Abstract
The mechanism of ventricular arrhythmias (VAs) occurring in the ventricular outflow tract (OT) is related to intracellular calcium overload and delayed afterdepolarizations that lead to triggered activity. The store overload-induced calcium release (SOICR) is thought to be one of the mechanisms of triggered activity, and inhibition of SOICR has been suggested as one of the antiarrhythmic effects of carvedilol.
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