SARS-CoV-2 induced myocarditis: Current knowledge about its molecular and pathophysiological mechanisms

The existence of an inflammatory process in the heart muscle, related to a progressive worsening of myocardial function, different etiopathogenetic mechanisms concur and often overlap, thus making the diagnosis and the therapeutic approach complex. As the COVID-19 pandemic progresses, the effects of the disease on the organ systems and in particular on the cardiovascular system are becoming more and more profound. Cardiac involvement is a well-known event with a high percentage of findings in the heart’s magnetic field, even in asymptomatic areas. There are numerous uncertainties regarding their evolution, in the long and short term, due not only to a difficult to determine the varied clinical expression and the rarely performed intramyocardial biopsy which additionally presents diagnostic problems but also in part to different clinical prognosis. Today, the new SARS-CoV-2 virus that uses the angiotensin converting enzyme 2 (ACE2) which is present at high levels in myocardial cells as its entrance it can create even severe heart injury. The pathophysiology in all of these cases can involve multiple immune and non-immune mechanisms within organs and vessels and can be occur in the clinical phases. Possible mechanisms of direct and indirect myocardial infarction in patients with COVID-19 include additional lesion and oxygen-rich and generalized inflammation response with myocardial immune hyperactivity (myocarditis). Therefore, these can occur through the excessive release of cytokines, the presence of thrombocytopenia, endocrine damage, heart failure, arrhythmias and more. Patients can show average signs of myocardial damage, and some develop spontaneous cardiac complications, such as heart failure, arrhythmias and, rarely, rare cardiogenic disorders. Pathophysiology in all of these may involve multiple mechanisms within the cytokine cephalic membrane, endocrine damage and thrombogenicity. The diagnosis of this myocardial injuri is mainly based on the myocardial enzyme troponin. This viewpoint paper explains today’s knowledge on viral myocarditis, in particular that from SARS-CoV-2 infection, if there is a connection with other possible biomolecular pathogenetic factors that can influence its natural course. In fact, it is for this reason that the pathogenetic mechanisms are analyzed and described. At the same time, its possible interaction with other parameters that are documented risk factors for cardiovascular disease was examined. Although these biomolecular findings were mainly related to necrotic parts of the myocardium, it is important to recognize that myocardial damage early for a better approach and prognosis.