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Ann N Y Acad Sci. 2007 Mar;1099:339-48.

Na/Ca exchange and cardiac ventricular arrhythmias.

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Laboratory of Experimental Cardiology, KUL, Campus Gasthuisberg O/N1, 704, Herestraat 49, B-3000 Leuven, Belgium.


Ventricular arrhythmias are a major cause of death in cardiovascular disease. Ca2+ removal from the cell by the electrogenic Na/Ca exchanger is essential for the Ca2+ 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 Ca2+ 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 Ca2+ balance.

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