IJCS | Volume 33, Nº3, May / June 2020

Almost 5% of the infections will have a severe course with acute respiratory distress syndrome, pulmonary bleeding, severe lymphopenia, kidney failure, circulatory shock, and failure of multiple organs. 3,5 The case-fatality rates by age group in Italy (1,625 cases) and China (1,023 cases) differed substantially, 7.2% and 2.3%, respectively, which can be partially explained by the older age distribution in Italy, as well as the presence of more comorbidities among Italians. 6 One fourth to half of the patients with COVID-19 have chronic conditions, especially cardiovascular (CVD) and cerebrovascular diseases, which increase the risk for a severe course of disease and death. A meta-analysis of six studies conducted in China, including 1,527 patients with COVID-19, has assessed the prevalence of CVD and reported the following proportions: hypertension, 17.1%; heart and cerebrovascular diseases, 16.4%; and diabetes, 9.7%. 7 Another study with 44,672 confirmed cases of COVID-19 in China has shown preexisting comorbidities, such as CVD (10.5%), diabetes (7.3%), and hypertension (6%), which related to a case‑fatality rate of 2.3%. 3 Those studies have evidenced the importance of not only chronic diseases but also of age and host immune status to COVID-19-related mortality, characterizing a complex, multifactorial and bidirectional model that can comprise the drugs used to treat those pathologies. 8,9 Acute and chronic cardiovascular complications have been observed and attributed to several mechanisms, such as relative ischemia, systemic inflammation and pathogen-mediated damage, with increased levels of biomarkers, such as troponin I, BNP, and d-dimer. 9-11 Myocardial damage was observed in 7.2% of patients with SARS-CoV-2 pneumonia, shock in 8.7%, and arrhythmia in 16.7%, leading to intensive care admission. 9 Ameta-analysis with four studies, including 341 COVID-19 patients, has reported a significantly higher standardizedmean difference in cardiac troponin I levels in patients with severe disease as compared to those with milder disease (25.6; 95%CI: 6.8-44.5 ng/L). 10 In a retrospective multicenter cohort study in China, elevated d-dimer levels at admission (> 1µg/mL) have been associated with in-hospital death even after adjustments (OR 18.4; 95% CI: 2.6-128.6 µg/mL). 11 Venous thromboembolism in COVID-19 has been reported, probably due to vascular inflammation, hypercoagulable states and endothelial dysfunction. 8 Fulminant myocarditis and heart failure have been associated with SARS-CoV-2 infection; moreover, preexisting coronary artery disease has been associated with a possible predisposition to that infection. .12-14 In a case series with 150 patients with COVID-19, 7% of the 68 deaths were attributed to myocarditis with circulatory failure. 12 Other studies have described fulminant myocarditis with high viral load and the post-mortem finding of mononuclear inflammatory infiltrates in the heart tissue. 13,14 New and important knowledge was recently presented in a case report: the lack of any pulmonary manifestation in a patient with myopericarditis and significant left ventricular dysfunction, who tested positive for SARS-CoV-2 and was successfully treated with dobutamine, lopinavir/ ritonavir, steroids, chloroquine, and the usual medical therapy for heart failure. 15 In another study, heart failure has been observed in 23.0% of the COVID-19 patients, being associated with non-survivors (51.9% vs. 11.7%); in addition, the contribution of previous ventricular dysfunction to that outcome remains inconclusive. 11 Murinemodels and human post-mortemsamples have shown that SARS-CoV can regulate the myocardial and pulmonary angiotensin-converting-enzyme 2 (ACE2), mediating myocardial inflammation, pulmonary edema and acute respiratory failure, and might explain the cardiovascular involvement of severely ill patients. 16 However, data available are still insufficient to determine whether these observations readily translate to humans, andno studyhas evaluated the effects of renin-angiotensin- aldosterone system inhibitors inpatientswithCOVID-19. 17 Some studies have suggested that ACE inhibitors (ACEI) and angiotensin-receptor blockers (ARB) can up-regulate ACE2, thus increasing susceptibility to the virus; other studies, however, have shown that ACEI / ARB can potentialize the pulmonary protective function of ACE2. 18,19 The Brazilian Society of Cardiology, the European Society of Cardiology and the American College of Cardiology recommend the individualized assessment of the patient, suggesting that the abrupt withdrawal of therapeutic schemes currently being practiced should not be performed, as that might cause clinical instability and adverse health outcomes. At the current time there is neither a vaccine against nor a specific treatment for COVID-19. Chloroquine blocks the viral infection by increasing the endosomal pH necessary for the virus/cell fusion and has shown an inhibitory effect on SARS-CoV-2 in vitro . Ribavirin, lopinavir/ritonavir and remdesivir are antiviral drugs being tested in prospective studies. It is worth noting that the lopinavir/ritonavir 200 Moraes & Pinto COVID-19: A matter close to heart Int J Cardiovasc Sci. 2020; 33(3):199-202 Editorial