Cryosurgical versus catheter ablation of the atrioventricular junction.

Results of catheter ablation of the atrioventricular (AV) junction in 41 patients were compared with results of cryosurgical ablation in 42 patients. Mean follow-up was 29 months among patients who underwent catheter ablation and 53 months among those who underwent cryosurgical ablation. In both groups complete heart block was produced in most patients (88% in the catheter ablation group, 86% in the cryosurgery group), and similar proportions of patients continued to receive antiarrhythmic drugs (27% in the catheter ablation group, 36% in the cryosurgery group). However, the short-term morbidity rate was significantly lower among patients who underwent catheter ablation (12% vs 42%) (p = 0.004). Long-term mortality and morbidity rates were not significantly different; most deaths were related to underlying cardiopulmonary disease and morbidity to problems with permanent pacemakers. Both catheter ablation and cryosurgical ablation of the AV junction are effective in creating complete AV block and controlling supraventricular tachycardia in medically refractory patients. Because catheter ablation is associated with lower short-term morbidity and avoids the need for a major surgical procedure, it is preferable to cryosurgical ablation of the AV junction when permanent abolition of AV conduction is necessary.

Frequency-dependent effects of verapamil on atrioventricular nodal conduction in man.

We sought to determine if verapamil induces frequency-dependent prolongation of atrioventricular nodal conduction in 10 consecutive patients studied in the electrophysiology laboratory. We used a maintenance infusion of verapamil designed to produce plasma concentrations of verapamil in the "therapeutic" range and that did not alter heart rate or blood pressure significantly. Frequency-dependent prolongation of atrioventricular nodal conduction (AH interval) was demonstrated in all 10 patients (p less than .001), and no change in HV conduction time with decreasing cycle length was noted in any patients while receiving verapamil. Two patterns of use-dependent response were seen. In four patients frequency-dependent prolongation of the delta(AH) interval [delta(AH) = AHverapamil - AHcontrol at a given cycle length] was seen with each decrement in pacing cycle length. In six patients frequency-dependent prolongation of the delta(AH) interval was not manifest until the fifth to eighth pacing cycle length tested. There was no association between the pattern observed and the initial heart rate or AH interval. After an abrupt change in pacing cycle length, the kinetics of delta (AH) interval prolongation were rapid; equilibrium was achieved by five to eight pulses in all patients. There was no correlation between the magnitude of prolongation of the AH interval noted at a particular cycle length and the concentration of verapamil during the maintenance infusion. These results indicate that verapamil causes use-dependent prolongation of atrioventricular nodal conduction in man.

Electrophysiologic effects of amiloride in canine Purkinje fibers: evidence for a delayed effect on repolarization.

Amiloride, a potassium-sparing diuretic, inhibits Na+ transport, Na+-H+ exchange and possibly Na+-Ca++ exchange in a variety of cellular and epithelial tissues. Similar membrane ion transport mechanisms exist in cardiac tissue, yet there are little data on possible interference by amiloride with ion transport in the heart. Given recent evidence for a delay in amiloride uptake into erythroid cells, we studied the electrophysiologic effects of amiloride after prolonged drug exposure in canine Purkinje fibers using standard microelectrode techniques. Amiloride (1-10 microM) led to a progressive lengthening of action potential duration with a tau of 1.8 +/- 0.5 hr (n = 15). At long cycle lengths (greater than or equal to 2000 msec) early afterdepolarizations and oscillations around the plateau were seen. To determine the etiology of the afterdepolarizations, Purkinje fibers treated for 2 hr with 10 microM amiloride were then exposed to tetrodotoxin, manganese and nisoldipine. Tetrodotoxin (7.8 X 10(-7) M) reversed completely all amiloride effects rapidly and reversibly. MnCl2 (4 mM) increased the afterdepolarizations, and arrest occurred at the plateau potential routinely. Nisoldipine (10(-6) M), a more selective blocker of slow inward current, shortened action potential duration somewhat but did not reverse fully the effects of amiloride. We conclude that amiloride has a pronounced effect on repolarization in the canine Purkinje fiber and this effect is manifest only after prolonged exposure to the drug.