The first observational studies and data analyses from China found a high prevalence of elevated troponin levels in patients with COVID-19, which also correlated with higher mortality rates. Several hypotheses have emerged to to explain the troponin rise, including viral myocarditis, cytokine-driven myocardial damage, microangiopathy, and unmasked severe coronary artery disease.
The comprehensive and timely review by Tersalvi et al, slated for upcoming publication in the Heart Failure Society of America publication, the Journal of Cardiac Failure, explores the available evidence regarding the association between COVID-19 and myocardial injury, and is designed to help clinicians and researchers understand the implications of an elevated troponin. The authors posit that although COVID-19 infection initially presents as a primarily respiratory condition, it quickly involves the cardiovascular system through an imbalance in the renin-angiotensin-aldosterone system mediated by ACE2 depletion. Though multiple additional mechanisms for troponin elevation are plausible, none have been proven as the main cause. The authors conclude that triaging patients with COVID-19 according to the presence of underlying cardiovascular disease and elevated troponin is a vital step in order to direct patients for prioritized and aggressive treatment strategies.
The full paper is currently available for preview in the Provider Resources section of the HFSA Coronavirus Resource Center.