Key result
Procainamide fails to reduce ventricular arrhythmias overall, with increased ectopy during complete vagal blockade.
Why the study?
The influence of the vagolytic effect of procainamide on early ventricular arrhythmias induced by LAD coronary occlusion was unclear.
Does procainamide pretreatment exacerbate ventricular arrhythmias induced by coronary occlusion in a feline model?
Does procainamide pretreatment exacerbate ventricular arrhythmias induced by coronary occlusion in a feline model?
The degree of vagal blockade induced by procainamide is a critical factor that can exacerbate ventricular arrhythmias during acute myocardial ischemia.
Answers are grounded in this paper and cite their sources.
Procainamide may worsen ectopy and VF via vagal blockade in feline ischemia models; leaves open autonomic modulation as arrhythmia target.
The influence of the vagolytic effect of procainamide on the early ventricular arrhythmias induced by left anterior descending coronary (LAD) occlusion was studied in chloraloseanaesthetised cats. All control animals developed a ventricular arrhythmia (1119 +/- 166 PVCs per hour), with a consistent onset time, duration, and overall mortality due to ventricular fibrillation (ie 20%). In 18 animals pretreated with procainamide (0.5 mg.kg-1.min-1 for 50 min), there was no effect on the ventricular arrhythmia in terms of ectopic frequency (1020 +/- 180 PVCs per hour), time to onset of arrhythmia, duration of arrhythmia, and mortality incidence (ie 16.7%). However, subdividing the data according to whether or not vagal blockade had been produced by procainamide revealed that animals exhibiting complete vagal blockade demonstrated significantly more ectopic beats (1606 +/- 310 PVCs per hour) and 33% developed ventricular fibrillation. Treated animals without complete vagal blockade exhibited an ectopic frequency rate of 620 +/- 98 PVCs per hour and none of the animals developed ventricular fibrillation. The haemodynamic parameters were similar between both procainamide treated subgroups. These results suggest that an important factor in response of the ischaemic heart to the cardiac rhythm effects of procainamide is the degree of vagal blockade induced by this agent.
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Corr et al. (1978) studied Ventricular arrhythmias induced by coronary occlusion. Procainamide vs. Control was evaluated on Ventricular arrhythmia (PVCs per hour). Procainamide did not reduce overall ventricular arrhythmias, but animals exhibiting complete vagal blockade had significantly more ectopic beats (1606 vs 620 PVCs per hour) and higher VF incidence.
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