The Hospitalist

Background: Previous trials have shown a reduction in composite outcomes if STEMI patients undergo staged PCI of nonculprit lesions discovered incidentally at the time of primary PCI for STEMI. However, no randomized trial has had the power to assess if staged PCI of nonculprit lesions reduces cardiovascular death or MI.

Overall, 4,041 patients from 140 centers were randomized with median 3-year follow-up. The complete revascularization group had lower rates of the primary composite outcome of death from cardiovascular disease or new MI (absolute reduction, 2.7%; 7.8% vs. 10.5%; number needed to treat, 37; hazard ratio, 0.74; 95% confidence interval, 0.60-0.91; P = .004). This finding was driven by lower incidence of new MI in the complete revascularization group – the incidence of death was similar between the groups. A coprimary composite outcome of death from cardiovascular causes, new MI, or ischemia-driven revascularization also favored complete revascularization, with an absolute risk reduction of 7.8% (8.9% vs. 16.7%; NNT, 13; HR, 0.51; 95% CI, 0.43-0.61; P less than .001). No statistically significant differences between groups were noted for the safety outcomes of major bleeding, stroke, stent thrombosis, or contrast-induced kidney injury.

Bottom line: Patients with STEMI who have multivessel disease incidentally discovered during primary PCI have a lower incidence of new MI and ischemia-driven revascularization when they undergo complete revascularization of all suitable lesions, as opposed to PCI of only their culprit lesion.

Citation: Mehta SR et al. Complete revascularization with multivessel PCI for myocardial infarction. N Engl J Med. 2019 Oct 10;381:1411-21.

Dr. Porter is chief quality and safety resident at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: Previous trials have shown a reduction in composite outcomes if STEMI patients undergo staged PCI of nonculprit lesions discovered incidentally at the time of primary PCI for STEMI. However, no randomized trial has had the power to assess if staged PCI of nonculprit lesions reduces cardiovascular death or MI.

Overall, 4,041 patients from 140 centers were randomized with median 3-year follow-up. The complete revascularization group had lower rates of the primary composite outcome of death from cardiovascular disease or new MI (absolute reduction, 2.7%; 7.8% vs. 10.5%; number needed to treat, 37; hazard ratio, 0.74; 95% confidence interval, 0.60-0.91; P = .004). This finding was driven by lower incidence of new MI in the complete revascularization group – the incidence of death was similar between the groups. A coprimary composite outcome of death from cardiovascular causes, new MI, or ischemia-driven revascularization also favored complete revascularization, with an absolute risk reduction of 7.8% (8.9% vs. 16.7%; NNT, 13; HR, 0.51; 95% CI, 0.43-0.61; P less than .001). No statistically significant differences between groups were noted for the safety outcomes of major bleeding, stroke, stent thrombosis, or contrast-induced kidney injury.

Bottom line: Patients with STEMI who have multivessel disease incidentally discovered during primary PCI have a lower incidence of new MI and ischemia-driven revascularization when they undergo complete revascularization of all suitable lesions, as opposed to PCI of only their culprit lesion.

Citation: Mehta SR et al. Complete revascularization with multivessel PCI for myocardial infarction. N Engl J Med. 2019 Oct 10;381:1411-21.

Dr. Porter is chief quality and safety resident at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: Previous trials have shown a reduction in composite outcomes if STEMI patients undergo staged PCI of nonculprit lesions discovered incidentally at the time of primary PCI for STEMI. However, no randomized trial has had the power to assess if staged PCI of nonculprit lesions reduces cardiovascular death or MI.

Overall, 4,041 patients from 140 centers were randomized with median 3-year follow-up. The complete revascularization group had lower rates of the primary composite outcome of death from cardiovascular disease or new MI (absolute reduction, 2.7%; 7.8% vs. 10.5%; number needed to treat, 37; hazard ratio, 0.74; 95% confidence interval, 0.60-0.91; P = .004). This finding was driven by lower incidence of new MI in the complete revascularization group – the incidence of death was similar between the groups. A coprimary composite outcome of death from cardiovascular causes, new MI, or ischemia-driven revascularization also favored complete revascularization, with an absolute risk reduction of 7.8% (8.9% vs. 16.7%; NNT, 13; HR, 0.51; 95% CI, 0.43-0.61; P less than .001). No statistically significant differences between groups were noted for the safety outcomes of major bleeding, stroke, stent thrombosis, or contrast-induced kidney injury.

Bottom line: Patients with STEMI who have multivessel disease incidentally discovered during primary PCI have a lower incidence of new MI and ischemia-driven revascularization when they undergo complete revascularization of all suitable lesions, as opposed to PCI of only their culprit lesion.

Citation: Mehta SR et al. Complete revascularization with multivessel PCI for myocardial infarction. N Engl J Med. 2019 Oct 10;381:1411-21.

Dr. Porter is chief quality and safety resident at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.

In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.

In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.

“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.

“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.

The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.

Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.

The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.

Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm² in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm², but <1 cm²).

“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.

In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.

Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
 

COVID-19 vs. non–COVID-19 thrombi

Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).

The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.

“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
 

Anticoagulation, yes, but dose unclear

These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.

“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.

“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.

Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.

Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.

However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.

Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”

It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”

All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.

The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.

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

Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.

In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.

In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.

“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.

“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.

The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.

Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.

The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.

Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm² in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm², but <1 cm²).

“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.

In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.

Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
 

COVID-19 vs. non–COVID-19 thrombi

Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).

The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.

“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
 

Anticoagulation, yes, but dose unclear

These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.

“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.

“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.

Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.

Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.

However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.

Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”

It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”

All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.

The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.

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

Autopsies on patients who died from COVID-19 are providing important clues on how to treat the disease. In an analysis of 40 hearts from COVID-19 patients who died early in the pandemic, myocyte necrosis was seen in 14 hearts, or 35%.

In the majority of these hearts, pathologists found both small areas of focal necrosis and cardiac thrombi, most of which were microthrombi in myocardial capillaries, arterioles, and small muscular cells.

In an interview, senior author Aloke V. Finn, MD, CVPath Institute, Gaithersburg, Md., stressed the importance of understanding what they saw, but also what they didn’t see.

“What we saw in the majority of patients with myocardial injury were these small areas of infarct and microthrombi in small vessels. What we didn’t see was any evidence of myocarditis and or huge infarcts in, like, the LAD artery,” he said.

“What we’re seeing here is not clinically detectable. ... There is no test that will tell you there are microthrombi and no imaging tests that will show these focal areas of necrosis, but that doesn’t mean it’s not there,” he added.

The finding of myocyte necrosis in about one-third of samples is consistent with another study that showed that 30%-40% of patients hospitalized with COVID-19 have elevated troponins, noted Dr. Finn. The investigators were unable to obtain troponin levels on their patients, which could limit the clinical translation of myocardial necrosis detected at autopsy.

Dr. Finn and colleagues, including first author Dario Pellegrini, MD, from Ospedale Papa Giovanni XXIII in Bergamo, Italy, published their findings online in Circulation on Jan. 22, 2020.

The report is a follow-up to another just published by Dr. Finn’s group in the Journal of the American College of Cardiology, which showed that myocarditis is a very rare finding in COVID-19 autopsies.

Only three of 14 individuals (21.4%) with evidence of myocyte necrosis showed evidence of acute MI, which Dr. Finn and colleagues define as an area of necrosis at least 1 cm² in size. The remaining 11 (78.6%) had only discrete areas of myocyte necrosis (>20 necrotic myocytes with an area of ≥0.05 mm², but <1 cm²).

“This makes sense when we saw what type of thrombus there was in these cases; it wasn’t thrombus in major epicardial vessels but microthombi in small vessels,” said Dr. Finn.

In those with necrosis, cardiac thrombi were present in 11 of 14 (78.6%) cases, with 2 of 14 (14.2%) having epicardial coronary artery thrombi and 0 of 14 (64.3%) having microthrombi in myocardial capillaries, arterioles, and small muscular arteries.

Further supporting the role of COVID-19–related hypercoagulability as the cause of myocardial injury in many patients, the investigators noted that the incidence of severe coronary artery disease (defined as >75% cross sectional narrowing) did not differ significantly between those with and without necrosis.
 

COVID-19 vs. non–COVID-19 thrombi

Going one step further, Dr. Finn’s team compared cardiac microthrombi from their COVID-19–positive autopsy cases with intramyocardial thromboemboli from COVID-19 cases. They also compared the samples with aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19–infected patients presenting with ST-segment elevation MI (STEMI).

The autopsy-obtained microthrombi had significantly more fibrin and terminal complement C5b-9 immunostaining than intramyocardial thromboemboli from COVID-19–negative subjects and than aspirated thrombi from either COVID-positive or COVID-negative STEMI patients.

“Basically, what we’re seeing in these thrombi is evidence of an immune-mediated reaction,” said Dr. Finn, explaining that complement C5b-9 is an innate immune system protein that circulates in the blood in response to any kind of activation of the immune system. “It is nonspecific but can also lead to coagulation problems,” he said.
 

Anticoagulation, yes, but dose unclear

These findings clearly support the use of anticoagulation in hospitalized COVID patients, said Jeffrey Weitz, MD, director of the Thrombosis & Atherosclerosis Research Institute, McMaster University, Hamilton, Ont. But the details of how much anticoagulation, what kind, and for whom are still a moving target.

“I think what we can say at this point is that these autopsy findings fit with previous studies that have shown microthrombi in the lungs and thrombi in the legs and gut, and support the notion that these patients should receive prophylactic doses of anticoagulants if they’re sick enough to be hospitalized,” said Dr. Weitz.

“But it’s not as simple as to say that this study shows clots form in the heart of COVID patients and therefore more anticoagulation is going to be better than less anticoagulation,” he said in an interview.

Recent top-line findings from three linked clinical trials – REMAP-CAP, ACTIV-4, and ATTACC – show that full-dose anticoagulation was beneficial in moderately ill patients hospitalized for COVID-19 and reduced the need for mechanical ventilation.

Moderately ill patients are those not in intensive care and who did not require organ support, such as mechanical ventilation, at the time of enrollment.

However, the same group reported findings in December that showed that routine use of full-dose anticoagulation when started in the ICU in critically ill patients was not beneficial and possibly harmful.

Dr. Weitz was only a little bit surprised by this finding of potential harm in the sickest patients. “I figured everybody should get prophylaxis but I wasn’t sure that everybody should get intensified anticoagulant. But my assumption was that if anybody is going to benefit from it, it would be the ICU patients.”

It was notable, said Dr. Weitz, that levels of D-dimer, a fibrin degradation product, were not associated with outcomes. “So, it doesn’t seem to be that patients with evidence of more clotting are more likely to benefit, which might indicate that it’s not the anticoagulant effect of the heparin that’s helping, but maybe the anti-inflammatory effect. At this point, we just don’t know.”

All three studies have paused enrollment of the critically ill subgroup, but are continuing to enroll patients with moderate illness and expect to publish results in the coming months, according to previous coverage from this news organization.

The study was funded by CVPath, a nonprofit institute that receives funding from a number of different industry entities. Dr. Finn and Dr. Weitz reported no relevant conflicts of interest.

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

The Blitz was a Nazi bombing campaign targeting London. It was designed to break the spirit of the British. Knowing London would be the centerpiece of the campaign, the British rather hastily established several psychiatric hospitals for the expected panic in the streets. However, despite 9 months of bombing, 43,000 civilians killed and 139,000 more wounded, the predicted chaos in the streets did not manifest. Civilians continued to work, industry continued to churn, and eventually, Hitler’s eye turned east toward Russia.

H. F. Davis/Wikimedia Commons/Public Domain

The surprising lack of pandemonium in London inspired Dr. John T. MacCurdy, who chronicled his findings in a book The Structure of Morale, more recently popularized in Malcolm Gladwell’s David and Goliath. A brief summary of Dr. MacCurdy’s theory divides the targeted Londoners into the following categories:

• Direct hit
• Near miss
• Remote miss

The direct hit group was defined as those killed by the bombing. However, As Dr. MacCurdy stated, “The morale of the community depends on the reaction of the survivors…Put this way, the fact is obvious, corpses do not run about spreading panic.”

