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Positive phase 3 top-line results for migraine prevention drug
AbbVie, the company developing the drug, has announced.
Top-line results from the ADVANCE trial, which evaluated atogepant 10, 30, and 60 mg, showed all three doses were associated with a significant reduction from baseline in mean monthly migraine days, compared with placebo.
There were also significant improvements in all six secondary endpoints with the two higher doses.
Data from the ADVANCE trial and a previous phase 2/3 trial will be the basis for regulatory submissions in the United States and other countries, AbbVie reported.
Decreased migraine days
The phase 3, multicenter, randomized, double-blind, placebo-controlled, parallel-group trial was designed to evaluate the efficacy, safety, and tolerability of oral atogepant for the prevention of migraine in those who experienced 4-14 migraine days per month.
A total of 910 patients were randomized to one of four treatment groups: 10 mg, 30 mg, or 60 mg of atogepant once daily or placebo. Efficacy analyses were based on the modified intent-to-treat population of 873 patients.
The primary endpoint was change from baseline in mean monthly migraine days during the 12-week treatment period. All atogepant dose groups met the primary endpoint and demonstrated significantly greater decreases in mean monthly migraine days, compared with placebo.
Mean monthly migraine days were reduced by 3.69 days with the 10-mg dose, 3.86 days with the 30-mg dose, and 4.2 days with the 60-mg dose of atogepant, compared with a reduction of 2.48 migraine days in the placebo group (P < .0001, all dose groups vs. placebo).
A key secondary endpoint measured the proportion of patients who achieved at least a 50% reduction in mean monthly migraine days over 12 weeks. This outcome occurred in 55.6% of the 10-mg atogepant group, 58.7% of the 30-mg group, and 60.8% of the 60-mg group, compared with 29% of the placebo group (P < .0001, all dose groups vs. placebo).
Significant improvements
Additional secondary endpoints measured during the 12-week treatment period included change from baseline in mean monthly headache days, mean monthly acute–medication use days, mean monthly performance of daily activities and physical impairment domain scores on the Activity Impairment in Migraine-Diary, and change from baseline in the Migraine-Specific Quality of Life Questionnaire Role Function-Restrictive domain score at week 12. Treatment with the 30-mg and 60-mg doses resulted in significant improvements in all secondary endpoints, and treatment with the 10-mg dose resulted in significant improvements in four of the six secondary endpoints.
No new safety risks were observed when compared with the safety profile of atogepant observed in previous trials, AbbVie said. Serious adverse events occurred in 0.9% of patients in the atogepant 10-mg group versus 0.9% of patients in the placebo group. No patients in the atogepant 30-mg or 60-mg groups experienced a serious adverse event. The most common adverse events (reported in at least 5% of patients and at least one atogepant group and at a rate greater than placebo), across all doses versus placebo, were constipation (6.9%-7.7% vs. 0.5%), nausea (4.4%-6.1% vs. 1.8%), and upper respiratory tract infection (3.9%-5.7% vs. 4.5%).
Most cases of constipation, nausea, and upper respiratory tract infection were mild or moderate in severity and did not lead to discontinuation. There were no hepatic safety issues identified in the trial.
Full data results will be presented at an upcoming medical congress and/or published in a peer-reviewed journal, the company said.
A version of this article originally appeared on Medscape.com.
AbbVie, the company developing the drug, has announced.
Top-line results from the ADVANCE trial, which evaluated atogepant 10, 30, and 60 mg, showed all three doses were associated with a significant reduction from baseline in mean monthly migraine days, compared with placebo.
There were also significant improvements in all six secondary endpoints with the two higher doses.
Data from the ADVANCE trial and a previous phase 2/3 trial will be the basis for regulatory submissions in the United States and other countries, AbbVie reported.
Decreased migraine days
The phase 3, multicenter, randomized, double-blind, placebo-controlled, parallel-group trial was designed to evaluate the efficacy, safety, and tolerability of oral atogepant for the prevention of migraine in those who experienced 4-14 migraine days per month.
A total of 910 patients were randomized to one of four treatment groups: 10 mg, 30 mg, or 60 mg of atogepant once daily or placebo. Efficacy analyses were based on the modified intent-to-treat population of 873 patients.
The primary endpoint was change from baseline in mean monthly migraine days during the 12-week treatment period. All atogepant dose groups met the primary endpoint and demonstrated significantly greater decreases in mean monthly migraine days, compared with placebo.
Mean monthly migraine days were reduced by 3.69 days with the 10-mg dose, 3.86 days with the 30-mg dose, and 4.2 days with the 60-mg dose of atogepant, compared with a reduction of 2.48 migraine days in the placebo group (P < .0001, all dose groups vs. placebo).
A key secondary endpoint measured the proportion of patients who achieved at least a 50% reduction in mean monthly migraine days over 12 weeks. This outcome occurred in 55.6% of the 10-mg atogepant group, 58.7% of the 30-mg group, and 60.8% of the 60-mg group, compared with 29% of the placebo group (P < .0001, all dose groups vs. placebo).
Significant improvements
Additional secondary endpoints measured during the 12-week treatment period included change from baseline in mean monthly headache days, mean monthly acute–medication use days, mean monthly performance of daily activities and physical impairment domain scores on the Activity Impairment in Migraine-Diary, and change from baseline in the Migraine-Specific Quality of Life Questionnaire Role Function-Restrictive domain score at week 12. Treatment with the 30-mg and 60-mg doses resulted in significant improvements in all secondary endpoints, and treatment with the 10-mg dose resulted in significant improvements in four of the six secondary endpoints.
No new safety risks were observed when compared with the safety profile of atogepant observed in previous trials, AbbVie said. Serious adverse events occurred in 0.9% of patients in the atogepant 10-mg group versus 0.9% of patients in the placebo group. No patients in the atogepant 30-mg or 60-mg groups experienced a serious adverse event. The most common adverse events (reported in at least 5% of patients and at least one atogepant group and at a rate greater than placebo), across all doses versus placebo, were constipation (6.9%-7.7% vs. 0.5%), nausea (4.4%-6.1% vs. 1.8%), and upper respiratory tract infection (3.9%-5.7% vs. 4.5%).
Most cases of constipation, nausea, and upper respiratory tract infection were mild or moderate in severity and did not lead to discontinuation. There were no hepatic safety issues identified in the trial.
Full data results will be presented at an upcoming medical congress and/or published in a peer-reviewed journal, the company said.
A version of this article originally appeared on Medscape.com.
AbbVie, the company developing the drug, has announced.
Top-line results from the ADVANCE trial, which evaluated atogepant 10, 30, and 60 mg, showed all three doses were associated with a significant reduction from baseline in mean monthly migraine days, compared with placebo.
There were also significant improvements in all six secondary endpoints with the two higher doses.
Data from the ADVANCE trial and a previous phase 2/3 trial will be the basis for regulatory submissions in the United States and other countries, AbbVie reported.
Decreased migraine days
The phase 3, multicenter, randomized, double-blind, placebo-controlled, parallel-group trial was designed to evaluate the efficacy, safety, and tolerability of oral atogepant for the prevention of migraine in those who experienced 4-14 migraine days per month.
A total of 910 patients were randomized to one of four treatment groups: 10 mg, 30 mg, or 60 mg of atogepant once daily or placebo. Efficacy analyses were based on the modified intent-to-treat population of 873 patients.
The primary endpoint was change from baseline in mean monthly migraine days during the 12-week treatment period. All atogepant dose groups met the primary endpoint and demonstrated significantly greater decreases in mean monthly migraine days, compared with placebo.
Mean monthly migraine days were reduced by 3.69 days with the 10-mg dose, 3.86 days with the 30-mg dose, and 4.2 days with the 60-mg dose of atogepant, compared with a reduction of 2.48 migraine days in the placebo group (P < .0001, all dose groups vs. placebo).
A key secondary endpoint measured the proportion of patients who achieved at least a 50% reduction in mean monthly migraine days over 12 weeks. This outcome occurred in 55.6% of the 10-mg atogepant group, 58.7% of the 30-mg group, and 60.8% of the 60-mg group, compared with 29% of the placebo group (P < .0001, all dose groups vs. placebo).
Significant improvements
Additional secondary endpoints measured during the 12-week treatment period included change from baseline in mean monthly headache days, mean monthly acute–medication use days, mean monthly performance of daily activities and physical impairment domain scores on the Activity Impairment in Migraine-Diary, and change from baseline in the Migraine-Specific Quality of Life Questionnaire Role Function-Restrictive domain score at week 12. Treatment with the 30-mg and 60-mg doses resulted in significant improvements in all secondary endpoints, and treatment with the 10-mg dose resulted in significant improvements in four of the six secondary endpoints.
No new safety risks were observed when compared with the safety profile of atogepant observed in previous trials, AbbVie said. Serious adverse events occurred in 0.9% of patients in the atogepant 10-mg group versus 0.9% of patients in the placebo group. No patients in the atogepant 30-mg or 60-mg groups experienced a serious adverse event. The most common adverse events (reported in at least 5% of patients and at least one atogepant group and at a rate greater than placebo), across all doses versus placebo, were constipation (6.9%-7.7% vs. 0.5%), nausea (4.4%-6.1% vs. 1.8%), and upper respiratory tract infection (3.9%-5.7% vs. 4.5%).
Most cases of constipation, nausea, and upper respiratory tract infection were mild or moderate in severity and did not lead to discontinuation. There were no hepatic safety issues identified in the trial.
Full data results will be presented at an upcoming medical congress and/or published in a peer-reviewed journal, the company said.
A version of this article originally appeared on Medscape.com.
Heart damage even after COVID-19 ‘recovery’ evokes specter of later heart failure
Evidence that the heart can take a major hit in patients hospitalized with COVID-19, especially those already with cardiovascular disease (CV) or its risk factors, has been sadly apparent from the pandemic’s earliest days.
Less clear from case studies and small series to date has been whether SARS-CoV-2 directly attacks the heart and whether acute cardiac effects of the illness may lead to some kind of lingering cardiomyopathy.
The field’s grasp of those issues advanced a bit in two new reports published July 27 in JAMA Cardiology that seem to validate concerns the virus can infect the myocardium, without necessarily causing myocarditis and the possibility that some “recovered” patients may be left with persisting myocardial injury and inflammation that potentially could later manifest as heart failure.
Persisting inflammation by cardiac magnetic resonance
A prospective cohort study with 100 patients recovered from a recent bout of the disease showed evidence of ventricular dysfunction, greater ventricular mass, and in 78% of the cohort, signs of myocardial inflammation by cardiac magnetic resonance (CMR) imaging. The CMR findings correlated with elevations in troponin T by high-sensitivity assay (hs-TnT).
Two-thirds of the cohort, whose acute COVID-19 severity had “ranged from asymptomatic to minor-to-moderate symptoms,” had recovered at home, whereas the remaining “severely unwell patients” had been hospitalized, wrote the authors, led by Valentina O. Püntmann, MD, PhD, University Hospital Frankfurt (Germany).
None of the patients had a history of heart failure or cardiomyopathy, although some had hypertension, diabetes, or evidence of coronary disease.
“Our findings demonstrate that participants with a relative paucity of preexisting cardiovascular condition and with mostly home-based recovery had frequent cardiac inflammatory involvement, which was similar to the hospitalized subgroup with regards to severity and extent,” the group noted.
“There is a considerable ongoing myocardial inflammation in the heart muscle weeks after recovery from COVID-19 illness. This finding is important because it may herald a considerable burden of heart failure in a few years down the line,” Dr. Püntmann said in an interview.
Early diagnosis would offer “a good chance that early treatment could reduce the relentless course of inflammatory damage or even halt it,” she said.
“The relatively clear onset of COVID-19 illness provides an opportunity, which we often do not have with other conditions, to take a proactive action and to look for heart involvement early, within a few weeks of recovery.”
The study’s CMR evidence of inflammation edema, scarring, and pericardial effusion are among “the major diagnostic criteria for inflammatory and viral myocarditis,” observed Biykem Bozkurt, MD, PhD, from Baylor College of Medicine, Houston, who wasn’t part of either new study.
The findings suggest – consistent with previous evidence – that some patients with recent COVID-19 may be left with ongoing myocardial inflammation, and this study further adds that it could potentially become subacute or even chronic and in some may not be totally reversible, she said in an interview. How long the effects are likely to persist “remains to be determined. We need longer-term outcomes data.”
Viral presence without myocarditis
The accompanying report featured a postmortem analysis of hearts from 39 patients with mostly severe COVID-19 that pointed to a significant SARS-CoV-2 presence and signs that the virus vigorously replicated in the myocardium.
But there was no evidence that the infection led to fulminant myocarditis. Rather, the virus had apparently infiltrated the heart by localizing in interstitial cells or in macrophages that took up in the myocardium without actually entering myocytes, concluded the report’s authors, led by Diana Lindner, PhD, from the University Heart and Vascular Centre, Hamburg (Germany).
The findings suggest “that the presence of SARS-CoV-2 in cardiac tissue does not necessarily cause an inflammatory reaction consistent with clinical myocarditis,” the group wrote.
Previously in the literature, in “cases in which myocardial inflammation was present, there was also evidence of clinical myocarditis, and therefore the current cases underlie a different pathophysiology,” they concluded.
No evidence of the virus was seen in 15 cases, about 61% of the group. In 16 of the remaining 24 hearts, the viral load exceeded 1,000 copies per mcg of RNA, a substantial presence. Those 16 showed increased expression of inflammatory cytokines but no inflammatory cell infiltrates or changes in leukocyte counts, the researchers noted.
“Findings of suggested viral replication in the cases with a very high viral load are showing that we need to do more studies to find out long-term consequences, which we do not know right now,” senior author Dirk Westermann, MD, also from the University Heart and Vascular Centre, Hamburg, said.
Implications for heart failure
The postmortem findings from Dr. Lindner and associates “provide intriguing evidence that COVID-19 is associated with at least some component of myocardial injury, perhaps as the result of direct viral infection of the heart,” wrote Clyde W. Yancy, MD, MSc, from Northwestern University, Chicago, and Gregg C. Fonarow, MD, from the University of California, Los Angeles, in an editorial accompanying both reports.
The CMR study from Dr. Püntmann and colleagues – on the backdrop of earlier COVID-19 observations – suggests the potential for “residual left ventricular dysfunction and ongoing inflammation” in the months following a COVID-19 diagnosis. Both developments may be “of sufficient concern to represent a nidus for new-onset heart failure and other cardiovascular complications,” contend Dr. Yancy and Dr. Fonarow.
“When added to the postmortem pathological findings from Lindner et al, we see the plot thickening and we are inclined to raise a new and very evident concern that cardiomyopathy and heart failure related to COVID-19 may potentially evolve as the natural history of this infection becomes clearer,” they wrote.
Some patients, having recovered from the acute illness, may be left with a chronic inflammatory state that probably puts them at increased risk for future heart failure, agreed Dr. Bozkurt when interviewed. “They could show further decline in cardiac function, and their recovery might take longer than with the usual viral illnesses that we see,” she said.
“There could also be a risk of sudden death. Inflammation sometimes gives rise to sudden death and ventricular arrhythmia, which I would be very worried about, especially if the myocardium is stressed,” Dr. Bozkurt said. “So competitive sports in those patients potentially could be risky.”
COVID-19 cohort vs. matched control subjects
The CMR study from Dr. Püntmann and colleagues prospectively entered 100 patients recently recovered from an acute bout of COVID-19, either at home or at a hospital, who were followed in a registry based at University Hospital Frankfurt. Their median age was 49 years; 47% were female. They were compared with 50 age- and sex-matched control patients and 50 apparently healthy volunteers matched for risk factors, the group noted.
On the same day as the CMR assessment, the recently recovered patients, compared with the healthy control subjects and risk-factor matched control subjects, respectively, showed (P ≤ .001 in each case):
- A reduced left ventricular (LV) ejection fraction: 56% vs. 60% and 61%.
- A higher LV end-diastolic volume index: 86 mL/m2 vs. 80 mL/m2 and 75 mL/m2.
- A greater LV mass index: 51 g/m2 vs. 47 g/m2 and 53 g/m2.
- A higher hs-TnT level: 5.6 pg/mL vs. 3.2 pg/mL and 3.9 pg/mL.
- A greater prevalence of hs-TnT levels 3 pg/mL or more: 71% vs. 11% and 31%.
At CMR, 78% of the recovered COVID-19 patients showed abnormalities that included raised myocardial native T1 and T2 mapping, which is suggestive of fibrosis and edema from inflammation, compared with the two control groups (P < .001 for all differences), “independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis,” the group wrote. Native T1 and T2 mapping correlated significantly with hs-TnT.
“We now have the diagnostic means to detect cardiac inflammation early, and we need make every effort to apply them in every day practice,”Dr. Püntmann said in the interview.
“Using cardiac MRI will allow us to raise our game against COVID-19 and proactively develop efficient cardioprotective treatments,” she said. “Until we have effective means of protecting from the infection, that is vaccination, we must act swiftly and within the means at hand.”
The analysis evokes several other ways patients with COVID-19 might be screened for significant myocardial involvement.
“Strategies could include checking troponins, not only at admission but maybe at discharge and perhaps even those individuals who are at home and are not necessarily requiring care,” Dr. Bozkurt said.
“Biomarker profiling and screening for ongoing inflammation probably are going to be important components of COVID-19, especially for those with subclinical risk and disease.”
Dr. Westermann proposed that troponin elevations at discharge “might be a good starting point” for selecting COVID-19 patients for functional testing or imaging to screen for cardiac sequelae. Performing such tests routinely now “would be overwhelming given the massive increase in patients we still see today.”
