The right ventricular outflow tract is highly vulnerable to arrhythmogenesis due to distinct developmental origins, complex myocardial architecture, and cellular vulnerability to ion overload.
The right ventricular outflow tract (RVOT) is the major origin of ventricular arrhythmias, including premature ventricular contractions, idiopathic ventricular arrhythmias, Brugada syndrome, torsade de pointes, long QT syndrome, and arrhythmogenic right ventricular cardiomyopathy. The RVOT has distinct developmental origins and cellular characteristics and a complex myocardial architecture with high shear wall stress, which may lead to its high vulnerability to arrhythmogenesis. RVOT myocytes are vulnerable to intracellular sodium and calcium overload due to calcium handling protein modulation, enhanced CaMKII activity, ryanodine receptor phosphorylation, and a higher cAMP level activated by predisposing factors or pathological conditions. A reduction in Cx43 and Scn5a expression may lead to electrical uncoupling in RVOT. The purpose of this review is to update the current understanding of the cellular and molecular mechanisms of RVOT arrhythmogenesis.
Lu et al. (Sat,) conducted a review in Right ventricular outflow tract arrhythmogenesis. The right ventricular outflow tract is highly vulnerable to arrhythmogenesis due to distinct developmental origins, complex myocardial architecture, and cellular vulnerability to ion overload.