected the parasite’s DNA by real-time quantitative polymerase chain reaction (qPCR). They analyzed 23 different single-nucleotide polymorphisms (SNPs) in six genes, and quantified the prevalence of resistance markers, including genes that provoke resistance to the most common antimalarial drugs: chloroquine, mefloquine, atovaquone/proguanil, and the artemisinins.
They analyzed SNPs at atpase6 (pfATPase6), pfcrt (chloroquine resistance transporter, cytb (cytochrome b), dhfr (dihydrofolate reductase), dhps (dihydropteroate synthetase), mdr1 (multidrug resistance protein) and mdr1 copy number, and kelch13 (kelch protein gene on chromosome 13).
Over time, they detected increasing mutant genotypes for dhfr S108N (P = .001) and dhps A613T (P = .029) but decreasing mutant genotypes for mdr1 N86Y (P < .001), D1246Y (P = .003), pfcrt K76T (P = .011), and pfcrt 74-75 (P = .014). They found no kelch13 mutations. They detected fewer mutations indicating chloroquine resistance over time, suggesting less chloroquine pressure in specimens from travelers to Africa, but mutations that provided proguanil resistance increased.
“Antimalarial resistance – particularly resistance to the powerful artemisinins – continues to expand globally, and it is important to conduct routine surveillance for resistant parasites in order to inform appropriate prevention and treatment guidelines,” Dr. Boggild explained. “It cannot be presumed that a drug’s efficacy will be durable over time given the global landscape of antimalarial resistance.”
Dr. Boggild acknowledged limitations to the study, including incomplete travel history in about half of the patients, relatively few patients from Southeast Asia, and the small sample set.
“Clinicians caring for travelers before or after travel should familiarize themselves with the options for malaria prevention and treatment and understand the risk–benefit profile of each drug,” Dr. Boggild advised.
“Resistance to proguanil means that we are reliant on the partner drug atovaquone for the antimalarial action of this formulation, which is effective only when taken with food,” she added.
Anne N. Cowell, MD, MPH, of the division of infectious diseases at the University of California, San Diego, was not surprised by the findings.
“The study demonstrates how quickly malaria parasites adapt and evolve to survive changes in malaria treatment,” Dr. Cowell, who was not involved in the study, told this news organization.
“These changes reflect changing malaria treatment and thus drug pressure during the time period,” she said in an email. “Because the majority of the clinical samples with a known travel history came from West Africa, and there was no clear evidence of artemisinin resistance in the area during the final time period studied, it is not surprising that they did not find kelch13 resistance mutations.
“The increase in mutations associated with proguanil resistance is concerning because atovaquone-proguanil is frequently used for prophylaxis during travel,” Dr. Cowell added. “There is no widespread evidence of resistance in travelers at this time, but it warrants monitoring.”
Sean C. Murphy, MD, PhD, an associate professor of laboratory medicine and the director of the malaria molecular diagnostic laboratory at the University of Washington in Seattle, also was not surprised by the study’s results.
“It may be just a matter of time before evidence of artemisinin resistance crops up among returning travelers,” he said in an email. “When that happens, we may lose the opportunity to easily use common go-to drugs like atovaquone/proguanil to treat these patients.
“The biggest takeaway of this study is the reminder that drug-resistant malaria (including the future potential for artemisinin-resistant malaria) is just an airplane flight or two away from nonendemic places like Canada and the United States,” Dr. Murphy noted. He was not involved with this Canadian study.
“Continued investment is needed to support malaria control, drug resistance monitoring, and vaccine efforts in order to fight this relentless, terrible parasite,” he urged.
The Project Initiation Fund of Public Health Ontario funded the study. The study authors, Dr. Cowell, and Dr. Murphy have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Testing the DNA of antimicrobial-resistant Plasmodium falciparum in the blood of travelers from malaria-endemic regions may help researchers monitor how drug resistance changes over time, a study from Canada reports.
“Malaria remains the deadliest vector-borne infectious disease worldwide. Plasmodium spp., most commonly P. falciparum, are responsible for [approximately] 229 million cases and 500,000 deaths from malaria annually,” the authors write in Emerging Infectious Diseases.
“Our findings demonstrate an absence of genetic markers of resistance to the most powerful antimalarials on the planet – the artemisinins – in potentially deadly malaria imported primarily from sub-Saharan Africa over time. This is good news,” senior study author Andrea K. Boggild, MD, MSc, DTMH, told this news organization.