A near miss were those for whom wounds were inflicted or loved ones were killed. This group felt the real repercussions of the bombing. However, with 139,000 wounded out of a city of 8 million people, they were a small minority.

The majority of Londoners, then, fit into the third group – the remote miss. These people faced a serious fear, but survived, often totally unscathed. The process of facing that fear without having panicked or having been harmed, then, led to “a feeling of excitement with a flavour of invulnerability.”

Therefore, rather than a city of millions running in fear in the streets, requiring military presence to control the chaos, London became a city of people who felt themselves, perhaps, invincible.

A similar threat passed through the world in the first several months of the COVID-19 pandemic. Hospitals were expected to be overrun, and ethics committees convened to discuss allocation of scarce ventilators. However, due, at least in part, to the impressive efforts of the populace of the United States, the majority of civilians did not feel the burden of this frightening disease. Certainly, in a few places, hospitals were overwhelmed, and resources were unavailable due to sheer numbers. These places saw those who suffered direct hits with the highest frequency. However, a disease with an infection fatality ratio recently estimated at 0.5-1%, with a relatively high rate of asymptomatic disease, led to a large majority of people who experienced the first wave of COVID-19 in the United States as a remote miss. COVID-19’s flattened first peak gave much of the population a sense of relief, and, perhaps, a “flavour of invulnerability.”

An anonymous, but concerned, household contact wrote The New York Times and illustrated perfectly the invulnerable feelings of a remote miss:

“I’m doing my best to avoid social contact, along with two other members of my household. We have sufficient supplies for a month. Despite that, one member insists on going out for trivial reasons, such as not liking the kind of apples we have. He’s 92. I’ve tried explaining and cajoling, using graphs and anecdotes to make the danger to all of us seem ‘real.’ It doesn’t take. His risk of death is many times greater than mine, and he’s poking holes in a lifeboat we all have to rely on. What is the correct path?”

American culture expects certainty from science. Therein lies the problem with a new disease no medical provider or researcher had seen prior to November 2019. Action was required in the effort to slow the spread with little to no data as a guide. Therefore, messages that seemed contradictory reached the public. “A mask less than N-95 grade will not protect you,” evolved to, “everyone should wear a homemade cloth mask.” As the pandemic evolved and data was gathered, new recommendations were presented. Unfortunately, such well-meaning and necessary changes led to confusion, mistrust, and conspiracy theories.

Medicine’s response

The science of COVID-19 carries phenomenal uncertainties, but the psychology of those who have suffered direct hits or near misses are the daily bedside challenge of all physicians, but particularly of hospitalists. We live at the front lines of disease – as one colleague put it to me, “we are the watchers on the wall.” Though we do not yet have our hoped-for, evidence-based treatment for this virus, we are familiar with acute illness. We know the rapid change of health to disease, and we know the chronically ill who suffer exacerbations of such illness. Supporting patients and their loved ones through those times is our daily practice.

On the other hand, those who have experienced only remote misses remain vulnerable in this pandemic, despite their feelings of invincibility. Those that feel invincible may be the least interested in our advice. This, too, is no strange position for a physician. We have tools to reach patients who do not reach out to us. Traditional media outlets have been saturated with headlines and talking points about this disease. Physicians who have taken to social media have been met with appreciation in some situations, but ignored, doubted, or shunned in others. In May 2020, NBC News reported an ED doctor’s attempt to dispel some COVID myths on social media. Unfortunately, his remarks were summarily dismissed. Through the frustration, we persevere.

Out of the many responsible authorities who help battle misinformation, the World Health Organization’s mythbusting website (www.who.int/emergencies/diseases/novel-coronavirus-2019/advice-for-public/myth-busters) directly confronts many incorrect circulating ideas. My personal favorite at the time of this writing is: “Being able to hold your breath for 10 seconds or more without coughing or feeling discomfort DOES NOT mean you are free from COVID-19.”

For the policy and communication side of medicine in the midst of this pandemic, I will not claim to have a silver bullet. There are many intelligent, policy-minded people who are working on that very problem. However, as individual practitioners and as individual citizens, I can see two powerful tools that may help us move forward.

1) Confidence and humility: We live in a world of uncertainty, and we struggle against that every day. This pandemic has put our uncertainty clearly on display. However, we may also be confident in providing the best currently known care, even while holding the humility that what we know will likely change. Before COVID-19, we have all seen patients who received multiple different answers from multiple different providers. When I am willing to admit my uncertainty, I have witnessed patients’ skepticism transform into assuming an active role in their care.

For those who have suffered a direct hit or a near miss, honest conversations are vital to build a trusting physician-patient relationship. For the remote miss group, speaking candidly about our uncertainty displays our authenticity and helps combat conspiracy-type theories of ulterior motives. This becomes all the more crucial when new technologies are being deployed – for instance, a September 2020 CBS News survey showed only 21% of Americans planned to get a COVID-19 vaccine “as soon as possible.”

2) Insight into our driving emotions: While the near miss patients are likely ready to continue prevention measures, the remote miss group is often more difficult. When we do have the opportunity to discuss actions to impede the virus’ spread with the remote miss group, understanding their potentially unrecognized motivations helps with that conversation. I have shared the story of the London Blitz and the remote miss and seen people connect the dots with their own emotions. Effective counseling – expecting the feelings of invulnerability amongst the remote miss group – can support endurance with prevention measures amongst that group and help flatten the curve.

Communicating our strengths, transparently discussing our weaknesses, and better understanding underlying emotions for ourselves and our patients may help save lives. As physicians, that is our daily practice, unchanged even as medicine takes center stage in our national conversation.

Dr. Walthall completed his internal medicine residency at the Medical University of South Carolina in Charleston, SC. After residency, he joined the faculty at MUSC in the Division of Hospital Medicine. He is also interested in systems-based care and has taken on the role of physician advisor. This essay appeared first on The Hospital Leader, the official blog of SHM.

The Blitz was a Nazi bombing campaign targeting London. It was designed to break the spirit of the British. Knowing London would be the centerpiece of the campaign, the British rather hastily established several psychiatric hospitals for the expected panic in the streets. However, despite 9 months of bombing, 43,000 civilians killed and 139,000 more wounded, the predicted chaos in the streets did not manifest. Civilians continued to work, industry continued to churn, and eventually, Hitler’s eye turned east toward Russia.

H. F. Davis/Wikimedia Commons/Public Domain

The surprising lack of pandemonium in London inspired Dr. John T. MacCurdy, who chronicled his findings in a book The Structure of Morale, more recently popularized in Malcolm Gladwell’s David and Goliath. A brief summary of Dr. MacCurdy’s theory divides the targeted Londoners into the following categories:

• Direct hit
• Near miss
• Remote miss

The direct hit group was defined as those killed by the bombing. However, As Dr. MacCurdy stated, “The morale of the community depends on the reaction of the survivors…Put this way, the fact is obvious, corpses do not run about spreading panic.”

A near miss were those for whom wounds were inflicted or loved ones were killed. This group felt the real repercussions of the bombing. However, with 139,000 wounded out of a city of 8 million people, they were a small minority.

The majority of Londoners, then, fit into the third group – the remote miss. These people faced a serious fear, but survived, often totally unscathed. The process of facing that fear without having panicked or having been harmed, then, led to “a feeling of excitement with a flavour of invulnerability.”

Therefore, rather than a city of millions running in fear in the streets, requiring military presence to control the chaos, London became a city of people who felt themselves, perhaps, invincible.

A similar threat passed through the world in the first several months of the COVID-19 pandemic. Hospitals were expected to be overrun, and ethics committees convened to discuss allocation of scarce ventilators. However, due, at least in part, to the impressive efforts of the populace of the United States, the majority of civilians did not feel the burden of this frightening disease. Certainly, in a few places, hospitals were overwhelmed, and resources were unavailable due to sheer numbers. These places saw those who suffered direct hits with the highest frequency. However, a disease with an infection fatality ratio recently estimated at 0.5-1%, with a relatively high rate of asymptomatic disease, led to a large majority of people who experienced the first wave of COVID-19 in the United States as a remote miss. COVID-19’s flattened first peak gave much of the population a sense of relief, and, perhaps, a “flavour of invulnerability.”

An anonymous, but concerned, household contact wrote The New York Times and illustrated perfectly the invulnerable feelings of a remote miss:

“I’m doing my best to avoid social contact, along with two other members of my household. We have sufficient supplies for a month. Despite that, one member insists on going out for trivial reasons, such as not liking the kind of apples we have. He’s 92. I’ve tried explaining and cajoling, using graphs and anecdotes to make the danger to all of us seem ‘real.’ It doesn’t take. His risk of death is many times greater than mine, and he’s poking holes in a lifeboat we all have to rely on. What is the correct path?”

American culture expects certainty from science. Therein lies the problem with a new disease no medical provider or researcher had seen prior to November 2019. Action was required in the effort to slow the spread with little to no data as a guide. Therefore, messages that seemed contradictory reached the public. “A mask less than N-95 grade will not protect you,” evolved to, “everyone should wear a homemade cloth mask.” As the pandemic evolved and data was gathered, new recommendations were presented. Unfortunately, such well-meaning and necessary changes led to confusion, mistrust, and conspiracy theories.

Medicine’s response

The science of COVID-19 carries phenomenal uncertainties, but the psychology of those who have suffered direct hits or near misses are the daily bedside challenge of all physicians, but particularly of hospitalists. We live at the front lines of disease – as one colleague put it to me, “we are the watchers on the wall.” Though we do not yet have our hoped-for, evidence-based treatment for this virus, we are familiar with acute illness. We know the rapid change of health to disease, and we know the chronically ill who suffer exacerbations of such illness. Supporting patients and their loved ones through those times is our daily practice.

On the other hand, those who have experienced only remote misses remain vulnerable in this pandemic, despite their feelings of invincibility. Those that feel invincible may be the least interested in our advice. This, too, is no strange position for a physician. We have tools to reach patients who do not reach out to us. Traditional media outlets have been saturated with headlines and talking points about this disease. Physicians who have taken to social media have been met with appreciation in some situations, but ignored, doubted, or shunned in others. In May 2020, NBC News reported an ED doctor’s attempt to dispel some COVID myths on social media. Unfortunately, his remarks were summarily dismissed. Through the frustration, we persevere.

Out of the many responsible authorities who help battle misinformation, the World Health Organization’s mythbusting website (www.who.int/emergencies/diseases/novel-coronavirus-2019/advice-for-public/myth-busters) directly confronts many incorrect circulating ideas. My personal favorite at the time of this writing is: “Being able to hold your breath for 10 seconds or more without coughing or feeling discomfort DOES NOT mean you are free from COVID-19.”

For the policy and communication side of medicine in the midst of this pandemic, I will not claim to have a silver bullet. There are many intelligent, policy-minded people who are working on that very problem. However, as individual practitioners and as individual citizens, I can see two powerful tools that may help us move forward.

1) Confidence and humility: We live in a world of uncertainty, and we struggle against that every day. This pandemic has put our uncertainty clearly on display. However, we may also be confident in providing the best currently known care, even while holding the humility that what we know will likely change. Before COVID-19, we have all seen patients who received multiple different answers from multiple different providers. When I am willing to admit my uncertainty, I have witnessed patients’ skepticism transform into assuming an active role in their care.

For those who have suffered a direct hit or a near miss, honest conversations are vital to build a trusting physician-patient relationship. For the remote miss group, speaking candidly about our uncertainty displays our authenticity and helps combat conspiracy-type theories of ulterior motives. This becomes all the more crucial when new technologies are being deployed – for instance, a September 2020 CBS News survey showed only 21% of Americans planned to get a COVID-19 vaccine “as soon as possible.”

2) Insight into our driving emotions: While the near miss patients are likely ready to continue prevention measures, the remote miss group is often more difficult. When we do have the opportunity to discuss actions to impede the virus’ spread with the remote miss group, understanding their potentially unrecognized motivations helps with that conversation. I have shared the story of the London Blitz and the remote miss and seen people connect the dots with their own emotions. Effective counseling – expecting the feelings of invulnerability amongst the remote miss group – can support endurance with prevention measures amongst that group and help flatten the curve.

