ABC | Volume 114, Nº5, May 2020

Review Article Askin et al. COVID-19 and cardiovascular diseases Arq Bras Cardiol. 2020; 114(5):817-822 common (46% overall, 72% in intensive care patients). Of these, 31% had HT (58% in intensive care patients); 15% had CVD (25% in intensive care patients), and 10% had DM (22% intensive care patients). 13 In a cohort analysis of 1,099 outpatients and inpatients, 24% had some comorbidity (58% among intubation or death); 15% had HT (36% among intubation or death); 7.4% had DM (27% among intubation or death), and 2.5% had KVH (9% among those with intubation or death). 14 The Chinese National Health Commission reported that 35% of patients diagnosed with COVID-19 had HT, and 17% had coronary heart disease. 15 A metaanalysis in China showed that, in 46,248 infected patients, the most common comorbidity was HT. 16 The possible mechanism of these associations is considered to be more common in people with advanced age, impaired immune system, high ACE2 levels, or predisposition to CVD. Another study conducted in China indicated that the most common comorbidity seen in patients who died from COVID-19 was CVD with 10.5% (Figure 2). 17 COVID-19 and myocardial damage Myocardial damage, with increased cardiac biomarkers, was among the first cases in China. In a study with 138 patients with COVID-19 in Wuhan, cardiac damage with high sensitivity Troponin I (hs-cTnI) and ECG or echocardiographic abnormalities were generally present in 7.2% of patients and 22% of patients in need of intensive care. 13 The Chinese national health report stated that approximately 12% of patients without CVD have increased troponin levels or arrest rates during hospitalization. 15 Hs-cTnI, in particular, was above the 99th percentile upper reference limit in 46% of survivors. 12 Initial results show that there are two myocardial damage patterns with COVID-19. One study showed that on the fourth day following the onset of symptoms, the median hs-cTnI level in survivors was 8.8 pg/mL and 2.5 pg/mL in those who died. During follow-up, mean hs-cTnI between survivors did not change significantly (2.5 – 4.4 pg/mL), but on the seventh day, hs-cTnI values ​were 24.7 pg/mL; 55.7 pg/mL on the 13th day; 134.5 pg/mL on the 19th day, and 290.6 pg/mL on the 22nd day. In particular, average time from onset of symptoms to death was 18.5 days (IQR 15 – 20 days). 12 The increased hs-cTnI level was associated with other inflammatory biomarkers (D-dimer, ferritin, interleukin-6 [IL‑6], lactate dehydrogenase). This was the reason for the cytokine storm or secondary hemophagocytosis. Viral myocarditis or stress cardiomyopathy is mostly reported in the cases who mostly present with cardiac symptoms. Recently, a case with chest pain with ST-segment elevation on ECG but normal coronaries was reported. The patient had reduced ejection fraction (EF) (27%), increased left ventricular diameters, and high cardiac biomarkers (troponin T > 10 ng/mL, NT-proBNP > 21,000 pg/mL). 18 Intravenous immunoglobulin and steroids improved his cardiac capacity within three weeks. In another report from China, a 63-year-old male with no cardiac history had severe respiratory symptoms, enlarged left ventricle (LVEDD 6.1 cm), and fulminant myocarditis with reduced EF. He had higher troponin-I (> 11 ng/mL) and NT- proBNP (> 22,000 pg/ml) levels. Extracorporeal membrane oxygenation and intravenous immunoglobulin, steroids, antiviral treatment regimens were applied because of the cardiogenic shock situation. Ventricular function improved significantly within 2 weeks. 19 Glucocorticoid therapy is not recommended by the world health organization because the effect of this therapy is still uncertain. 20,21 China’s national report also reported that symptoms might be palpitations and chest pain rarely. 15 Limited data showed a lower incidence of fulminant myocarditis and Figure 2 – Comorbidity rates in patients who died from COVID-19 in China. 818