“We also showed that over 90% of falciparum malaria imports were resistant to the proguanil component of the fixed drug combination atovaquone-proguanil, a popular oral antimalarial that is first-line treatment for uncomplicated malaria in Canada,” Dr. Boggild, an associate professor in the department of medicine at the University of Toronto, Canada, added in an email. “We documented no genetic markers of atovaquone resistance.”
Search for global patterns of emerging drug resistance
Dr. Boggild, the medical director of the tropical disease unit at Toronto General Hospital, and colleagues analyzed 243 whole-blood specimens that contained P. falciparum and no other Plasmodium species from the malaria biobank at the Public Health Ontario Laboratory in Toronto. They analyzed specimens from the years 2008-2009, 2013-2014, and 2017-2018 from patients ranging in age from 3 to 88 years. Of the 186 patients with a documented travel history, 81 had traveled in West Africa, the most common region, and 40 in Nigeria, the most common country. Five specimens came from travelers to Southeast Asia, and one came from a traveler to the Caribbean.
The researchers extracted DNA from whole blood and detected the parasite’s DNA by real-time quantitative polymerase chain reaction (qPCR). They analyzed 23 different single-nucleotide polymorphisms (SNPs) in six genes, and quantified the prevalence of resistance markers, including genes that provoke resistance to the most common antimalarial drugs: chloroquine, mefloquine, atovaquone/proguanil, and the artemisinins.
They analyzed SNPs at atpase6 (pfATPase6), pfcrt (chloroquine resistance transporter, cytb (cytochrome b), dhfr (dihydrofolate reductase), dhps (dihydropteroate synthetase), mdr1 (multidrug resistance protein) and mdr1 copy number, and kelch13 (kelch protein gene on chromosome 13).
Over time, they detected increasing mutant genotypes for dhfr S108N (P = .001) and dhps A613T (P = .029) but decreasing mutant genotypes for mdr1 N86Y (P < .001), D1246Y (P = .003), pfcrt K76T (P = .011), and pfcrt 74-75 (P = .014). They found no kelch13 mutations. They detected fewer mutations indicating chloroquine resistance over time, suggesting less chloroquine pressure in specimens from travelers to Africa, but mutations that provided proguanil resistance increased.
“Antimalarial resistance – particularly resistance to the powerful artemisinins – continues to expand globally, and it is important to conduct routine surveillance for resistant parasites in order to inform appropriate prevention and treatment guidelines,” Dr. Boggild explained. “It cannot be presumed that a drug’s efficacy will be durable over time given the global landscape of antimalarial resistance.”
Dr. Boggild acknowledged limitations to the study, including incomplete travel history in about half of the patients, relatively few patients from Southeast Asia, and the small sample set.
“Clinicians caring for travelers before or after travel should familiarize themselves with the options for malaria prevention and treatment and understand the risk–benefit profile of each drug,” Dr. Boggild advised.
“Resistance to proguanil means that we are reliant on the partner drug atovaquone for the antimalarial action of this formulation, which is effective only when taken with food,” she added.
Anne N. Cowell, MD, MPH, of the division of infectious diseases at the University of California, San Diego, was not surprised by the findings.
“The study demonstrates how quickly malaria parasites adapt and evolve to survive changes in malaria treatment,” Dr. Cowell, who was not involved in the study, told this news organization.
“These changes reflect changing malaria treatment and thus drug pressure during the time period,” she said in an email. “Because the majority of the clinical samples with a known travel history came from West Africa, and there was no clear evidence of artemisinin resistance in the area during the final time period studied, it is not surprising that they did not find kelch13 resistance mutations.
“The increase in mutations associated with proguanil resistance is concerning because atovaquone-proguanil is frequently used for prophylaxis during travel,” Dr. Cowell added. “There is no widespread evidence of resistance in travelers at this time, but it warrants monitoring.”
Sean C. Murphy, MD, PhD, an associate professor of laboratory medicine and the director of the malaria molecular diagnostic laboratory at the University of Washington in Seattle, also was not surprised by the study’s results.
“It may be just a matter of time before evidence of artemisinin resistance crops up among returning travelers,” he said in an email. “When that happens, we may lose the opportunity to easily use common go-to drugs like atovaquone/proguanil to treat these patients.
“The biggest takeaway of this study is the reminder that drug-resistant malaria (including the future potential for artemisinin-resistant malaria) is just an airplane flight or two away from nonendemic places like Canada and the United States,” Dr. Murphy noted. He was not involved with this Canadian study.
“Continued investment is needed to support malaria control, drug resistance monitoring, and vaccine efforts in order to fight this relentless, terrible parasite,” he urged.
