COVID-19–Associated Nonocclusive Fibrin Microthrombi in the Heart

Cardiac injury as detected by blood troponin levels or wall motion abnormalities is not uncommonly seen in people with COVID-19 infection and portends poorer prognosis. Although several mechanisms, including viral myocarditis, thrombotic occlusion of epicardial coronary vessels, and microthrombotic occlusion of myocardial arterioles and capillaries have been postulated, the nature of cardiac injury in these patients remains incompletely understood but at the same time is essential to the development of therapies. Although quite a few studies have been published showing cardiac abnormalities on noninvasive imaging in patients recovering from COVID-19, specific mechanisms by which the virus causes cardiac injury cannot be easily ascertained using such techniques. Ultimately, autopsy studies are be the best avenue to learn how the virus affects the heart. In a recently published paper, Bois et al studied 15 autopsy hearts from COVID-19 victims (12 with active infection and 3 with cleared infection) and compared findings with those from individuals who died from influenza A/B (n = 6) as well as those who died non–virally mediated deaths (n = 6). Although abnormal nonocclusive fibrin microthrombi formation were detected in most of the COVID-19 hearts (12/16; 75.0%), acute ischemic injury to the myocardium was present in only 1 of these cases and troponin levels were reported in 8/15 (median [range], 19.5 [0–461] ng/L; without electrocardiographic or echocardiographic findings). The incidence of fibrin microthrombi was extremely high versus in the hearts of influenza victims (2/6; 33.3%) and control cases (2/6, 33.3%; P = .006). In addition, a relatively high number of cases was reported to have acute lymphocytic myocarditis (33.3% of COVID-19 cases). No evidence of SARS-CoV-2 virus in the heart was detected by multiple diagnostic modalities, including immunohistochemistry, electron microscopy, and droplet digital polymerase chain reaction. Although this paper suggests microthrombi as an important mechanism of cardiac injury, most cases studied did not have evidence of ischemic injury, raising the question of whether the reported findings have important clinical significance. Moreover, the rather high rate of myocarditis reported here is much higher than reported in the literature, and, in the absence of detectable virus, such findings raise the question of whether myocarditis was related to COVID-19 infection or some other cause. In the future, it will be important to determine in a systematic manner the relationship between myocardial injury as determined by blood troponin electrocardiography/ echocardiography and/ or evidence of myocyte necrosis and cardiac findings to demonstrate underlying causes responsible for myocyte injury in patients with COVID-19 infection.