Communicating our strengths, transparently discussing our weaknesses, and better understanding underlying emotions for ourselves and our patients may help save lives. As physicians, that is our daily practice, unchanged even as medicine takes center stage in our national conversation.

Dr. Walthall completed his internal medicine residency at the Medical University of South Carolina in Charleston, SC. After residency, he joined the faculty at MUSC in the Division of Hospital Medicine. He is also interested in systems-based care and has taken on the role of physician advisor. This essay appeared first on The Hospital Leader, the official blog of SHM.

The Blitz was a Nazi bombing campaign targeting London. It was designed to break the spirit of the British. Knowing London would be the centerpiece of the campaign, the British rather hastily established several psychiatric hospitals for the expected panic in the streets. However, despite 9 months of bombing, 43,000 civilians killed and 139,000 more wounded, the predicted chaos in the streets did not manifest. Civilians continued to work, industry continued to churn, and eventually, Hitler’s eye turned east toward Russia.

H. F. Davis/Wikimedia Commons/Public Domain

The surprising lack of pandemonium in London inspired Dr. John T. MacCurdy, who chronicled his findings in a book The Structure of Morale, more recently popularized in Malcolm Gladwell’s David and Goliath. A brief summary of Dr. MacCurdy’s theory divides the targeted Londoners into the following categories:

• Direct hit
• Near miss
• Remote miss

The direct hit group was defined as those killed by the bombing. However, As Dr. MacCurdy stated, “The morale of the community depends on the reaction of the survivors…Put this way, the fact is obvious, corpses do not run about spreading panic.”

A near miss were those for whom wounds were inflicted or loved ones were killed. This group felt the real repercussions of the bombing. However, with 139,000 wounded out of a city of 8 million people, they were a small minority.

The majority of Londoners, then, fit into the third group – the remote miss. These people faced a serious fear, but survived, often totally unscathed. The process of facing that fear without having panicked or having been harmed, then, led to “a feeling of excitement with a flavour of invulnerability.”

Therefore, rather than a city of millions running in fear in the streets, requiring military presence to control the chaos, London became a city of people who felt themselves, perhaps, invincible.

A similar threat passed through the world in the first several months of the COVID-19 pandemic. Hospitals were expected to be overrun, and ethics committees convened to discuss allocation of scarce ventilators. However, due, at least in part, to the impressive efforts of the populace of the United States, the majority of civilians did not feel the burden of this frightening disease. Certainly, in a few places, hospitals were overwhelmed, and resources were unavailable due to sheer numbers. These places saw those who suffered direct hits with the highest frequency. However, a disease with an infection fatality ratio recently estimated at 0.5-1%, with a relatively high rate of asymptomatic disease, led to a large majority of people who experienced the first wave of COVID-19 in the United States as a remote miss. COVID-19’s flattened first peak gave much of the population a sense of relief, and, perhaps, a “flavour of invulnerability.”

An anonymous, but concerned, household contact wrote The New York Times and illustrated perfectly the invulnerable feelings of a remote miss:

“I’m doing my best to avoid social contact, along with two other members of my household. We have sufficient supplies for a month. Despite that, one member insists on going out for trivial reasons, such as not liking the kind of apples we have. He’s 92. I’ve tried explaining and cajoling, using graphs and anecdotes to make the danger to all of us seem ‘real.’ It doesn’t take. His risk of death is many times greater than mine, and he’s poking holes in a lifeboat we all have to rely on. What is the correct path?”

American culture expects certainty from science. Therein lies the problem with a new disease no medical provider or researcher had seen prior to November 2019. Action was required in the effort to slow the spread with little to no data as a guide. Therefore, messages that seemed contradictory reached the public. “A mask less than N-95 grade will not protect you,” evolved to, “everyone should wear a homemade cloth mask.” As the pandemic evolved and data was gathered, new recommendations were presented. Unfortunately, such well-meaning and necessary changes led to confusion, mistrust, and conspiracy theories.

Medicine’s response

The science of COVID-19 carries phenomenal uncertainties, but the psychology of those who have suffered direct hits or near misses are the daily bedside challenge of all physicians, but particularly of hospitalists. We live at the front lines of disease – as one colleague put it to me, “we are the watchers on the wall.” Though we do not yet have our hoped-for, evidence-based treatment for this virus, we are familiar with acute illness. We know the rapid change of health to disease, and we know the chronically ill who suffer exacerbations of such illness. Supporting patients and their loved ones through those times is our daily practice.

On the other hand, those who have experienced only remote misses remain vulnerable in this pandemic, despite their feelings of invincibility. Those that feel invincible may be the least interested in our advice. This, too, is no strange position for a physician. We have tools to reach patients who do not reach out to us. Traditional media outlets have been saturated with headlines and talking points about this disease. Physicians who have taken to social media have been met with appreciation in some situations, but ignored, doubted, or shunned in others. In May 2020, NBC News reported an ED doctor’s attempt to dispel some COVID myths on social media. Unfortunately, his remarks were summarily dismissed. Through the frustration, we persevere.

Out of the many responsible authorities who help battle misinformation, the World Health Organization’s mythbusting website (www.who.int/emergencies/diseases/novel-coronavirus-2019/advice-for-public/myth-busters) directly confronts many incorrect circulating ideas. My personal favorite at the time of this writing is: “Being able to hold your breath for 10 seconds or more without coughing or feeling discomfort DOES NOT mean you are free from COVID-19.”

For the policy and communication side of medicine in the midst of this pandemic, I will not claim to have a silver bullet. There are many intelligent, policy-minded people who are working on that very problem. However, as individual practitioners and as individual citizens, I can see two powerful tools that may help us move forward.

1) Confidence and humility: We live in a world of uncertainty, and we struggle against that every day. This pandemic has put our uncertainty clearly on display. However, we may also be confident in providing the best currently known care, even while holding the humility that what we know will likely change. Before COVID-19, we have all seen patients who received multiple different answers from multiple different providers. When I am willing to admit my uncertainty, I have witnessed patients’ skepticism transform into assuming an active role in their care.

For those who have suffered a direct hit or a near miss, honest conversations are vital to build a trusting physician-patient relationship. For the remote miss group, speaking candidly about our uncertainty displays our authenticity and helps combat conspiracy-type theories of ulterior motives. This becomes all the more crucial when new technologies are being deployed – for instance, a September 2020 CBS News survey showed only 21% of Americans planned to get a COVID-19 vaccine “as soon as possible.”

2) Insight into our driving emotions: While the near miss patients are likely ready to continue prevention measures, the remote miss group is often more difficult. When we do have the opportunity to discuss actions to impede the virus’ spread with the remote miss group, understanding their potentially unrecognized motivations helps with that conversation. I have shared the story of the London Blitz and the remote miss and seen people connect the dots with their own emotions. Effective counseling – expecting the feelings of invulnerability amongst the remote miss group – can support endurance with prevention measures amongst that group and help flatten the curve.

Communicating our strengths, transparently discussing our weaknesses, and better understanding underlying emotions for ourselves and our patients may help save lives. As physicians, that is our daily practice, unchanged even as medicine takes center stage in our national conversation.

Dr. Walthall completed his internal medicine residency at the Medical University of South Carolina in Charleston, SC. After residency, he joined the faculty at MUSC in the Division of Hospital Medicine. He is also interested in systems-based care and has taken on the role of physician advisor. This essay appeared first on The Hospital Leader, the official blog of SHM.

Background: The PARTHENON clinical development program has conducted several clinical trials to assess the effectiveness of ticagrelor in multiple cardiovascular diseases. A prior study revealed the addition of ticagrelor to aspirin in patients with history of MI showed a small benefit in cardiovascular outcomes but with increased bleeding risk. While this effect was seen in both patients with and without diabetes, the absolute benefit for those with diabetes was considered large because of their higher baseline risk. Given this, investigators wanted to know if addition of ticagrelor to aspirin could also be beneficial in diabetics with known coronary disease but without history of MI or stroke.

Further studies into risk stratification based on prothrombotic versus bleeding risk could be beneficial in identifying specific groups that could benefit from DAPT. Conclusions from this study suggest the benefit of DAPT in diabetics does not outweigh its risk.

Bottom line: Addition of ticagrelor to aspirin in diabetic patients with stable coronary disease and no prior MI or stroke is not recommended.

Citation: Steg PG et al. Ticagrelor in patients with stable coronary disease and diabetes. N Eng J Med. 2019 Oct 3;381(14):1309-20.

Dr. Breitbach is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: The PARTHENON clinical development program has conducted several clinical trials to assess the effectiveness of ticagrelor in multiple cardiovascular diseases. A prior study revealed the addition of ticagrelor to aspirin in patients with history of MI showed a small benefit in cardiovascular outcomes but with increased bleeding risk. While this effect was seen in both patients with and without diabetes, the absolute benefit for those with diabetes was considered large because of their higher baseline risk. Given this, investigators wanted to know if addition of ticagrelor to aspirin could also be beneficial in diabetics with known coronary disease but without history of MI or stroke.

Further studies into risk stratification based on prothrombotic versus bleeding risk could be beneficial in identifying specific groups that could benefit from DAPT. Conclusions from this study suggest the benefit of DAPT in diabetics does not outweigh its risk.

Bottom line: Addition of ticagrelor to aspirin in diabetic patients with stable coronary disease and no prior MI or stroke is not recommended.

Citation: Steg PG et al. Ticagrelor in patients with stable coronary disease and diabetes. N Eng J Med. 2019 Oct 3;381(14):1309-20.

Dr. Breitbach is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: The PARTHENON clinical development program has conducted several clinical trials to assess the effectiveness of ticagrelor in multiple cardiovascular diseases. A prior study revealed the addition of ticagrelor to aspirin in patients with history of MI showed a small benefit in cardiovascular outcomes but with increased bleeding risk. While this effect was seen in both patients with and without diabetes, the absolute benefit for those with diabetes was considered large because of their higher baseline risk. Given this, investigators wanted to know if addition of ticagrelor to aspirin could also be beneficial in diabetics with known coronary disease but without history of MI or stroke.

Further studies into risk stratification based on prothrombotic versus bleeding risk could be beneficial in identifying specific groups that could benefit from DAPT. Conclusions from this study suggest the benefit of DAPT in diabetics does not outweigh its risk.

Bottom line: Addition of ticagrelor to aspirin in diabetic patients with stable coronary disease and no prior MI or stroke is not recommended.

Citation: Steg PG et al. Ticagrelor in patients with stable coronary disease and diabetes. N Eng J Med. 2019 Oct 3;381(14):1309-20.

Dr. Breitbach is assistant professor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Once upon a time, physicians wrote letters to peers and colleagues around the world, sharing their medical discoveries, theories, case reports, and questions; conferring on problems; and then waiting for return mail to bring a reply. And the science of medicine advanced at a glacial pace.

Today, communication in multiple mediums flows much faster, almost instantaneously, between many more physicians, regardless of distance, addressing a much greater complexity of medical topics and treatments. And one of the chief mediums for this rapid electronic conversation among doctors is Twitter, according to Charlie Wray, DO, MS, a hospitalist at the University of California, San Francisco.

Dr. Wray, associate editor and digital media editor for the Journal of Hospital Medicine, is one of the moderators of #JHMchat, a monthly get-together on Twitter for interested hospitalists to link up virtually; respond to questions posed by JHM editors and other moderators; exchange perspectives, experiences, and tips with their peers; and build professional relationships and personal friendships. Relationship building has become particularly important in the age of COVID-19, when opportunities to connect in person at events such as SHM’s annual conferences have been curtailed.

The online #JHMchat community began in 2015, shortly after Dr. Wray completed a hospitalist research fellowship at the University of Chicago. His fellowship mentor, Vineet Arora, MD, MAPP, MHM, associate chief medical officer for the clinical learning environment at University of Chicago Medicine, had noticed how other online medical communities were engaging in discussions around different topics.

“She thought it could be a great way for hospitalists to meet online and talk about the articles published in JHM,” Dr. Wray explained. “We were all getting into social media and learning how to moderate interactive discussions such as Twitter.”