Dr. Püntmann had no disclosures; statements of potential conflict for the other authors are in the report. Dr. Bozkurt has previously disclosed receiving consultant fees or honoraria from Bayer Healthcare, Bristol-Myers Squibb, Lantheus Medical Imaging, and Respicardia; serving on a data safety monitoring board for LivaNova USA ; and having unspecified relationships with Abbott Laboratories. Dr. Lindner had no disclosures; Dr. Westermann reported receiving personal fees from AstraZeneca, Bayer, Novartis, and Medtronic. Dr. Yancy is a deputy editor and Dr. Fonarow a section editor for JAMA Cardiology. Dr. Yancy had no other disclosures. Dr. Fonarow reported receiving personal fees from Abbott Laboratories, Amgen, AstraZeneca, Bayer, CHF Solutions, Edwards Lifesciences, Janssen, Medtronic, Merck, and Novartis.
A version of this article originally appeared on Medscape.com.
Evidence that the heart can take a major hit in patients hospitalized with COVID-19, especially those already with cardiovascular disease (CV) or its risk factors, has been sadly apparent from the pandemic’s earliest days.
Less clear from case studies and small series to date has been whether SARS-CoV-2 directly attacks the heart and whether acute cardiac effects of the illness may lead to some kind of lingering cardiomyopathy.
The field’s grasp of those issues advanced a bit in two new reports published July 27 in JAMA Cardiology that seem to validate concerns the virus can infect the myocardium, without necessarily causing myocarditis and the possibility that some “recovered” patients may be left with persisting myocardial injury and inflammation that potentially could later manifest as heart failure.
Persisting inflammation by cardiac magnetic resonance
A prospective cohort study with 100 patients recovered from a recent bout of the disease showed evidence of ventricular dysfunction, greater ventricular mass, and in 78% of the cohort, signs of myocardial inflammation by cardiac magnetic resonance (CMR) imaging. The CMR findings correlated with elevations in troponin T by high-sensitivity assay (hs-TnT).
Two-thirds of the cohort, whose acute COVID-19 severity had “ranged from asymptomatic to minor-to-moderate symptoms,” had recovered at home, whereas the remaining “severely unwell patients” had been hospitalized, wrote the authors, led by Valentina O. Püntmann, MD, PhD, University Hospital Frankfurt (Germany).
None of the patients had a history of heart failure or cardiomyopathy, although some had hypertension, diabetes, or evidence of coronary disease.
“Our findings demonstrate that participants with a relative paucity of preexisting cardiovascular condition and with mostly home-based recovery had frequent cardiac inflammatory involvement, which was similar to the hospitalized subgroup with regards to severity and extent,” the group noted.
“There is a considerable ongoing myocardial inflammation in the heart muscle weeks after recovery from COVID-19 illness. This finding is important because it may herald a considerable burden of heart failure in a few years down the line,” Dr. Püntmann said in an interview.
Early diagnosis would offer “a good chance that early treatment could reduce the relentless course of inflammatory damage or even halt it,” she said.
“The relatively clear onset of COVID-19 illness provides an opportunity, which we often do not have with other conditions, to take a proactive action and to look for heart involvement early, within a few weeks of recovery.”
The study’s CMR evidence of inflammation edema, scarring, and pericardial effusion are among “the major diagnostic criteria for inflammatory and viral myocarditis,” observed Biykem Bozkurt, MD, PhD, from Baylor College of Medicine, Houston, who wasn’t part of either new study.
The findings suggest – consistent with previous evidence – that some patients with recent COVID-19 may be left with ongoing myocardial inflammation, and this study further adds that it could potentially become subacute or even chronic and in some may not be totally reversible, she said in an interview. How long the effects are likely to persist “remains to be determined. We need longer-term outcomes data.”
Viral presence without myocarditis
The accompanying report featured a postmortem analysis of hearts from 39 patients with mostly severe COVID-19 that pointed to a significant SARS-CoV-2 presence and signs that the virus vigorously replicated in the myocardium.
But there was no evidence that the infection led to fulminant myocarditis. Rather, the virus had apparently infiltrated the heart by localizing in interstitial cells or in macrophages that took up in the myocardium without actually entering myocytes, concluded the report’s authors, led by Diana Lindner, PhD, from the University Heart and Vascular Centre, Hamburg (Germany).
The findings suggest “that the presence of SARS-CoV-2 in cardiac tissue does not necessarily cause an inflammatory reaction consistent with clinical myocarditis,” the group wrote.
Previously in the literature, in “cases in which myocardial inflammation was present, there was also evidence of clinical myocarditis, and therefore the current cases underlie a different pathophysiology,” they concluded.
No evidence of the virus was seen in 15 cases, about 61% of the group. In 16 of the remaining 24 hearts, the viral load exceeded 1,000 copies per mcg of RNA, a substantial presence. Those 16 showed increased expression of inflammatory cytokines but no inflammatory cell infiltrates or changes in leukocyte counts, the researchers noted.
“Findings of suggested viral replication in the cases with a very high viral load are showing that we need to do more studies to find out long-term consequences, which we do not know right now,” senior author Dirk Westermann, MD, also from the University Heart and Vascular Centre, Hamburg, said.
Implications for heart failure
The postmortem findings from Dr. Lindner and associates “provide intriguing evidence that COVID-19 is associated with at least some component of myocardial injury, perhaps as the result of direct viral infection of the heart,” wrote Clyde W. Yancy, MD, MSc, from Northwestern University, Chicago, and Gregg C. Fonarow, MD, from the University of California, Los Angeles, in an editorial accompanying both reports.
The CMR study from Dr. Püntmann and colleagues – on the backdrop of earlier COVID-19 observations – suggests the potential for “residual left ventricular dysfunction and ongoing inflammation” in the months following a COVID-19 diagnosis. Both developments may be “of sufficient concern to represent a nidus for new-onset heart failure and other cardiovascular complications,” contend Dr. Yancy and Dr. Fonarow.
“When added to the postmortem pathological findings from Lindner et al, we see the plot thickening and we are inclined to raise a new and very evident concern that cardiomyopathy and heart failure related to COVID-19 may potentially evolve as the natural history of this infection becomes clearer,” they wrote.
Some patients, having recovered from the acute illness, may be left with a chronic inflammatory state that probably puts them at increased risk for future heart failure, agreed Dr. Bozkurt when interviewed. “They could show further decline in cardiac function, and their recovery might take longer than with the usual viral illnesses that we see,” she said.
“There could also be a risk of sudden death. Inflammation sometimes gives rise to sudden death and ventricular arrhythmia, which I would be very worried about, especially if the myocardium is stressed,” Dr. Bozkurt said. “So competitive sports in those patients potentially could be risky.”
COVID-19 cohort vs. matched control subjects
The CMR study from Dr. Püntmann and colleagues prospectively entered 100 patients recently recovered from an acute bout of COVID-19, either at home or at a hospital, who were followed in a registry based at University Hospital Frankfurt. Their median age was 49 years; 47% were female. They were compared with 50 age- and sex-matched control patients and 50 apparently healthy volunteers matched for risk factors, the group noted.
On the same day as the CMR assessment, the recently recovered patients, compared with the healthy control subjects and risk-factor matched control subjects, respectively, showed (P ≤ .001 in each case):
- A reduced left ventricular (LV) ejection fraction: 56% vs. 60% and 61%.
- A higher LV end-diastolic volume index: 86 mL/m2 vs. 80 mL/m2 and 75 mL/m2.
- A greater LV mass index: 51 g/m2 vs. 47 g/m2 and 53 g/m2.
- A higher hs-TnT level: 5.6 pg/mL vs. 3.2 pg/mL and 3.9 pg/mL.
- A greater prevalence of hs-TnT levels 3 pg/mL or more: 71% vs. 11% and 31%.
At CMR, 78% of the recovered COVID-19 patients showed abnormalities that included raised myocardial native T1 and T2 mapping, which is suggestive of fibrosis and edema from inflammation, compared with the two control groups (P < .001 for all differences), “independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis,” the group wrote. Native T1 and T2 mapping correlated significantly with hs-TnT.
“We now have the diagnostic means to detect cardiac inflammation early, and we need make every effort to apply them in every day practice,”Dr. Püntmann said in the interview.
“Using cardiac MRI will allow us to raise our game against COVID-19 and proactively develop efficient cardioprotective treatments,” she said. “Until we have effective means of protecting from the infection, that is vaccination, we must act swiftly and within the means at hand.”
The analysis evokes several other ways patients with COVID-19 might be screened for significant myocardial involvement.
“Strategies could include checking troponins, not only at admission but maybe at discharge and perhaps even those individuals who are at home and are not necessarily requiring care,” Dr. Bozkurt said.
“Biomarker profiling and screening for ongoing inflammation probably are going to be important components of COVID-19, especially for those with subclinical risk and disease.”
Dr. Westermann proposed that troponin elevations at discharge “might be a good starting point” for selecting COVID-19 patients for functional testing or imaging to screen for cardiac sequelae. Performing such tests routinely now “would be overwhelming given the massive increase in patients we still see today.”
Dr. Püntmann had no disclosures; statements of potential conflict for the other authors are in the report. Dr. Bozkurt has previously disclosed receiving consultant fees or honoraria from Bayer Healthcare, Bristol-Myers Squibb, Lantheus Medical Imaging, and Respicardia; serving on a data safety monitoring board for LivaNova USA ; and having unspecified relationships with Abbott Laboratories. Dr. Lindner had no disclosures; Dr. Westermann reported receiving personal fees from AstraZeneca, Bayer, Novartis, and Medtronic. Dr. Yancy is a deputy editor and Dr. Fonarow a section editor for JAMA Cardiology. Dr. Yancy had no other disclosures. Dr. Fonarow reported receiving personal fees from Abbott Laboratories, Amgen, AstraZeneca, Bayer, CHF Solutions, Edwards Lifesciences, Janssen, Medtronic, Merck, and Novartis.
A version of this article originally appeared on Medscape.com.
Evidence that the heart can take a major hit in patients hospitalized with COVID-19, especially those already with cardiovascular disease (CV) or its risk factors, has been sadly apparent from the pandemic’s earliest days.
Less clear from case studies and small series to date has been whether SARS-CoV-2 directly attacks the heart and whether acute cardiac effects of the illness may lead to some kind of lingering cardiomyopathy.
The field’s grasp of those issues advanced a bit in two new reports published July 27 in JAMA Cardiology that seem to validate concerns the virus can infect the myocardium, without necessarily causing myocarditis and the possibility that some “recovered” patients may be left with persisting myocardial injury and inflammation that potentially could later manifest as heart failure.
Persisting inflammation by cardiac magnetic resonance
A prospective cohort study with 100 patients recovered from a recent bout of the disease showed evidence of ventricular dysfunction, greater ventricular mass, and in 78% of the cohort, signs of myocardial inflammation by cardiac magnetic resonance (CMR) imaging. The CMR findings correlated with elevations in troponin T by high-sensitivity assay (hs-TnT).
Two-thirds of the cohort, whose acute COVID-19 severity had “ranged from asymptomatic to minor-to-moderate symptoms,” had recovered at home, whereas the remaining “severely unwell patients” had been hospitalized, wrote the authors, led by Valentina O. Püntmann, MD, PhD, University Hospital Frankfurt (Germany).
None of the patients had a history of heart failure or cardiomyopathy, although some had hypertension, diabetes, or evidence of coronary disease.
“Our findings demonstrate that participants with a relative paucity of preexisting cardiovascular condition and with mostly home-based recovery had frequent cardiac inflammatory involvement, which was similar to the hospitalized subgroup with regards to severity and extent,” the group noted.
“There is a considerable ongoing myocardial inflammation in the heart muscle weeks after recovery from COVID-19 illness. This finding is important because it may herald a considerable burden of heart failure in a few years down the line,” Dr. Püntmann said in an interview.
Early diagnosis would offer “a good chance that early treatment could reduce the relentless course of inflammatory damage or even halt it,” she said.
“The relatively clear onset of COVID-19 illness provides an opportunity, which we often do not have with other conditions, to take a proactive action and to look for heart involvement early, within a few weeks of recovery.”
The study’s CMR evidence of inflammation edema, scarring, and pericardial effusion are among “the major diagnostic criteria for inflammatory and viral myocarditis,” observed Biykem Bozkurt, MD, PhD, from Baylor College of Medicine, Houston, who wasn’t part of either new study.
The findings suggest – consistent with previous evidence – that some patients with recent COVID-19 may be left with ongoing myocardial inflammation, and this study further adds that it could potentially become subacute or even chronic and in some may not be totally reversible, she said in an interview. How long the effects are likely to persist “remains to be determined. We need longer-term outcomes data.”
Viral presence without myocarditis
The accompanying report featured a postmortem analysis of hearts from 39 patients with mostly severe COVID-19 that pointed to a significant SARS-CoV-2 presence and signs that the virus vigorously replicated in the myocardium.
But there was no evidence that the infection led to fulminant myocarditis. Rather, the virus had apparently infiltrated the heart by localizing in interstitial cells or in macrophages that took up in the myocardium without actually entering myocytes, concluded the report’s authors, led by Diana Lindner, PhD, from the University Heart and Vascular Centre, Hamburg (Germany).
The findings suggest “that the presence of SARS-CoV-2 in cardiac tissue does not necessarily cause an inflammatory reaction consistent with clinical myocarditis,” the group wrote.
Previously in the literature, in “cases in which myocardial inflammation was present, there was also evidence of clinical myocarditis, and therefore the current cases underlie a different pathophysiology,” they concluded.
No evidence of the virus was seen in 15 cases, about 61% of the group. In 16 of the remaining 24 hearts, the viral load exceeded 1,000 copies per mcg of RNA, a substantial presence. Those 16 showed increased expression of inflammatory cytokines but no inflammatory cell infiltrates or changes in leukocyte counts, the researchers noted.
“Findings of suggested viral replication in the cases with a very high viral load are showing that we need to do more studies to find out long-term consequences, which we do not know right now,” senior author Dirk Westermann, MD, also from the University Heart and Vascular Centre, Hamburg, said.
Implications for heart failure
The postmortem findings from Dr. Lindner and associates “provide intriguing evidence that COVID-19 is associated with at least some component of myocardial injury, perhaps as the result of direct viral infection of the heart,” wrote Clyde W. Yancy, MD, MSc, from Northwestern University, Chicago, and Gregg C. Fonarow, MD, from the University of California, Los Angeles, in an editorial accompanying both reports.
The CMR study from Dr. Püntmann and colleagues – on the backdrop of earlier COVID-19 observations – suggests the potential for “residual left ventricular dysfunction and ongoing inflammation” in the months following a COVID-19 diagnosis. Both developments may be “of sufficient concern to represent a nidus for new-onset heart failure and other cardiovascular complications,” contend Dr. Yancy and Dr. Fonarow.
“When added to the postmortem pathological findings from Lindner et al, we see the plot thickening and we are inclined to raise a new and very evident concern that cardiomyopathy and heart failure related to COVID-19 may potentially evolve as the natural history of this infection becomes clearer,” they wrote.
Some patients, having recovered from the acute illness, may be left with a chronic inflammatory state that probably puts them at increased risk for future heart failure, agreed Dr. Bozkurt when interviewed. “They could show further decline in cardiac function, and their recovery might take longer than with the usual viral illnesses that we see,” she said.
“There could also be a risk of sudden death. Inflammation sometimes gives rise to sudden death and ventricular arrhythmia, which I would be very worried about, especially if the myocardium is stressed,” Dr. Bozkurt said. “So competitive sports in those patients potentially could be risky.”
COVID-19 cohort vs. matched control subjects
The CMR study from Dr. Püntmann and colleagues prospectively entered 100 patients recently recovered from an acute bout of COVID-19, either at home or at a hospital, who were followed in a registry based at University Hospital Frankfurt. Their median age was 49 years; 47% were female. They were compared with 50 age- and sex-matched control patients and 50 apparently healthy volunteers matched for risk factors, the group noted.
On the same day as the CMR assessment, the recently recovered patients, compared with the healthy control subjects and risk-factor matched control subjects, respectively, showed (P ≤ .001 in each case):
- A reduced left ventricular (LV) ejection fraction: 56% vs. 60% and 61%.
- A higher LV end-diastolic volume index: 86 mL/m2 vs. 80 mL/m2 and 75 mL/m2.
- A greater LV mass index: 51 g/m2 vs. 47 g/m2 and 53 g/m2.
- A higher hs-TnT level: 5.6 pg/mL vs. 3.2 pg/mL and 3.9 pg/mL.
- A greater prevalence of hs-TnT levels 3 pg/mL or more: 71% vs. 11% and 31%.
At CMR, 78% of the recovered COVID-19 patients showed abnormalities that included raised myocardial native T1 and T2 mapping, which is suggestive of fibrosis and edema from inflammation, compared with the two control groups (P < .001 for all differences), “independent of preexisting conditions, severity and overall course of the acute illness, and the time from the original diagnosis,” the group wrote. Native T1 and T2 mapping correlated significantly with hs-TnT.
“We now have the diagnostic means to detect cardiac inflammation early, and we need make every effort to apply them in every day practice,”Dr. Püntmann said in the interview.
“Using cardiac MRI will allow us to raise our game against COVID-19 and proactively develop efficient cardioprotective treatments,” she said. “Until we have effective means of protecting from the infection, that is vaccination, we must act swiftly and within the means at hand.”
The analysis evokes several other ways patients with COVID-19 might be screened for significant myocardial involvement.
“Strategies could include checking troponins, not only at admission but maybe at discharge and perhaps even those individuals who are at home and are not necessarily requiring care,” Dr. Bozkurt said.
“Biomarker profiling and screening for ongoing inflammation probably are going to be important components of COVID-19, especially for those with subclinical risk and disease.”
Dr. Westermann proposed that troponin elevations at discharge “might be a good starting point” for selecting COVID-19 patients for functional testing or imaging to screen for cardiac sequelae. Performing such tests routinely now “would be overwhelming given the massive increase in patients we still see today.”