The Project Initiation Fund of Public Health Ontario funded the study. The study authors, Dr. Cowell, and Dr. Murphy have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Testing the DNA of antimicrobial-resistant Plasmodium falciparum in the blood of travelers from malaria-endemic regions may help researchers monitor how drug resistance changes over time, a study from Canada reports.
“Malaria remains the deadliest vector-borne infectious disease worldwide. Plasmodium spp., most commonly P. falciparum, are responsible for [approximately] 229 million cases and 500,000 deaths from malaria annually,” the authors write in Emerging Infectious Diseases.
“Our findings demonstrate an absence of genetic markers of resistance to the most powerful antimalarials on the planet – the artemisinins – in potentially deadly malaria imported primarily from sub-Saharan Africa over time. This is good news,” senior study author Andrea K. Boggild, MD, MSc, DTMH, told this news organization.
“We also showed that over 90% of falciparum malaria imports were resistant to the proguanil component of the fixed drug combination atovaquone-proguanil, a popular oral antimalarial that is first-line treatment for uncomplicated malaria in Canada,” Dr. Boggild, an associate professor in the department of medicine at the University of Toronto, Canada, added in an email. “We documented no genetic markers of atovaquone resistance.”
Search for global patterns of emerging drug resistance
Dr. Boggild, the medical director of the tropical disease unit at Toronto General Hospital, and colleagues analyzed 243 whole-blood specimens that contained P. falciparum and no other Plasmodium species from the malaria biobank at the Public Health Ontario Laboratory in Toronto. They analyzed specimens from the years 2008-2009, 2013-2014, and 2017-2018 from patients ranging in age from 3 to 88 years. Of the 186 patients with a documented travel history, 81 had traveled in West Africa, the most common region, and 40 in Nigeria, the most common country. Five specimens came from travelers to Southeast Asia, and one came from a traveler to the Caribbean.
The researchers extracted DNA from whole blood and detected the parasite’s DNA by real-time quantitative polymerase chain reaction (qPCR). They analyzed 23 different single-nucleotide polymorphisms (SNPs) in six genes, and quantified the prevalence of resistance markers, including genes that provoke resistance to the most common antimalarial drugs: chloroquine, mefloquine, atovaquone/proguanil, and the artemisinins.
They analyzed SNPs at atpase6 (pfATPase6), pfcrt (chloroquine resistance transporter, cytb (cytochrome b), dhfr (dihydrofolate reductase), dhps (dihydropteroate synthetase), mdr1 (multidrug resistance protein) and mdr1 copy number, and kelch13 (kelch protein gene on chromosome 13).
Over time, they detected increasing mutant genotypes for dhfr S108N (P = .001) and dhps A613T (P = .029) but decreasing mutant genotypes for mdr1 N86Y (P < .001), D1246Y (P = .003), pfcrt K76T (P = .011), and pfcrt 74-75 (P = .014). They found no kelch13 mutations. They detected fewer mutations indicating chloroquine resistance over time, suggesting less chloroquine pressure in specimens from travelers to Africa, but mutations that provided proguanil resistance increased.
“Antimalarial resistance – particularly resistance to the powerful artemisinins – continues to expand globally, and it is important to conduct routine surveillance for resistant parasites in order to inform appropriate prevention and treatment guidelines,” Dr. Boggild explained. “It cannot be presumed that a drug’s efficacy will be durable over time given the global landscape of antimalarial resistance.”
Dr. Boggild acknowledged limitations to the study, including incomplete travel history in about half of the patients, relatively few patients from Southeast Asia, and the small sample set.
“Clinicians caring for travelers before or after travel should familiarize themselves with the options for malaria prevention and treatment and understand the risk–benefit profile of each drug,” Dr. Boggild advised.
“Resistance to proguanil means that we are reliant on the partner drug atovaquone for the antimalarial action of this formulation, which is effective only when taken with food,” she added.
Anne N. Cowell, MD, MPH, of the division of infectious diseases at the University of California, San Diego, was not surprised by the findings.
“The study demonstrates how quickly malaria parasites adapt and evolve to survive changes in malaria treatment,” Dr. Cowell, who was not involved in the study, told this news organization.
“These changes reflect changing malaria treatment and thus drug pressure during the time period,” she said in an email. “Because the majority of the clinical samples with a known travel history came from West Africa, and there was no clear evidence of artemisinin resistance in the area during the final time period studied, it is not surprising that they did not find kelch13 resistance mutations.
