Myocarditis and asymptomatic Covid-19 in college athletes

[jim mcnamara]

TL;DR

NIH Directors blog: summary of a heart study on college age student athletes

https://directorsblog.nih.gov/2020/10/01/covid-19-can-damage-hearts-of-some-college-athletes/

Myocarditis (heart damage and inflammation) was found in a study group of 25 male & female college athletes. This population tested positive for Covid-19, but were asymptomatic. 4 males in the group were found to have myocarditis as a result of Covid-19 infections. Subsequent imaging verified the extent of the disease process.

Myocarditis is a known outcome of Covid-19, some cases resolve with no problems. Other cases follow steps in the disease process that may lead to very serious problems, including death especially during extended exercise. The article gives more detail.

The article is not very technical, and should be accessible for everyone.

As a side note - the NIH Director has other interesting blog entries.

 

[berkeman]

The article is not very technical, and should be accessible for everyone.

TBH, the popular article left me pretty confused. I'll circle back when I have time and try to read the technical articles, but I have some confusions...

• How did these student athletes end up in quarantine if they were asymptomatic? Via a testing protocol?
• If they did not stop training until after the virus was in their system, did that add to the myocarditis damage?
• Or is the main concern how long after the virus symptoms disappear should the athlete wait before resuming normal training and competition in order to avoid long-term damage?

 

[jim mcnamara]

The JAMA Cardiology paper line #1:
Investigating the use of imaging, e.g., on asymptomatic athletes to determine their readiness to safely resume playing their sport. It does in fact work well to show cardiac problems is their conclusion. That was their goal.

I do not think it implies a wait after quarantine, rather imaging after quarantine. Problems get referred to cardiologist. Who then determines when it is reasonable to resume. I would hope, anyway.

The population was tested and found to be Covid-19 positive, in quarantine I assume == how they ended up in the test group.

I think the researchers assert that asymptomatic sports team members should get screened before they resume. This is just case report, a much larger study is required. Not all colleges and high schools have easy access to imaging facilities. But they can have sick athletes.

The other 2 papers are about imaging and criteria so that physicians can learn about the CMR methodology for a cardiac evaluation.

#2 discusses what criteria to consider when making decisions for patient resumption of play.

 

[Ygggdrasil]

A new study of ~789 professional athletes with COVID-19 suggests myocardiotits and inflammatory heart disease are rare among those infected by COVID-19 (less than 1%):

Five of 789 professional athletes infected with COVID-19 were later found to have suffered inflammatory heart disease in the largest study to date on the cardiac impact of the virus in sports.

In data published Thursday in JAMA Cardiology, doctors affiliated with six U.S.-based leagues followed the 789 infected players last year between May and October.

Before returning to play, the athletes underwent three noninvasive tests that tracked heart rhythms, took an ultrasound of their hearts and measured a protein in their blood that can be a signal of heart damage. Thirty athletes had abnormal test results and were referred for a cardiac MRI. Doctors diagnosed five cases of inflammatory heart disease (0.6% of the total), with three cases identified as myocarditis and two as pericarditis

https://www.espn.com/espn/story/_/i...covid-19-developed-inflammatory-heart-disease

Here's the published study:
Prevalence of Inflammatory Heart Disease Among Professional Athletes With Prior COVID-19 Infection Who Received Systematic Return-to-Play Cardiac Screening
https://jamanetwork.com/journals/jamacardiology/fullarticle/2777308

Question What is the prevalence of inflammatory heart disease identified through implementation of recent return-to-play (RTP) cardiac screening recommendations in professional athletes with prior Coronavirus disease 2019 (COVID-19) infection?

Findings In this cross-sectional study of RTP cardiac testing performed on 789 professional athletes with COVID-19 infection, imaging evidence of inflammatory heart disease that resulted in restriction from play was identified in 5 athletes (0.6%). No adverse cardiac events occurred in the athletes who underwent cardiac screening and resumed professional sport participation.

