COVID-19 and Cardiac Arrhythmias: Lesson Learned and Dilemmas

Abstract

Over the last few years, COVID-19 has attracted medical attention both in terms of healthcare system reorganization and research. Among the different cardiovascular complications of the SARS-CoV-2 infection, cardiac arrhythmias represent an important clinical manifestation requiring proper therapy both in the acute and post-acute phase. The multiparametric in-hospital monitoring of COVID-19 patients frequently detects new-onset or recurrent cardiac arrhythmias. As many patients are monitored remotely from cardiology departments, this setting calls for proper arrhythmia interpretation and management, especially in critically ill patients in the intensive care unit. From this perspective, the possible pathophysiologic mechanisms and the main clinical manifestations of brady- and tachyarrhythmias in COVID-19 patients are briefly presented. The progressively increasing body of evidence on pathophysiology helps to identify the reversible causes of arrhythmias, better clarify the setting in which they occur, and establish their impact on prognosis, which are of paramount importance to orient decision making. Despite the accumulating knowledge on this disease, some dilemmas in the management of these patients may remain, such as the need to implant in the acute or post-acute phase a permanent pacemaker or cardioverter/defibrillation in patients presenting with brady- or tachyarrhythmias and lifelong oral anticoagulation in new-onset atrial fibrillation detected during SARS-CoV-2 infection.

Keywords: COVID-19; SARS-CoV-2 infection; bradyarrhythmia; cardiac arrhythmias; oral anticoagulation; tachyarrhythmias.

Figure 1

Possible mechanisms of cardiac arrhythmias in COVID-19. Asterisk indicates the influence of ACE system imbalance. Abbreviations: ACE: angiotensin converting enzyme; ARDS: acute respiratory distress syndrome; DIC: diffuse intravascular coagulation; PE: pulmonary embolism; SIRS: systemic inflammatory response syndrome.

Figure 2

Most accredited mechanisms involved in COVID-19 to generate bradyarrhythmias and supraventricular and ventricular tachyarrhythmias. Abbreviations: AVB: atrioventricular block; SSS: sick sinus syndrome.

Figure 3

Types of bradyarrhythmia in COVID-19. Data are extracted from references [57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96,97,98,99,100,101,102]. Abbreviations: AVB: atrioventricular block; SA: sinus arrest; SB: sinus bradycardia.

Figure 4

(A,B) Twelve-lead electrocardiogram of a case with atrial fibrillation (A) and typical atrial flutter (B). In (A), the absence of distinct repeating P-waves with irregular atrial activation, which are diagnostic criteria for atrial fibrillation, is evident; the ventricular response is modulated by pharmacologic agents acting on the atrioventricular conduction. In (B), P-waves with sawtooth morphology (negative in the inferior and left precordial leads and positive in aVL and V1) is clearly observed in the right-hand side; importantly, during the increased sympathetic tone, possibly during infections, the atrioventricular conduction ratio is frequently 2:1 with a ventricular response of 140–150 bpm, as in the right-hand side of this figure. In both arrhythmias, 12-lead electrocardiographic recording is essential for a correct diagnosis.