COVID-19, cardiovascular diseases and cardiac troponins
Chan W Kim1, Wilbert S Aronow1
1Cardiology Department, & The Department of Medicine, Westchester Medical Center & New York Medical College, Valhalla, NY 10595, USA.
Insights
COVID-19 patients show significant myocardial injury, indicated by elevated cardiac troponin (cTn). This study explores the mechanisms behind this injury and the role of cTn as a prognostic biomarker.
Area of Science:
- Cardiology
- Infectious Diseases
- Pathology
Background:
- COVID-19 is associated with significant myocardial injury, evidenced by elevated serum cardiac troponin (cTn).
- The precise mechanisms driving this cardiac damage remain incompletely understood.
- Potential pathways include direct viral effects, systemic inflammation, and hypoxemia.
Purpose of the Study:
- To discuss the pathological mechanisms contributing to myocardial injury in COVID-19.
- To explore the causes of elevated cardiac troponin (cTn) in these patients.
- To evaluate the utility of cTn as a biomarker and prognostic indicator for clinical outcomes.
Main Methods:
- Review and synthesis of existing literature on COVID-19 and myocardial injury.
- Discussion of proposed pathological mechanisms.
- Analysis of the role of cardiac troponin as a biomarker.
Main Results:
- Elevated serum cardiac troponin (cTn) is a strong indicator of myocardial injury in COVID-19.
- Potential injury mechanisms include viral invasion, cytokine storm, hypercoagulability, and hypoxemia.
- Elevated cTn may result from myocarditis, microangiopathy, or myocardial infarction.
Conclusions:
- Cardiac troponin (cTn) is a valuable biomarker for assessing myocardial injury in COVID-19 patients.
- Understanding the mechanisms of injury is crucial for patient management.
- cTn levels may serve as a prognostic factor for clinical outcomes in COVID-19.
Abstract:
There has been strong evidence of myocardial injury in COVID-19 patients with significantly elevated serum cardiac troponin (cTn). While the exact mechanism of injury is unclear, possible suggested pathological mechanisms of injury are discussed. These include increased susceptibility of the myocardium and endothelium to viral invasion, underlying hyperinflammatory state and subsequent cytokine storm, a hypercoagulable and prothrombotic state, and indirect myocardial injury due to hypoxemia. As a result of these pathological mechanisms in COVID-19 patients, cTn may be elevated largely due to myocarditis, microangiopathy or myocardial infarction. The utility of cTn as a biomarker for measuring myocardial injury in these patients and assessing its ability as a prognostic factor for clinical outcome is also discussed.
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