Introduction
Sars-COV-2 is a novel betacoronavirus that have infected over 177 million individuals and claimed 3.9 million deaths globally (1,2). Cardiac involvement in patients with moderate to severe COVID-19 infection could range from asymptomatic myocardial damage to overt myocarditis and myocardial infarction secondary to epicardial coronary artery disease (CAD) (3-7). Myocardial damage is somewhat common in patients hospitalized for COVID-19; while some cases can be explained with histologically proven myocarditis or epicardial CAD, in most cases the origin of this damage is uncertain (8). Coronary microvascular dysfunction has been suggested as a possible cause of myocardial ischemia in COVID-19 patients, as studies have suggested presence of microvascular dysfunction in other vascular beds and there is histologic evidence for Sars-COV-2 associated endothelitis in specimens obtained from heart, lung, kidney, liver and other tissues (9,10). However, this is an indirect assumption as there are no data so far to suggest CMD in COVID-19 patients.
Cardiac microvascular dysfunction could be measured with several invasive or non-invasive methods (11-14). Coronary flow velocity reserve (CFVR), which can be obtained by comparing velocities obtained before and after administration of a vasodilator agent, is the primary method of assessing CMD with echocardiography. Importantly, echocardiography allows making bedside measurements, which is usually the optimal method for assessing CMD in critically ill patients.
In the present study, we aimed to understand whether patients hospitalized with COVID-19 had echocardiographically demonstrable CMD as compared to healthy individuals, and whether the severity of the disease correlates with the severity of CMD.