The chat’s founders approached JHM’s then-editor Andrew Auerbach, MD, MHM, a hospitalist at UCSF, who agreed that it was a great idea. They asked Christopher Moriates, MD, author of a recently published paper on the advisability of nebulized bronchodilators for obstructive pulmonary symptoms and assistant dean for health care value at the University of Texas, Austin, to come on the chat and talk about his paper. Visiting Dr. Arora at the time, he joined her in her living room for the first chat on Oct. 12, 2015. Seventy-five participants posted 431 tweets, with a total of 2 million Twitter impressions, suggesting that they had tapped a latent need.

How the chat works

To participate in the JHM chats on Twitter, one needs to open an account on the platform (it’s free) and follow the Journal’s Twitter feed (@jhospmedicine). But that’s pretty much it, Dr. Wray said. The group convenes on a Monday evening each month for an hour, starting at 9 p.m. Eastern time. Upcoming chats and topics are announced on Twitter and at SHM’s website.

The chats have grown and evolved since 2015, shifting in focus given recent social upheavals over the pandemic and heated discussions about diversity, equity, and racial justice in medicine, he said. “When COVID hit, the journal’s editor – Dr. Samir Shah – recognized that we were in a unique moment with the pandemic. The journal took advantage of the opportunity to publish a lot more personal perspectives and viewpoints around COVID, along with a special issue devoted to social justice.”

Moderators for the chat typically choose three or four questions based on recently published articles or other relevant topics, such as racial inequities in health care or how to apply military principles to hospital medicine leadership. “We reach out to authors and tell them they can explain their articles to interested readers through the chat. I can’t think of a single one who said no. They see the opportunity to highlight their work and engage with readers who want to ask them questions,” Dr. Wray said.

The moderators’ questions are posed to stimulate participation, but another goal is to use that hour for networking. “It’s a powerful tool to allow SHM members to engage with each other,” he said. “Sometimes the chat has the feeling of trying to drink water from a fire hose – with the messages flashing past so quickly. But the key is not to try to respond to everything but rather to follow those threads that particularly interest you. We encourage you to engage, but it’s totally fine if you just sit back and observe. One thing we have done to make it a little more formal is to offer CME credits for participants.”

The chat welcomes hospitalists and nonhospitalists, nurse practitioners, physician assistants, academics, and nonacademics. “No matter how engaged you are with Twitter, if you have 10,000 followers or 10, we’ll amplify your voice,” he said. “We also have medical students participating and consider their perspectives valuable, too.”

Dr. Wray identified three main types of participants in the monthly chats. The first are regulars who come every month, rain or shine. Like the character Norm in the old television comedy “Cheers,” everybody knows their name. They become friends, sharing and reveling in each other’s accomplishments. “These are people who have multiple connections, personally and professionally, at a lot of different levels. I probably know a hundred or more people who I’ve primarily gotten to know online.”

A second and larger group might be drawn in because of an interest in a specific topic or article, but they’re also welcome to participate in the chat. And the third group may lurk in the background, following along but not commenting. The size of that third group is unknown, but metrics from SHM show a total of 796 participants posting 4,088 tweets during chats in 2020 (for an average of 132 participants and 681 tweets per chat). This adds up to a total of 34 million impressions across the platform for #JHMchat tweets for the year.
 

Creating community online

“Why do we do it? It’s difficult to read all of the relevant published articles and keep up to date,” said Dr. Arora, a medical educator whose job at Chicago Medicine is to improve the clinical learning environment for trainees and staff by aligning learning with the health system’s institutional quality, safety and value missions.

“Our idea was to bring together a kind of virtual journal club and have discussions around topics such as: how do you create a shared vision on rounds? How do you integrate that into clinical practice? How do we preserve work/life balance or address structural racism?” she said. Other topics have included work flow concerns, burnout, difficult conversations with patients, and career planning.

“The people we’re trying to reach are hospitalists – and they’re busy at the front lines of care. We also thought this was an interesting way to raise the journal’s profile and spark broader interest in the articles it publishes. But it’s really about creating community, with people who look forward to talking and connecting with each other each month through the chats,” Dr. Arora said. If they miss a chat, they feel they’ve missed important interactions.

“Many times when people log onto the chat, they give a status report on where they are at, such as ‘I’m home putting my kids to bed,’ or ‘I’m on call tonight,’ ” she added. “People are willing to engage with the medium because it’s easy to engage with. We can forget that physicians are like everyone else. They like to learn, but they want that learning to be fun.”

On Dec. 14, 2020, at 9 p.m. Eastern time, the first question for the monthly #JHMchat was posted: How will caring for COVID-19 patients this winter differ from caring for patients in the first wave? Given that another surge of hospitalized COVID patients is looming, participants posted that they feel familiar and more confident with effective clinical strategies for hospitalized COVID patients, having learned so much more about the virus. But they’re facing greater numbers of patients than in prior surges. “In March, we were in crisis, now we’re in complexity,” one noted.

Joining the moderators was the Pediatric Overflow Planning Contingency Response Network (POPCoRN), a group formed earlier this year to help mobilize pediatric medical capacity for COVID patients during pandemic surges (see “POPCoRN network mobilizes pediatric capacity during pandemic,” The Hospitalist, April 30, 2020). One of its questions involved the redeployment of physicians in response to COVID demands and what, for example, pediatric hospitalists need as resources and tools when they are reassigned to adult patients or to new roles in unfamiliar settings. A variety of educational resources were cited from POPCoRN, SHM, and ImproveDX, among others.
 

Defining medical communication

Another chat moderator is Angela Castellanos, MD, a pediatric hospitalist at Tufts Medical Center in Boston. Dr. Castellanos did a 1-year, full-time fellowship right after residency at the New England Journal of Medicine, participating hands-on as a member of the editorial team for the print and online editions of the venerable journal. She is now doing a digital media fellowship with JHM, a part-time commitment while holding down a full-time job as a hospitalist. She also puts together a Spanish language podcast covering primary care pediatric issues for parents and families.

“I’m interested in medical communication generally, as I try to figure out what that means,” she said. “I have continued to look for ways to be part of the social media community and to be more creative about it. The JHM fellowship came at a perfect time for me to learn to do more in digital media.”

COVID has created new opportunities for more immediate dialogue with colleagues – what are they seeing and what’s working in the absence of clinical trials, she explained. “That’s how we communicate, as a way to get information out fast, such as when hospitals began proning COVID patients to make it easier for them to breathe.”

Dr. Castellanos said she grew up with text messaging and social media and wants to continue to grow her skills in this area. “I think I developed some skills at NEJM, but the opportunity to see how they do things at another journal with a different mission was also valuable. I get to share the space with people in academic settings and leaders in my field. I tweet at them; they tweet at me. These two fellowships have given me unique insights and mentorships. I know I want to continue doing pediatric hospital medicine and to engage academically and learn how to do research.”

Twitter sometimes gets a bad reputation for hostile or incendiary posts, Dr. Wray noted. “If you look at social media writ large, it can sometimes seem like a dumpster fire.” But what has happened in the medical community and in most medical Twitter encounters is a more cordial approach to conversations. “People who work in medicine converse with each other, with room for respectful disagreements. We’re extra supportive of each other,” he said.

“I think if hospitalists are looking for a community of peers, to engage with them and network and to find colleagues in similar circumstances, the JHM chat is such a fantastic place,” Dr. Wray concluded. “Don’t just come once, come several times, meet people along the way. For me, one of the most beneficial ways to advance my career has been by connecting with people through the chat. It allows me to share my work and success with the hospitalist community, as well as highlighting my trainees’ and colleagues’ successes, and it has created opportunities I never would have expected for getting involved in other projects.”

Once upon a time, physicians wrote letters to peers and colleagues around the world, sharing their medical discoveries, theories, case reports, and questions; conferring on problems; and then waiting for return mail to bring a reply. And the science of medicine advanced at a glacial pace.

Today, communication in multiple mediums flows much faster, almost instantaneously, between many more physicians, regardless of distance, addressing a much greater complexity of medical topics and treatments. And one of the chief mediums for this rapid electronic conversation among doctors is Twitter, according to Charlie Wray, DO, MS, a hospitalist at the University of California, San Francisco.

Dr. Wray, associate editor and digital media editor for the Journal of Hospital Medicine, is one of the moderators of #JHMchat, a monthly get-together on Twitter for interested hospitalists to link up virtually; respond to questions posed by JHM editors and other moderators; exchange perspectives, experiences, and tips with their peers; and build professional relationships and personal friendships. Relationship building has become particularly important in the age of COVID-19, when opportunities to connect in person at events such as SHM’s annual conferences have been curtailed.

The online #JHMchat community began in 2015, shortly after Dr. Wray completed a hospitalist research fellowship at the University of Chicago. His fellowship mentor, Vineet Arora, MD, MAPP, MHM, associate chief medical officer for the clinical learning environment at University of Chicago Medicine, had noticed how other online medical communities were engaging in discussions around different topics.

“She thought it could be a great way for hospitalists to meet online and talk about the articles published in JHM,” Dr. Wray explained. “We were all getting into social media and learning how to moderate interactive discussions such as Twitter.”

The chat’s founders approached JHM’s then-editor Andrew Auerbach, MD, MHM, a hospitalist at UCSF, who agreed that it was a great idea. They asked Christopher Moriates, MD, author of a recently published paper on the advisability of nebulized bronchodilators for obstructive pulmonary symptoms and assistant dean for health care value at the University of Texas, Austin, to come on the chat and talk about his paper. Visiting Dr. Arora at the time, he joined her in her living room for the first chat on Oct. 12, 2015. Seventy-five participants posted 431 tweets, with a total of 2 million Twitter impressions, suggesting that they had tapped a latent need.

How the chat works

To participate in the JHM chats on Twitter, one needs to open an account on the platform (it’s free) and follow the Journal’s Twitter feed (@jhospmedicine). But that’s pretty much it, Dr. Wray said. The group convenes on a Monday evening each month for an hour, starting at 9 p.m. Eastern time. Upcoming chats and topics are announced on Twitter and at SHM’s website.

The chats have grown and evolved since 2015, shifting in focus given recent social upheavals over the pandemic and heated discussions about diversity, equity, and racial justice in medicine, he said. “When COVID hit, the journal’s editor – Dr. Samir Shah – recognized that we were in a unique moment with the pandemic. The journal took advantage of the opportunity to publish a lot more personal perspectives and viewpoints around COVID, along with a special issue devoted to social justice.”

Moderators for the chat typically choose three or four questions based on recently published articles or other relevant topics, such as racial inequities in health care or how to apply military principles to hospital medicine leadership. “We reach out to authors and tell them they can explain their articles to interested readers through the chat. I can’t think of a single one who said no. They see the opportunity to highlight their work and engage with readers who want to ask them questions,” Dr. Wray said.

The moderators’ questions are posed to stimulate participation, but another goal is to use that hour for networking. “It’s a powerful tool to allow SHM members to engage with each other,” he said. “Sometimes the chat has the feeling of trying to drink water from a fire hose – with the messages flashing past so quickly. But the key is not to try to respond to everything but rather to follow those threads that particularly interest you. We encourage you to engage, but it’s totally fine if you just sit back and observe. One thing we have done to make it a little more formal is to offer CME credits for participants.”

The chat welcomes hospitalists and nonhospitalists, nurse practitioners, physician assistants, academics, and nonacademics. “No matter how engaged you are with Twitter, if you have 10,000 followers or 10, we’ll amplify your voice,” he said. “We also have medical students participating and consider their perspectives valuable, too.”

Dr. Wray identified three main types of participants in the monthly chats. The first are regulars who come every month, rain or shine. Like the character Norm in the old television comedy “Cheers,” everybody knows their name. They become friends, sharing and reveling in each other’s accomplishments. “These are people who have multiple connections, personally and professionally, at a lot of different levels. I probably know a hundred or more people who I’ve primarily gotten to know online.”

A second and larger group might be drawn in because of an interest in a specific topic or article, but they’re also welcome to participate in the chat. And the third group may lurk in the background, following along but not commenting. The size of that third group is unknown, but metrics from SHM show a total of 796 participants posting 4,088 tweets during chats in 2020 (for an average of 132 participants and 681 tweets per chat). This adds up to a total of 34 million impressions across the platform for #JHMchat tweets for the year.
 

