Nicotine infusion in canine hearts with healed myocardial infarction lengthened the pacing cycle length at which ventricular fibrillation was induced from 171 to 210 ms (P<0.01).
Does nicotine infusion increase vulnerability to ventricular fibrillation in a canine model of healed myocardial infarction?
Nicotine facilitates conduction block, reentry, and ventricular fibrillation in canine hearts with healed myocardial infarction by increasing depolarization and repolarization alternans.
Absolute Event Rate: 210% vs 171%
p-value: p=<0.01
The vulnerability of the infarcted hearts to ventricular fibrillation (VF) was tested in in situ canine hearts during nicotine infusion. The activation pattern was mapped with 477 bipolar electrodes in open-chest anesthetized dogs (n = 8) 5-6 wk after permanent occlusion of the left anterior descending coronary artery. Nicotine (129 +/- 76 ng/ml) lengthened (P 1. We conclude that nicotine facilitates conduction block, reentry, and VF in hearts with healed myocardial infarction by increasing the magnitude of depolarization and repolarization alternans consistent with the restitution hypothesis of vulnerability to VF.
Yashima et al. (Thu,) conducted a other in Healed myocardial infarction (n=8). Nicotine vs. Baseline was evaluated on Pacing cycle length at which ventricular fibrillation was induced (p=<0.01). Nicotine infusion in canine hearts with healed myocardial infarction lengthened the pacing cycle length at which ventricular fibrillation was induced from 171 to 210 ms (P<0.01).