Pathophysiology of heart failure in patients with COVID-19

Introduction: the mechanisms that are suggested as determinant in the vulnerability of patients with heart failure to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and which cause the respiratory syndrome labeled COVID-19 (Coronavirus Infectious Disease-19), has revealed controversial. Objective: to gather information on the pathophysiological features of acute heart failure in the context of COVID-19. Method: concerning this topic, from September to November 2020 at the Policlínico Comunitario “Ramón López Peña” in Santiago de Cuba, a narrative review was carried out. The search was conducted checking the databases Pubmed, Infomed and SciELO, without date restriction, and in Spanish and English language. Development: the mechanisms involved on the pathophysiological features of heart failure in patients with this infectious disease revealed uncertainty. Myocardial damage is achievement of two aspects, the direct effect of viral respiratory infection on the myocyte, which is expressed as a local inflammatory response, and the heart participation as a target organ to the systemic and inappropriate inflammatory response, generated by a marked cytokines release. The last aspect referred also causes endothelial damage that triggers thromboembolic and ischemic complications, systolic and diastolic dysfunction of the heart, and ultimately leads to multiorgan system failure. Conclusions: despite the advances in understanding the etiopathogenesis of this disease, the pathophysiological mechanisms that determine on the heart failure still require to be precisely clarified, although the influence of the inappropriate inflammatory response, induced by cytokines, it is recognized in the onset myocardial damage.