Meaning Using expert consensus RTP screening recommendations for athletes testing positive for COVID-19, few cases of inflammatory heart disease were detected and safe return to professional sport activity has thus far been achieved.

Of course, professional athletes are not reflective of the general population, so it's hard to know if these results can be extrapolated to college athletes or the general population.

 

[Ygggdrasil]

Of course, professional athletes are not reflective of the general population, so it's hard to know if these results can be extrapolated to college athletes or the general population.

Here's a study of a population likely more reflective of the general public that finds that cardiovascular abnormalities are rare after mild or asymptomatic disease:

Prospective Case-Control Study of Cardiovascular Abnormalities 6 Months Following Mild COVID-19 in Healthcare Workers
https://www.sciencedirect.com/science/article/pii/S1936878X21003569

Abstract:

Objectives
The purpose of this study was to detect cardiovascular changes after mild severe acute respiratory syndrome Coronavirus 2 infection.

Background
Concern exists that mild Coronavirus disease 2019 may cause myocardial and vascular disease.

Methods
Participants were recruited from COVIDsortium, a 3-hospital prospective study of 731 health care workers who underwent first-wave weekly symptom, polymerase chain reaction, and serology assessment over 4 months, with seroconversion in 21.5% (n = 157). At 6 months post-infection, 74 seropositive and 75 age-, sex-, and ethnicity-matched seronegative control subjects were recruited for cardiovascular phenotyping (comprehensive phantom-calibrated cardiovascular magnetic resonance and blood biomarkers). Analysis was blinded, using objective artificial intelligence analytics where available.

Results
A total of 149 subjects (mean age 37 years, range 18 to 63 years, 58% women) were recruited. Seropositive infections had been mild with case definition, noncase definition, and asymptomatic disease in 45 (61%), 18 (24%), and 11 (15%), respectively, with 1 person hospitalized (for 2 days). Between seropositive and seronegative groups, there were no differences in cardiac structure (left ventricular volumes, mass, atrial area), function (ejection fraction, global longitudinal shortening, aortic distensibility), tissue characterization (T1, T2, extracellular volume fraction mapping, late gadolinium enhancement) or biomarkers (troponin, N-terminal pro–B-type natriuretic peptide). With abnormal defined by the 75 seronegatives (2 SDs from mean, e.g., ejection fraction <54%, septal T1 >1,072 ms, septal T2 >52.4 ms), individuals had abnormalities including reduced ejection fraction (n = 2, minimum 50%), T1 elevation (n = 6), T2 elevation (n = 9), late gadolinium enhancement (n = 13, median 1%, max 5% of myocardium), biomarker elevation (borderline troponin elevation in 4; all N-terminal pro–B-type natriuretic peptide normal). These were distributed equally between seropositive and seronegative individuals.

Conclusions
Cardiovascular abnormalities are no more common in seropositive versus seronegative otherwise healthy, workforce representative individuals 6 months post–mild severe acute respiratory syndrome Coronavirus 2 infection.

Here's an opinion piece in STAT news about how initial warnings of cardiovascular harm from COVID-19 were overblown and based on bad science:

We take away two lessons from the Covid-19 myocarditis story. One is that SARS-CoV-2 can sometimes, though rarely, cause heart inflammation — just as many other viruses do. Clinicians, therefore, can appeal to sound medicine; further testing can be decided on an individual basis. Screening low-risk patients with MRI and other fancy tests is neither necessary nor wise.

The broader lesson is that science communication in times of crisis must keep a level head. The public, and decision-makers, need properly controlled studies instead of early sensational reports. In a world where success is measured by clicks, the idea that even mild cases of Covid-19 could pose a new and unprecedented threat to the heart took off. That fear has largely been unsubstantiated, though news of it won’t spread nearly as quickly.

https://www.statnews.com/2021/05/14/setting-the-record-straight-there-is-no-covid-heart/