Samuel D. Moscavitch et al. Jefferson L. Vieira Peter Libby
Why COVID-19 became an issue for cardiovascular specialists? SARS-CoV-2- related myocardial injury and myocarditis
Approximately 20-30% of hospitalized patients with COVID-19 have evidence of cardiac injury, as indicated by elevated levels of high-sensitivity troponins. The presence and magnitude of troponin elevation is associated with more severe disease and worse outcomes, even after adjusting for relevant risk factors. Myocardial injury portends a fatal outcome of COVID-19, while the prognosis of patients without myocardial injury, even with underlying cardiovascular disease, is more favorable.
The pathophysiology of SARS-CoV-2-induced myocardial injury remains a topic of active research. COVID-19 can unfavorably affect the balance between myocardial oxygen supply and demand, as with other overwhelming viral or bacterial infections (). Fever, metabolic stress, sympathetic activation, and tachycardia increase the energy expenditure and oxygen consumption of the myocardium., This imbalance can provoke type 2 (or “demand” type) myocardial infarction. Hypoxia from respiratory impairment can favor the production of reactive oxygen species and oxidative stress, acidosis, mitochondrial damage, and cell death.,, Other mechanisms of myocardial injury during COVID-19 include ischemia from microvascular thrombi and toxic levels of cytokines. Cardiac damage due to direct SARS-CoV-2 infection of cardiac myocytes appears uncommon.– Indeed, the pericytes, smooth-muscle like cells that surround microvessels, express high levels of the receptor for SARS-CoV-2, angiotensin converting enzyme 2 (ACE2), while cardiac myocytes themselves have few, if any, of these portals of entry used by the virus.
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