ABC | Volume 114, Nº6, June 2020

Review Article Figueiredo Neto et al. Coronavirus and Myocardium Arq Bras Cardiol. 2020; 114(6):1051-1057 of the renin-angiotensin system, such as systemic arterial hypertension (SAH), heart failure (HF), and atherosclerosis, by converting angiotensin II into angiotensin I-VII, which has a cardioprotective effect. In addition to the heart and lungs, ACE-2 is expressed in the intestinal epithelium, vascular endothelium, and kidneys, providing a mechanism for multiple organ dysfunction, which can be observed in SARS-CoV-2 infection. 3- COVID-19 and Myocardial Injury Increased troponin upon admission to the hospital has been associated with higher mortality in two studies involving patients hospitalized with COVID-19. 7-8 One of these studies, which was conducted in a hospital at Wuhan University, evaluated a cohort of 416 patients hospitalized for COVID-19, with a mean age of 64 years, 50% of whom were female; the most frequent CVD was SAH (30.5%). Of the patients included, 82 (19.7%) had myocardial injury, defined as high-sensitivity troponin I above the 99th percentile. Patients with hypertension had more myocardial injury than those without hypertension (59% vs. 23%). The same was the case patients for patients with coronary artery disease (CAD) (29.3% vs. 6.0%); cerebrovascular disease (15.9% vs. 2.7%), and HF (14.6% vs. 1.5%) (p < 0.001 for all variables). The authors observed greater frequency of acute respiratory distress syndrome (58.5% vs. 14.7%, p < 0.001) and greater mortality among patients with myocardial injury (51% x 4.5%, p < 0.001). 7 The second, a single-center retrospective study, evaluated a cohort of 187 patients with COVID-19. Mean age was 58 years; 35% had some CVD (SAH, CAD, or cardiomyopathy), and 43 patients progressed to death (23%). The authors observed increased troponin T in 27.8% of cases. Mortality rate was around 7% for patients without CVD and negative troponin T; this value was ten-fold when the presence of CVD was associated with the presence of cardiac injury. 7 It is worth underscoring that mortality in patients with CVD, who nonetheless had negative troponin T during infection, was not as expressive (13.3%) as mortality in those with increased troponin. 8 Patients with increased troponin were more elderly. They had more comorbidities; higher levels of leukocytes, NT- pro-BNP, C-reactive protein, and procalcitonin; and lower lymphocyte counts. Another study demonstrated that, on the fourth day after onset of symptoms, mean troponin levels were 8.8 pg/mL in patients who did not survive, in comparison with 2.5 pg/mL in those who survived. During follow-up, median troponin among survivors did not change significantly (2.5 – 4.4 pg/ mL), while it rose to 24.7 pg/mL on the seventh day, 55.7 pg/ mL on the thirteenth day, 134.5 pg/mL on the nineteenth day, and 290.6 pg/mL on the twenty-second day among patients who did not survive. Average time to death after onset of symptoms was 18.5 days (IQR 15 - 20 days). 9 The increase in troponin was accompanied by an increase in other inflammatory biomarkers (D dimer, ferritin, interleukin-6 (IL-6), and lactate dehydrogenase), thus Figure 1 – By means of its surface spike protein, SARS-CoV-2 binds to the human ACE-2 receptor following activation of the spike protein by TMPRSS2. SARS-CoV: severe acute respiratory syndrome coronavirus; SARS-COV-2: severe acute respiratory syndrome coronavirus 2; COVID-19: coronavirus disease 2019;ACE-2: angiotensin- converting enzyme-2; TMPRSS2: transmembrane protease, serine 2. Source: Costa IBSS, Brittar CS, Rizk SI, et al., 2020. 1052