The existing outbreak of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) also called coronavirus disease 2019 (COVID-19) has quickly progressed to a worldwide pandemic

The existing outbreak of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) also called coronavirus disease 2019 (COVID-19) has quickly progressed to a worldwide pandemic. in December 2019 origin, based on the Johns Hopkins COVID-19 Source Middle [1]. Respiratory stress is the most crucial manifestation of COVID-19. In addition, there are well-documented cardiac complications of COVID-19 Vernakalant HCl in patients with and without prior cardiovascular disease. The cardiac complications include myocarditis, heart failure, and acute coronary syndrome resulting from coronary artery thrombosis or SARS-CoV-2-related plaque ruptures [2]. There is growing evidence showing that arrhythmias are also one of the major complications. Liu et al. reported that about 7% of patients report palpitations as a presenting symptom [3]. In a recent report from Wuhan, China, 16.7% of hospitalized and 44.4% of ICU patients with COVID-19 had cardiac arrhythmias [4]. Recent studies have suggested that myocardial injury is common especially in critically ill COVID-19-infected patients through different mechanisms mainly due to direct damage of cardiomyocytes and systemic inflammation [2]. There are more than 20 viruses that have been implicated in myocardial inflammation and myocarditis, the most common are parvovirus B19, human herpesvirus 6, adenovirus, and coxsackievirus B3 [5]. The proposed mechanisms for arrhythmogenicity in viral infections in general are through the interplay between host factors and viral characteristics. These mechanisms include altered intercellular coupling, interstitial edema, and cardiac fibrosis that lead to abnormal conduction in addition to abnormal Ca2+ handling and downregulation of K+ channels that results in repolarization abnormalities and action potential conduction abnormalities [6]. Gaaloul et al. reported that myocardial inflammation caused by viral contamination leads to ion channel dysfunction or electrophysiological and structural remodeling as a mechanism for arrhythmia [5]. In vivo studies on mice and rabbits infected with SARS-CoV exhibited direct viral RNA inclusion in cardiomyocytes and conduction system disease [7]. Furthermore, it has been reported that patients with the SARS-CoV contamination experience different cardiac manifestations including Vernakalant HCl arrhythmias and sudden death [8]. To date, our knowledge of arrhythmia complications of COVID-19 is within its infancy even now. Nevertheless, our understanding relating to arrhythmogenicity from the book coronavirus is quickly changing and there keeps growing proof demonstrating different arrhythmia manifestations of COVID-19. Within this paper, we summarize essential studies relating to arrhythmia manifestations of COVID-19 and reveal this possibly fatal problem (Fig.?1). Open up in another home window Fig. 1 Arrhythmia manifestations?of COVID-19 and feasible mechanisms Arrhythmias in Viral Infections Cardiac conduction program disease relating to the sinoatrial (SA) node and atrioventricular (AV) node has been proven to be due to various infections including viral myocarditis [9]. According to Liu et al., the myocarditis process has three phases: phase one, viral contamination, the entry of the computer virus and proliferation in the myocardium that may lead to the second phase (autoimmune phase) with T cell activation, cytokine production, and cross-reacting antibodies formation and ultimately lead to phase 3, cardiac remodeling and progressive cardiac dilatation [10]. Acute viral myocarditis and acute pericarditis are self-limiting conditions that ordinarily have a benign course with minimal symptoms. However, ventricular arrhythmia is usually a frequent complication in viral myocarditis [11]. Case reports have exhibited the occurrence of arrhythmias in association with many viral infections including the influenza computer virus, Epstein-Barr computer virus (EBV), human immuno-deficiency computer virus (HIV), as well as others [12C17]. In a study by Sardana et al., over 17 million people with HIV were followed for a median CDK7 period of 4.7?years and they found that people with HIV were at an increased risk of developing atrial fibrillation AF with a hazard ratio of 1 1.46 after adjusting for race, age, gender, socio-economic status, Vernakalant HCl obesity, etc. [18]. A case of a 45-year-old male who had transient non-sustained ventricular tachycardia reported by Andrea Frustaci et al. indicated influenza computer virus focal myositis with inflammatory infiltration of conduction tissue on samples of left ventricular endomyocardial biopsy [12]. Another.