Cardiac MAO-A inhibition protects against catecholamine-induced ventricular arrhythmias via enhanced diastolic calcium control.

This study implicates catecholamine metabolism in arrhythmogenesis and reveals that monoamine oxidase is linked to Ca2+ regulation in the heart. It further illustrates therapeutic potential of cardiac MAO-A inhibition as a dual-purpose drug target to simultaneously manage depression and lower arrhythmia risk in affected patients.