Dr. Püntmann had no disclosures; statements of potential conflict for the other authors are in the report. Dr. Bozkurt has previously disclosed receiving consultant fees or honoraria from Bayer Healthcare, Bristol-Myers Squibb, Lantheus Medical Imaging, and Respicardia; serving on a data safety monitoring board for LivaNova USA ; and having unspecified relationships with Abbott Laboratories. Dr. Lindner had no disclosures; Dr. Westermann reported receiving personal fees from AstraZeneca, Bayer, Novartis, and Medtronic. Dr. Yancy is a deputy editor and Dr. Fonarow a section editor for JAMA Cardiology. Dr. Yancy had no other disclosures. Dr. Fonarow reported receiving personal fees from Abbott Laboratories, Amgen, AstraZeneca, Bayer, CHF Solutions, Edwards Lifesciences, Janssen, Medtronic, Merck, and Novartis.
A version of this article originally appeared on Medscape.com.
More data needed to better understand COVID-19 skin manifestations
Qing Zhao, MD, Xiaokai Fang, MD, and their colleagues at the Shandong Provincial Hospital for Skin Diseases & Shandong Provincial Institute of Dermatology and Venereology, in Jinan, China, reported the results of a literature review of 44 articles published through May 2020 that included 507 patients with cutaneous manifestations of COVID-19. The review was published in the Journal of The European Academy of Dermatology and Venereology.
Nearly all of the patients (96%) were from Europe, and more than half were women (60%), with an average age of 49 years. Most patients had multiple skin symptoms, with the most common being erythema (44%), chilblain-like lesions (20%), urticaria-like lesions (16%), vesicular manifestations (13%), livedo/necrosis (6%), and petechiae (almost 2%). The authors described erythema as being present in specific sites, such as the trunk, extremities, flexural regions, face, and mucous membranes. Slightly less than half of all patients had significant pruritus.
Data on systemic COVID-19 symptoms were available for 431 patients and included fever in about two-thirds of patients and cough in almost 70%, with dyspnea in almost half of patients. Almost 60% had fatigue, and almost 60% had asthenia. Information about the onset of skin symptoms was available in 88 patients; of these patients, lesions were seen an average of almost 10 days after systemic symptoms appeared and, in almost 15%, were the first symptoms noted.
Histopathologic exams were done for only 23 patients and, in all cases, showed “inflammatory features without specific pathological changes, such as lymphocyte infiltration.” In one study, reverse transcription polymerase chain reaction testing of skin biopsy specimens tested negative for SARS-CoV-2.
Expression of ACE2, the receptor of SARS-CoV-2, in the skin was evaluated in six of the studies. “Higher ACE2 expression was identified in keratinocytes, mainly in differentiating keratinocytes and basal cells compared to the other cells of skin tissues,” the authors wrote. These results were confirmed with immunohistochemistry, which, they said, found “ACE2-positive keratinocytes in the stratum basal, the stratum spinosum, and the stratum granulosum of epiderma.” They added that this provides evidence “for percutaneous infection or the entry of virus into patients through skin tissues,” but cautioned that more research is needed.
The authors acknowledged that there are still many unanswered questions about COVID-19, and that more clinical data and research are needed, to improve the understanding of the cutaneous manifestations associated with COVID-19.
In an interview, Alisa N. Femia, MD, director of inpatient dermatology in the department of dermatology at New York University, said that the cutaneous signs described in the review align well with what she has seen in patients with COVID-19.
At this point, it is unclear whether cutaneous manifestations of COVID-19 are a result of SARS-CoV-2 invading the skin or an immune response related to SARS-CoV-2, noted Dr. Femia, who was not involved in the research. One method of entry could be through transmitting virus present on the skin to another part of the body where infection is more likely.
While it is possible COVID-19 could be contracted through the skin, she noted, it is much more likely an individual would be infected by SARS-CoV-2 through more traditionally understood means of transmission, such as through respiratory droplets in person-to-person contact. “I think we are far away from drawing that conclusion, that one could touch a surface or a person who has COVID and contract it through their skin,” Dr. Femia said. “The skin has a lot of other ways to protect against that from occurring,” she added.
“SAR-CoV-2 obviously enters through the ACE2 receptor, which is fairly ubiquitous, and it has been seen in keratinocytes,” she said. “But the skin is one of our biggest barriers ... and further, studies to date have shown that that receptor is expressed in relatively low levels of the keratinocytes.”
Pathogenesis of different cutaneous manifestations may be different, Dr. Femia said. For example, urticaria and morbilliform eruption were described by the authors of the review as more benign eruptions, but pathogenesis may differ from that of so-called COVID toes and from the pathogenesis of purpura and ulcerations seen in patients with more severe disease, she noted. It is plausible, she added, that purpura and ulcerations may be a “direct invasion of SARS-CoV-2 into endothelial cells,” which creates secondary processes “that ultimately destroy the skin.”
Urticaria and morbilliform eruptions, on the other hand, “are more simply that the immune system is recognizing COVID, and in doing so, is also recognizing some antigens in the skin and creating a hypersensitive response to the skin” and has “nothing to do with the SARS-CoV-2 virus actually being in that location,” she said.
It is important to differentiate between patients who have skin manifestations attributed to COVID-19 and those with manifestations independent of COVID-19, which is difficult, Dr. Femia noted. A patient with COVID-19 and a cutaneous manifestation may be having a reaction to a medication. “It’s important to have a critical eye and to remember that, when we see these manifestations, we should always be investigating whether there was an alternative cause so that we can better learn what exactly we should be attributing to this infection,” she said
Adam Friedman, MD, professor and interim chair of dermatology at George Washington University, Washington, said the authors of the review had presented interesting work, but made some “assumptions that need to be proven.” Dr. Friedman also was not involved in the research, but agreed in an interview with the assessment that it is unlikely SARS-CoV-2 would penetrate the skin. While some viruses – such as the poxvirus that causes molluscum contagiosum and the herpes simplex virus – invade keratinocytes specifically, there is a particular clinical phenotype that results that is associated with changes in the epidermis. However, “the skin manifestations of COVID-19 do not fit with direct skin invasion, [but] rather the immune response to systemic disease,” he said.
“[I]n terms of systemic invasion through the skin, it is possible, but this study certainly doesn’t show that. The presence/expression of ACE2 in the epidermis doesn’t translate to route of infection,” Dr. Friedman said..
The study received financial support from Shandong First Medical University, the Innovation Project of Shandong Academy of Medical Sciences and the Shandong Province Taishan Scholar Project. The authors report no relevant financial disclosures. Dr. Femia and Dr. Friedman had no relevant financial disclosures.
SOURCE: Zhao Q et al. J Eur Acad Dermatol Venereol. 2020 Jun 28. doi: 10.1111/jdv.16778.
Qing Zhao, MD, Xiaokai Fang, MD, and their colleagues at the Shandong Provincial Hospital for Skin Diseases & Shandong Provincial Institute of Dermatology and Venereology, in Jinan, China, reported the results of a literature review of 44 articles published through May 2020 that included 507 patients with cutaneous manifestations of COVID-19. The review was published in the Journal of The European Academy of Dermatology and Venereology.
Nearly all of the patients (96%) were from Europe, and more than half were women (60%), with an average age of 49 years. Most patients had multiple skin symptoms, with the most common being erythema (44%), chilblain-like lesions (20%), urticaria-like lesions (16%), vesicular manifestations (13%), livedo/necrosis (6%), and petechiae (almost 2%). The authors described erythema as being present in specific sites, such as the trunk, extremities, flexural regions, face, and mucous membranes. Slightly less than half of all patients had significant pruritus.
Data on systemic COVID-19 symptoms were available for 431 patients and included fever in about two-thirds of patients and cough in almost 70%, with dyspnea in almost half of patients. Almost 60% had fatigue, and almost 60% had asthenia. Information about the onset of skin symptoms was available in 88 patients; of these patients, lesions were seen an average of almost 10 days after systemic symptoms appeared and, in almost 15%, were the first symptoms noted.
Histopathologic exams were done for only 23 patients and, in all cases, showed “inflammatory features without specific pathological changes, such as lymphocyte infiltration.” In one study, reverse transcription polymerase chain reaction testing of skin biopsy specimens tested negative for SARS-CoV-2.
Expression of ACE2, the receptor of SARS-CoV-2, in the skin was evaluated in six of the studies. “Higher ACE2 expression was identified in keratinocytes, mainly in differentiating keratinocytes and basal cells compared to the other cells of skin tissues,” the authors wrote. These results were confirmed with immunohistochemistry, which, they said, found “ACE2-positive keratinocytes in the stratum basal, the stratum spinosum, and the stratum granulosum of epiderma.” They added that this provides evidence “for percutaneous infection or the entry of virus into patients through skin tissues,” but cautioned that more research is needed.
The authors acknowledged that there are still many unanswered questions about COVID-19, and that more clinical data and research are needed, to improve the understanding of the cutaneous manifestations associated with COVID-19.
In an interview, Alisa N. Femia, MD, director of inpatient dermatology in the department of dermatology at New York University, said that the cutaneous signs described in the review align well with what she has seen in patients with COVID-19.
At this point, it is unclear whether cutaneous manifestations of COVID-19 are a result of SARS-CoV-2 invading the skin or an immune response related to SARS-CoV-2, noted Dr. Femia, who was not involved in the research. One method of entry could be through transmitting virus present on the skin to another part of the body where infection is more likely.
While it is possible COVID-19 could be contracted through the skin, she noted, it is much more likely an individual would be infected by SARS-CoV-2 through more traditionally understood means of transmission, such as through respiratory droplets in person-to-person contact. “I think we are far away from drawing that conclusion, that one could touch a surface or a person who has COVID and contract it through their skin,” Dr. Femia said. “The skin has a lot of other ways to protect against that from occurring,” she added.
“SAR-CoV-2 obviously enters through the ACE2 receptor, which is fairly ubiquitous, and it has been seen in keratinocytes,” she said. “But the skin is one of our biggest barriers ... and further, studies to date have shown that that receptor is expressed in relatively low levels of the keratinocytes.”
Pathogenesis of different cutaneous manifestations may be different, Dr. Femia said. For example, urticaria and morbilliform eruption were described by the authors of the review as more benign eruptions, but pathogenesis may differ from that of so-called COVID toes and from the pathogenesis of purpura and ulcerations seen in patients with more severe disease, she noted. It is plausible, she added, that purpura and ulcerations may be a “direct invasion of SARS-CoV-2 into endothelial cells,” which creates secondary processes “that ultimately destroy the skin.”
Urticaria and morbilliform eruptions, on the other hand, “are more simply that the immune system is recognizing COVID, and in doing so, is also recognizing some antigens in the skin and creating a hypersensitive response to the skin” and has “nothing to do with the SARS-CoV-2 virus actually being in that location,” she said.
It is important to differentiate between patients who have skin manifestations attributed to COVID-19 and those with manifestations independent of COVID-19, which is difficult, Dr. Femia noted. A patient with COVID-19 and a cutaneous manifestation may be having a reaction to a medication. “It’s important to have a critical eye and to remember that, when we see these manifestations, we should always be investigating whether there was an alternative cause so that we can better learn what exactly we should be attributing to this infection,” she said
Adam Friedman, MD, professor and interim chair of dermatology at George Washington University, Washington, said the authors of the review had presented interesting work, but made some “assumptions that need to be proven.” Dr. Friedman also was not involved in the research, but agreed in an interview with the assessment that it is unlikely SARS-CoV-2 would penetrate the skin. While some viruses – such as the poxvirus that causes molluscum contagiosum and the herpes simplex virus – invade keratinocytes specifically, there is a particular clinical phenotype that results that is associated with changes in the epidermis. However, “the skin manifestations of COVID-19 do not fit with direct skin invasion, [but] rather the immune response to systemic disease,” he said.
“[I]n terms of systemic invasion through the skin, it is possible, but this study certainly doesn’t show that. The presence/expression of ACE2 in the epidermis doesn’t translate to route of infection,” Dr. Friedman said..
The study received financial support from Shandong First Medical University, the Innovation Project of Shandong Academy of Medical Sciences and the Shandong Province Taishan Scholar Project. The authors report no relevant financial disclosures. Dr. Femia and Dr. Friedman had no relevant financial disclosures.
SOURCE: Zhao Q et al. J Eur Acad Dermatol Venereol. 2020 Jun 28. doi: 10.1111/jdv.16778.
Qing Zhao, MD, Xiaokai Fang, MD, and their colleagues at the Shandong Provincial Hospital for Skin Diseases & Shandong Provincial Institute of Dermatology and Venereology, in Jinan, China, reported the results of a literature review of 44 articles published through May 2020 that included 507 patients with cutaneous manifestations of COVID-19. The review was published in the Journal of The European Academy of Dermatology and Venereology.
Nearly all of the patients (96%) were from Europe, and more than half were women (60%), with an average age of 49 years. Most patients had multiple skin symptoms, with the most common being erythema (44%), chilblain-like lesions (20%), urticaria-like lesions (16%), vesicular manifestations (13%), livedo/necrosis (6%), and petechiae (almost 2%). The authors described erythema as being present in specific sites, such as the trunk, extremities, flexural regions, face, and mucous membranes. Slightly less than half of all patients had significant pruritus.
Data on systemic COVID-19 symptoms were available for 431 patients and included fever in about two-thirds of patients and cough in almost 70%, with dyspnea in almost half of patients. Almost 60% had fatigue, and almost 60% had asthenia. Information about the onset of skin symptoms was available in 88 patients; of these patients, lesions were seen an average of almost 10 days after systemic symptoms appeared and, in almost 15%, were the first symptoms noted.
Histopathologic exams were done for only 23 patients and, in all cases, showed “inflammatory features without specific pathological changes, such as lymphocyte infiltration.” In one study, reverse transcription polymerase chain reaction testing of skin biopsy specimens tested negative for SARS-CoV-2.
Expression of ACE2, the receptor of SARS-CoV-2, in the skin was evaluated in six of the studies. “Higher ACE2 expression was identified in keratinocytes, mainly in differentiating keratinocytes and basal cells compared to the other cells of skin tissues,” the authors wrote. These results were confirmed with immunohistochemistry, which, they said, found “ACE2-positive keratinocytes in the stratum basal, the stratum spinosum, and the stratum granulosum of epiderma.” They added that this provides evidence “for percutaneous infection or the entry of virus into patients through skin tissues,” but cautioned that more research is needed.
The authors acknowledged that there are still many unanswered questions about COVID-19, and that more clinical data and research are needed, to improve the understanding of the cutaneous manifestations associated with COVID-19.
In an interview, Alisa N. Femia, MD, director of inpatient dermatology in the department of dermatology at New York University, said that the cutaneous signs described in the review align well with what she has seen in patients with COVID-19.
At this point, it is unclear whether cutaneous manifestations of COVID-19 are a result of SARS-CoV-2 invading the skin or an immune response related to SARS-CoV-2, noted Dr. Femia, who was not involved in the research. One method of entry could be through transmitting virus present on the skin to another part of the body where infection is more likely.
While it is possible COVID-19 could be contracted through the skin, she noted, it is much more likely an individual would be infected by SARS-CoV-2 through more traditionally understood means of transmission, such as through respiratory droplets in person-to-person contact. “I think we are far away from drawing that conclusion, that one could touch a surface or a person who has COVID and contract it through their skin,” Dr. Femia said. “The skin has a lot of other ways to protect against that from occurring,” she added.
“SAR-CoV-2 obviously enters through the ACE2 receptor, which is fairly ubiquitous, and it has been seen in keratinocytes,” she said. “But the skin is one of our biggest barriers ... and further, studies to date have shown that that receptor is expressed in relatively low levels of the keratinocytes.”
Pathogenesis of different cutaneous manifestations may be different, Dr. Femia said. For example, urticaria and morbilliform eruption were described by the authors of the review as more benign eruptions, but pathogenesis may differ from that of so-called COVID toes and from the pathogenesis of purpura and ulcerations seen in patients with more severe disease, she noted. It is plausible, she added, that purpura and ulcerations may be a “direct invasion of SARS-CoV-2 into endothelial cells,” which creates secondary processes “that ultimately destroy the skin.”
Urticaria and morbilliform eruptions, on the other hand, “are more simply that the immune system is recognizing COVID, and in doing so, is also recognizing some antigens in the skin and creating a hypersensitive response to the skin” and has “nothing to do with the SARS-CoV-2 virus actually being in that location,” she said.
It is important to differentiate between patients who have skin manifestations attributed to COVID-19 and those with manifestations independent of COVID-19, which is difficult, Dr. Femia noted. A patient with COVID-19 and a cutaneous manifestation may be having a reaction to a medication. “It’s important to have a critical eye and to remember that, when we see these manifestations, we should always be investigating whether there was an alternative cause so that we can better learn what exactly we should be attributing to this infection,” she said
Adam Friedman, MD, professor and interim chair of dermatology at George Washington University, Washington, said the authors of the review had presented interesting work, but made some “assumptions that need to be proven.” Dr. Friedman also was not involved in the research, but agreed in an interview with the assessment that it is unlikely SARS-CoV-2 would penetrate the skin. While some viruses – such as the poxvirus that causes molluscum contagiosum and the herpes simplex virus – invade keratinocytes specifically, there is a particular clinical phenotype that results that is associated with changes in the epidermis. However, “the skin manifestations of COVID-19 do not fit with direct skin invasion, [but] rather the immune response to systemic disease,” he said.
“[I]n terms of systemic invasion through the skin, it is possible, but this study certainly doesn’t show that. The presence/expression of ACE2 in the epidermis doesn’t translate to route of infection,” Dr. Friedman said..
