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.