ABC | Volume 114, Nº5, May 2020

Review Article Costa et al. The heart and COVID-19 Arq Bras Cardiol. 2020; 114(5):805-816 4.26 and 7.89, respectively). 11 In a recent study, Guo et al. have reported elevated troponin levels in 27.8% of 187 patients with COVID-19. Among patients without CVD and with normal troponin levels, mortality was 7.6%; among patients with CVD and normal troponin levels, mortality was 13.3%; among patients without CVD and with elevated troponin levels, mortality was 37.5%; and among patients with CVD and elevated troponin levels, mortality was 69.4%. There was a strong correlation between high troponin levels and increased C-reactive protein and NT-proBNP levels. Patients with increased troponin levels had a higher incidence of ventricular arrhythmias and higher need for mechanical ventilation. 10 Cardiovascular complications, such as HF, myocarditis, acute myocardial infarction, shock and arrhythmias, are also frequent in patients with myocardial injury. In a cohort with 150 patients, 7% of them developed irreversible myocardial damage and HF, associated with significant elevations in troponin levels. 17 Malignant arrhythmias (ventricular tachycardia with degeneration to ventricular fibrillation or hemodynamic instability) have been most frequently observed in individuals with troponin elevation (11.5% vs 5.2%). 10 Patients with severe COVID-19 can rapidly develop important cardiovascular impairment, shock and failure of multiple organs. In two Chinese cohorts of hospitalized patients with COVID-19, up to 20% developed the severe form of disease with shock. 9,12 Myocarditis can be related to acute HF in patients with COVID-19. Cases of COVID-19-related myocarditis have been described, with fulminant myocarditis, rapid progression and significant ventricular dysfunction, associated with diffuse myocardial edema. Those patients had electrocardiographic changes and troponin elevation. 14,18,19 Although TS has not been directly linked to COVID-19, some cases of ventricular dysfunction in COVID-19 patients might be attributed to that syndrome, which is a frequent complication in individuals with exacerbated systemic inflammatory response, inwhom the stress and severity of the viral infection trigger the TS. 20 Interaction of SARS-CoV-2 with angiotensin-converting enzyme-2 Some studies have suggested that the damage to the cardiovascular system secondary to SARS-CoV-2 can be linked to the angiotensin-converting enzyme-2 (ACE2), 13,15 which is related to the immune system and present in high concentration in the lungs and heart. The ACE2 down- regulates the angiotensin-renin system by inactivating angiotensin-2, and ACE2 might have a protective role against the development of respiratory failure and its progression. SARS-CoV-2 has four main structural proteins: spike (S), nucleocapsid (N), membrane (M), and envelope (E) proteins. The coronavirus spike protein binds to the Figure 2 - The SARS-CoV-2, via its surface spike protein, binds to the human ACE2 receptor after spike protein activation by TMPRSS2. SARS-CoV: severe acute respiratory syndrome coronavirus; SARS-COV-2: severe acute respiratory syndrome coronavirus 2; COVID-19: coronavirus disease 2019;ACE2: angiotensin-converting enzyme-2; TMPRSS2: transmembrane protease serine-2. 807