Sars-Cov-2 and cardiovascular diseases: major considerations and systematic review

Introduction: In the new coronavirus (SARS-CoV-2) scenario, COVID-19 disease is associated with vascular inflammatory processes, myocarditis, and cardiac arrhythmias, thus, its mortality is associated with cardiovascular diseases (CVD), diabetes, and hypertension. The mechanisms are that cardiovascular disease and pharmacological inhibition of SARS-CoV-2 can increase ACE2 levels, and coronavirus infection can decrease ACE2. Among patients with COVID-19, there is a high prevalence of cardiovascular disease and over 7% of patients have a myocardial injury from infection (22% of critically ill patients). Objective: Therefore, the present study aimed to conduct a systematic review of the main clinical outcomes of cardiovascular effects in patients infected with COVID-19. Methods: Literary search criteria were followed with the use of the MeSH Terms that were cited in the item on "Search strategies". A total of 65 clinical studies that were submitted to the eligibility analysis were checked, and after that, 31 studies were selected. The search strategy was performed in PubMed, Embase, Ovid and Cochrane Library, Web of Science, Science Direct Journals (Elsevier), Scopus (Elsevier), OneFile (Gale). Major considerations and conclusion: Therefore, patients with COVID-19 combined with cardiovascular disease are associated with an increased risk of mortality. Critical patients are characterized by fewer lymphocytes. A COVID-19 disease is associated with a high inflammatory load that can induce vascular inflammation, myocarditis, and cardiac arrhythmias. Thus, cardiovascular risk factors and conditions must be carefully controlled according to the evidence-based guidelines. Cardiovascular disease and COVID-19 pharmacological inhibition increase ACE2 levels, which can increase coronavirus virulence in the lung and heart (7). On the other hand, there is evidence that coronavirus infection can decrease ACE2, leading to toxic over-accumulation of angiotensin II, which induces acute respiratory distress syndrome and fulminant myocarditis. The inhibition of SARS-CoV-2 can reduce this effect.