[Acute ischemia, autonomic reflexes, and ventricular fibrillation]

The effects of the autonomic nervous system on malignant arrhythmias, particularly in the setting of ischemic heart disease, have been widely investigated and described. Specifically, while sympathetic hyperactivity is arrhythmogenic, an increased vagal activity often exerts a beneficial effect. New insights on the relationship between autonomic activity and sudden cardiac death have been obtained in conscious dogs in which a healed myocardial infarction, acute myocardial ischemia and exercise are combined. In this chronic animal model myocardial infarction reduces baroreflex sensitivity and heart rate variability (markers of vagal reflex and tonic activity to the heart) and a depressed baroreflex sensitivity or a reduced heart rate variability after myocardial infarction indicates an increased risk for ventricular fibrillation. The clinical relevance of these experimental observations was confirmed in studies in patients with myocardial infarction. Exercise training increases vagal control of heart rate and concomitantly prevents recurrence of ventricular fibrillation during acute ischemia in dogs susceptible to sudden death. The protective effect of vagal activity is further confirmed by the experimental evidence that electrical stimulation of the vagus is able to prevent ventricular fibrillation during acute myocardial ischemia. The possibility of modulating the autonomic control of cardiac activity by means of pharmacologic and non pharmacologic interventions able to increase cardiac vagal activity represents a rational and promising approach to reduce risk for lethal events after myocardial infarction.