Abstract

Introduction Since December 31, 2019, when China reported the appearance of cases of acute respiratory failure caused by a new species of coronavirus, SARS-CoV-2, which causes the disease called COVID-19, almost 20 million cases were confirmed, causing 726 thousand deaths worldwide. In Brazil, on August 8th, 2020, there was approximately 3 million cases and 100 thousand death by the disease. Its rapid spread, its high potential for hospitalization, and its high lethality, especially in the most fragile groups such as [...]

Highlights

  • Since December 31, 2019, when China reported the appearance of cases of acute respiratory failure caused by a new species of coronavirus, SARS-CoV-2, which causes the disease called COVID-19, almost 20 million cases were confirmed, causing 726 thousand deaths worldwide.[1]

  • The medications used are described in case records, with no solid scientific evidence for their use, and with a COVID-19/complications; Pandemics; Betacoronavirus; Cardiovascular Diseases/complications; Arrhythmias, Cardiac; Stroke Volume; Death, Sudden; Chloroquine; Hydroxychloroquine; Azythromycin

  • It was demonstrated that approximately 20% of patients with COVID-19 have myocardial injury, 10% have myocarditis, and 10 to 30% evolve with shock,[18] which would multiply the probability of adverse effects in a proinflammatory and pro-thrombotic environment

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Summary

Introduction

Since December 31, 2019, when China reported the appearance of cases of acute respiratory failure caused by a new species of coronavirus, SARS-CoV-2, which causes the disease called COVID-19, almost 20 million cases were confirmed, causing 726 thousand deaths worldwide.[1]. It is observed that the highest incidence of events occurs in people with other predisposing factors, such as long QT syndrome, structural cardiovascular diseases, or the use of other drugs that prolong QT.[17] In addition, it was demonstrated that approximately 20% of patients with COVID-19 have myocardial injury, 10% have myocarditis, and 10 to 30% evolve with shock,[18] which would multiply the probability of adverse effects in a proinflammatory and pro-thrombotic environment These patients possibly have greater substrates for arrhythmia and electrolyte disturbances, and still in the critical phase of the disease, most patients admitted to intensive care units are treated with multiple combined therapies, such as vasoactive amines, diuretics, and serotonin 5-ht[3] receptor antagonists, among others.

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