Influence of Atropine and of Vagally Mediated Bradycardia on the Occurrence of Ventricular Arrhythmias following Acute Coronary Occlusion in Closed-Chest Dogs

Abstract

In contrast to previous opinions, recent investigations have suggested that increasing heart rate (HR) with atropine when moderate sinus bradycardia accompanies acute myocardial infarction is not necessarily beneficial. To further characterize the influence of vagally mediated changes in HR during ischemia, we evaluated the effects of atropine and of electric stimulation of the vagus nerves on the incidence of ventricular arrhythmias during acute coronary occlusion in closed-chest dogs. Protection from occlusion-induced arrhythmia was not observed when 28 dogs receiving atropine were compared with 27 control dogs. Rather, the total incidence of ventricular arrhythmias was significantly higher ( P < 0.05) and ventricular fibrillation tended to occur more frequently in the atropine-treated group. Moreover, fewer ventricular arrhythmias (and total absence of ventricular fibrillation or close-coupled premature beats) were noted in 12 control animals with spontaneous bradycardia (HR<60 beats/min) compared with 15 nonbradycardic animals. When vagal stimulation produced bradycardia (HR = 40-60 beats/min) during coronary occlusion, occurrence and character of ventricular arrhythmias were the same as in dogs with normal rates (HR = 80-100 beats/min). Although these results may not necessarily apply to man, further studies are needed before it can be assumed that all individuals with moderate bradycardia during acute myocardial infarction should receive vagolytic agents.

Neuro-cardiac interaction in malignant ventricular arrhythmia and sudden cardiac death

“…In autonomically-intact dogs, spontaneous ischaemia-induced VF increased in vivo following i.v. atropine (Goldstein et al 1973), with similar conclusions drawn from control experiments in the dog model of SCD (Schwartz et al 1984;Vanoli et al 1991). This is supported by data during direct VNS where atropine abolished protection (Yoon et al 1977).…”

“…The anti-arrhythmic action of VNS was later reproduced by Scherlag's group (Scherlag et al 1970) who showed that VNS interrupted the spontaneous occurrence of VT during coronary artery occlusion . Other studies in the 1970's (Goldstein et al 1973;Myers et al 1974;Kent et al 1973) confirmed the anti-arrhythmic action of VNS in the ventricle during ischaemia. Several studies provided evidence that VNS is also protective against experimental induced VF -with the demonstration of a VNS dependent increase in the current required to induce VF, i.e.…”

“…Nonetheless, the protective effect of VNS during coronary artery occlusion in the postinfarct canine exercise experiments was either reduced (Goldstein et al 1973) or abolished (Schwartz et al 1984) when heart rate was controlled. VNS prevented VF in 55% of animals that were rate controlled vs. 92% of control dogs in sinus rhythm, suggesting that bradycardia 'is important but not essential'.…”

“…There is evidence from in vivo studies under anaesthesia in experimentally induced VF, that VNS is protective under these conditions (Scherlag et al 1970;Goldstein et al 1973). Conversely, bilateral vagotomy or atropine perfusion increases arrhythmic mortality in anaesthetised cats during (Corr & Gillis 1974) and following coronary artery occlusion (Zuanetti et al 1987) suggesting that intrinsic vagal activity was protective.…”

Intravenous Cocaine Decreases Cardiac Vagal Tone, Vagal Index (Derived in Lorenz Space), and Heart Period Complexity (Approximate Entropy) in Cocaine Abusers

“…Evidence that tonic parasympathetic inhibitory control of the heart normally suppresses arrhythmiagenesis (Kamarck and Jennings 1991) may be directly relevant. Withdrawal of vagal tone is associated with several different cardiac arrhythmias (Corr and Gillis 1974;Goldstein et al 1973;Kent et al 1973;Myers et al 1974). Therefore, the relatively pronounced release of vagal inhibition produced by moderate dosages of cocaine may play a direct etiologic role in overdose of this drug.…”