The study received financial support from Shandong First Medical University, the Innovation Project of Shandong Academy of Medical Sciences and the Shandong Province Taishan Scholar Project. The authors report no relevant financial disclosures. Dr. Femia and Dr. Friedman had no relevant financial disclosures.
SOURCE: Zhao Q et al. J Eur Acad Dermatol Venereol. 2020 Jun 28. doi: 10.1111/jdv.16778.
FROM THE JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY AND VENEREOLOGY
COVID-19 bits and pieces
It turns out that a pandemic, at least this COVID-19 version, can be a challenge for folks like me who are seldom at a loss for words. The pandemic has so overwhelmed every corner of our lives that it is hard to think of another topic on which to pontificate and still not tromp on someone’s political toes. One can always write about the pandemic itself, and I’ve tried that, but as the curtain is gradually being pulled back on this crafty little germ one runs the risk of making an observation today that will be disproved in a week or 2. However, I can’t suppress my urge to write, and so I have decided to share a few brief random observations. Of course they are related to the pandemic. And of course I realize that there is a better than fifty percent chance that they will be proved wrong by the time you read my next Letters from Maine.
Under the radar
Two of the many mysteries about SARS-CoV-2 involve young children who as a group appear to be less easily infected than adults and even when infected seem to be less likely to spread the disease to other people, particularly adults. One explanation posited by some researchers in France is that young children are less likely to have symptoms such as cough and are less powerful speakers and so might be less likely to spew out a significant number of infected aerosolized droplets (“How to Reopen Schools: What Science and Other Countries Teach Us.” By Pam Belluck, Apoorva Mandavill, and Benedict Carey. New York Times, July 11, 2020). While there are probably several factors to explain this observation, one may be that young children are short, seldom taller than an adult waistline. I suspect the majority of aerosols they emit fall and inactivate harmlessly to the floor several feet below an adult’s nose and mouth. Regardless of the explanation, it appears to be good news for the opening of schools, at least for the early grades.
Forget the deep cleaning
There has been a glut of news stories about reopening schools, and many of these stories are accompanied by images of school custodians with buckets, mops, spray bottles, and sponges scouring desks and walls. The most recent image in our local newspaper was of someone scrubbing the underside of a desk. I know it’s taking the World Health Organization an unconscionable period of time to acknowledge that SARS-CoV-2 is airborne, but the rest of us should have gotten the message long ago and been directing our attention to air handling and ventilation. The urge to scrub and deep clean is a hard habit to break, but this nasty bug is not like influenza or a flesh eating bacteria in which deep cleaning might help. A better image to attach to a story on school reopening would be one of a custodian with a screwdriver struggling to pry open a classroom window that had been painted shut a decade ago.
Managing the inevitable
Middlebury College in Vermont and Bowdoin College here in Brunswick, Maine, are similar in many respects because they are small and situated in relatively isolated small New England towns with good track records for pandemic management. Middlebury has elected to invite all its 2,750 students back to campus, whereas Bowdoin has decided to allow only incoming first years and transfer students (for a total of about 600) to return. Both schools will institute similar testing and social distancing protocols and restrict students from access to their respective towns (“A Tale of 2 Colleges.” By Bill Burger. Inside Higher Ed, June 29,2020). It will be an interesting experiment. I’m voting for Middlebury and not because my son and daughter-in-law are alums, but because I think Middlebury seems to have acknowledged that no matter how diligent one is in creating a SARS-CoV-2–free environment at the outset, these are college kids and there will be some cases on both campuses. It is on how those inevitable realities are managed and contained that an institution should be judged.
Patience
Unfortunately, We always have been a restless and impatient population eager to get moving and it has driven us to greatness. Hopefully, patience will be a lesson that we will learn, along with many others.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
It turns out that a pandemic, at least this COVID-19 version, can be a challenge for folks like me who are seldom at a loss for words. The pandemic has so overwhelmed every corner of our lives that it is hard to think of another topic on which to pontificate and still not tromp on someone’s political toes. One can always write about the pandemic itself, and I’ve tried that, but as the curtain is gradually being pulled back on this crafty little germ one runs the risk of making an observation today that will be disproved in a week or 2. However, I can’t suppress my urge to write, and so I have decided to share a few brief random observations. Of course they are related to the pandemic. And of course I realize that there is a better than fifty percent chance that they will be proved wrong by the time you read my next Letters from Maine.
Under the radar
Two of the many mysteries about SARS-CoV-2 involve young children who as a group appear to be less easily infected than adults and even when infected seem to be less likely to spread the disease to other people, particularly adults. One explanation posited by some researchers in France is that young children are less likely to have symptoms such as cough and are less powerful speakers and so might be less likely to spew out a significant number of infected aerosolized droplets (“How to Reopen Schools: What Science and Other Countries Teach Us.” By Pam Belluck, Apoorva Mandavill, and Benedict Carey. New York Times, July 11, 2020). While there are probably several factors to explain this observation, one may be that young children are short, seldom taller than an adult waistline. I suspect the majority of aerosols they emit fall and inactivate harmlessly to the floor several feet below an adult’s nose and mouth. Regardless of the explanation, it appears to be good news for the opening of schools, at least for the early grades.
Forget the deep cleaning
There has been a glut of news stories about reopening schools, and many of these stories are accompanied by images of school custodians with buckets, mops, spray bottles, and sponges scouring desks and walls. The most recent image in our local newspaper was of someone scrubbing the underside of a desk. I know it’s taking the World Health Organization an unconscionable period of time to acknowledge that SARS-CoV-2 is airborne, but the rest of us should have gotten the message long ago and been directing our attention to air handling and ventilation. The urge to scrub and deep clean is a hard habit to break, but this nasty bug is not like influenza or a flesh eating bacteria in which deep cleaning might help. A better image to attach to a story on school reopening would be one of a custodian with a screwdriver struggling to pry open a classroom window that had been painted shut a decade ago.
Managing the inevitable
Middlebury College in Vermont and Bowdoin College here in Brunswick, Maine, are similar in many respects because they are small and situated in relatively isolated small New England towns with good track records for pandemic management. Middlebury has elected to invite all its 2,750 students back to campus, whereas Bowdoin has decided to allow only incoming first years and transfer students (for a total of about 600) to return. Both schools will institute similar testing and social distancing protocols and restrict students from access to their respective towns (“A Tale of 2 Colleges.” By Bill Burger. Inside Higher Ed, June 29,2020). It will be an interesting experiment. I’m voting for Middlebury and not because my son and daughter-in-law are alums, but because I think Middlebury seems to have acknowledged that no matter how diligent one is in creating a SARS-CoV-2–free environment at the outset, these are college kids and there will be some cases on both campuses. It is on how those inevitable realities are managed and contained that an institution should be judged.
Patience
Unfortunately, We always have been a restless and impatient population eager to get moving and it has driven us to greatness. Hopefully, patience will be a lesson that we will learn, along with many others.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
It turns out that a pandemic, at least this COVID-19 version, can be a challenge for folks like me who are seldom at a loss for words. The pandemic has so overwhelmed every corner of our lives that it is hard to think of another topic on which to pontificate and still not tromp on someone’s political toes. One can always write about the pandemic itself, and I’ve tried that, but as the curtain is gradually being pulled back on this crafty little germ one runs the risk of making an observation today that will be disproved in a week or 2. However, I can’t suppress my urge to write, and so I have decided to share a few brief random observations. Of course they are related to the pandemic. And of course I realize that there is a better than fifty percent chance that they will be proved wrong by the time you read my next Letters from Maine.
Under the radar
Two of the many mysteries about SARS-CoV-2 involve young children who as a group appear to be less easily infected than adults and even when infected seem to be less likely to spread the disease to other people, particularly adults. One explanation posited by some researchers in France is that young children are less likely to have symptoms such as cough and are less powerful speakers and so might be less likely to spew out a significant number of infected aerosolized droplets (“How to Reopen Schools: What Science and Other Countries Teach Us.” By Pam Belluck, Apoorva Mandavill, and Benedict Carey. New York Times, July 11, 2020). While there are probably several factors to explain this observation, one may be that young children are short, seldom taller than an adult waistline. I suspect the majority of aerosols they emit fall and inactivate harmlessly to the floor several feet below an adult’s nose and mouth. Regardless of the explanation, it appears to be good news for the opening of schools, at least for the early grades.
Forget the deep cleaning
There has been a glut of news stories about reopening schools, and many of these stories are accompanied by images of school custodians with buckets, mops, spray bottles, and sponges scouring desks and walls. The most recent image in our local newspaper was of someone scrubbing the underside of a desk. I know it’s taking the World Health Organization an unconscionable period of time to acknowledge that SARS-CoV-2 is airborne, but the rest of us should have gotten the message long ago and been directing our attention to air handling and ventilation. The urge to scrub and deep clean is a hard habit to break, but this nasty bug is not like influenza or a flesh eating bacteria in which deep cleaning might help. A better image to attach to a story on school reopening would be one of a custodian with a screwdriver struggling to pry open a classroom window that had been painted shut a decade ago.
Managing the inevitable
Middlebury College in Vermont and Bowdoin College here in Brunswick, Maine, are similar in many respects because they are small and situated in relatively isolated small New England towns with good track records for pandemic management. Middlebury has elected to invite all its 2,750 students back to campus, whereas Bowdoin has decided to allow only incoming first years and transfer students (for a total of about 600) to return. Both schools will institute similar testing and social distancing protocols and restrict students from access to their respective towns (“A Tale of 2 Colleges.” By Bill Burger. Inside Higher Ed, June 29,2020). It will be an interesting experiment. I’m voting for Middlebury and not because my son and daughter-in-law are alums, but because I think Middlebury seems to have acknowledged that no matter how diligent one is in creating a SARS-CoV-2–free environment at the outset, these are college kids and there will be some cases on both campuses. It is on how those inevitable realities are managed and contained that an institution should be judged.
Patience
Unfortunately, We always have been a restless and impatient population eager to get moving and it has driven us to greatness. Hopefully, patience will be a lesson that we will learn, along with many others.
Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Email him at pdnews@mdedge.com.
Higher death rate seen in cancer patients with nosocomial COVID-19
, according to researchers.
In an observational study of patients with COVID-19 and cancer, 19% of patients had COVID-19 acquired during a non-COVID-related hospital stay, and 81% had community-acquired COVID-19.
At a median follow-up of 23 days, the overall mortality rate was 28%. However, the all-cause mortality rate in patients with nosocomial COVID-19 was more than double that of patients with community-acquired COVID-19, at 47% and 23%, respectively.
Arielle Elkrief, MD, of the University of Montreal, reported these results during the AACR virtual meeting: COVID-19 and Cancer.
“This is the first report that describes a high rate of hospital-acquired COVID-19 in patients with cancer, at a rate of 19%,” Dr. Elkrief said. “This was associated with high mortality in both univariate and multivariate analyses.”
The study included 250 adults and 3 children with COVID-19 and cancer who were identified between March 3 and May 23, 2020. They ranged in age from 4 to 95 years, but the median age was 73 years.
All patients had either laboratory-confirmed (95%) or presumed COVID-19 (5%) and invasive cancer. The most common cancer types were similar to those seen in the general population. Lung and breast cancer were the most common, followed by lymphoma, prostate cancer, and colorectal cancer. Most patients were on active anticancer therapy, most often chemotherapy.
Most patients (n = 236) were residents of Quebec, but 17 patients were residents of British Columbia.
“It is important to note that Quebec was one of the most heavily affected areas in North America at the time of the study,” Dr. Elkrief said.
Outcomes by group
There were 206 patients (81%) who had community-acquired COVID-19 and 47 (19%) who had nosocomial COVID-19. The two groups were similar with respect to sex, performance status, and cancer stage. A small trend toward more patients on active therapy was seen in the nosocomial group, but the difference did not reach statistical significance.
The median overall survival was 27 days in the nosocomial group and 71 days in the community-acquired group (hazard ratio, 2.2; P = .002).
A multivariate analysis showed that nosocomial infection was “strongly and independently associated with death,” Dr. Elkrief said. “Other risk factors for poor prognosis included age, poor [performance] status, and advanced stage of cancer.”
There were no significant differences between the hospital-acquired and community-acquired groups for other outcomes, including oxygen requirements (43% and 47%, respectively), ICU admission (13% and 11%), need for mechanical ventilation (6% and 5%), or length of stay (median, 9.5 days and 8.5 days).
The low rate of ICU admission, considering the mortality rate of 28%, “could reflect that patients with cancer are less likely to be admitted to the ICU,” Dr. Elkrief noted.
Applying the findings to practice
The findings reinforce the importance of adherence to stringent infection control guidelines to protect vulnerable patients, such as those with cancer, Dr. Elkrief said.
In ambulatory settings, this means decreasing in-person visits through increased use of teleconsultations, and for those who need to be seen in person, screening for symptoms or use of polymerase chain reaction testing should be used when resources are available, she said.
“Similar principles apply to chemotherapy treatment units,” Dr. Elkrief said. She added that staff must avoid cross-contamination between COVID and COVID-free zones, and that “dedicated personnel and equipment should be maintained and separate between these two zones.
“Adequate protective personal equipment and strict hand hygiene protocols are also of utmost importance,” Dr. Elkrief said. “The threat of COVID-19 is not behind us, and so we continue to enforce these strategies to protect our patients.”
Session moderator Gypsyamber D’Souza, PhD, an infectious disease epidemiologist at Johns Hopkins University in Baltimore, raised the question of whether the high nosocomial infection and death rate in this study was related to patients having more severe disease because of underlying comorbidities.
Dr. Elkrief explained that the overall mortality rate was indeed higher than the 13% reported in other studies, and it may reflect an overrepresentation of hospitalized or more severely ill patients in the cohort.
However, the investigators made every effort to include all patients with both cancer and COVID-19 by using systematic screening of inpatient and outpatients lists and registries.
Further, the multivariate analysis included both inpatients and outpatients and adjusted for known negative prognostic factors for COVID-19 outcomes. These included increasing age, poor performance status, and different comorbidities.
The finding that nosocomial infection was an independent predictor of death “pushed us to look at nosocomial infection as a new independent risk factor,” Dr. Elkrief said.
Dr. Elkrief reported grant support from AstraZeneca. Dr. D’Souza did not report any disclosures.
SOURCE: Elkrief A et al. AACR: COVID and Cancer, Abstract S12-01.
, according to researchers.
In an observational study of patients with COVID-19 and cancer, 19% of patients had COVID-19 acquired during a non-COVID-related hospital stay, and 81% had community-acquired COVID-19.
At a median follow-up of 23 days, the overall mortality rate was 28%. However, the all-cause mortality rate in patients with nosocomial COVID-19 was more than double that of patients with community-acquired COVID-19, at 47% and 23%, respectively.
Arielle Elkrief, MD, of the University of Montreal, reported these results during the AACR virtual meeting: COVID-19 and Cancer.
“This is the first report that describes a high rate of hospital-acquired COVID-19 in patients with cancer, at a rate of 19%,” Dr. Elkrief said. “This was associated with high mortality in both univariate and multivariate analyses.”
The study included 250 adults and 3 children with COVID-19 and cancer who were identified between March 3 and May 23, 2020. They ranged in age from 4 to 95 years, but the median age was 73 years.
All patients had either laboratory-confirmed (95%) or presumed COVID-19 (5%) and invasive cancer. The most common cancer types were similar to those seen in the general population. Lung and breast cancer were the most common, followed by lymphoma, prostate cancer, and colorectal cancer. Most patients were on active anticancer therapy, most often chemotherapy.
Most patients (n = 236) were residents of Quebec, but 17 patients were residents of British Columbia.
“It is important to note that Quebec was one of the most heavily affected areas in North America at the time of the study,” Dr. Elkrief said.
Outcomes by group
There were 206 patients (81%) who had community-acquired COVID-19 and 47 (19%) who had nosocomial COVID-19. The two groups were similar with respect to sex, performance status, and cancer stage. A small trend toward more patients on active therapy was seen in the nosocomial group, but the difference did not reach statistical significance.
The median overall survival was 27 days in the nosocomial group and 71 days in the community-acquired group (hazard ratio, 2.2; P = .002).
A multivariate analysis showed that nosocomial infection was “strongly and independently associated with death,” Dr. Elkrief said. “Other risk factors for poor prognosis included age, poor [performance] status, and advanced stage of cancer.”
There were no significant differences between the hospital-acquired and community-acquired groups for other outcomes, including oxygen requirements (43% and 47%, respectively), ICU admission (13% and 11%), need for mechanical ventilation (6% and 5%), or length of stay (median, 9.5 days and 8.5 days).
The low rate of ICU admission, considering the mortality rate of 28%, “could reflect that patients with cancer are less likely to be admitted to the ICU,” Dr. Elkrief noted.
Applying the findings to practice
The findings reinforce the importance of adherence to stringent infection control guidelines to protect vulnerable patients, such as those with cancer, Dr. Elkrief said.
In ambulatory settings, this means decreasing in-person visits through increased use of teleconsultations, and for those who need to be seen in person, screening for symptoms or use of polymerase chain reaction testing should be used when resources are available, she said.
“Similar principles apply to chemotherapy treatment units,” Dr. Elkrief said. She added that staff must avoid cross-contamination between COVID and COVID-free zones, and that “dedicated personnel and equipment should be maintained and separate between these two zones.
“Adequate protective personal equipment and strict hand hygiene protocols are also of utmost importance,” Dr. Elkrief said. “The threat of COVID-19 is not behind us, and so we continue to enforce these strategies to protect our patients.”
Session moderator Gypsyamber D’Souza, PhD, an infectious disease epidemiologist at Johns Hopkins University in Baltimore, raised the question of whether the high nosocomial infection and death rate in this study was related to patients having more severe disease because of underlying comorbidities.