“The increase in mutations associated with proguanil resistance is concerning because atovaquone-proguanil is frequently used for prophylaxis during travel,” Dr. Cowell added. “There is no widespread evidence of resistance in travelers at this time, but it warrants monitoring.”
Sean C. Murphy, MD, PhD, an associate professor of laboratory medicine and the director of the malaria molecular diagnostic laboratory at the University of Washington in Seattle, also was not surprised by the study’s results.
“It may be just a matter of time before evidence of artemisinin resistance crops up among returning travelers,” he said in an email. “When that happens, we may lose the opportunity to easily use common go-to drugs like atovaquone/proguanil to treat these patients.
“The biggest takeaway of this study is the reminder that drug-resistant malaria (including the future potential for artemisinin-resistant malaria) is just an airplane flight or two away from nonendemic places like Canada and the United States,” Dr. Murphy noted. He was not involved with this Canadian study.
“Continued investment is needed to support malaria control, drug resistance monitoring, and vaccine efforts in order to fight this relentless, terrible parasite,” he urged.
The Project Initiation Fund of Public Health Ontario funded the study. The study authors, Dr. Cowell, and Dr. Murphy have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM EMERGING INFECTIOUS DISEASES
2020 presidential election tied to spike in cardiac events
The analysis of nearly 6.4 million adults showed that the rate of hospitalization for acute cardiovascular disease (CVD) was 17% higher in the 5 days after the election than in a 5-day period 2 weeks earlier.
The rate of acute myocardial infarction (AMI) was 42% higher, with no significant difference for heart failure or stroke hospital admissions.
“These findings suggest that awareness of the heightened risk of CVD and strategies to mitigate risk during notable political events are needed,” write Matthew T. Mefford, PhD, of Kaiser Permanente Southern California, Pasadena, and colleagues.
The study was published in the April issue of JAMA Network Open.
Stress and the heart
In the American Psychological Association Stress in America 2020 survey conducted roughly 3 months before the 2020 presidential election, 77% of adults cited the future of the country as a substantial source of stress, enhanced by the ongoing COVID-19 pandemic, the authors note. More than two-thirds said the election was a substantial source of stress.
Dr. Mefford and colleagues compared CVD hospitalizations at Kaiser Permanente Southern and Northern California hospitals in the 5-day risk window of Nov. 4-8, 2020, with the control window of Oct. 21-25, 2020.
There were 666 CVD hospitalizations (760.47 per 100,000 person-years [PY]) in the risk window, compared with 569 (647.97 per 100,000 PY) in the control window (rate ratio, 1.17; 95% confidence interval, 1.05-1.31).
There were also significantly more hospitalizations for AMI immediately after the election than before (179 vs. 126 AMI hospitalizations; 204.4 vs. 143.5 per 100,000 PY; RR, 1.42; 95% CI, 1.13-1.79).
There was no significant difference between the risk and control periods for hospitalizations because of stroke or heart failure.
The study also suggests higher rates of acute CVD after the election in older adults, men, and White individuals. Political affiliation was not examined in the study.
“Importantly, results were consistent before and after excluding patients with confirmed COVID-19 infection,” the study team notes.
Yet, the potential influence of COVID-19 stressors on increasing CVD risk cannot be ruled out, they say.
However, COVID-19 stressors occurred over a much longer period and are less likely to explain the transient risks observed in the defined risk and control windows that are in close proximity to the 2020 election, the investigators point out.
There is growing evidence that psychological health contributes to CVD.
Previous studies shown a higher risk for acute CVD around population-wide psychosocial or environmental stressors, but less was known about acute CVD risk in relation to political events.
The researchers note future studies evaluating stress-relieving interventions may be important for understanding the intersection of political events, associated stress, and acute CVD risk.
Partial funding for the study was provided by a grant from the W.K. Kellogg Foundation. The authors have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The analysis of nearly 6.4 million adults showed that the rate of hospitalization for acute cardiovascular disease (CVD) was 17% higher in the 5 days after the election than in a 5-day period 2 weeks earlier.
The rate of acute myocardial infarction (AMI) was 42% higher, with no significant difference for heart failure or stroke hospital admissions.
“These findings suggest that awareness of the heightened risk of CVD and strategies to mitigate risk during notable political events are needed,” write Matthew T. Mefford, PhD, of Kaiser Permanente Southern California, Pasadena, and colleagues.
The study was published in the April issue of JAMA Network Open.
