Cross-sectional study explores differences in biomarkers in fulminant and non-fulminant COVID-19 myocarditis

Coronavirus disease 2019 (COVID-19) myocarditis is increasingly becoming a common complication of the disease. COVID-19 predominantly causes respiratory illness but, in some cases, may also affect the cardiovascular system and cause myocarditis.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to the angiotensin-converting enzyme 2 (ACE-2) receptor present on the surface of cardiac cells, which likely explains the direct cardiac involvement in COVID-19 patients.

Myocarditis and its clinical presentation in COVID-19

Myocarditis is an inflammatory disease that has both infectious and non-infectious etiologies. The most severe type of myocarditis is fulminant myocarditis, which is predominantly caused by viral infections.

Fulminant myocarditis is characterized by severe and sudden inflammation of the myocardium that leads to cardiogenic shock, ventricular bradyarrhythmias or tachyarrhythmias.

Although the clinical presentation of COVID-19 patients with myocarditis varies greatly, the usual symptoms include chest pain, fatigue, acute heart failure, and cardiogenic shock.

Previous studies have reported increased levels of inflammatory markers including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), lactate, and procalcitonin.

Several electrocardiogram (ECG) abnormalities are seen in myocarditis patients ranging from PR depression and ST elevation to new-onset bundle branch block, brady- or tachyarrhythmias, and QT prolongation.

Patient instability, resource limitations, or isolation precautions are the hurdles to a formal diagnosis of myocarditis with endomyocardial biopsy or cardiac MRI. Hence, exploratory analysis is necessary to clinically define the characteristics and severity of COVID-19-related myocarditis.

Studying the clinical course and echocardiographic / lab findings in fulminant and non-fulminant COVID-19 myocarditis

Researchers from the US recently conducted a study to examine the clinical course and echocardiographic and lab testing across clinically defined fulminant and non-fulminant COVID-19 myocarditis. This study is published on the preprint server, medRxiv.*

The cross-sectional, observational study had 19 patients with COVID-19 myocarditis and reports clinical course, presenting symptoms, lab findings, and echocardiographic results stratified by fulminant and non-fulminant myocarditis.

The researchers used student t-test and univariate logistic regression to compare lab findings across fulminant and non-fulminant cases of myocarditis.

None of the 19 patients had a prior history of atrial fibrillation, coronary artery disease, or heart failure. 78.9% of cases required supplemental oxygen and 21.1% of patients died. Patients with fulminant myocarditis had a significantly higher geometric mean D-dimer and ferritin compared to those with non-fulminant suspected myocarditis.

10 out of the 16 patients with available echocardiographic data had normal left ventricular systolic function and 26.3% of cases had pericardial effusions.

“As the absolute values of troponin elevation are remarkable in this cross-sectional study, further research may investigate the clinical significance of different levels of troponin elevation.”

Study highlights the significance of exploratory analysis to investigate the extent of direct or indirect COVID-19-mediated injury

This study characterizes clinical COVID-19-related myocarditis using descriptive analysis. It is important to characterize clinical COVID-19 myocarditis as its signs and symptoms overlap with demand-mediated ischemia, sepsis-induced cardiomyopathy, and ARDS, and it may have unidentified clinical implications.

This study is a relatively small cross-sectional study in a convenience sample and is limited to generating hypotheses. Therefore, statistical inference cannot be made to a generalized population based on the observations of this study. Statistical extremes in the observations show that the results call for further investigation and the authors hope this can motivate variable selection in future studies.

To summarize, this work on clinically suspected COVID-19 myocarditis substantiates the significance of investigating the extent of COVID-19-mediated direct injury or indirect systemic inflammation with the help of exploratory analysis. Future works may determine whether direct vs indirect mechanisms predominate and how the difference affects clinical outcomes in covid-19 patients.

“In summary, the present study better characterizes the entity of clinically suspected COVID-19 myocarditis and substantiates the importance of investigating the extent to which COVID-19 is mediated by direct viral injury and/or indirect systemic inflammation through exploratory analysis.”

*Important Notice

medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.

Journal reference:
Susha Cheriyedath

Written by

Susha Cheriyedath

Susha has a Bachelor of Science (B.Sc.) degree in Chemistry and Master of Science (M.Sc) degree in Biochemistry from the University of Calicut, India. She always had a keen interest in medical and health science. As part of her masters degree, she specialized in Biochemistry, with an emphasis on Microbiology, Physiology, Biotechnology, and Nutrition. In her spare time, she loves to cook up a storm in the kitchen with her super-messy baking experiments.


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