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Complications in Patients With COVID-19.

Complications in Patients With COVID-19 To the Editor In their excellent article, Madjid et al1 provide a comprehensive overview of all the latest data regarding coronaviruses, with a focus on their effects on the cardiovascular system. The authors present several reports suggesting evidence of myocardial injury in patients with coronavirus disease 2019 (COVID-19) infection, manifested by elevation of high-sensitivity troponin T and I. They propose that myocardial injury in these patients is likely associated with infectionrelated myocarditis, based on sporadic autopsy cases as well as 2 cases of severe myocarditis with reduced systolic function. Nonetheless, the autopsy study by Xu et al that is cited1 reports no obvious histological changes seen in heart tissue, suggesting that severe acute respiratory syndrome coronavirus 2 might directly affect the heart. Additionally, the 2 definite myocarditis case reports by Inciardi et al and Hu et al that are also cited1 did not show any respiratory involvement during the clinical course, which is a quite different clinical presentation from most critically ill patients. During the previous 2003 severe acute respiratory syndrome and Middle East respiratory syndrome epidemic, myocarditis was not documented as a proven complication of coronavirus infection, and only subclinical reversible diastolic impairment without any systolic involvement was observed in most patients.2 Troponin elevation in the context of COVID-19 infection may as well be related to various other mechanisms,3 including acute myocardial infarction type I (ie, plaque rupture induced by arterial wall inflammation), acute myocardial infarction type II (supply-demand mismatch) triggered by infection, or even Takotsubo stress cardiomyopathy, which is observed with increasing frequency in patients with sepsis.4 Furthermore, troponin elevation may originate from right ventricle injury related to respiratory failure or pulmonary thromboembolic phenomena, which have also been reported as a common feature of this disease, or from transient cytosolic leakage of cardiac troponin T due to increased myocardial membrane permeability induced by systemic inflammatory response. Finally, multiple pathways may cooperate in some cases, with myocarditis remaining a challenging diagnosis, especially when echocardiography or electrocardiographic data are limited due to conditions in the isolation ward. From this perspective, troponin elevation should not be regarded as equivalent to myocarditis or, even worse, to left ventricle impairment, which could potentially mislead clinical judgment in severely ill patients, but rather as a significant prognosticator. This is also supported by data suggesting that patients with elevated troponin T levels but without any underlying cardiovascular disease may experience a more dismal outcome compared with patients with preexisting cardiac disease but with normal troponin T levels during the course of COVID-19 infection.5