COVID-19 and the Beat-To-Beat Heart

Abstract

other factors than myocardial damage, such as sinus tachycardia, atrial fibrillation, atrial flutter, and monomorphic or polymorphic ventricular tachycardia can be involved in development of arrhythmias in these patients. 4,5 Evidence has shown that in the first 5-9 days, patients with COVID-19 have a uniform disease progression, without major changes in inflammatory or cardiac biomarkers; however, after 10-24 days, there is an increase in pro-inflammatory cytokines, mainly interleukin-6 and 1, and TNF alpha, along with increases in myoglobin, D-dimer, and C-reactive protein. 5,6 Data from basic and clinical studies have shown that inflammation plays an important role as a risk factor for long QT syndrome and Torsades de Pointes, mainly through the increase of cytokines. This directly affects myocardial electrophysiology and can lead to unfavorable outcomes of cardiac arrhythmia by increasing oxidative stress in cardiomyocytes and resident macrophages, destabilizing electrical activity, leading to prolongation of the cardiomyocyte action potential and causing lethal ventricular arrhythmias. 6 Furtehermore, Zhou et. al. 2 demonstrated an increase in D-dimer (a marker of thrombotic events) in patients with an unfavorable outcome (Figure 1).