SARS-CoV-2-Induced Myocarditis: A State-of-the-Art Review

Abstract

In this review, we investigated whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can directly cause myocarditis with severe myocardial damage induced by viral particles. A review of the major data published from 2020 to 2022 was performed by consulting the major databases alongside first-hand experiences that emerged from the cardiac biopsies and autopsy examinations of patients who died of SARS-CoV-2 infections. From this study, a significantly large amount of data suggests that the Dallas criteria were met in a residual percentage of patients, demonstrating that SARS-CoV-2 myocarditis was a rare clinical and pathological entity that occurred in a small percentage of subjects. All cases described here were highly selected and subjected to autopsies or endomyocardial biopsies (EMBs). The most important discovery, through the detection of the SARS-CoV-2 genome using the polymerase chain reaction, consisted in the presence of the viral genome in the lung tissue of most of the patients who died from COVID-19. However, the discovery of the SARS-CoV-2 viral genome was a rare event in cardiac tissue from autopsy findings of patients who died of myocarditis It is important to emphasize that myocardial inflammation alone, as promoted by macrophages and T cell infiltrations, can be observed in noninfectious deaths and COVID-19 cases, but the extent of each cause is varied, and in neither case have such findings been reported to support clinically relevant myocarditis. Therefore, in the different infected vs. non-infected samples examined, none of our findings provide a definitive histochemical assessment for the diagnosis of myocarditis in the majority of cases evaluated. We report evidence suggesting an extremely low frequency of viral myocarditis that has also been associated with unclear therapeutic implications. These two key factors strongly point towards the use of an endomyocardial biopsy to irrefutably reach a diagnosis of viral myocarditis in the context of COVID-19.

Comparison of left ventricular deformation abnormalities by echocardiography with cardiac magnetic resonance imaging in patients with acute myocarditis and preserved left ventricular ejection fraction

“…Of note, despite the small number of pts with acute myocarditis, pathological findings were found by both cMRI and STE in all pts, whereas no pathological findings were found by either cMRI or STE in controls during this time. However, this small cohort of pts from the pre-SARS-CoV-2 era seems noteworthy, as pts after SARS-CoV-2 infection often present with cardiac symptoms suggestive for concomitant myocardial involvement ( 16 , 39 – 42 ). Because residual cardiac findings after unrecognized concomitant myocarditis secondary to SARS-CoV-2 infection are likely to cause changes in LV rotation, even this highly selected group of pre-SARS-CoV-2 era pts may be valuable for future investigation.…”

“…Even after mild and subclinical courses of acute myocarditis, subepicardial fibrosis can act as an arrhythmogenic substrate for malignant arrhythmias, which may result in an unfavorable prognosis in these pts ( 1 , 3 , 15 ). However, data on patient outcome depending on the severity of myocardial injury in pts with myocardial involvement due to viral infections are sparse ( 1 – 3 , 28 , 39 , 43 , 44 ). Despite their primary lack of functional relevance, small areas of fibrosis may cause persistent impairments of regional LV deformation, especially of rCS.…”

The Impact of Cardiovascular Antecedents on the Prognosis of COVID-19 Critically Ill Patients

“…The histological lesions described during the autopsy included limited interstitial fibrosis and mononuclear inflammatory infiltrates in the heart, with evidence of the macrophages (CD68) and T-cells (CD4) [ 8 ]. These lesions did not meet the Dallas criteria for myocarditis [ 9 ]. Thus, the severity of cardiac damage in COVID-19 could not be correlated with the extensive myocardial cell damage or massive monocytic inflammatory infiltrates.…”

Persistence of SARS-CoV-2 colonization and high expression of inflammatory factors in cardiac tissue 6 months after COVID-19 recovery: a prospective cohort study

“…In some case reports involving post-infection myocardial biopsy, the SARS-CoV-2 genome was detected in patients with heart failure symptoms, and an endocardial biopsy was performed four weeks after the onset of pulmonary symptoms. SARS-CoV-2 infection was accompanied by myocarditis, indicating myocardial infection ( 15 ). Thus, the timing of viral colonization or clearance in the cardiac tissues of patients recovering from COVID-19, as well as the relevant myocardial inflammatory infiltrates, remains uncertain at present.…”