Stress and the heart
In the American Psychological Association Stress in America 2020 survey conducted roughly 3 months before the 2020 presidential election, 77% of adults cited the future of the country as a substantial source of stress, enhanced by the ongoing COVID-19 pandemic, the authors note. More than two-thirds said the election was a substantial source of stress.
Dr. Mefford and colleagues compared CVD hospitalizations at Kaiser Permanente Southern and Northern California hospitals in the 5-day risk window of Nov. 4-8, 2020, with the control window of Oct. 21-25, 2020.
There were 666 CVD hospitalizations (760.47 per 100,000 person-years [PY]) in the risk window, compared with 569 (647.97 per 100,000 PY) in the control window (rate ratio, 1.17; 95% confidence interval, 1.05-1.31).
There were also significantly more hospitalizations for AMI immediately after the election than before (179 vs. 126 AMI hospitalizations; 204.4 vs. 143.5 per 100,000 PY; RR, 1.42; 95% CI, 1.13-1.79).
There was no significant difference between the risk and control periods for hospitalizations because of stroke or heart failure.
The study also suggests higher rates of acute CVD after the election in older adults, men, and White individuals. Political affiliation was not examined in the study.
“Importantly, results were consistent before and after excluding patients with confirmed COVID-19 infection,” the study team notes.
Yet, the potential influence of COVID-19 stressors on increasing CVD risk cannot be ruled out, they say.
However, COVID-19 stressors occurred over a much longer period and are less likely to explain the transient risks observed in the defined risk and control windows that are in close proximity to the 2020 election, the investigators point out.
There is growing evidence that psychological health contributes to CVD.
Previous studies shown a higher risk for acute CVD around population-wide psychosocial or environmental stressors, but less was known about acute CVD risk in relation to political events.
The researchers note future studies evaluating stress-relieving interventions may be important for understanding the intersection of political events, associated stress, and acute CVD risk.
Partial funding for the study was provided by a grant from the W.K. Kellogg Foundation. The authors have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
The analysis of nearly 6.4 million adults showed that the rate of hospitalization for acute cardiovascular disease (CVD) was 17% higher in the 5 days after the election than in a 5-day period 2 weeks earlier.
The rate of acute myocardial infarction (AMI) was 42% higher, with no significant difference for heart failure or stroke hospital admissions.
“These findings suggest that awareness of the heightened risk of CVD and strategies to mitigate risk during notable political events are needed,” write Matthew T. Mefford, PhD, of Kaiser Permanente Southern California, Pasadena, and colleagues.
The study was published in the April issue of JAMA Network Open.
Stress and the heart
In the American Psychological Association Stress in America 2020 survey conducted roughly 3 months before the 2020 presidential election, 77% of adults cited the future of the country as a substantial source of stress, enhanced by the ongoing COVID-19 pandemic, the authors note. More than two-thirds said the election was a substantial source of stress.
Dr. Mefford and colleagues compared CVD hospitalizations at Kaiser Permanente Southern and Northern California hospitals in the 5-day risk window of Nov. 4-8, 2020, with the control window of Oct. 21-25, 2020.
There were 666 CVD hospitalizations (760.47 per 100,000 person-years [PY]) in the risk window, compared with 569 (647.97 per 100,000 PY) in the control window (rate ratio, 1.17; 95% confidence interval, 1.05-1.31).
There were also significantly more hospitalizations for AMI immediately after the election than before (179 vs. 126 AMI hospitalizations; 204.4 vs. 143.5 per 100,000 PY; RR, 1.42; 95% CI, 1.13-1.79).
There was no significant difference between the risk and control periods for hospitalizations because of stroke or heart failure.
The study also suggests higher rates of acute CVD after the election in older adults, men, and White individuals. Political affiliation was not examined in the study.
“Importantly, results were consistent before and after excluding patients with confirmed COVID-19 infection,” the study team notes.
Yet, the potential influence of COVID-19 stressors on increasing CVD risk cannot be ruled out, they say.
However, COVID-19 stressors occurred over a much longer period and are less likely to explain the transient risks observed in the defined risk and control windows that are in close proximity to the 2020 election, the investigators point out.
There is growing evidence that psychological health contributes to CVD.
Previous studies shown a higher risk for acute CVD around population-wide psychosocial or environmental stressors, but less was known about acute CVD risk in relation to political events.
The researchers note future studies evaluating stress-relieving interventions may be important for understanding the intersection of political events, associated stress, and acute CVD risk.
Partial funding for the study was provided by a grant from the W.K. Kellogg Foundation. The authors have no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
FROM JAMA NETWORK OPEN