Cardiac Troponin in COVID-19: Elevated but Mostly Stable, Not Acute Coronary Syndrome
This early-pandemic review examined the pattern of cardiac troponin elevation in COVID-19 patients, finding that most demonstrated stable rather than dynamically rising values typical of acute myocardial infarction. Elevated troponin was associated with disease severity and mortality, likely reflecting myocardial injury from systemic inflammation rather than coronary events. The findings guided laboratory interpretation strategies for troponin results during the pandemic.
The original study
Clinical utility of cardiac troponin measurement in COVID-19 infection.
- Authors
- Gaze DC
- Journal
- Annals of clinical biochemistry
- Type
- Journal Article, Review
- PMID
- 32255359
Original abstract
The novel coronavirus SARS-CoV-2 causes the disease COVID-19, a severe acute respiratory syndrome. COVID-19 is now a global pandemic and public health emergency due to rapid human-to-human transmission. The impact is far-reaching, with enforced social distancing and isolation, detrimental effects on individual physical activity and mental wellbeing, education in the young and economic impact to business. Whilst most COVID-19 patients demonstrate mild-to-moderate symptoms, those with severe disease progression are at a higher risk of mortality. As more is learnt about this novel disease, it is becoming evident that comorbid cardiovascular disease is associated with a greater severity and increased mortality. Many patients positive for COVID-19 demonstrate increased concentrations of cardiac troponin, creating confusion in clinical interpretation. While myocardial infarction is associated with acute infectious respiratory disease, the majority of COVID-19 patients demonstrate stable cTn rather than the dynamically changing values indicative of an acute coronary syndrome. Although full understanding of the mechanism of cTn release in COVID-19 is currently lacking, this mini-review assesses the limited published literature with a view to offering insight to pathophysiological mechanisms and reported treatment regimens.