Dr. Elkrief explained that the overall mortality rate was indeed higher than the 13% reported in other studies, and it may reflect an overrepresentation of hospitalized or more severely ill patients in the cohort.
However, the investigators made every effort to include all patients with both cancer and COVID-19 by using systematic screening of inpatient and outpatients lists and registries.
Further, the multivariate analysis included both inpatients and outpatients and adjusted for known negative prognostic factors for COVID-19 outcomes. These included increasing age, poor performance status, and different comorbidities.
The finding that nosocomial infection was an independent predictor of death “pushed us to look at nosocomial infection as a new independent risk factor,” Dr. Elkrief said.
Dr. Elkrief reported grant support from AstraZeneca. Dr. D’Souza did not report any disclosures.
SOURCE: Elkrief A et al. AACR: COVID and Cancer, Abstract S12-01.
, according to researchers.
In an observational study of patients with COVID-19 and cancer, 19% of patients had COVID-19 acquired during a non-COVID-related hospital stay, and 81% had community-acquired COVID-19.
At a median follow-up of 23 days, the overall mortality rate was 28%. However, the all-cause mortality rate in patients with nosocomial COVID-19 was more than double that of patients with community-acquired COVID-19, at 47% and 23%, respectively.
Arielle Elkrief, MD, of the University of Montreal, reported these results during the AACR virtual meeting: COVID-19 and Cancer.
“This is the first report that describes a high rate of hospital-acquired COVID-19 in patients with cancer, at a rate of 19%,” Dr. Elkrief said. “This was associated with high mortality in both univariate and multivariate analyses.”
The study included 250 adults and 3 children with COVID-19 and cancer who were identified between March 3 and May 23, 2020. They ranged in age from 4 to 95 years, but the median age was 73 years.
All patients had either laboratory-confirmed (95%) or presumed COVID-19 (5%) and invasive cancer. The most common cancer types were similar to those seen in the general population. Lung and breast cancer were the most common, followed by lymphoma, prostate cancer, and colorectal cancer. Most patients were on active anticancer therapy, most often chemotherapy.
Most patients (n = 236) were residents of Quebec, but 17 patients were residents of British Columbia.
“It is important to note that Quebec was one of the most heavily affected areas in North America at the time of the study,” Dr. Elkrief said.
Outcomes by group
There were 206 patients (81%) who had community-acquired COVID-19 and 47 (19%) who had nosocomial COVID-19. The two groups were similar with respect to sex, performance status, and cancer stage. A small trend toward more patients on active therapy was seen in the nosocomial group, but the difference did not reach statistical significance.
The median overall survival was 27 days in the nosocomial group and 71 days in the community-acquired group (hazard ratio, 2.2; P = .002).
A multivariate analysis showed that nosocomial infection was “strongly and independently associated with death,” Dr. Elkrief said. “Other risk factors for poor prognosis included age, poor [performance] status, and advanced stage of cancer.”
There were no significant differences between the hospital-acquired and community-acquired groups for other outcomes, including oxygen requirements (43% and 47%, respectively), ICU admission (13% and 11%), need for mechanical ventilation (6% and 5%), or length of stay (median, 9.5 days and 8.5 days).
The low rate of ICU admission, considering the mortality rate of 28%, “could reflect that patients with cancer are less likely to be admitted to the ICU,” Dr. Elkrief noted.
Applying the findings to practice
The findings reinforce the importance of adherence to stringent infection control guidelines to protect vulnerable patients, such as those with cancer, Dr. Elkrief said.
In ambulatory settings, this means decreasing in-person visits through increased use of teleconsultations, and for those who need to be seen in person, screening for symptoms or use of polymerase chain reaction testing should be used when resources are available, she said.
“Similar principles apply to chemotherapy treatment units,” Dr. Elkrief said. She added that staff must avoid cross-contamination between COVID and COVID-free zones, and that “dedicated personnel and equipment should be maintained and separate between these two zones.
“Adequate protective personal equipment and strict hand hygiene protocols are also of utmost importance,” Dr. Elkrief said. “The threat of COVID-19 is not behind us, and so we continue to enforce these strategies to protect our patients.”
Session moderator Gypsyamber D’Souza, PhD, an infectious disease epidemiologist at Johns Hopkins University in Baltimore, raised the question of whether the high nosocomial infection and death rate in this study was related to patients having more severe disease because of underlying comorbidities.
Dr. Elkrief explained that the overall mortality rate was indeed higher than the 13% reported in other studies, and it may reflect an overrepresentation of hospitalized or more severely ill patients in the cohort.
However, the investigators made every effort to include all patients with both cancer and COVID-19 by using systematic screening of inpatient and outpatients lists and registries.
Further, the multivariate analysis included both inpatients and outpatients and adjusted for known negative prognostic factors for COVID-19 outcomes. These included increasing age, poor performance status, and different comorbidities.
The finding that nosocomial infection was an independent predictor of death “pushed us to look at nosocomial infection as a new independent risk factor,” Dr. Elkrief said.
Dr. Elkrief reported grant support from AstraZeneca. Dr. D’Souza did not report any disclosures.
SOURCE: Elkrief A et al. AACR: COVID and Cancer, Abstract S12-01.
FROM AACR: COVID-19 AND CANCER
Low vitamin D linked to increased COVID-19 risk
Low plasma vitamin D levels emerged as an independent risk factor for COVID-19 infection and hospitalization in a large, population-based study.
Participants positive for COVID-19 were 50% more likely to have low vs normal 25(OH)D levels in a multivariate analysis that controlled for other confounders, for example.
The take home message for physicians is to “test patients’ vitamin D levels and keep them optimal for the overall health – as well as for a better immunoresponse to COVID-19,” senior author Milana Frenkel-Morgenstern, PhD, head of the Cancer Genomics and BioComputing of Complex Diseases Lab at Bar-Ilan University in Ramat Gan, Israel, said in an interview.
The study was published online July 23 in The FEBS Journal.
Previous and ongoing studies are evaluating a potential role for vitamin D to prevent or minimize the severity of SARS-CoV-2 infection, building on years of research addressing vitamin D for other viral respiratory infections. The evidence to date regarding COVID-19, primarily observational studies, has yielded mixed results.
Multiple experts weighed in on the controversy in a previous report. Many point out the limitations of observational data, particularly when it comes to ruling out other factors that could affect the severity of COVID-19 infection. In addition, in a video report, JoAnn E. Manson, MD, DrPH, of Harvard Medical School in Boston, cited an observational study from three South Asian hospitals that found more severe COVID-19 patients had lower vitamin D levels, as well as other “compelling evidence” suggesting an association.
Dr. Frenkel-Morgenstern and colleagues studied data for 7,807 people, of whom 10.1% were COVID-19 positive. They assessed electronic health records for demographics, potential confounders, and outcomes between February 1 and April 30.
Participants positive for COVID-19 tended to be younger and were more likely to be men and live in a lower socioeconomic area, compared with the participants who were negative for COVID-19, in a univariate analysis.
Key findings
A higher proportion of COVID-19–positive patients had low plasma 25(OH)D concentrations, about 90% versus 85% of participants who were negative for COVID-19. The difference was statistically significant (P < .001). Furthermore, the increased likelihood for low vitamin D levels among those positive for COVID-19 held in a multivariate analysis that controlled for demographics and psychiatric and somatic disorders (adjusted odds ratio, 1.50). The difference remained statistically significant (P < .001).
The study also was noteworthy for what it did not find among participants with COVID-19. For example, the prevalence of dementia, cardiovascular disease, chronic lung disorders, and hypertension were significantly higher among the COVID-19 negative participants.
“Severe social contacts restrictions that were imposed on all the population and were even more emphasized in this highly vulnerable population” could explain these findings, the researchers noted.
“We assume that following the Israeli Ministry of Health instructions, patients with chronic medical conditions significantly reduced their social contacts” and thereby reduced their infection risk.
In contrast to previous reports, obesity was not a significant factor associated with increased likelihood for COVID-19 infection or hospitalization in the current study.
The researchers also linked low plasma 25(OH)D level to an increased likelihood of hospitalization for COVID-19 infection (crude OR, 2.09; P < .05).
After controlling for demographics and chronic disorders, the aOR decreased to 1.95 (P = .061) in a multivariate analysis. The only factor that remained statistically significant for hospitalization was age over 50 years (aOR, 2.71; P < .001).
Implications and future plans
The large number of participants and the “real world,” population-based design are strengths of the study. Considering potential confounders is another strength, the researchers noted. The retrospective database design was a limitation.
Going forward, Dr. Frenkel-Morgenstern and colleagues will “try to decipher the potential role of vitamin D in prevention and/or treatment of COVID-19” through three additional studies, she said. Also, they would like to conduct a meta-analysis to combine data from different countries to further explore the potential role of vitamin D in COVID-19.
“A compelling case”
“This is a strong study – large, adjusted for confounders, consistent with the biology and other clinical studies of vitamin D, infections, and COVID-19,” Wayne Jonas, MD, a practicing family physician and executive director of Samueli Integrative Health Programs, said in an interview.
Because the research was retrospective and observational, a causative link between vitamin D levels and COVID-19 risk cannot be interpreted from the findings. “That would need a prospective, randomized study,” said Dr. Jonas, who was not involved with the current study.
However, “the study makes a compelling case for possibly screening vitamin D levels for judging risk of COVID infection and hospitalization,” Dr. Jonas said, “and the compelling need for a large, randomized vitamin D supplement study to see if it can help prevent infection.”
“Given that vitamin D is largely safe, such a study could be done quickly and on healthy people with minimal risk for harm,” he added.
More confounders likely?
“I think the study is of interest,” Naveed Sattar, PhD, professor of metabolic medicine at the University of Glasgow, who also was not affiliated with the research, said in an interview.
“Whilst the authors adjusted for some confounders, there is a strong potential for residual confounding,” said Dr. Sattar, a coauthor of a UK Biobank study that did not find an association between vitamin D stages and COVID-19 infection in multivariate models.
For example, Dr. Sattar said, “Robust adjustment for social class is important since both Vitamin D levels and COVID-19 severity are both strongly associated with social class.” Further, it remains unknown when and what time of year the vitamin D concentrations were measured in the current study.
“In the end, only a robust randomized trial can tell us whether vitamin D supplementation helps lessen COVID-19 severity,” Dr. Sattar added. “I am not hopeful we will find this is the case – but I am glad some such trials are [ongoing].”
Dr. Frenkel-Morgenstern received a COVID-19 Data Sciences Institute grant to support this work. Dr. Frenkel-Morgenstern, Dr. Jonas, and Dr. Sattar have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Low plasma vitamin D levels emerged as an independent risk factor for COVID-19 infection and hospitalization in a large, population-based study.
Participants positive for COVID-19 were 50% more likely to have low vs normal 25(OH)D levels in a multivariate analysis that controlled for other confounders, for example.
The take home message for physicians is to “test patients’ vitamin D levels and keep them optimal for the overall health – as well as for a better immunoresponse to COVID-19,” senior author Milana Frenkel-Morgenstern, PhD, head of the Cancer Genomics and BioComputing of Complex Diseases Lab at Bar-Ilan University in Ramat Gan, Israel, said in an interview.
The study was published online July 23 in The FEBS Journal.
Previous and ongoing studies are evaluating a potential role for vitamin D to prevent or minimize the severity of SARS-CoV-2 infection, building on years of research addressing vitamin D for other viral respiratory infections. The evidence to date regarding COVID-19, primarily observational studies, has yielded mixed results.
Multiple experts weighed in on the controversy in a previous report. Many point out the limitations of observational data, particularly when it comes to ruling out other factors that could affect the severity of COVID-19 infection. In addition, in a video report, JoAnn E. Manson, MD, DrPH, of Harvard Medical School in Boston, cited an observational study from three South Asian hospitals that found more severe COVID-19 patients had lower vitamin D levels, as well as other “compelling evidence” suggesting an association.
Dr. Frenkel-Morgenstern and colleagues studied data for 7,807 people, of whom 10.1% were COVID-19 positive. They assessed electronic health records for demographics, potential confounders, and outcomes between February 1 and April 30.
Participants positive for COVID-19 tended to be younger and were more likely to be men and live in a lower socioeconomic area, compared with the participants who were negative for COVID-19, in a univariate analysis.
Key findings
A higher proportion of COVID-19–positive patients had low plasma 25(OH)D concentrations, about 90% versus 85% of participants who were negative for COVID-19. The difference was statistically significant (P < .001). Furthermore, the increased likelihood for low vitamin D levels among those positive for COVID-19 held in a multivariate analysis that controlled for demographics and psychiatric and somatic disorders (adjusted odds ratio, 1.50). The difference remained statistically significant (P < .001).
The study also was noteworthy for what it did not find among participants with COVID-19. For example, the prevalence of dementia, cardiovascular disease, chronic lung disorders, and hypertension were significantly higher among the COVID-19 negative participants.
“Severe social contacts restrictions that were imposed on all the population and were even more emphasized in this highly vulnerable population” could explain these findings, the researchers noted.
“We assume that following the Israeli Ministry of Health instructions, patients with chronic medical conditions significantly reduced their social contacts” and thereby reduced their infection risk.
In contrast to previous reports, obesity was not a significant factor associated with increased likelihood for COVID-19 infection or hospitalization in the current study.
The researchers also linked low plasma 25(OH)D level to an increased likelihood of hospitalization for COVID-19 infection (crude OR, 2.09; P < .05).
After controlling for demographics and chronic disorders, the aOR decreased to 1.95 (P = .061) in a multivariate analysis. The only factor that remained statistically significant for hospitalization was age over 50 years (aOR, 2.71; P < .001).
Implications and future plans
The large number of participants and the “real world,” population-based design are strengths of the study. Considering potential confounders is another strength, the researchers noted. The retrospective database design was a limitation.
Going forward, Dr. Frenkel-Morgenstern and colleagues will “try to decipher the potential role of vitamin D in prevention and/or treatment of COVID-19” through three additional studies, she said. Also, they would like to conduct a meta-analysis to combine data from different countries to further explore the potential role of vitamin D in COVID-19.
“A compelling case”
“This is a strong study – large, adjusted for confounders, consistent with the biology and other clinical studies of vitamin D, infections, and COVID-19,” Wayne Jonas, MD, a practicing family physician and executive director of Samueli Integrative Health Programs, said in an interview.
Because the research was retrospective and observational, a causative link between vitamin D levels and COVID-19 risk cannot be interpreted from the findings. “That would need a prospective, randomized study,” said Dr. Jonas, who was not involved with the current study.
However, “the study makes a compelling case for possibly screening vitamin D levels for judging risk of COVID infection and hospitalization,” Dr. Jonas said, “and the compelling need for a large, randomized vitamin D supplement study to see if it can help prevent infection.”
“Given that vitamin D is largely safe, such a study could be done quickly and on healthy people with minimal risk for harm,” he added.
More confounders likely?
“I think the study is of interest,” Naveed Sattar, PhD, professor of metabolic medicine at the University of Glasgow, who also was not affiliated with the research, said in an interview.
“Whilst the authors adjusted for some confounders, there is a strong potential for residual confounding,” said Dr. Sattar, a coauthor of a UK Biobank study that did not find an association between vitamin D stages and COVID-19 infection in multivariate models.
For example, Dr. Sattar said, “Robust adjustment for social class is important since both Vitamin D levels and COVID-19 severity are both strongly associated with social class.” Further, it remains unknown when and what time of year the vitamin D concentrations were measured in the current study.
“In the end, only a robust randomized trial can tell us whether vitamin D supplementation helps lessen COVID-19 severity,” Dr. Sattar added. “I am not hopeful we will find this is the case – but I am glad some such trials are [ongoing].”
Dr. Frenkel-Morgenstern received a COVID-19 Data Sciences Institute grant to support this work. Dr. Frenkel-Morgenstern, Dr. Jonas, and Dr. Sattar have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
Low plasma vitamin D levels emerged as an independent risk factor for COVID-19 infection and hospitalization in a large, population-based study.
Participants positive for COVID-19 were 50% more likely to have low vs normal 25(OH)D levels in a multivariate analysis that controlled for other confounders, for example.
The take home message for physicians is to “test patients’ vitamin D levels and keep them optimal for the overall health – as well as for a better immunoresponse to COVID-19,” senior author Milana Frenkel-Morgenstern, PhD, head of the Cancer Genomics and BioComputing of Complex Diseases Lab at Bar-Ilan University in Ramat Gan, Israel, said in an interview.
The study was published online July 23 in The FEBS Journal.
Previous and ongoing studies are evaluating a potential role for vitamin D to prevent or minimize the severity of SARS-CoV-2 infection, building on years of research addressing vitamin D for other viral respiratory infections. The evidence to date regarding COVID-19, primarily observational studies, has yielded mixed results.
Multiple experts weighed in on the controversy in a previous report. Many point out the limitations of observational data, particularly when it comes to ruling out other factors that could affect the severity of COVID-19 infection. In addition, in a video report, JoAnn E. Manson, MD, DrPH, of Harvard Medical School in Boston, cited an observational study from three South Asian hospitals that found more severe COVID-19 patients had lower vitamin D levels, as well as other “compelling evidence” suggesting an association.
Dr. Frenkel-Morgenstern and colleagues studied data for 7,807 people, of whom 10.1% were COVID-19 positive. They assessed electronic health records for demographics, potential confounders, and outcomes between February 1 and April 30.
Participants positive for COVID-19 tended to be younger and were more likely to be men and live in a lower socioeconomic area, compared with the participants who were negative for COVID-19, in a univariate analysis.
Key findings
A higher proportion of COVID-19–positive patients had low plasma 25(OH)D concentrations, about 90% versus 85% of participants who were negative for COVID-19. The difference was statistically significant (P < .001). Furthermore, the increased likelihood for low vitamin D levels among those positive for COVID-19 held in a multivariate analysis that controlled for demographics and psychiatric and somatic disorders (adjusted odds ratio, 1.50). The difference remained statistically significant (P < .001).