Creating community online

“Why do we do it? It’s difficult to read all of the relevant published articles and keep up to date,” said Dr. Arora, a medical educator whose job at Chicago Medicine is to improve the clinical learning environment for trainees and staff by aligning learning with the health system’s institutional quality, safety and value missions.

“Our idea was to bring together a kind of virtual journal club and have discussions around topics such as: how do you create a shared vision on rounds? How do you integrate that into clinical practice? How do we preserve work/life balance or address structural racism?” she said. Other topics have included work flow concerns, burnout, difficult conversations with patients, and career planning.

“The people we’re trying to reach are hospitalists – and they’re busy at the front lines of care. We also thought this was an interesting way to raise the journal’s profile and spark broader interest in the articles it publishes. But it’s really about creating community, with people who look forward to talking and connecting with each other each month through the chats,” Dr. Arora said. If they miss a chat, they feel they’ve missed important interactions.

“Many times when people log onto the chat, they give a status report on where they are at, such as ‘I’m home putting my kids to bed,’ or ‘I’m on call tonight,’ ” she added. “People are willing to engage with the medium because it’s easy to engage with. We can forget that physicians are like everyone else. They like to learn, but they want that learning to be fun.”

On Dec. 14, 2020, at 9 p.m. Eastern time, the first question for the monthly #JHMchat was posted: How will caring for COVID-19 patients this winter differ from caring for patients in the first wave? Given that another surge of hospitalized COVID patients is looming, participants posted that they feel familiar and more confident with effective clinical strategies for hospitalized COVID patients, having learned so much more about the virus. But they’re facing greater numbers of patients than in prior surges. “In March, we were in crisis, now we’re in complexity,” one noted.

Joining the moderators was the Pediatric Overflow Planning Contingency Response Network (POPCoRN), a group formed earlier this year to help mobilize pediatric medical capacity for COVID patients during pandemic surges (see “POPCoRN network mobilizes pediatric capacity during pandemic,” The Hospitalist, April 30, 2020). One of its questions involved the redeployment of physicians in response to COVID demands and what, for example, pediatric hospitalists need as resources and tools when they are reassigned to adult patients or to new roles in unfamiliar settings. A variety of educational resources were cited from POPCoRN, SHM, and ImproveDX, among others.
 

Defining medical communication

Another chat moderator is Angela Castellanos, MD, a pediatric hospitalist at Tufts Medical Center in Boston. Dr. Castellanos did a 1-year, full-time fellowship right after residency at the New England Journal of Medicine, participating hands-on as a member of the editorial team for the print and online editions of the venerable journal. She is now doing a digital media fellowship with JHM, a part-time commitment while holding down a full-time job as a hospitalist. She also puts together a Spanish language podcast covering primary care pediatric issues for parents and families.

“I’m interested in medical communication generally, as I try to figure out what that means,” she said. “I have continued to look for ways to be part of the social media community and to be more creative about it. The JHM fellowship came at a perfect time for me to learn to do more in digital media.”

COVID has created new opportunities for more immediate dialogue with colleagues – what are they seeing and what’s working in the absence of clinical trials, she explained. “That’s how we communicate, as a way to get information out fast, such as when hospitals began proning COVID patients to make it easier for them to breathe.”

Dr. Castellanos said she grew up with text messaging and social media and wants to continue to grow her skills in this area. “I think I developed some skills at NEJM, but the opportunity to see how they do things at another journal with a different mission was also valuable. I get to share the space with people in academic settings and leaders in my field. I tweet at them; they tweet at me. These two fellowships have given me unique insights and mentorships. I know I want to continue doing pediatric hospital medicine and to engage academically and learn how to do research.”

Twitter sometimes gets a bad reputation for hostile or incendiary posts, Dr. Wray noted. “If you look at social media writ large, it can sometimes seem like a dumpster fire.” But what has happened in the medical community and in most medical Twitter encounters is a more cordial approach to conversations. “People who work in medicine converse with each other, with room for respectful disagreements. We’re extra supportive of each other,” he said.

“I think if hospitalists are looking for a community of peers, to engage with them and network and to find colleagues in similar circumstances, the JHM chat is such a fantastic place,” Dr. Wray concluded. “Don’t just come once, come several times, meet people along the way. For me, one of the most beneficial ways to advance my career has been by connecting with people through the chat. It allows me to share my work and success with the hospitalist community, as well as highlighting my trainees’ and colleagues’ successes, and it has created opportunities I never would have expected for getting involved in other projects.”

Once upon a time, physicians wrote letters to peers and colleagues around the world, sharing their medical discoveries, theories, case reports, and questions; conferring on problems; and then waiting for return mail to bring a reply. And the science of medicine advanced at a glacial pace.

Today, communication in multiple mediums flows much faster, almost instantaneously, between many more physicians, regardless of distance, addressing a much greater complexity of medical topics and treatments. And one of the chief mediums for this rapid electronic conversation among doctors is Twitter, according to Charlie Wray, DO, MS, a hospitalist at the University of California, San Francisco.

Dr. Wray, associate editor and digital media editor for the Journal of Hospital Medicine, is one of the moderators of #JHMchat, a monthly get-together on Twitter for interested hospitalists to link up virtually; respond to questions posed by JHM editors and other moderators; exchange perspectives, experiences, and tips with their peers; and build professional relationships and personal friendships. Relationship building has become particularly important in the age of COVID-19, when opportunities to connect in person at events such as SHM’s annual conferences have been curtailed.

The online #JHMchat community began in 2015, shortly after Dr. Wray completed a hospitalist research fellowship at the University of Chicago. His fellowship mentor, Vineet Arora, MD, MAPP, MHM, associate chief medical officer for the clinical learning environment at University of Chicago Medicine, had noticed how other online medical communities were engaging in discussions around different topics.

“She thought it could be a great way for hospitalists to meet online and talk about the articles published in JHM,” Dr. Wray explained. “We were all getting into social media and learning how to moderate interactive discussions such as Twitter.”

The chat’s founders approached JHM’s then-editor Andrew Auerbach, MD, MHM, a hospitalist at UCSF, who agreed that it was a great idea. They asked Christopher Moriates, MD, author of a recently published paper on the advisability of nebulized bronchodilators for obstructive pulmonary symptoms and assistant dean for health care value at the University of Texas, Austin, to come on the chat and talk about his paper. Visiting Dr. Arora at the time, he joined her in her living room for the first chat on Oct. 12, 2015. Seventy-five participants posted 431 tweets, with a total of 2 million Twitter impressions, suggesting that they had tapped a latent need.

How the chat works

To participate in the JHM chats on Twitter, one needs to open an account on the platform (it’s free) and follow the Journal’s Twitter feed (@jhospmedicine). But that’s pretty much it, Dr. Wray said. The group convenes on a Monday evening each month for an hour, starting at 9 p.m. Eastern time. Upcoming chats and topics are announced on Twitter and at SHM’s website.

The chats have grown and evolved since 2015, shifting in focus given recent social upheavals over the pandemic and heated discussions about diversity, equity, and racial justice in medicine, he said. “When COVID hit, the journal’s editor – Dr. Samir Shah – recognized that we were in a unique moment with the pandemic. The journal took advantage of the opportunity to publish a lot more personal perspectives and viewpoints around COVID, along with a special issue devoted to social justice.”

Moderators for the chat typically choose three or four questions based on recently published articles or other relevant topics, such as racial inequities in health care or how to apply military principles to hospital medicine leadership. “We reach out to authors and tell them they can explain their articles to interested readers through the chat. I can’t think of a single one who said no. They see the opportunity to highlight their work and engage with readers who want to ask them questions,” Dr. Wray said.

The moderators’ questions are posed to stimulate participation, but another goal is to use that hour for networking. “It’s a powerful tool to allow SHM members to engage with each other,” he said. “Sometimes the chat has the feeling of trying to drink water from a fire hose – with the messages flashing past so quickly. But the key is not to try to respond to everything but rather to follow those threads that particularly interest you. We encourage you to engage, but it’s totally fine if you just sit back and observe. One thing we have done to make it a little more formal is to offer CME credits for participants.”

The chat welcomes hospitalists and nonhospitalists, nurse practitioners, physician assistants, academics, and nonacademics. “No matter how engaged you are with Twitter, if you have 10,000 followers or 10, we’ll amplify your voice,” he said. “We also have medical students participating and consider their perspectives valuable, too.”

Dr. Wray identified three main types of participants in the monthly chats. The first are regulars who come every month, rain or shine. Like the character Norm in the old television comedy “Cheers,” everybody knows their name. They become friends, sharing and reveling in each other’s accomplishments. “These are people who have multiple connections, personally and professionally, at a lot of different levels. I probably know a hundred or more people who I’ve primarily gotten to know online.”

A second and larger group might be drawn in because of an interest in a specific topic or article, but they’re also welcome to participate in the chat. And the third group may lurk in the background, following along but not commenting. The size of that third group is unknown, but metrics from SHM show a total of 796 participants posting 4,088 tweets during chats in 2020 (for an average of 132 participants and 681 tweets per chat). This adds up to a total of 34 million impressions across the platform for #JHMchat tweets for the year.
 

Creating community online

“Why do we do it? It’s difficult to read all of the relevant published articles and keep up to date,” said Dr. Arora, a medical educator whose job at Chicago Medicine is to improve the clinical learning environment for trainees and staff by aligning learning with the health system’s institutional quality, safety and value missions.

“Our idea was to bring together a kind of virtual journal club and have discussions around topics such as: how do you create a shared vision on rounds? How do you integrate that into clinical practice? How do we preserve work/life balance or address structural racism?” she said. Other topics have included work flow concerns, burnout, difficult conversations with patients, and career planning.

“The people we’re trying to reach are hospitalists – and they’re busy at the front lines of care. We also thought this was an interesting way to raise the journal’s profile and spark broader interest in the articles it publishes. But it’s really about creating community, with people who look forward to talking and connecting with each other each month through the chats,” Dr. Arora said. If they miss a chat, they feel they’ve missed important interactions.

“Many times when people log onto the chat, they give a status report on where they are at, such as ‘I’m home putting my kids to bed,’ or ‘I’m on call tonight,’ ” she added. “People are willing to engage with the medium because it’s easy to engage with. We can forget that physicians are like everyone else. They like to learn, but they want that learning to be fun.”

On Dec. 14, 2020, at 9 p.m. Eastern time, the first question for the monthly #JHMchat was posted: How will caring for COVID-19 patients this winter differ from caring for patients in the first wave? Given that another surge of hospitalized COVID patients is looming, participants posted that they feel familiar and more confident with effective clinical strategies for hospitalized COVID patients, having learned so much more about the virus. But they’re facing greater numbers of patients than in prior surges. “In March, we were in crisis, now we’re in complexity,” one noted.

Joining the moderators was the Pediatric Overflow Planning Contingency Response Network (POPCoRN), a group formed earlier this year to help mobilize pediatric medical capacity for COVID patients during pandemic surges (see “POPCoRN network mobilizes pediatric capacity during pandemic,” The Hospitalist, April 30, 2020). One of its questions involved the redeployment of physicians in response to COVID demands and what, for example, pediatric hospitalists need as resources and tools when they are reassigned to adult patients or to new roles in unfamiliar settings. A variety of educational resources were cited from POPCoRN, SHM, and ImproveDX, among others.
 

Defining medical communication

Another chat moderator is Angela Castellanos, MD, a pediatric hospitalist at Tufts Medical Center in Boston. Dr. Castellanos did a 1-year, full-time fellowship right after residency at the New England Journal of Medicine, participating hands-on as a member of the editorial team for the print and online editions of the venerable journal. She is now doing a digital media fellowship with JHM, a part-time commitment while holding down a full-time job as a hospitalist. She also puts together a Spanish language podcast covering primary care pediatric issues for parents and families.

“I’m interested in medical communication generally, as I try to figure out what that means,” she said. “I have continued to look for ways to be part of the social media community and to be more creative about it. The JHM fellowship came at a perfect time for me to learn to do more in digital media.”

