Table 3.
Virus | Arrhythmias reported | Proposed mechanism of action |
---|---|---|
Dengue virus |
Sinus bradycardia AV block AF |
Direct invasion, immune mediated cardiomyocyte damage direct involvement of conduction system Prodromal phase in acute myocarditis leading to arrhythmia |
Chikungunya | AF, brady-arrhythmias, AV block | Penetrates myocytes and directly damaging muscle fibers; prodromal phase in acute myocarditis leading to arrhythmia |
Zika | AF, atrial tachycardia, ventricular arrhythmias | Invasion of cardiac cells, leading to autoimmune induced apoptosis |
SARS-CoV-2 | AF, VT | Binds to ACE2 of myocardial cells, leading to myocarditis via direct toxicity, induced inflammatory response |
Coxsackie B | Ventricular arrhythmias | Binds to CAR and DAF of cardiac myocytes, cleavage of dystrophin leading to DCM; alteration of cardiac ion channels |
Adenovirus | Ventricular arrhythmias | Binds to CAR and integrins αvβ3 and αvβ5 of cardiac myocytes; alteration of cardiac ion channels |
Rubella | AV block | Unclear, likely from myocardial inflammation and scarring |
HIV | AF, atrial arrhythmias | Release of Nef, leading to dysregulation of autophagy causing cardiomyocyte death; HIV tat protein causing inactivation of hERG K+ channels |
Influenza A | AF, AV block, ventricular arrhythmias | Infection of cardiomyocytes, Purkinje cells, and endothelial cells |
HHV-6 | AV block, ventricular arrhythmias | Direct infection of cardiomyocytes (HHV-6A), infection of vascular endothelium leading to endothelial/diastolic dysfunction (HHV-6B) |
Parvovirus B19 | Ventricular arrhythmias | Infection of endothelial cells of small cardiac vessels leading to diastolic dysfunction |
HSV | AF, sinus node dysfunction | Inflammation (AF); CNS dysfunction from HSV encephalitis |
CMV | AV block | Invasion of cardiomyocytes; inflammation and edema of conduction system from myocarditis |
EBV | Ventricular arrhythmias, AV block | Invasion of cardiomyocytes and vascular endothelium |
VZV |
Ventricular arrhythmias AF, AV block |
Inflammation (AF); resultant fibrosis and scarring leading to conduction blocks and reentry circuits |