The study also was noteworthy for what it did not find among participants with COVID-19. For example, the prevalence of dementia, cardiovascular disease, chronic lung disorders, and hypertension were significantly higher among the COVID-19 negative participants.
“Severe social contacts restrictions that were imposed on all the population and were even more emphasized in this highly vulnerable population” could explain these findings, the researchers noted.
“We assume that following the Israeli Ministry of Health instructions, patients with chronic medical conditions significantly reduced their social contacts” and thereby reduced their infection risk.
In contrast to previous reports, obesity was not a significant factor associated with increased likelihood for COVID-19 infection or hospitalization in the current study.
The researchers also linked low plasma 25(OH)D level to an increased likelihood of hospitalization for COVID-19 infection (crude OR, 2.09; P < .05).
After controlling for demographics and chronic disorders, the aOR decreased to 1.95 (P = .061) in a multivariate analysis. The only factor that remained statistically significant for hospitalization was age over 50 years (aOR, 2.71; P < .001).
Implications and future plans
The large number of participants and the “real world,” population-based design are strengths of the study. Considering potential confounders is another strength, the researchers noted. The retrospective database design was a limitation.
Going forward, Dr. Frenkel-Morgenstern and colleagues will “try to decipher the potential role of vitamin D in prevention and/or treatment of COVID-19” through three additional studies, she said. Also, they would like to conduct a meta-analysis to combine data from different countries to further explore the potential role of vitamin D in COVID-19.
“A compelling case”
“This is a strong study – large, adjusted for confounders, consistent with the biology and other clinical studies of vitamin D, infections, and COVID-19,” Wayne Jonas, MD, a practicing family physician and executive director of Samueli Integrative Health Programs, said in an interview.
Because the research was retrospective and observational, a causative link between vitamin D levels and COVID-19 risk cannot be interpreted from the findings. “That would need a prospective, randomized study,” said Dr. Jonas, who was not involved with the current study.
However, “the study makes a compelling case for possibly screening vitamin D levels for judging risk of COVID infection and hospitalization,” Dr. Jonas said, “and the compelling need for a large, randomized vitamin D supplement study to see if it can help prevent infection.”
“Given that vitamin D is largely safe, such a study could be done quickly and on healthy people with minimal risk for harm,” he added.
More confounders likely?
“I think the study is of interest,” Naveed Sattar, PhD, professor of metabolic medicine at the University of Glasgow, who also was not affiliated with the research, said in an interview.
“Whilst the authors adjusted for some confounders, there is a strong potential for residual confounding,” said Dr. Sattar, a coauthor of a UK Biobank study that did not find an association between vitamin D stages and COVID-19 infection in multivariate models.
For example, Dr. Sattar said, “Robust adjustment for social class is important since both Vitamin D levels and COVID-19 severity are both strongly associated with social class.” Further, it remains unknown when and what time of year the vitamin D concentrations were measured in the current study.
“In the end, only a robust randomized trial can tell us whether vitamin D supplementation helps lessen COVID-19 severity,” Dr. Sattar added. “I am not hopeful we will find this is the case – but I am glad some such trials are [ongoing].”
Dr. Frenkel-Morgenstern received a COVID-19 Data Sciences Institute grant to support this work. Dr. Frenkel-Morgenstern, Dr. Jonas, and Dr. Sattar have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
NFL’s only physician player opts out of 2020 season over COVID
Canadian-born Duvernay-Tardif, right guard for the Kansas City Chiefs, announced on Twitter on July 24 what he called “one of the most difficult decisions I have had to make in my life.”
“There is no doubt in my mind the Chiefs’ medical staff have put together a strong plan to minimize the health risks associated with COVID-19, but some risks will remain,” he posted.
“Being at the frontline during this offseason has given me a different perspective on this pandemic and the stress it puts on individuals and our healthcare system. I cannot allow myself to potentially transmit the virus in our communities simply to play the sport that I love. If I am to take risks, I will do it caring for patients.”
According to CNN, Duvernay-Tardif, less than 3 months after helping the Chiefs win the Super Bowl in February, began working at a long-term care facility near Montreal in what he described as a “nursing role.”
Duvernay-Tardif wrote recently in an article for Sports Illustrated that he has not completed his residency and is not yet licensed to practice.
“My first day back in the hospital was April 24,” Duvernay-Tardif wrote. “I felt nervous the night before, but a good nervous, like before a game.”
Duvernay-Tardif has also served on the NFL Players’ Association COVID-19 task force, according to Yahoo News .
A spokesperson for Duvernay-Tardif told Medscape Medical News he was unavailable to comment about the announcement.
Starting His Dual Career
Duvernay-Tardif, 29, was drafted in the sixth round by the Chiefs in 2014.
According to Forbes , he spent 8 years (2010-2018) pursuing his medical degree while still playing college football for McGill University in Montreal. Duvernay-Tardif played offensive tackle for the Redmen and in his senior year (2013) won the Metras Trophy as most outstanding lineman in Canadian college football.
He explained in a previous Medscape interview how he managed his dual career; as a doctor he said he would like to focus on emergency medicine:
“I would say that at around 16-17 years of age, I was pretty convinced that medicine was for me,” he told Medscape.
“I was lucky that I didn’t have to do an undergrad program,” he continued. “In Canada, they have a fast-track program where instead of doing a full undergrad before getting into medical school, you can do a 1-year program where you can do all your physiology and biology classes all together.
“I had the chance to get into that program, and that’s how I was able to manage football and medicine at the same time. There’s no way I could have finished my med school doing part-time med school like I did for the past 4 years.”
ESPN explained the opt-out option: “According to an agreement approved by both the league and the union on [July 24], players considered high risk for COVID-19 can earn $350,000 and an accrued NFL season if they choose to opt out of the 2020 season. Players without risk can earn $150,000 for opting out. Duvernay-Tardif was scheduled to make $2.75 million this season.”
The danger of COVID-19 in professional sports has already been seen in Major League Baseball.
According to USA Today, the Miami Marlins have at least 14 players and staff who have tested positive for COVID-19, and major league baseball Commissioner Rob Manfred must decide whether to further delay the shortened season, cancel it, or allow it to continue.
MLB postponed the Marlins’ home opener July 27 against the Baltimore Orioles as well as the New York Yankees game in Philadelphia against the Phillies.
COVID-19 also shut down professional, college, high school, and recreational sports throughout much of the country beginning in March.
Medicine, Football Intersect
In the previous Medscape interview, Duvernay-Tardif talked about how medicine influenced his football career.
“For me, medicine was really helpful in the sense that I was better able to build a routine and question what works for me and what doesn’t. It gave me the ability to structure my work in order to optimize my time and to make sure that it’s pertinent.
“Another thing is the psychology and the sports psychology. I think there’s a little bit of a stigma around mental health issues in professional sports and everywhere, actually. I think because of medicine, I was more willing to question myself and more willing to use different tools in order to be a better football player.”
A version of this article first appeared on Medscape.com.
Canadian-born Duvernay-Tardif, right guard for the Kansas City Chiefs, announced on Twitter on July 24 what he called “one of the most difficult decisions I have had to make in my life.”
“There is no doubt in my mind the Chiefs’ medical staff have put together a strong plan to minimize the health risks associated with COVID-19, but some risks will remain,” he posted.
“Being at the frontline during this offseason has given me a different perspective on this pandemic and the stress it puts on individuals and our healthcare system. I cannot allow myself to potentially transmit the virus in our communities simply to play the sport that I love. If I am to take risks, I will do it caring for patients.”
According to CNN, Duvernay-Tardif, less than 3 months after helping the Chiefs win the Super Bowl in February, began working at a long-term care facility near Montreal in what he described as a “nursing role.”
Duvernay-Tardif wrote recently in an article for Sports Illustrated that he has not completed his residency and is not yet licensed to practice.
“My first day back in the hospital was April 24,” Duvernay-Tardif wrote. “I felt nervous the night before, but a good nervous, like before a game.”
Duvernay-Tardif has also served on the NFL Players’ Association COVID-19 task force, according to Yahoo News .
A spokesperson for Duvernay-Tardif told Medscape Medical News he was unavailable to comment about the announcement.
Starting His Dual Career
Duvernay-Tardif, 29, was drafted in the sixth round by the Chiefs in 2014.
According to Forbes , he spent 8 years (2010-2018) pursuing his medical degree while still playing college football for McGill University in Montreal. Duvernay-Tardif played offensive tackle for the Redmen and in his senior year (2013) won the Metras Trophy as most outstanding lineman in Canadian college football.
He explained in a previous Medscape interview how he managed his dual career; as a doctor he said he would like to focus on emergency medicine:
“I would say that at around 16-17 years of age, I was pretty convinced that medicine was for me,” he told Medscape.
“I was lucky that I didn’t have to do an undergrad program,” he continued. “In Canada, they have a fast-track program where instead of doing a full undergrad before getting into medical school, you can do a 1-year program where you can do all your physiology and biology classes all together.
“I had the chance to get into that program, and that’s how I was able to manage football and medicine at the same time. There’s no way I could have finished my med school doing part-time med school like I did for the past 4 years.”
ESPN explained the opt-out option: “According to an agreement approved by both the league and the union on [July 24], players considered high risk for COVID-19 can earn $350,000 and an accrued NFL season if they choose to opt out of the 2020 season. Players without risk can earn $150,000 for opting out. Duvernay-Tardif was scheduled to make $2.75 million this season.”
The danger of COVID-19 in professional sports has already been seen in Major League Baseball.
According to USA Today, the Miami Marlins have at least 14 players and staff who have tested positive for COVID-19, and major league baseball Commissioner Rob Manfred must decide whether to further delay the shortened season, cancel it, or allow it to continue.
MLB postponed the Marlins’ home opener July 27 against the Baltimore Orioles as well as the New York Yankees game in Philadelphia against the Phillies.
COVID-19 also shut down professional, college, high school, and recreational sports throughout much of the country beginning in March.
Medicine, Football Intersect
In the previous Medscape interview, Duvernay-Tardif talked about how medicine influenced his football career.
“For me, medicine was really helpful in the sense that I was better able to build a routine and question what works for me and what doesn’t. It gave me the ability to structure my work in order to optimize my time and to make sure that it’s pertinent.
“Another thing is the psychology and the sports psychology. I think there’s a little bit of a stigma around mental health issues in professional sports and everywhere, actually. I think because of medicine, I was more willing to question myself and more willing to use different tools in order to be a better football player.”
A version of this article first appeared on Medscape.com.
Canadian-born Duvernay-Tardif, right guard for the Kansas City Chiefs, announced on Twitter on July 24 what he called “one of the most difficult decisions I have had to make in my life.”
“There is no doubt in my mind the Chiefs’ medical staff have put together a strong plan to minimize the health risks associated with COVID-19, but some risks will remain,” he posted.
“Being at the frontline during this offseason has given me a different perspective on this pandemic and the stress it puts on individuals and our healthcare system. I cannot allow myself to potentially transmit the virus in our communities simply to play the sport that I love. If I am to take risks, I will do it caring for patients.”
According to CNN, Duvernay-Tardif, less than 3 months after helping the Chiefs win the Super Bowl in February, began working at a long-term care facility near Montreal in what he described as a “nursing role.”
Duvernay-Tardif wrote recently in an article for Sports Illustrated that he has not completed his residency and is not yet licensed to practice.
“My first day back in the hospital was April 24,” Duvernay-Tardif wrote. “I felt nervous the night before, but a good nervous, like before a game.”
Duvernay-Tardif has also served on the NFL Players’ Association COVID-19 task force, according to Yahoo News .
A spokesperson for Duvernay-Tardif told Medscape Medical News he was unavailable to comment about the announcement.
Starting His Dual Career
Duvernay-Tardif, 29, was drafted in the sixth round by the Chiefs in 2014.
According to Forbes , he spent 8 years (2010-2018) pursuing his medical degree while still playing college football for McGill University in Montreal. Duvernay-Tardif played offensive tackle for the Redmen and in his senior year (2013) won the Metras Trophy as most outstanding lineman in Canadian college football.
He explained in a previous Medscape interview how he managed his dual career; as a doctor he said he would like to focus on emergency medicine:
“I would say that at around 16-17 years of age, I was pretty convinced that medicine was for me,” he told Medscape.
“I was lucky that I didn’t have to do an undergrad program,” he continued. “In Canada, they have a fast-track program where instead of doing a full undergrad before getting into medical school, you can do a 1-year program where you can do all your physiology and biology classes all together.
“I had the chance to get into that program, and that’s how I was able to manage football and medicine at the same time. There’s no way I could have finished my med school doing part-time med school like I did for the past 4 years.”
ESPN explained the opt-out option: “According to an agreement approved by both the league and the union on [July 24], players considered high risk for COVID-19 can earn $350,000 and an accrued NFL season if they choose to opt out of the 2020 season. Players without risk can earn $150,000 for opting out. Duvernay-Tardif was scheduled to make $2.75 million this season.”
The danger of COVID-19 in professional sports has already been seen in Major League Baseball.
According to USA Today, the Miami Marlins have at least 14 players and staff who have tested positive for COVID-19, and major league baseball Commissioner Rob Manfred must decide whether to further delay the shortened season, cancel it, or allow it to continue.
MLB postponed the Marlins’ home opener July 27 against the Baltimore Orioles as well as the New York Yankees game in Philadelphia against the Phillies.
COVID-19 also shut down professional, college, high school, and recreational sports throughout much of the country beginning in March.
Medicine, Football Intersect
In the previous Medscape interview, Duvernay-Tardif talked about how medicine influenced his football career.
“For me, medicine was really helpful in the sense that I was better able to build a routine and question what works for me and what doesn’t. It gave me the ability to structure my work in order to optimize my time and to make sure that it’s pertinent.
“Another thing is the psychology and the sports psychology. I think there’s a little bit of a stigma around mental health issues in professional sports and everywhere, actually. I think because of medicine, I was more willing to question myself and more willing to use different tools in order to be a better football player.”
A version of this article first appeared on Medscape.com.
Diary of a rheumatologist who briefly became a COVID hospitalist
When the coronavirus pandemic hit New York City in early March, the Hospital for Special Surgery leadership decided that the best way to serve the city was to stop elective orthopedic procedures temporarily and use the facility to take on patients from its sister institution, NewYork–Presbyterian Hospital.
As in other institutions, it was all hands on deck. , other internal medicine subspecialists were asked to volunteer, including rheumatologists and primary care sports medicine doctors.
As a rheumatologist, it had been well over 10 years since I had last done any inpatient work. I was filled with trepidation, but I was also excited to dive in.
April 4:
Feeling very unmoored. I am in unfamiliar territory, and it’s terrifying. There are so many things that I no longer know how to do. Thankfully, the hospitalists are gracious, extremely supportive, and helpful.
My N95 doesn’t fit well. It’s never fit — not during residency or fellowship, not in any job I’ve had, and not today. The lady fit-testing me said she was sorry, but the look on her face said, “I’m sorry, but you’re going to die.”
April 7:
We don’t know how to treat coronavirus. I’ve sent some patients home, others I’ve sent to the ICU. Thank goodness for treatment algorithms from leadership, but we are sorely lacking good-quality data.
Our infectious disease doctor doesn’t think hydroxychloroquine works at all; I suspect he is right. The guidance right now is to give hydroxychloroquine and azithromycin to everyone who is sick enough to be admitted, but there are methodologic flaws in the early enthusiastic preprints, and so far, I’ve not noticed any demonstrable benefit.
The only thing that seems to be happening is that I am seeing more QT prolongation — not something I previously counseled my rheumatology patients on.
April 9:
The patients have been, with a few exceptions, alone in the room. They’re not allowed to have visitors and are required to wear masks all the time. Anyone who enters their rooms is fully covered up so you can barely see them. It’s anonymous and dehumanizing.
We’re instructed to take histories by phone in order to limit the time spent in each room. I buck this instruction; I still take histories in person because human contact seems more important now than ever.
Except maybe I should be smarter about this. One of my patients refuses any treatment, including oxygen support. She firmly believes this is a result of 5G networks — something I later discovered was a common conspiracy theory. She refused to wear a mask despite having a very bad cough. She coughed in my face a lot when we were chatting. My face with my ill-fitting N95 mask. Maybe the fit-testing lady’s eyes weren’t lying and I will die after all.
April 15:
On the days when I’m not working as a hospitalist, I am still doing remote visits with my rheumatology patients. It feels good to be doing something familiar and something I’m actually good at. But it is surreal to be faced with the quotidian on one hand and life and death on the other.
I recently saw a fairly new patient, and I still haven’t figured out if she has a rheumatic condition or if her symptoms all stem from an alcohol use disorder. In our previous visits, she could barely acknowledge that her drinking was an issue. On today’s visit, she told me she was 1½ months sober.
I don’t know her very well, but it was the happiest news I’d heard in a long time. I was so beside myself with joy that I cried, which says more about my current emotional state than anything else, really.
April 21:
On my panel of patients, I have three women with COVID-19 — all of whom lost their husbands to COVID-19, and none of whom were able to say their goodbyes. I cannot even begin to imagine what it must be like to survive this period of illness, isolation, and fear, only to be met on the other side by grief.
Rheumatology doesn’t lend itself too well to such existential concerns; I am not equipped for this. Perhaps my only advantage as a rheumatologist is that I know how to use IVIG, anakinra, and tocilizumab.
Someone on my panel was started on anakinra, and it turned his case around. Would he have gotten better without it anyway? We’ll never know for sure.
