Na/Ca Exchange and Cardiac Ventricular Arrhythmias

摘要

Ventricular arrhythmias are a major cause of death in cardiovascular disease. Ca~(2+) removal from the cell by the electrogenic Na/Ca exchanger is essential for the Ca~(2+) flux balance during excitation-contraction coupling but also contributes to the electrical events. "Classic" views on the exchanger in arrhythmias include its well-recognized role as depolarizing current underlying delayed afterdepolarizations (DADs) during spontaneous Ca~(2+) release and the alterations in expression in certain forms of cardiac hypertrophy and heart failure. "Novel" views relate to more subtle roles for the exchanger in arrhythmias. Na/Ca exchange function in disease could be modulated indirectly, through phosphorylation or anchoring proteins. Ongoing studies relate Na/Ca exchange to variability in action potential duration (APD) and early afterdepolarizations (EADs) in a dog model of cardiac hypertrophy and arrhythmias. Further research on drugs that target Na/Ca exchange will have to carefully examine the effects on Ca~(2+) balance.