COVID has created new opportunities for more immediate dialogue with colleagues – what are they seeing and what’s working in the absence of clinical trials, she explained. “That’s how we communicate, as a way to get information out fast, such as when hospitals began proning COVID patients to make it easier for them to breathe.”

Dr. Castellanos said she grew up with text messaging and social media and wants to continue to grow her skills in this area. “I think I developed some skills at NEJM, but the opportunity to see how they do things at another journal with a different mission was also valuable. I get to share the space with people in academic settings and leaders in my field. I tweet at them; they tweet at me. These two fellowships have given me unique insights and mentorships. I know I want to continue doing pediatric hospital medicine and to engage academically and learn how to do research.”

Twitter sometimes gets a bad reputation for hostile or incendiary posts, Dr. Wray noted. “If you look at social media writ large, it can sometimes seem like a dumpster fire.” But what has happened in the medical community and in most medical Twitter encounters is a more cordial approach to conversations. “People who work in medicine converse with each other, with room for respectful disagreements. We’re extra supportive of each other,” he said.

“I think if hospitalists are looking for a community of peers, to engage with them and network and to find colleagues in similar circumstances, the JHM chat is such a fantastic place,” Dr. Wray concluded. “Don’t just come once, come several times, meet people along the way. For me, one of the most beneficial ways to advance my career has been by connecting with people through the chat. It allows me to share my work and success with the hospitalist community, as well as highlighting my trainees’ and colleagues’ successes, and it has created opportunities I never would have expected for getting involved in other projects.”

The Janssen/Johnson & Johnson single-dose adenovirus vaccine provides 85% efficacy globally against severe COVID-19 illness, according to the highly anticipated interim phase 3 results announced this morning.

The efficacy against severe disease provided by the Janssen/J&J vaccine held true regardless of age, race/ethnicity, absence or presence of comorbidities, and geography. The 44,000-participant ENSEMBLE study was conducted in the United States, South America, and South Africa.

“The team is very diligently monitoring all the variants that come up, and there are literally thousands of these. We are acting in anticipation of a variant being a potential problem. The South African variant we too acted on right away. So we too are preparing that antigen for testing.

“With data today, we do see that not a single South African, after 28 days post vaccination, ended up needing to go to the hospital, no South African died who was vaccinated.

“We do see that 85%-plus protection in South African against severe disease. That is one of the most exciting results in the dataset today,” said Mathai Mammen, MD, PhD, global head of Janssen Research & Development.

The overall efficacy was 66% globally, 72% in the United States, 66% in Latin America, and 57% in South Africa against moderate to severe SARS-CoV-2 28 days post vaccination, officials from the National Institutes of Health and Janssen reported during a media briefing.

But the J&J vaccine has potential advantages over the existing two-dose Pfizer/BioNTech and Moderna mRNA vaccines because it’s single dose and has less stringent storage requirements – only regular refrigeration is needed versus a need to freeze the two-dose Pfizer/BioNTech and Moderna COVID-19 vaccines. The J&J vaccine can be refrigerated for up to 3 months at 36°-46° F (2°-8° C).

But the difference between these just-released efficacy figures and the 94%-95% efficacy provided by the existing Pfizer/BioNTech and Moderna mRNA vaccines generated many questions during the briefing.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said the focus should not just be on the overall numbers. “The most important thing from a public health standpoint domestically is to keep people out of the hospital and prevent them from getting severe illness,” he said. “Many in the general public might look at a number and want to know if they get symptomatic disease or not.”

“More important than preventing someone from getting some aches and a sore throat is to prevent people – particularly people who have underlying conditions and the elderly, the ones most susceptible to a severe outcome – [from getting] severe disease,” Dr. Fauci added. Prevention of severe outcomes in a high percentage of individuals “will alleviate so much of the stress, human suffering, and death.”

Dr. Fauci acknowledged that many people will naturally focus on the distinction between 72% efficacy and 94%-95% efficacy. “This could be a messaging challenge [but] you have to make sure people understand the implications.”

It is more complex, he added, than just asking people: “If you go to the door on the left, you get 94% or 95%. If you go to the door to the right, you get 72%. What door do you want to go to?”

Instead, the messaging should be that “this and the other vaccines we have are actually preventing severe disease to a very substantial degree.”
 

Company defends numbers

Janssen defended their efficacy findings, pointing out that it is not a fair comparison.

“The vaccine programs that went a couple of months ago, they ran their studies during different times, when the pandemic was less complex. There were not these variants, and there was not the same level of incidence, which puts pressure on vaccine efficacy,” said Mathai Mammen, MD, PhD, global head of research and development for Janssen.

“So the numbers cannot really be compared, and that does pose a messaging challenge,” he said. “But the reality is, if one was to run the same studies [for the Pfizer and Moderna vaccines] today you would likely see different results.”

Asked if the efficacy figures could affect vaccine hesitancy, National Institutes of Health Director Francis Collins, MD, PhD, said at the announcement that most reluctance among people to get vaccinated against SARS-CoV-2 stems from concerns about safety. “The safety record is extremely good for this vaccine, as it is for the others that have received emergency use authorization.”

Janssen/J&J plans to submit for emergency use authorization from the U.S. Food and Drug Administration next week, at which point the company plans to release more information on side effects, deaths, and patient subpopulation efficacy, and more from the ENSEMBLE trial.

Janssen is aiming to provide 1 billion doses by the end of this year.

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

The Janssen/Johnson & Johnson single-dose adenovirus vaccine provides 85% efficacy globally against severe COVID-19 illness, according to the highly anticipated interim phase 3 results announced this morning.

The efficacy against severe disease provided by the Janssen/J&J vaccine held true regardless of age, race/ethnicity, absence or presence of comorbidities, and geography. The 44,000-participant ENSEMBLE study was conducted in the United States, South America, and South Africa.

“The team is very diligently monitoring all the variants that come up, and there are literally thousands of these. We are acting in anticipation of a variant being a potential problem. The South African variant we too acted on right away. So we too are preparing that antigen for testing.

“With data today, we do see that not a single South African, after 28 days post vaccination, ended up needing to go to the hospital, no South African died who was vaccinated.

“We do see that 85%-plus protection in South African against severe disease. That is one of the most exciting results in the dataset today,” said Mathai Mammen, MD, PhD, global head of Janssen Research & Development.

The overall efficacy was 66% globally, 72% in the United States, 66% in Latin America, and 57% in South Africa against moderate to severe SARS-CoV-2 28 days post vaccination, officials from the National Institutes of Health and Janssen reported during a media briefing.

But the J&J vaccine has potential advantages over the existing two-dose Pfizer/BioNTech and Moderna mRNA vaccines because it’s single dose and has less stringent storage requirements – only regular refrigeration is needed versus a need to freeze the two-dose Pfizer/BioNTech and Moderna COVID-19 vaccines. The J&J vaccine can be refrigerated for up to 3 months at 36°-46° F (2°-8° C).

But the difference between these just-released efficacy figures and the 94%-95% efficacy provided by the existing Pfizer/BioNTech and Moderna mRNA vaccines generated many questions during the briefing.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said the focus should not just be on the overall numbers. “The most important thing from a public health standpoint domestically is to keep people out of the hospital and prevent them from getting severe illness,” he said. “Many in the general public might look at a number and want to know if they get symptomatic disease or not.”

“More important than preventing someone from getting some aches and a sore throat is to prevent people – particularly people who have underlying conditions and the elderly, the ones most susceptible to a severe outcome – [from getting] severe disease,” Dr. Fauci added. Prevention of severe outcomes in a high percentage of individuals “will alleviate so much of the stress, human suffering, and death.”

Dr. Fauci acknowledged that many people will naturally focus on the distinction between 72% efficacy and 94%-95% efficacy. “This could be a messaging challenge [but] you have to make sure people understand the implications.”

It is more complex, he added, than just asking people: “If you go to the door on the left, you get 94% or 95%. If you go to the door to the right, you get 72%. What door do you want to go to?”

Instead, the messaging should be that “this and the other vaccines we have are actually preventing severe disease to a very substantial degree.”
 

Company defends numbers

Janssen defended their efficacy findings, pointing out that it is not a fair comparison.

“The vaccine programs that went a couple of months ago, they ran their studies during different times, when the pandemic was less complex. There were not these variants, and there was not the same level of incidence, which puts pressure on vaccine efficacy,” said Mathai Mammen, MD, PhD, global head of research and development for Janssen.

“So the numbers cannot really be compared, and that does pose a messaging challenge,” he said. “But the reality is, if one was to run the same studies [for the Pfizer and Moderna vaccines] today you would likely see different results.”

Asked if the efficacy figures could affect vaccine hesitancy, National Institutes of Health Director Francis Collins, MD, PhD, said at the announcement that most reluctance among people to get vaccinated against SARS-CoV-2 stems from concerns about safety. “The safety record is extremely good for this vaccine, as it is for the others that have received emergency use authorization.”

Janssen/J&J plans to submit for emergency use authorization from the U.S. Food and Drug Administration next week, at which point the company plans to release more information on side effects, deaths, and patient subpopulation efficacy, and more from the ENSEMBLE trial.

Janssen is aiming to provide 1 billion doses by the end of this year.

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

The Janssen/Johnson & Johnson single-dose adenovirus vaccine provides 85% efficacy globally against severe COVID-19 illness, according to the highly anticipated interim phase 3 results announced this morning.

The efficacy against severe disease provided by the Janssen/J&J vaccine held true regardless of age, race/ethnicity, absence or presence of comorbidities, and geography. The 44,000-participant ENSEMBLE study was conducted in the United States, South America, and South Africa.

“The team is very diligently monitoring all the variants that come up, and there are literally thousands of these. We are acting in anticipation of a variant being a potential problem. The South African variant we too acted on right away. So we too are preparing that antigen for testing.

“With data today, we do see that not a single South African, after 28 days post vaccination, ended up needing to go to the hospital, no South African died who was vaccinated.

“We do see that 85%-plus protection in South African against severe disease. That is one of the most exciting results in the dataset today,” said Mathai Mammen, MD, PhD, global head of Janssen Research & Development.

The overall efficacy was 66% globally, 72% in the United States, 66% in Latin America, and 57% in South Africa against moderate to severe SARS-CoV-2 28 days post vaccination, officials from the National Institutes of Health and Janssen reported during a media briefing.

But the J&J vaccine has potential advantages over the existing two-dose Pfizer/BioNTech and Moderna mRNA vaccines because it’s single dose and has less stringent storage requirements – only regular refrigeration is needed versus a need to freeze the two-dose Pfizer/BioNTech and Moderna COVID-19 vaccines. The J&J vaccine can be refrigerated for up to 3 months at 36°-46° F (2°-8° C).

But the difference between these just-released efficacy figures and the 94%-95% efficacy provided by the existing Pfizer/BioNTech and Moderna mRNA vaccines generated many questions during the briefing.

Anthony Fauci, MD, director of the National Institute of Allergy and Infectious Diseases, said the focus should not just be on the overall numbers. “The most important thing from a public health standpoint domestically is to keep people out of the hospital and prevent them from getting severe illness,” he said. “Many in the general public might look at a number and want to know if they get symptomatic disease or not.”

“More important than preventing someone from getting some aches and a sore throat is to prevent people – particularly people who have underlying conditions and the elderly, the ones most susceptible to a severe outcome – [from getting] severe disease,” Dr. Fauci added. Prevention of severe outcomes in a high percentage of individuals “will alleviate so much of the stress, human suffering, and death.”

Dr. Fauci acknowledged that many people will naturally focus on the distinction between 72% efficacy and 94%-95% efficacy. “This could be a messaging challenge [but] you have to make sure people understand the implications.”

It is more complex, he added, than just asking people: “If you go to the door on the left, you get 94% or 95%. If you go to the door to the right, you get 72%. What door do you want to go to?”

Instead, the messaging should be that “this and the other vaccines we have are actually preventing severe disease to a very substantial degree.”
 

Company defends numbers

Janssen defended their efficacy findings, pointing out that it is not a fair comparison.

“The vaccine programs that went a couple of months ago, they ran their studies during different times, when the pandemic was less complex. There were not these variants, and there was not the same level of incidence, which puts pressure on vaccine efficacy,” said Mathai Mammen, MD, PhD, global head of research and development for Janssen.