April 28:
Patients seem to be requiring prolonged intubation. We have now reached the stage where patients are alive but trached and PEGed. One of my patients had been intubated for close to 3 weeks. She was one of four people in her family who contracted the illness (they had had a dinner party before New York’s state of emergency was declared). We thought she might die once she was extubated, but she is still fighting. Unconscious, unarousable, but breathing on her own.
Will she ever wake up? We don’t know. We put the onus on her family to make decisions about placing a PEG tube in. They can only do so from a distance with imperfect information gleaned from periodic, brief FaceTime interactions — where no interaction happens at all.
May 4:
It’s my last day as a “COVID hospitalist.” When I first started, I felt like I was being helpful. Walking home in the middle of the 7 PM cheers for healthcare workers frequently left me teary eyed. As horrible as the situation was, I was proud of myself for volunteering to help and appreciative of a broken city’s gratitude toward all healthcare workers in general. Maybe I bought into the idea that, like many others around me, I am a hero.
I don’t feel like a hero, though. The stuff I saw was easy compared with the stuff that my colleagues in critical care saw. Our hospital accepted the more stable patient transfers from our sister hospitals. Patients who remained in the NewYork–Presbyterian system were sicker, with encephalitis, thrombotic complications, multiorgan failure, and cytokine release syndrome. It’s the doctors who took care of those patients who deserve to be called heroes.
No, I am no hero. But did my volunteering make a difference? It made a difference to me. The overwhelming feeling I am left with isn’t pride; it’s humility. I feel humbled that I could feel so unexpectedly touched by the lives of people that I had no idea I could feel touched by.
Postscript:
My patient Esther [name changed to hide her identity] died from COVID-19. She was MY patient — not a patient I met as a COVID hospitalist, but a patient with rheumatoid arthritis whom I cared for for years.
She had scleromalacia and multiple failed scleral grafts, which made her profoundly sad. She fought her anxiety fiercely and always with poise and panache. One way she dealt with her anxiety was that she constantly messaged me via our EHR portal. She ran everything by me and trusted me to be her rock.
The past month has been so busy that I just now noticed it had been a month since I last heard from her. I tried to call her but got her voicemail. It wasn’t until I exchanged messages with her ophthalmologist that I found out she had passed away from complications of COVID-19.
She was taking rituximab and mycophenolate. I wonder if these drugs made her sicker than she would have been otherwise; it fills me with sadness. I wonder if she was alone like my other COVID-19 patients. I wonder if she was afraid. I am sorry that I wasn’t able to say goodbye.
Karmela Kim Chan, MD, is an assistant professor at Weill Cornell Medical College and an attending physician at Hospital for Special Surgery and Memorial Sloan Kettering Cancer Center in New York City. Before moving to New York City, she spent 7 years in private practice in Rhode Island and was a columnist for this rheumatology publication, writing about the challenges of starting life as a full-fledged rheumatologist in a private practice.
A version of this article originally appeared on Medscape.com. This article is part of a partnership between Medscape and Hospital for Special Surgery.
When the coronavirus pandemic hit New York City in early March, the Hospital for Special Surgery leadership decided that the best way to serve the city was to stop elective orthopedic procedures temporarily and use the facility to take on patients from its sister institution, NewYork–Presbyterian Hospital.
As in other institutions, it was all hands on deck. , other internal medicine subspecialists were asked to volunteer, including rheumatologists and primary care sports medicine doctors.
As a rheumatologist, it had been well over 10 years since I had last done any inpatient work. I was filled with trepidation, but I was also excited to dive in.
April 4:
Feeling very unmoored. I am in unfamiliar territory, and it’s terrifying. There are so many things that I no longer know how to do. Thankfully, the hospitalists are gracious, extremely supportive, and helpful.
My N95 doesn’t fit well. It’s never fit — not during residency or fellowship, not in any job I’ve had, and not today. The lady fit-testing me said she was sorry, but the look on her face said, “I’m sorry, but you’re going to die.”
April 7:
We don’t know how to treat coronavirus. I’ve sent some patients home, others I’ve sent to the ICU. Thank goodness for treatment algorithms from leadership, but we are sorely lacking good-quality data.
Our infectious disease doctor doesn’t think hydroxychloroquine works at all; I suspect he is right. The guidance right now is to give hydroxychloroquine and azithromycin to everyone who is sick enough to be admitted, but there are methodologic flaws in the early enthusiastic preprints, and so far, I’ve not noticed any demonstrable benefit.
The only thing that seems to be happening is that I am seeing more QT prolongation — not something I previously counseled my rheumatology patients on.
April 9:
The patients have been, with a few exceptions, alone in the room. They’re not allowed to have visitors and are required to wear masks all the time. Anyone who enters their rooms is fully covered up so you can barely see them. It’s anonymous and dehumanizing.
We’re instructed to take histories by phone in order to limit the time spent in each room. I buck this instruction; I still take histories in person because human contact seems more important now than ever.
Except maybe I should be smarter about this. One of my patients refuses any treatment, including oxygen support. She firmly believes this is a result of 5G networks — something I later discovered was a common conspiracy theory. She refused to wear a mask despite having a very bad cough. She coughed in my face a lot when we were chatting. My face with my ill-fitting N95 mask. Maybe the fit-testing lady’s eyes weren’t lying and I will die after all.
April 15:
On the days when I’m not working as a hospitalist, I am still doing remote visits with my rheumatology patients. It feels good to be doing something familiar and something I’m actually good at. But it is surreal to be faced with the quotidian on one hand and life and death on the other.
I recently saw a fairly new patient, and I still haven’t figured out if she has a rheumatic condition or if her symptoms all stem from an alcohol use disorder. In our previous visits, she could barely acknowledge that her drinking was an issue. On today’s visit, she told me she was 1½ months sober.
I don’t know her very well, but it was the happiest news I’d heard in a long time. I was so beside myself with joy that I cried, which says more about my current emotional state than anything else, really.
April 21:
On my panel of patients, I have three women with COVID-19 — all of whom lost their husbands to COVID-19, and none of whom were able to say their goodbyes. I cannot even begin to imagine what it must be like to survive this period of illness, isolation, and fear, only to be met on the other side by grief.
Rheumatology doesn’t lend itself too well to such existential concerns; I am not equipped for this. Perhaps my only advantage as a rheumatologist is that I know how to use IVIG, anakinra, and tocilizumab.
Someone on my panel was started on anakinra, and it turned his case around. Would he have gotten better without it anyway? We’ll never know for sure.
April 28:
Patients seem to be requiring prolonged intubation. We have now reached the stage where patients are alive but trached and PEGed. One of my patients had been intubated for close to 3 weeks. She was one of four people in her family who contracted the illness (they had had a dinner party before New York’s state of emergency was declared). We thought she might die once she was extubated, but she is still fighting. Unconscious, unarousable, but breathing on her own.
Will she ever wake up? We don’t know. We put the onus on her family to make decisions about placing a PEG tube in. They can only do so from a distance with imperfect information gleaned from periodic, brief FaceTime interactions — where no interaction happens at all.
May 4:
It’s my last day as a “COVID hospitalist.” When I first started, I felt like I was being helpful. Walking home in the middle of the 7 PM cheers for healthcare workers frequently left me teary eyed. As horrible as the situation was, I was proud of myself for volunteering to help and appreciative of a broken city’s gratitude toward all healthcare workers in general. Maybe I bought into the idea that, like many others around me, I am a hero.
I don’t feel like a hero, though. The stuff I saw was easy compared with the stuff that my colleagues in critical care saw. Our hospital accepted the more stable patient transfers from our sister hospitals. Patients who remained in the NewYork–Presbyterian system were sicker, with encephalitis, thrombotic complications, multiorgan failure, and cytokine release syndrome. It’s the doctors who took care of those patients who deserve to be called heroes.
No, I am no hero. But did my volunteering make a difference? It made a difference to me. The overwhelming feeling I am left with isn’t pride; it’s humility. I feel humbled that I could feel so unexpectedly touched by the lives of people that I had no idea I could feel touched by.
Postscript:
My patient Esther [name changed to hide her identity] died from COVID-19. She was MY patient — not a patient I met as a COVID hospitalist, but a patient with rheumatoid arthritis whom I cared for for years.
She had scleromalacia and multiple failed scleral grafts, which made her profoundly sad. She fought her anxiety fiercely and always with poise and panache. One way she dealt with her anxiety was that she constantly messaged me via our EHR portal. She ran everything by me and trusted me to be her rock.
The past month has been so busy that I just now noticed it had been a month since I last heard from her. I tried to call her but got her voicemail. It wasn’t until I exchanged messages with her ophthalmologist that I found out she had passed away from complications of COVID-19.
She was taking rituximab and mycophenolate. I wonder if these drugs made her sicker than she would have been otherwise; it fills me with sadness. I wonder if she was alone like my other COVID-19 patients. I wonder if she was afraid. I am sorry that I wasn’t able to say goodbye.
Karmela Kim Chan, MD, is an assistant professor at Weill Cornell Medical College and an attending physician at Hospital for Special Surgery and Memorial Sloan Kettering Cancer Center in New York City. Before moving to New York City, she spent 7 years in private practice in Rhode Island and was a columnist for this rheumatology publication, writing about the challenges of starting life as a full-fledged rheumatologist in a private practice.
A version of this article originally appeared on Medscape.com. This article is part of a partnership between Medscape and Hospital for Special Surgery.
When the coronavirus pandemic hit New York City in early March, the Hospital for Special Surgery leadership decided that the best way to serve the city was to stop elective orthopedic procedures temporarily and use the facility to take on patients from its sister institution, NewYork–Presbyterian Hospital.
As in other institutions, it was all hands on deck. , other internal medicine subspecialists were asked to volunteer, including rheumatologists and primary care sports medicine doctors.
As a rheumatologist, it had been well over 10 years since I had last done any inpatient work. I was filled with trepidation, but I was also excited to dive in.
April 4:
Feeling very unmoored. I am in unfamiliar territory, and it’s terrifying. There are so many things that I no longer know how to do. Thankfully, the hospitalists are gracious, extremely supportive, and helpful.
My N95 doesn’t fit well. It’s never fit — not during residency or fellowship, not in any job I’ve had, and not today. The lady fit-testing me said she was sorry, but the look on her face said, “I’m sorry, but you’re going to die.”
April 7:
We don’t know how to treat coronavirus. I’ve sent some patients home, others I’ve sent to the ICU. Thank goodness for treatment algorithms from leadership, but we are sorely lacking good-quality data.
Our infectious disease doctor doesn’t think hydroxychloroquine works at all; I suspect he is right. The guidance right now is to give hydroxychloroquine and azithromycin to everyone who is sick enough to be admitted, but there are methodologic flaws in the early enthusiastic preprints, and so far, I’ve not noticed any demonstrable benefit.
The only thing that seems to be happening is that I am seeing more QT prolongation — not something I previously counseled my rheumatology patients on.
April 9:
The patients have been, with a few exceptions, alone in the room. They’re not allowed to have visitors and are required to wear masks all the time. Anyone who enters their rooms is fully covered up so you can barely see them. It’s anonymous and dehumanizing.
We’re instructed to take histories by phone in order to limit the time spent in each room. I buck this instruction; I still take histories in person because human contact seems more important now than ever.
Except maybe I should be smarter about this. One of my patients refuses any treatment, including oxygen support. She firmly believes this is a result of 5G networks — something I later discovered was a common conspiracy theory. She refused to wear a mask despite having a very bad cough. She coughed in my face a lot when we were chatting. My face with my ill-fitting N95 mask. Maybe the fit-testing lady’s eyes weren’t lying and I will die after all.
April 15:
On the days when I’m not working as a hospitalist, I am still doing remote visits with my rheumatology patients. It feels good to be doing something familiar and something I’m actually good at. But it is surreal to be faced with the quotidian on one hand and life and death on the other.
I recently saw a fairly new patient, and I still haven’t figured out if she has a rheumatic condition or if her symptoms all stem from an alcohol use disorder. In our previous visits, she could barely acknowledge that her drinking was an issue. On today’s visit, she told me she was 1½ months sober.
I don’t know her very well, but it was the happiest news I’d heard in a long time. I was so beside myself with joy that I cried, which says more about my current emotional state than anything else, really.
April 21:
On my panel of patients, I have three women with COVID-19 — all of whom lost their husbands to COVID-19, and none of whom were able to say their goodbyes. I cannot even begin to imagine what it must be like to survive this period of illness, isolation, and fear, only to be met on the other side by grief.
Rheumatology doesn’t lend itself too well to such existential concerns; I am not equipped for this. Perhaps my only advantage as a rheumatologist is that I know how to use IVIG, anakinra, and tocilizumab.
Someone on my panel was started on anakinra, and it turned his case around. Would he have gotten better without it anyway? We’ll never know for sure.
April 28:
Patients seem to be requiring prolonged intubation. We have now reached the stage where patients are alive but trached and PEGed. One of my patients had been intubated for close to 3 weeks. She was one of four people in her family who contracted the illness (they had had a dinner party before New York’s state of emergency was declared). We thought she might die once she was extubated, but she is still fighting. Unconscious, unarousable, but breathing on her own.
Will she ever wake up? We don’t know. We put the onus on her family to make decisions about placing a PEG tube in. They can only do so from a distance with imperfect information gleaned from periodic, brief FaceTime interactions — where no interaction happens at all.
May 4:
It’s my last day as a “COVID hospitalist.” When I first started, I felt like I was being helpful. Walking home in the middle of the 7 PM cheers for healthcare workers frequently left me teary eyed. As horrible as the situation was, I was proud of myself for volunteering to help and appreciative of a broken city’s gratitude toward all healthcare workers in general. Maybe I bought into the idea that, like many others around me, I am a hero.
I don’t feel like a hero, though. The stuff I saw was easy compared with the stuff that my colleagues in critical care saw. Our hospital accepted the more stable patient transfers from our sister hospitals. Patients who remained in the NewYork–Presbyterian system were sicker, with encephalitis, thrombotic complications, multiorgan failure, and cytokine release syndrome. It’s the doctors who took care of those patients who deserve to be called heroes.
No, I am no hero. But did my volunteering make a difference? It made a difference to me. The overwhelming feeling I am left with isn’t pride; it’s humility. I feel humbled that I could feel so unexpectedly touched by the lives of people that I had no idea I could feel touched by.
Postscript:
My patient Esther [name changed to hide her identity] died from COVID-19. She was MY patient — not a patient I met as a COVID hospitalist, but a patient with rheumatoid arthritis whom I cared for for years.
She had scleromalacia and multiple failed scleral grafts, which made her profoundly sad. She fought her anxiety fiercely and always with poise and panache. One way she dealt with her anxiety was that she constantly messaged me via our EHR portal. She ran everything by me and trusted me to be her rock.
The past month has been so busy that I just now noticed it had been a month since I last heard from her. I tried to call her but got her voicemail. It wasn’t until I exchanged messages with her ophthalmologist that I found out she had passed away from complications of COVID-19.
She was taking rituximab and mycophenolate. I wonder if these drugs made her sicker than she would have been otherwise; it fills me with sadness. I wonder if she was alone like my other COVID-19 patients. I wonder if she was afraid. I am sorry that I wasn’t able to say goodbye.
Karmela Kim Chan, MD, is an assistant professor at Weill Cornell Medical College and an attending physician at Hospital for Special Surgery and Memorial Sloan Kettering Cancer Center in New York City. Before moving to New York City, she spent 7 years in private practice in Rhode Island and was a columnist for this rheumatology publication, writing about the challenges of starting life as a full-fledged rheumatologist in a private practice.
A version of this article originally appeared on Medscape.com. This article is part of a partnership between Medscape and Hospital for Special Surgery.
COVID-19 fears would keep most Hispanics with stroke, MI symptoms home
More than half of Hispanic adults would be afraid to go to a hospital for a possible heart attack or stroke because they might get infected with SARS-CoV-2, according to a new survey from the American Heart Association.
Compared with Hispanic respondents, 55% of whom said they feared COVID-19, significantly fewer Blacks (45%) and Whites (40%) would be scared to go to the hospital if they thought they were having a heart attack or stroke, the AHA said based on the survey of 2,050 adults, which was conducted May 29 to June 2, 2020, by the Harris Poll.
Hispanics also were significantly more likely to stay home if they thought they were experiencing a heart attack or stroke (41%), rather than risk getting infected at the hospital, than were Blacks (33%), who were significantly more likely than Whites (24%) to stay home, the AHA reported.
White respondents, on the other hand, were the most likely to believe (89%) that a hospital would give them the same quality of care provided to everyone else. Hispanics and Blacks had significantly lower rates, at 78% and 74%, respectively, the AHA noted.
These findings are “yet another challenge for Black and Hispanic communities, who are more likely to have underlying health conditions such as cardiovascular disease and diabetes and dying of COVID-19 at disproportionately high rates,” Rafael Ortiz, MD, American Heart Association volunteer medical expert and chief of neuro-endovascular surgery at Lenox Hill Hospital, New York, said in the AHA statement.
The survey was performed in conjunction with the AHA’s “Don’t Die of Doubt” campaign, which “reminds Americans, especially in Hispanic and Black communities, that the hospital remains the safest place to be if experiencing symptoms of a heart attack or a stroke.”
Among all the survey respondents, 57% said they would feel better if hospitals treated COVID-19 patients in a separate area. A number of other possible precautions ranked lower in helping them feel better:
- Screen all visitors, patients, and staff for COVID-19 symptoms when they enter the hospital: 39%.
- Require all patients, visitors, and staff to wear masks: 30%.
- Put increased cleaning protocols in place to disinfect multiple times per day: 23%.
- “Nothing would make me feel comfortable”: 6%.
Despite all the concerns about the risk of coronavirus infection, however, most Americans (77%) still believe that hospitals are the safest place to be in the event of a medical emergency, and 84% said that hospitals are prepared to safely treat emergencies that are not related to the pandemic, the AHA reported.
