Clinical aspects SARS-CoV-2 (COVID-19) infection
A viral epidemic caused by a new coronavirus SARS-CoV-2 (COVID-19) began in Wuhan (China) in November 2019. The epidemic quickly became a global pandemic (1). Knowledges of this viral infection is evolving rapidly, to date there are still no direct antivirals or effective vaccines and therapeutic treatments are on an empirical basis. At the time of writing this article, 10.7 million infected people and about 516,000 deaths are reported. (2) SARS-CoV-2 is a family of RNA viruses capable of infecting humans and causing severe respiratory tract infections that can be fatal in some cases. (3) Studies have shown that SARS-CoV-2 has about 80% of the SARS-CoV-like genome responsible for the 2003 outbreak. (4) SARS-CoV-2 penetrates into cells using the S protein via the angiotensin 2 conversion enzyme receptor (ACE-2) on the cell surface, which is widely present in the epithelial cells of the respiratory mucosa, (5). ACE-2 is also a conversion enzyme with a key role in the renin-angiotensin system (RAS). Clinical experts and scientists have described SARS-CoV-2 infection in three stages: the first asymptomatic or mildly symptomatic, the second moderately severe characterized by a pulmonary inflammatory state, the third very severe stage characterized by a generalized inflammatory state affecting all tissues causing multi-organ dysfunction. (6) In the most severe stages of infection, COVID-19 lung lesions are characterised by diffuse alveolar damage with irregular inflammatory cellular infiltration consisting of the presence of monocytes, macrophages and lymphocytes infiltrating the lung interstitium, and presence of intravascular thrombosis. (7). Severe inflammatory pulmonary infiltration prevents the exchange of alveolar gases, moreover, the most serious cases develop significant cardiovascular morbidity (8), (9). In this last direction, in fact data that have recently emerged do not only identify COVID-19 viral infection as a respiratory disease and risk of acute respiratory distress syndrome but also with acute myocardial damage that can be a critical component in the development of serious complications. These aspects are further confirmed by studies that show that patients with a history of cardiovascular disease are at increased risk of COVID-19 complications. (10) In fact, in a recent study (11) it was found that 77% of the deceased patients developed acute myocardial damage, other studies confirm these data. (12) (13) Some pathophysiological bases have been hypothesized, one of which is that the phenomenon of the ”cytokinic storm” (14) which occurs in the most severe stages of COVID-19 infection causes myocarditis which is the cause of acute heart failure, in addition, TNF-α and some other pro-inflammatory cytokines are capable of inducing typical cellular modifications of the decompensated heart, such as down-regulation of the sarcoplasmic reticulum ATPasica calcic pump (15), or decoupling of the beta-adrenergic receptors from activation of cyclic intracellular AMP (16) or death of heart cells.