ABC | Volume 114, Nº6, June 2020

Review Article Coronavirus Disease 2019 and the Myocardium José Albuquerque de Figueiredo Neto, 1 Fabiana G. Marcondes-Braga, 2 Lidia Zytinski Moura, 3 André Melo e Silva de Figueiredo, 1 Viviane Melo e Silva de Figueiredo, 1 Ricardo Mourilhe-Rocha, 4 Evandro Tinoco Mesquita 5 Universidade Federal do Maranhão, 1 São Luis, MA - Brazil Instituto do Coração do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, 2 São Paulo, SP - Brazil Pontifícia Universidade Católica do Paraná, 3 Curitiba, PR - Brazil Universidade do Estado do Rio de Janeiro e Hospital Pró-cardíaco. 4 Educador C.T.E.B./UHG. 5 Abstract Infection with the coronavirus known as COVID-19 has promoted growing interest on the part of cardiologists, emergency care specialists, intensive care specialists, and researchers, due to the study of myocardial involvement based on different clinical forms resulting from immunoinflammatory and neurohumoral demodulation. Myocardial involvement may be minimal and identifiable only by electrocardiographic changes, mainly increased cardiac troponins, or, on the other side of the spectrum, by forms of fulminant myocarditis and takotsubo syndrome. The description of probable acute myocarditis has been widely supported by the observation of increased troponin in association with dysfunction. Classical definition of myocarditis, supported by endomyocardial biopsy of inflammatory infiltrate, is rare; it has been observed in only one case report to date, and the virus has not been identified inside cardiomyocytes. Thus, the phenomenon that has been documented is acute myocardial injury, making it necessary to rule our obstructive coronary disease based on increased markers of myocardial necrosis, whether or not they are associated with ventricular dysfunction, likely associated with cytokine storms and other factors that may synergistically promote myocardial injury, such as sympathetic hyperactivation, hypoxemia, arterial hypotension, and microvascular thrombotic phenomena. Systemic inflammatory and myocardial phenomena following viral infection have been well documented, and they may progress to cardiac remodeling and myocardial dysfunction. Cardiac monitoring of these patients is, therefore, important in order to monitor the development of the phenotype of dilated myocardiopathy. This review presents the main etiological and physiopathological findings, a description of the taxonomy of these types of cardiac involvement, and their correlation with the main clinical forms of the myocardial component present in patients in the acute phase of COVID-19. Introduction Myocardial injury, as shown by increased cardiac biomarkers, was identified among the first cases of COVID-19 in China. The National Health Council of China reported that almost 12% of patients without known cardiovascular disease (CVD) showed elevated levels of troponin or cardiac arrest during hospitalization. 1 These findings have stimulated research and interest on the part of cardiologists, intensive care specialists, and clinical researchers, due to early recognition of these abnormalities, as well as the search for physiopathological mechanisms and their real impacts on prognosis. In addition to this, individuals with previous CVD have been shown to be at a higher risk of developing severe forms and higher mortality. Accordingly, it is of fundamental importance to understand the spectrum of myocardial involvement, whether primary or secondary, in addition to the etiological and physiopathological mechanisms involved, in order to promote the development of therapeutic strategies that can prevent and diminish myocardial aggression during the acute phase. SARS-CoV-2 and the mechanism of direct cellular aggression SARS-CoV-2 infection is caused by binding of the spike protein on the surface of the virus to the human angiotensin converting enzyme 2 (ACE-2) receptor after activation of the spike protein by transmembrane protease, serine 2 (TMPRSS2). ACE-2 is expressed in the lungs, mainly in the type-II alveolar cells, and it seems to be the predominant means of entry. 2-4 SARS-CoV-2, in binding to ACE-2, causes downregulation of this enzyme, determining an increase in levels of angiotensin II, which may lead to deleterious effects in the activation of the renin-angiotensin-aldosterone system, such as vessel constriction, changes in vascular permeability, myocardial remodeling, and acute pulmonary injury, which may partially justify the frequent pulmonary symptoms in this syndrome 5 (Figure 1). 6 ACE-2 is also highly expressed in the heart, neutralizing the effects of angiotensin II in states with excessive activation Keywords Myocardium/injuries; Troponin; Inflammatory Diseases; Myocarditis; Takotsubo Syndrome; Biomarkers; Coronavirus; COVID-19; Pandemics; Cardiomyopathy, Dilated; Thrombotic Microangiopathies Mailing Address: José Albuquerque de Figueiredo Neto • Avenida dos Holandeses, 1B, ap. 1202, Ponta D’Areia, São Luís - MA – Brazil E-mail: jafneto@terra.com.br Manuscript received April 23, 2020, revised manuscript May 04, 2020, accepted May 06, 2020 DOI: https://doi.org/10.36660/abc.20200373 1051