“So the numbers cannot really be compared, and that does pose a messaging challenge,” he said. “But the reality is, if one was to run the same studies [for the Pfizer and Moderna vaccines] today you would likely see different results.”

Asked if the efficacy figures could affect vaccine hesitancy, National Institutes of Health Director Francis Collins, MD, PhD, said at the announcement that most reluctance among people to get vaccinated against SARS-CoV-2 stems from concerns about safety. “The safety record is extremely good for this vaccine, as it is for the others that have received emergency use authorization.”

Janssen/J&J plans to submit for emergency use authorization from the U.S. Food and Drug Administration next week, at which point the company plans to release more information on side effects, deaths, and patient subpopulation efficacy, and more from the ENSEMBLE trial.

Janssen is aiming to provide 1 billion doses by the end of this year.

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

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

A version of this article first appeared on WebMD.com.

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

A version of this article first appeared on WebMD.com.

The United States is facing a “Category 5” storm as coronavirus variants begin to spread across the country, one of the nation’s top infectious disease experts said Sunday.

“We are going to see something like we have not seen yet in this country,” Michael Osterholm, PhD, MPH, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, Minneapolis, said on NBC’s Meet the Press.

The United States has reported 467 cases of the coronavirus variant first identified in the United Kingdom, across 32 states, according to the CDC variant tracker. The United States has also reported three cases of the variant first identified in South Africa in South Carolina and Maryland. One case of the variant first identified in Brazil has been found in Minnesota.

Although overall COVID-19 cases and hospitalizations have declined during the past few weeks, another storm is brewing on the horizon with the variants, Dr. Osterholm told host Chuck Todd. The U.K. variant will likely cause a surge in COVID-19 cases during the next 6-14 weeks, he said. “You and I are sitting on this beach where it’s 70 degrees, perfectly blue skies, gentle breeze. But I see that hurricane 5, Category 5 or higher, 450 miles offshore. And telling people to evacuate on that nice blue sky day is going to be hard. But I can also tell you that hurricane is coming.”

Dr. Osterholm urged federal and state officials to vaccinate as many people as possible to reduce the oncoming storm. The United States has distributed 49.9 million doses and administered 31.1 million doses, according to the latest CDC data updated Sunday, including 25.2 million first doses and 5.6 million second doses.

Doling out more doses to older Americans, rather than holding onto the second dose of the two-shot regimen, is an urgent decision, Dr. Osterholm said.

“I think right now, in advance of this surge, we need to get as many one doses in as many people over 65 as we possibly can to reduce serious illnesses and deaths that are going to occur over the weeks ahead,” he said.

The U.K. variant will likely become the dominant coronavirus strain in the United States in coming weeks, Dr. Osterholm said, adding that COVID-19 vaccines should be able to protect against it. In the meantime, however, he’s worried that the variant will cause more infections and deaths until more people get vaccinated.

“What we have to do now is also anticipate this and understand that we’re going to have change quickly,” he said. “As fast as we’re opening restaurants, we’re likely going to be closing them in the near term.”

A version of this article first appeared on WebMD.com.

Patients with an implantable cardioverter defibrillator (ICD) should be warned that some newer models of smartphones equipped with magnets, such as the iPhone 12, can disable their device, inhibiting its lifesaving functions, according to investigators who tested and confirmed this effect.

SL/Getty Images

“Once the iPhone was brought close to the ICD over the left chest area, immediate suspension of ICD therapies was noted which persisted for the duration of the test,” reported the investigating team led by Joshua C. Greenberg, MD, who is an electrophysiology fellow at Henry Ford Hospital, Detroit. The results were published in Heart Rhythm.

The American Heart Association has already cautioned that magnetic fields can inhibit the pulse generators for ICDs and pacemakers. On the AHA website, there is a list of devices and their potential for functional interference, but cell phones and other common devices are identified as posing a low risk.

The most recent iPhone and perhaps other advanced smartphones appear to be different. According to the authors of a study that tested the iPhone 12, this model has a circular array of magnets around a central charging coil. This array interacts with Apple’s proprietary MagSafe technology, which accelerates charging. The magnets also serve to orient the phone on the charger and enable other MagSafe accessories.

The authors of the new study were concerned that this array of magnets might be sufficiently strong to interfere with ICDs or other devices at risk. In a previously published study, the strength of a magnetic field sufficient to interfere with implantable cardiac devices was estimated to be at least 10 gauss.

Tests were performed on a patient wearing a Medtronic ICD.

“Once the iPhone was brought close to the ICD over the left chest area, immediate suspension of ICD therapies was noted,” according to the authors of the study. The functional loss of the ICS persisted for the duration of proximity. It was reproduced multiple times and with multiple phone positions.

Previous studies have provided evidence that earlier models do not share this risk. In a study testing the iPhone 6 and an Apple Watch in 148 patients with various types of implantable electronic devices, including pacemakers, cardioverter defibrillators, resynchronization defibrillators, and resynchronization pacemakers, only one instance of interference was observed in 1,352 tests.

With wand telemetry, iPhone-induced interferences could be detected with the iPhone 6 in 14% of the patients, but these did not appear to be clinically meaningful, and this type of interference could not be detected with the Apple Watch, according to the report. The single observed interaction, which was between an iPhone 6 and a dual-chamber pacemaker, suggested device-device interactions are uncommon.

More recently, a woman with a single-chamber Medtronic ICD who went to sleep wearing an Apple Watch was awoken by warning beeps from her cardiac device, according to a case report published online. The Apple watch became the prime suspect in causing the ICD warning when proximity of the watch reproduced the warning during clinical examination. However, the magnetic interference was ultimately found to be emanating from the wristband, not the watch.

This case prompted additional studies with Fitbit and other Apple Watch wristbands. Both wristbands contain magnets used to track heart rate. Both were found capable of deactivating ICDs at distances of approximately 2 cm. On the basis of these results, the authors concluded that patients should be counseled about the risk posed by wristbands used in fitness tracking, concluding that they should be kept at least 6 inches away from ICDs and not worn while sleeping.

On their website, Apple maintains a page that specifically warns about the potential for interactions between iPhone 12s and medical devices . Although there is an acknowledgment that the iPhone12 contains more magnets than prior iPhone models, it is stated that iPhone 12 models are “not expected to pose a greater risk of magnetic interference to medical devices than prior iPhone models.” Nevertheless, the Apple instructions advise keeping the iPhone and MagSafe accessories more than 6 inches away from medical devices.

Dr. Greenberg and coinvestigators concluded that the iPhone 12 does pose a greater risk to the dysfunction of ICDs and other medical devices because of the more powerful magnets. As a result, the study brings forward “an important public health issue concerning the newer generation iPhone 12.”

Well aware of this issue and this study, Bruce L. Wilkoff, MD, director of cardiac pacing and tachyarrhythmia devices, Cleveland Clinic, agreed. He said the focus should not be restricted to the iPhone 12 series but other wearable devices as alluded to in the study.

“Pacemakers and implantable defibrillators are designed to respond to magnets for important reasons, but magnets have many common uses,” he said. These can change the function of the implantable cardiac devise, but “it is temporary and only when placed in close proximity.”

The solution is simple. “Patients should be careful to avoid locating these objects near these devices,” Dr. Wilkoff said.

However, the first step is awareness. According to the study authors, devices with magnets powerful enough to impair function of implantable devices, such as the iPhone 12 “can potentially inhibit lifesaving therapy.”

Patients should be counseled and provided with practical steps, according to the authors. This includes keeping these devices out of pockets near implantable devices. They called for more noise from makers of smartphones and other devices with strong enough magnets to alter pacemaker and ICD function, and they advised physicians to draw awareness to this issue.

Dr. Greenberg reported no potential conflicts of interest.

Patients with an implantable cardioverter defibrillator (ICD) should be warned that some newer models of smartphones equipped with magnets, such as the iPhone 12, can disable their device, inhibiting its lifesaving functions, according to investigators who tested and confirmed this effect.

SL/Getty Images

“Once the iPhone was brought close to the ICD over the left chest area, immediate suspension of ICD therapies was noted which persisted for the duration of the test,” reported the investigating team led by Joshua C. Greenberg, MD, who is an electrophysiology fellow at Henry Ford Hospital, Detroit. The results were published in Heart Rhythm.

The American Heart Association has already cautioned that magnetic fields can inhibit the pulse generators for ICDs and pacemakers. On the AHA website, there is a list of devices and their potential for functional interference, but cell phones and other common devices are identified as posing a low risk.

The most recent iPhone and perhaps other advanced smartphones appear to be different. According to the authors of a study that tested the iPhone 12, this model has a circular array of magnets around a central charging coil. This array interacts with Apple’s proprietary MagSafe technology, which accelerates charging. The magnets also serve to orient the phone on the charger and enable other MagSafe accessories.

The authors of the new study were concerned that this array of magnets might be sufficiently strong to interfere with ICDs or other devices at risk. In a previously published study, the strength of a magnetic field sufficient to interfere with implantable cardiac devices was estimated to be at least 10 gauss.

Tests were performed on a patient wearing a Medtronic ICD.

“Once the iPhone was brought close to the ICD over the left chest area, immediate suspension of ICD therapies was noted,” according to the authors of the study. The functional loss of the ICS persisted for the duration of proximity. It was reproduced multiple times and with multiple phone positions.

Previous studies have provided evidence that earlier models do not share this risk. In a study testing the iPhone 6 and an Apple Watch in 148 patients with various types of implantable electronic devices, including pacemakers, cardioverter defibrillators, resynchronization defibrillators, and resynchronization pacemakers, only one instance of interference was observed in 1,352 tests.

With wand telemetry, iPhone-induced interferences could be detected with the iPhone 6 in 14% of the patients, but these did not appear to be clinically meaningful, and this type of interference could not be detected with the Apple Watch, according to the report. The single observed interaction, which was between an iPhone 6 and a dual-chamber pacemaker, suggested device-device interactions are uncommon.

More recently, a woman with a single-chamber Medtronic ICD who went to sleep wearing an Apple Watch was awoken by warning beeps from her cardiac device, according to a case report published online. The Apple watch became the prime suspect in causing the ICD warning when proximity of the watch reproduced the warning during clinical examination. However, the magnetic interference was ultimately found to be emanating from the wristband, not the watch.

This case prompted additional studies with Fitbit and other Apple Watch wristbands. Both wristbands contain magnets used to track heart rate. Both were found capable of deactivating ICDs at distances of approximately 2 cm. On the basis of these results, the authors concluded that patients should be counseled about the risk posed by wristbands used in fitness tracking, concluding that they should be kept at least 6 inches away from ICDs and not worn while sleeping.

On their website, Apple maintains a page that specifically warns about the potential for interactions between iPhone 12s and medical devices . Although there is an acknowledgment that the iPhone12 contains more magnets than prior iPhone models, it is stated that iPhone 12 models are “not expected to pose a greater risk of magnetic interference to medical devices than prior iPhone models.” Nevertheless, the Apple instructions advise keeping the iPhone and MagSafe accessories more than 6 inches away from medical devices.

Dr. Greenberg and coinvestigators concluded that the iPhone 12 does pose a greater risk to the dysfunction of ICDs and other medical devices because of the more powerful magnets. As a result, the study brings forward “an important public health issue concerning the newer generation iPhone 12.”

Well aware of this issue and this study, Bruce L. Wilkoff, MD, director of cardiac pacing and tachyarrhythmia devices, Cleveland Clinic, agreed. He said the focus should not be restricted to the iPhone 12 series but other wearable devices as alluded to in the study.

“Pacemakers and implantable defibrillators are designed to respond to magnets for important reasons, but magnets have many common uses,” he said. These can change the function of the implantable cardiac devise, but “it is temporary and only when placed in close proximity.”

The solution is simple. “Patients should be careful to avoid locating these objects near these devices,” Dr. Wilkoff said.

However, the first step is awareness. According to the study authors, devices with magnets powerful enough to impair function of implantable devices, such as the iPhone 12 “can potentially inhibit lifesaving therapy.”

