However, a recent pathological study found scarce interstitial mononuclear inflammatory infiltrates in heart tissue without substantial myocardial damage in a patient with COVID-19,13 suggesting that COVID-19 might not directly impair the heart.

Vice versa, we did not observe viral particles in cardiac myocytes and, therefore, we cannot infer on viral cardiotropism. Cardiac myocytes showed non‐specific damage that was mainly characterized by focal myofibrillar lysis. In addition, we did not observe cytopathic endothelia and small intramural vessel inflammation or thrombosis. Other cases are needed to confirm this observation.

Cardiac myocytes showed non‐specific features consisting of focal myofibrillar lysis, and lipid droplets. We did not observe viral particles in myocytes and endothelia. Small intramural vessels were free from vasculitis and thrombosis. EMB did not show significant myocyte hypertrophy or nuclear changes; interstitial fibrosis was minimal, focal, and mainly perivascular

The pathologic study showed low‐grade interstitial and endocardial inflammation (Figure 1A and 1B). Large (>20 μm), vacuolated, CD68‐positive macrophages were seen with immune‐light microscopy (Figure 1C and 1D); they were ultrastructurally characterized by cytopathy, with membrane damage and cytoplasmic vacuoles (Figure 1E). The ultrastructural study demonstrated single or small groups of viral particles with the morphology (dense round viral envelope and electron‐dense spike‐like structures on their surface) and size (variable between 70 and 120 nm) of coronaviruses (Figure 2). COVID‐19 infected Vero cells were used as control. The viral particles were observed in cytopathic, structurally damaged interstitial cells that demonstrated loss of the cytoplasmic membrane integrity (Figure 3)

There were no obvious histological changes seen in heart tissue, suggesting that SARS-CoV-2 infection might not directly impair the heart