Propranolol slowed mean heart rate by 20% and protected against arrhythmia during acute myocardial ischemia in dogs, but lost this effect when heart rate was increased to 184 ± 9 beats/min.
Do antiarrhythmic agents (lidocaine, procaine amide, propranolol) and heart rate influence ischemic zone epicardial activation delay and the onset of ventricular tachycardia during acute myocardial ischemia in dogs?
In a canine model of acute myocardial ischemia, the antiarrhythmic effect of propranolol is primarily mediated by heart rate reduction, whereas lidocaine and procaine amide do not delay the onset of ventricular tachycardia.
The influence of lidocaine, procaine amide, and propranolol on ventricular arrhythmias during acute myocardial ischemia in the dog was examined. Ischemic zone epicardial (IZE) activation delay and the time of onset of ventricular tachycardia (VT t ) were studied. Progressive IZE delay always preceded ventricular tachycardia (VT). Ventricular tachycardia occurred when IZE delay extended into the T wave of the standard electrocardiogram but areas of ischemic epicardium were found in which activation delayed beyond the T wave. Fast heart rates during acute ischemia were associated with an accelerated time course of IZE delay and early VT. Slow heart rates resulted in minimal IZE delay and delayed onset or absence of VT. Sympathectomized dogs with heart rates 32% slower than normal dogs did not develop significant IZE delay or VT during ischemia. When heart rates were increased by atrial pacing, these dogs behaved in the same fashion as the normal dogs with respect to IZE delay and VT t . Lidocaine was found to hasten the time course of IZE delay but to have no significant effect on VT t . Procaine amide did not influence IZE delay nor VT t during ischemia. Propranolol slowed the mean heart rate by 20% and appeared to protect against arrhythmia. When the heart rate (115 ± 10 beats/min; mean ± standard deviation) was increased by atrial pacing (184 ± 9 beats/min), propranolol did not significantly influence IZE delay or VT t as compared to the untreated controls. The clinical counterpart of our experiments during acute ischemia may relate to the prehospitalization phase of myocardial infarction.
Hope et al. (Sun,) conducted a other in Acute myocardial ischemia. Lidocaine, procaine amide, and propranolol vs. Untreated controls was evaluated on Ischemic zone epicardial (IZE) activation delay and time of onset of ventricular tachycardia (VT t). Propranolol slowed mean heart rate by 20% and protected against arrhythmia during acute myocardial ischemia in dogs, but lost this effect when heart rate was increased to 184 ± 9 beats/min.