Patients should be counseled and provided with practical steps, according to the authors. This includes keeping these devices out of pockets near implantable devices. They called for more noise from makers of smartphones and other devices with strong enough magnets to alter pacemaker and ICD function, and they advised physicians to draw awareness to this issue.

Dr. Greenberg reported no potential conflicts of interest.

Patients with an implantable cardioverter defibrillator (ICD) should be warned that some newer models of smartphones equipped with magnets, such as the iPhone 12, can disable their device, inhibiting its lifesaving functions, according to investigators who tested and confirmed this effect.

SL/Getty Images

“Once the iPhone was brought close to the ICD over the left chest area, immediate suspension of ICD therapies was noted which persisted for the duration of the test,” reported the investigating team led by Joshua C. Greenberg, MD, who is an electrophysiology fellow at Henry Ford Hospital, Detroit. The results were published in Heart Rhythm.

The American Heart Association has already cautioned that magnetic fields can inhibit the pulse generators for ICDs and pacemakers. On the AHA website, there is a list of devices and their potential for functional interference, but cell phones and other common devices are identified as posing a low risk.

The most recent iPhone and perhaps other advanced smartphones appear to be different. According to the authors of a study that tested the iPhone 12, this model has a circular array of magnets around a central charging coil. This array interacts with Apple’s proprietary MagSafe technology, which accelerates charging. The magnets also serve to orient the phone on the charger and enable other MagSafe accessories.

The authors of the new study were concerned that this array of magnets might be sufficiently strong to interfere with ICDs or other devices at risk. In a previously published study, the strength of a magnetic field sufficient to interfere with implantable cardiac devices was estimated to be at least 10 gauss.

Tests were performed on a patient wearing a Medtronic ICD.

“Once the iPhone was brought close to the ICD over the left chest area, immediate suspension of ICD therapies was noted,” according to the authors of the study. The functional loss of the ICS persisted for the duration of proximity. It was reproduced multiple times and with multiple phone positions.

Previous studies have provided evidence that earlier models do not share this risk. In a study testing the iPhone 6 and an Apple Watch in 148 patients with various types of implantable electronic devices, including pacemakers, cardioverter defibrillators, resynchronization defibrillators, and resynchronization pacemakers, only one instance of interference was observed in 1,352 tests.

With wand telemetry, iPhone-induced interferences could be detected with the iPhone 6 in 14% of the patients, but these did not appear to be clinically meaningful, and this type of interference could not be detected with the Apple Watch, according to the report. The single observed interaction, which was between an iPhone 6 and a dual-chamber pacemaker, suggested device-device interactions are uncommon.

More recently, a woman with a single-chamber Medtronic ICD who went to sleep wearing an Apple Watch was awoken by warning beeps from her cardiac device, according to a case report published online. The Apple watch became the prime suspect in causing the ICD warning when proximity of the watch reproduced the warning during clinical examination. However, the magnetic interference was ultimately found to be emanating from the wristband, not the watch.

This case prompted additional studies with Fitbit and other Apple Watch wristbands. Both wristbands contain magnets used to track heart rate. Both were found capable of deactivating ICDs at distances of approximately 2 cm. On the basis of these results, the authors concluded that patients should be counseled about the risk posed by wristbands used in fitness tracking, concluding that they should be kept at least 6 inches away from ICDs and not worn while sleeping.

On their website, Apple maintains a page that specifically warns about the potential for interactions between iPhone 12s and medical devices . Although there is an acknowledgment that the iPhone12 contains more magnets than prior iPhone models, it is stated that iPhone 12 models are “not expected to pose a greater risk of magnetic interference to medical devices than prior iPhone models.” Nevertheless, the Apple instructions advise keeping the iPhone and MagSafe accessories more than 6 inches away from medical devices.

Dr. Greenberg and coinvestigators concluded that the iPhone 12 does pose a greater risk to the dysfunction of ICDs and other medical devices because of the more powerful magnets. As a result, the study brings forward “an important public health issue concerning the newer generation iPhone 12.”

Well aware of this issue and this study, Bruce L. Wilkoff, MD, director of cardiac pacing and tachyarrhythmia devices, Cleveland Clinic, agreed. He said the focus should not be restricted to the iPhone 12 series but other wearable devices as alluded to in the study.

“Pacemakers and implantable defibrillators are designed to respond to magnets for important reasons, but magnets have many common uses,” he said. These can change the function of the implantable cardiac devise, but “it is temporary and only when placed in close proximity.”

The solution is simple. “Patients should be careful to avoid locating these objects near these devices,” Dr. Wilkoff said.

However, the first step is awareness. According to the study authors, devices with magnets powerful enough to impair function of implantable devices, such as the iPhone 12 “can potentially inhibit lifesaving therapy.”

Patients should be counseled and provided with practical steps, according to the authors. This includes keeping these devices out of pockets near implantable devices. They called for more noise from makers of smartphones and other devices with strong enough magnets to alter pacemaker and ICD function, and they advised physicians to draw awareness to this issue.

Dr. Greenberg reported no potential conflicts of interest.

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

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

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

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

More people with fever and body aches are turning to NSAIDs to ease symptoms, but the drugs have come under new scrutiny as investigators work to determine whether they are a safe way to relieve the pain of COVID-19 vaccination or symptoms of the disease.

Early on in the pandemic, French health officials warned that NSAIDs, such as ibuprofen, could worsen coronavirus disease, and they recommended switching to acetaminophen instead.

The National Health Service in the United Kingdom followed with a similar recommendation for acetaminophen.

But the European Medicines Agency took a different approach, reporting “no scientific evidence” that NSAIDs could worsen COVID-19. The U.S. Food and Drug Administration also opted not to take a stance.

The debate prompted discussion on social media, with various reactions from around the world. It also inspired Craig Wilen, MD, PhD, from Yale University, New Haven, Conn., and associates to examine the effect of NSAIDs on COVID-19 infection and immune response. Their findings were published online Jan.20 in the Journal of Virology.

“It really bothered me that non–evidence-based decisions were driving the conversation,” Dr. Wilen said. “Millions of people are taking NSAIDs every day and clinical decisions about their care shouldn’t be made on a hypothesis.”

One theory is that NSAIDs alter susceptibility to infection by modifying ACE2. The drugs might also change the cell entry receptor for SARS-CoV-2, alter virus replication, or even modify the immune response.

British researchers, also questioning the safety of NSAIDs in patients with COVID-19, delved into National Health Service records to study two large groups of patients, some of whom were taking the pain relievers.

“We were watching the controversy and the lack of evidence and wanted to contribute,” lead investigator Angel Wong, PhD, from the London School of Hygiene and Tropical Medicine, said in an interview.

And with nearly 11 million NSAID prescriptions dispensed in primary care in England alone in the past 12 months, the inconsistency was concerning.

The team compared COVID-19–related deaths in two groups: one group of more than 700,000 people taking NSAIDs, including patients with rheumatoid arthritis and osteoarthritis; and another of almost 3.5 million people not on the medication.

NSAIDs work by inhibiting cyclooxygenase-1 and COX-2 enzymes in the body, which are crucial for the generation of prostaglandins. These lipid molecules play a role in inflammation and are blocked by NSAIDs.

The investigators found no evidence of a harmful effect of NSAIDs on COVID-19-related deaths; their results were published online Jan. 21 in the Annals of the Rheumatic Diseases.

The results, they pointed out, are in line with a Danish study that also showed no evidence of a higher risk for severe COVID-19 outcomes with NSAID use.

“It’s reassuring,” Dr. Wong said, “that patients can safely continue treatment.”
 

More new evidence

Dr. Wilen’s team found that SARS-CoV-2 infection stimulated COX-2 expression in human and mice cells. However, suppression of COX-2 by two commonly used NSAIDs, ibuprofen and meloxicam, had no effect on ACE2 expression, viral entry, or viral replication.

In their mouse model of SARS-CoV-2 infection, the investigators saw that NSAIDs impaired the production of proinflammatory cytokines and neutralizing antibodies. The findings suggest that NSAIDs influence COVID-19 outcomes by dampening the inflammatory response and production of protective antibodies, rather than modifying susceptibility to infection or viral replication.

Understanding the effect of NSAIDs on cytokine production is critical, Dr. Wilen pointed out, because they might be protective early in COVID-19 but pathologic at later stages.

Timing is crucial in the case of other immunomodulatory drugs. For example, dexamethasone lowers mortality in COVID-19 patients on respiratory support but is potentially harmful for those with milder disease.

There still is a lot to learn, Dr. Wilen acknowledged. “We may be seeing something similar going on with NSAIDs, where the timing of treatment is important.”

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

Background: A new update to the Choosing Wisely Campaign was released September 2019.

• Not routinely using broad respiratory viral testing and instead using more targeted approaches to respiratory pathogen tests (e.g., respiratory syncytial virus, influenza A/B, or group A pharyngitis) unless the results will lead to changes to or discontinuations of antimicrobial therapy or isolation.
• Not routinely testing for community gastrointestinal pathogens in patients that develop diarrhea 3 days after hospitalization and to primarily test for Clostridiodes difficile in these patients, unless they are immunocompromised or older adults.
• Not checking procalcitonin unless a specific evidence-based guideline is used for antibiotic stewardship, as it is often used incorrectly without benefit to the patient.
• Not ordering serology for Helicobacter pylori and instead ordering the stool antigen or breath test to test for active infection given higher sensitivity and specificity.
• Not repeating antibody tests for patients with history of hepatitis C and instead ordering a viral load if there is concern for reinfection.

Bottom line: Only order infectious disease tests that will guide changes in clinical management.

Citation: ASCP Effective Test Utilization Steering Committee. Thirty things patients and physicians should question. 2019 Sep 9. Choosingwisely.org.

Dr. Blount is clinical instructor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: A new update to the Choosing Wisely Campaign was released September 2019.

• Not routinely using broad respiratory viral testing and instead using more targeted approaches to respiratory pathogen tests (e.g., respiratory syncytial virus, influenza A/B, or group A pharyngitis) unless the results will lead to changes to or discontinuations of antimicrobial therapy or isolation.
• Not routinely testing for community gastrointestinal pathogens in patients that develop diarrhea 3 days after hospitalization and to primarily test for Clostridiodes difficile in these patients, unless they are immunocompromised or older adults.
• Not checking procalcitonin unless a specific evidence-based guideline is used for antibiotic stewardship, as it is often used incorrectly without benefit to the patient.
• Not ordering serology for Helicobacter pylori and instead ordering the stool antigen or breath test to test for active infection given higher sensitivity and specificity.
• Not repeating antibody tests for patients with history of hepatitis C and instead ordering a viral load if there is concern for reinfection.

Bottom line: Only order infectious disease tests that will guide changes in clinical management.

Citation: ASCP Effective Test Utilization Steering Committee. Thirty things patients and physicians should question. 2019 Sep 9. Choosingwisely.org.

Dr. Blount is clinical instructor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.

Background: A new update to the Choosing Wisely Campaign was released September 2019.

• Not routinely using broad respiratory viral testing and instead using more targeted approaches to respiratory pathogen tests (e.g., respiratory syncytial virus, influenza A/B, or group A pharyngitis) unless the results will lead to changes to or discontinuations of antimicrobial therapy or isolation.
• Not routinely testing for community gastrointestinal pathogens in patients that develop diarrhea 3 days after hospitalization and to primarily test for Clostridiodes difficile in these patients, unless they are immunocompromised or older adults.
• Not checking procalcitonin unless a specific evidence-based guideline is used for antibiotic stewardship, as it is often used incorrectly without benefit to the patient.
• Not ordering serology for Helicobacter pylori and instead ordering the stool antigen or breath test to test for active infection given higher sensitivity and specificity.
• Not repeating antibody tests for patients with history of hepatitis C and instead ordering a viral load if there is concern for reinfection.

Bottom line: Only order infectious disease tests that will guide changes in clinical management.

Citation: ASCP Effective Test Utilization Steering Committee. Thirty things patients and physicians should question. 2019 Sep 9. Choosingwisely.org.

Dr. Blount is clinical instructor of medicine, hospital medicine, at the Rocky Mountain Veterans Affairs Regional Medical Center, Aurora, Colo.