Threshold, enzymatic, and pathologic changes associated with prolonged transcutaneous pacing in a chronic heart block model.

Abstract

Previous studies have shown that 30 minutes of transcutaneous cardiac pacing (TCP) can induce mild, clinically insignificant myocardial damage. Longer use of TCP may cause more severe cardiac damage which might result in an increase in the capture threshold for subsequent transvenous cardiac pacing (TVP). To assess this possibility, we examined changes induced by TCP in a canine chronic heart block model. Heart block was induced in conditioned dogs (n = 8) by His bundle ablation. Seven to 10 days after induction of heart block, six animals were paced. Cardiac enzymes were drawn before pacing and at 4, 24, 48, and 72 hours after pacing. Although there was a significant rise in CK at 4 and 24 hours (P less than 0.05), there was no detectable rise in the MB fraction in any of the paced animals. There was no elevation of LDH after pacing, although three animals did develop an LDH1/LDH2 isoenzyme flip indicative of myocardial damage. Animals were sacrificed 72 hours after pacing and their hearts were examined for gross and microscopic changes. The hearts of the paced animals revealed subendocardial, subepicardial, and perivascular areas of basophilic degeneration involving less than 1% of the myocardium in four of six animals. No evidence of such damage was seen in two heart-blocked control animals not undergoing pacing. TVP and TCP capture thresholds assessed before and after a 60-minute TCP pacing period showed no significant change. Hence, use of TCP for a 60-minute period prior to TVP appears to be a safe emergency pacing technique.