Effect of sodium and calcium channel blockers on short-term cardiac memory in humans

Cardiac memory (CM) can be induced by both short and long period of pacing from the right ventricle. Although several mechanisms have been proposed in animal studies, mechanisms of CM in humans are not well studied.

A total of 46 patients (20 females; mean age 46+/-13 years) with paroxysmal supraventricular tachycardia referred for catheter ablation were enrolled. After catheter ablation, CM was induced by 20 min of pacing from right ventricular apex (RVA). The CM was quantified as the difference of T wave area in each lead between baseline and after RVA pacing. After complete recovery from the induced CM, verapamil (1.5 mg/kg; 0.005 mg/kg/min), lidocaine (1 mg/kg; 2 mg/min), procainamide (10 mg/kg; 4 mg/min), and nitroglycerine (0.6 mg sublingually; 5 microg/min), were given in 14, 10, 12, and 10 patients respectively. The pacing procedure was repeated and the degrees of CM were compared before and after each drug administered.

The short-term CM was demonstrated by changes in T wave area after RVA pacing in all patients. The degrees of CM were suppressed in patients after verapamil and lidocaine. In contrast, procainamide and nitroglycerin had no significant effect on the degrees of CM expression.

The expression of short-term CM can be suppressed by verapamil and lidocaine but not by procainamide and nitroglycerin. The results may suggest that short-term CM in humans can be modulated by calcium dependent process and the functional alternations of sodium and potassium channels.