“Health care professionals know what to do even when things seem chaotic, and emergency departments have made plans behind the scenes to keep patients and healthcare workers safe even during a pandemic,” Dr. Ortiz pointed out.
More than half of Hispanic adults would be afraid to go to a hospital for a possible heart attack or stroke because they might get infected with SARS-CoV-2, according to a new survey from the American Heart Association.
Compared with Hispanic respondents, 55% of whom said they feared COVID-19, significantly fewer Blacks (45%) and Whites (40%) would be scared to go to the hospital if they thought they were having a heart attack or stroke, the AHA said based on the survey of 2,050 adults, which was conducted May 29 to June 2, 2020, by the Harris Poll.
Hispanics also were significantly more likely to stay home if they thought they were experiencing a heart attack or stroke (41%), rather than risk getting infected at the hospital, than were Blacks (33%), who were significantly more likely than Whites (24%) to stay home, the AHA reported.
White respondents, on the other hand, were the most likely to believe (89%) that a hospital would give them the same quality of care provided to everyone else. Hispanics and Blacks had significantly lower rates, at 78% and 74%, respectively, the AHA noted.
These findings are “yet another challenge for Black and Hispanic communities, who are more likely to have underlying health conditions such as cardiovascular disease and diabetes and dying of COVID-19 at disproportionately high rates,” Rafael Ortiz, MD, American Heart Association volunteer medical expert and chief of neuro-endovascular surgery at Lenox Hill Hospital, New York, said in the AHA statement.
The survey was performed in conjunction with the AHA’s “Don’t Die of Doubt” campaign, which “reminds Americans, especially in Hispanic and Black communities, that the hospital remains the safest place to be if experiencing symptoms of a heart attack or a stroke.”
Among all the survey respondents, 57% said they would feel better if hospitals treated COVID-19 patients in a separate area. A number of other possible precautions ranked lower in helping them feel better:
- Screen all visitors, patients, and staff for COVID-19 symptoms when they enter the hospital: 39%.
- Require all patients, visitors, and staff to wear masks: 30%.
- Put increased cleaning protocols in place to disinfect multiple times per day: 23%.
- “Nothing would make me feel comfortable”: 6%.
Despite all the concerns about the risk of coronavirus infection, however, most Americans (77%) still believe that hospitals are the safest place to be in the event of a medical emergency, and 84% said that hospitals are prepared to safely treat emergencies that are not related to the pandemic, the AHA reported.
“Health care professionals know what to do even when things seem chaotic, and emergency departments have made plans behind the scenes to keep patients and healthcare workers safe even during a pandemic,” Dr. Ortiz pointed out.
More than half of Hispanic adults would be afraid to go to a hospital for a possible heart attack or stroke because they might get infected with SARS-CoV-2, according to a new survey from the American Heart Association.
Compared with Hispanic respondents, 55% of whom said they feared COVID-19, significantly fewer Blacks (45%) and Whites (40%) would be scared to go to the hospital if they thought they were having a heart attack or stroke, the AHA said based on the survey of 2,050 adults, which was conducted May 29 to June 2, 2020, by the Harris Poll.
Hispanics also were significantly more likely to stay home if they thought they were experiencing a heart attack or stroke (41%), rather than risk getting infected at the hospital, than were Blacks (33%), who were significantly more likely than Whites (24%) to stay home, the AHA reported.
White respondents, on the other hand, were the most likely to believe (89%) that a hospital would give them the same quality of care provided to everyone else. Hispanics and Blacks had significantly lower rates, at 78% and 74%, respectively, the AHA noted.
These findings are “yet another challenge for Black and Hispanic communities, who are more likely to have underlying health conditions such as cardiovascular disease and diabetes and dying of COVID-19 at disproportionately high rates,” Rafael Ortiz, MD, American Heart Association volunteer medical expert and chief of neuro-endovascular surgery at Lenox Hill Hospital, New York, said in the AHA statement.
The survey was performed in conjunction with the AHA’s “Don’t Die of Doubt” campaign, which “reminds Americans, especially in Hispanic and Black communities, that the hospital remains the safest place to be if experiencing symptoms of a heart attack or a stroke.”
Among all the survey respondents, 57% said they would feel better if hospitals treated COVID-19 patients in a separate area. A number of other possible precautions ranked lower in helping them feel better:
- Screen all visitors, patients, and staff for COVID-19 symptoms when they enter the hospital: 39%.
- Require all patients, visitors, and staff to wear masks: 30%.
- Put increased cleaning protocols in place to disinfect multiple times per day: 23%.
- “Nothing would make me feel comfortable”: 6%.
Despite all the concerns about the risk of coronavirus infection, however, most Americans (77%) still believe that hospitals are the safest place to be in the event of a medical emergency, and 84% said that hospitals are prepared to safely treat emergencies that are not related to the pandemic, the AHA reported.
“Health care professionals know what to do even when things seem chaotic, and emergency departments have made plans behind the scenes to keep patients and healthcare workers safe even during a pandemic,” Dr. Ortiz pointed out.
Cleaner data confirm severe COVID-19 link to diabetes, hypertension
Further refinement of data from patients hospitalized worldwide for COVID-19 disease showed a 12% prevalence rate of patients with diabetes in this population and a 17% prevalence rate for hypertension.
These are lower rates than previously reported for COVID-19 patients with either of these two comorbidities, yet the findings still document important epidemiologic links between diabetes, hypertension, and COVID-19, said the study’s authors.
A meta-analysis of data from 15,794 patients hospitalized because of COVID-19 disease that was drawn from 65 carefully curated reports published from December 1, 2019, to April 6, 2020, also showed that, among the hospitalized COVID-19 patients with diabetes (either type 1 or type 2), the rate of patients who required ICU admission was 96% higher than among those without diabetes and mortality was 2.78-fold higher, both statistically significant differences.
The rate of ICU admissions among those hospitalized with COVID-19 who also had hypertension was 2.95-fold above those without hypertension, and mortality was 2.39-fold higher, also statistically significant differences, reported a team of researchers in the recently published report.
The new meta-analysis was notable for the extra effort investigators employed to eliminate duplicated patients from their database of COVID-19 patients included in various published reports, a potential source of bias that likely introduced errors into prior meta-analyses that used similar data. “We found an overwhelming proportion of studies at high risk of data repetition,” the report said. Virtually all of the included studies were retrospective case studies, nearly two-thirds had data from a single center, and 71% of the studies included only patients in China.
“We developed a method to identify reports that had a high risk for repetitions” of included patients, said Fady Hannah-Shmouni, MD, a senior author of the study. “We also used methods to minimize bias, we excluded certain patients populations, and we applied a uniform definition of COVID-19 disease severity,” specifically patients who died or needed ICU admission, because the definitions used originally by many of the reports were very heterogeneous, said Dr. Hannah-Shmouni, principal investigator for Endocrine, Genetics, and Hypertension at the National Institute of Child Health and Human Development.
Despite the effort to eliminate case duplications, the analysis remains subject to additional confounders, in part because of a lack of comprehensive patient information on factors such as smoking, body mass index, socioeconomic status, and the specific type of diabetes or hypertension a patient had. “Even with these limitations, we were able to show that the prevalence of hypertension and diabetes is elevated in patients with COVID-19, that patients with diabetes have increased risk for both death and ICU admissions, and that there is the potential for reverse causality in the reporting of hypertension as a risk factor for COVID-19,” Dr. Hannah-Shmouni said in an interview. “We believe the explosion of data that associated hypertension and COVID-19 may be partially the result of reverse causality.”
One possible example of this reverse causality is the overlap between hypertension and age as potential risk factors for COVID-19 disease or increased infection severity. People “older than 80 frequently develop severe disease if infected with the novel coronavirus, and 80% of people older than 80 have hypertension, so it’s not surprising that hypertension is highly prevalent among hospitalized COVID-19 patients,” but this “does not imply a causal relationship between hypertension and severe COVID-19; the risk of hypertension probably depends on older age,” noted Ernesto L. Schiffrin, MD, a coauthor of the study, as well as professor of medicine at McGill University and director of the Hypertension and Vascular Research Unit at the Lady Davis Institute for Medical Research, both in Montreal. “My current opinion, on the basis of the totality of data, is that hypertension does not worsen [COVID-19] outcomes, but patients who are elderly, obese, diabetic, or immunocompromised are susceptible to more severe COVID-19 and worse outcomes,” said Dr. Schiffrin in an interview.
The new findings show “there is certainly an interplay between the virus, diabetes, and hypertension and other risk factors,” and while still limited by biases, the new findings “get closer” to correctly estimating the COVID-19 risks associated with these comorbidities,” Dr. Hannah-Shmouni said.
The connections identified between COVID-19, diabetes, and hypertension mean that patients with these chronic diseases should receive education about their COVID-19 risks and should have adequate access to the drugs and supplies they need to control blood pressure and hyperglycemia. Patients with diabetes also need to be current on vaccinations to reduce their risk for pneumonia. And recognition of the heightened COVID-19 risk for people with these comorbidities is important among people who work in relevant government agencies, health care workers, and patient advocacy groups, he added.
The study received no commercial funding. Dr. Hannah-Shmouni and Dr. Schiffrin had no disclosures.
SOURCE: Barrera FJ et al. J Endocn Soc. 2020 July 21. doi: 10.1210/jendso/bvaa102.
Further refinement of data from patients hospitalized worldwide for COVID-19 disease showed a 12% prevalence rate of patients with diabetes in this population and a 17% prevalence rate for hypertension.
These are lower rates than previously reported for COVID-19 patients with either of these two comorbidities, yet the findings still document important epidemiologic links between diabetes, hypertension, and COVID-19, said the study’s authors.
A meta-analysis of data from 15,794 patients hospitalized because of COVID-19 disease that was drawn from 65 carefully curated reports published from December 1, 2019, to April 6, 2020, also showed that, among the hospitalized COVID-19 patients with diabetes (either type 1 or type 2), the rate of patients who required ICU admission was 96% higher than among those without diabetes and mortality was 2.78-fold higher, both statistically significant differences.
The rate of ICU admissions among those hospitalized with COVID-19 who also had hypertension was 2.95-fold above those without hypertension, and mortality was 2.39-fold higher, also statistically significant differences, reported a team of researchers in the recently published report.
The new meta-analysis was notable for the extra effort investigators employed to eliminate duplicated patients from their database of COVID-19 patients included in various published reports, a potential source of bias that likely introduced errors into prior meta-analyses that used similar data. “We found an overwhelming proportion of studies at high risk of data repetition,” the report said. Virtually all of the included studies were retrospective case studies, nearly two-thirds had data from a single center, and 71% of the studies included only patients in China.
“We developed a method to identify reports that had a high risk for repetitions” of included patients, said Fady Hannah-Shmouni, MD, a senior author of the study. “We also used methods to minimize bias, we excluded certain patients populations, and we applied a uniform definition of COVID-19 disease severity,” specifically patients who died or needed ICU admission, because the definitions used originally by many of the reports were very heterogeneous, said Dr. Hannah-Shmouni, principal investigator for Endocrine, Genetics, and Hypertension at the National Institute of Child Health and Human Development.
Despite the effort to eliminate case duplications, the analysis remains subject to additional confounders, in part because of a lack of comprehensive patient information on factors such as smoking, body mass index, socioeconomic status, and the specific type of diabetes or hypertension a patient had. “Even with these limitations, we were able to show that the prevalence of hypertension and diabetes is elevated in patients with COVID-19, that patients with diabetes have increased risk for both death and ICU admissions, and that there is the potential for reverse causality in the reporting of hypertension as a risk factor for COVID-19,” Dr. Hannah-Shmouni said in an interview. “We believe the explosion of data that associated hypertension and COVID-19 may be partially the result of reverse causality.”
One possible example of this reverse causality is the overlap between hypertension and age as potential risk factors for COVID-19 disease or increased infection severity. People “older than 80 frequently develop severe disease if infected with the novel coronavirus, and 80% of people older than 80 have hypertension, so it’s not surprising that hypertension is highly prevalent among hospitalized COVID-19 patients,” but this “does not imply a causal relationship between hypertension and severe COVID-19; the risk of hypertension probably depends on older age,” noted Ernesto L. Schiffrin, MD, a coauthor of the study, as well as professor of medicine at McGill University and director of the Hypertension and Vascular Research Unit at the Lady Davis Institute for Medical Research, both in Montreal. “My current opinion, on the basis of the totality of data, is that hypertension does not worsen [COVID-19] outcomes, but patients who are elderly, obese, diabetic, or immunocompromised are susceptible to more severe COVID-19 and worse outcomes,” said Dr. Schiffrin in an interview.
The new findings show “there is certainly an interplay between the virus, diabetes, and hypertension and other risk factors,” and while still limited by biases, the new findings “get closer” to correctly estimating the COVID-19 risks associated with these comorbidities,” Dr. Hannah-Shmouni said.
The connections identified between COVID-19, diabetes, and hypertension mean that patients with these chronic diseases should receive education about their COVID-19 risks and should have adequate access to the drugs and supplies they need to control blood pressure and hyperglycemia. Patients with diabetes also need to be current on vaccinations to reduce their risk for pneumonia. And recognition of the heightened COVID-19 risk for people with these comorbidities is important among people who work in relevant government agencies, health care workers, and patient advocacy groups, he added.
The study received no commercial funding. Dr. Hannah-Shmouni and Dr. Schiffrin had no disclosures.
SOURCE: Barrera FJ et al. J Endocn Soc. 2020 July 21. doi: 10.1210/jendso/bvaa102.
Further refinement of data from patients hospitalized worldwide for COVID-19 disease showed a 12% prevalence rate of patients with diabetes in this population and a 17% prevalence rate for hypertension.
These are lower rates than previously reported for COVID-19 patients with either of these two comorbidities, yet the findings still document important epidemiologic links between diabetes, hypertension, and COVID-19, said the study’s authors.
A meta-analysis of data from 15,794 patients hospitalized because of COVID-19 disease that was drawn from 65 carefully curated reports published from December 1, 2019, to April 6, 2020, also showed that, among the hospitalized COVID-19 patients with diabetes (either type 1 or type 2), the rate of patients who required ICU admission was 96% higher than among those without diabetes and mortality was 2.78-fold higher, both statistically significant differences.
The rate of ICU admissions among those hospitalized with COVID-19 who also had hypertension was 2.95-fold above those without hypertension, and mortality was 2.39-fold higher, also statistically significant differences, reported a team of researchers in the recently published report.
The new meta-analysis was notable for the extra effort investigators employed to eliminate duplicated patients from their database of COVID-19 patients included in various published reports, a potential source of bias that likely introduced errors into prior meta-analyses that used similar data. “We found an overwhelming proportion of studies at high risk of data repetition,” the report said. Virtually all of the included studies were retrospective case studies, nearly two-thirds had data from a single center, and 71% of the studies included only patients in China.
“We developed a method to identify reports that had a high risk for repetitions” of included patients, said Fady Hannah-Shmouni, MD, a senior author of the study. “We also used methods to minimize bias, we excluded certain patients populations, and we applied a uniform definition of COVID-19 disease severity,” specifically patients who died or needed ICU admission, because the definitions used originally by many of the reports were very heterogeneous, said Dr. Hannah-Shmouni, principal investigator for Endocrine, Genetics, and Hypertension at the National Institute of Child Health and Human Development.
Despite the effort to eliminate case duplications, the analysis remains subject to additional confounders, in part because of a lack of comprehensive patient information on factors such as smoking, body mass index, socioeconomic status, and the specific type of diabetes or hypertension a patient had. “Even with these limitations, we were able to show that the prevalence of hypertension and diabetes is elevated in patients with COVID-19, that patients with diabetes have increased risk for both death and ICU admissions, and that there is the potential for reverse causality in the reporting of hypertension as a risk factor for COVID-19,” Dr. Hannah-Shmouni said in an interview. “We believe the explosion of data that associated hypertension and COVID-19 may be partially the result of reverse causality.”
One possible example of this reverse causality is the overlap between hypertension and age as potential risk factors for COVID-19 disease or increased infection severity. People “older than 80 frequently develop severe disease if infected with the novel coronavirus, and 80% of people older than 80 have hypertension, so it’s not surprising that hypertension is highly prevalent among hospitalized COVID-19 patients,” but this “does not imply a causal relationship between hypertension and severe COVID-19; the risk of hypertension probably depends on older age,” noted Ernesto L. Schiffrin, MD, a coauthor of the study, as well as professor of medicine at McGill University and director of the Hypertension and Vascular Research Unit at the Lady Davis Institute for Medical Research, both in Montreal. “My current opinion, on the basis of the totality of data, is that hypertension does not worsen [COVID-19] outcomes, but patients who are elderly, obese, diabetic, or immunocompromised are susceptible to more severe COVID-19 and worse outcomes,” said Dr. Schiffrin in an interview.
The new findings show “there is certainly an interplay between the virus, diabetes, and hypertension and other risk factors,” and while still limited by biases, the new findings “get closer” to correctly estimating the COVID-19 risks associated with these comorbidities,” Dr. Hannah-Shmouni said.
The connections identified between COVID-19, diabetes, and hypertension mean that patients with these chronic diseases should receive education about their COVID-19 risks and should have adequate access to the drugs and supplies they need to control blood pressure and hyperglycemia. Patients with diabetes also need to be current on vaccinations to reduce their risk for pneumonia. And recognition of the heightened COVID-19 risk for people with these comorbidities is important among people who work in relevant government agencies, health care workers, and patient advocacy groups, he added.
The study received no commercial funding. Dr. Hannah-Shmouni and Dr. Schiffrin had no disclosures.
SOURCE: Barrera FJ et al. J Endocn Soc. 2020 July 21. doi: 10.1210/jendso/bvaa102.
FROM JOURNAL OF THE ENDOCRINE SOCIETY