Task Force 4 : Sudden cardiac death Nonpharmacologic interventions

FEW WOULD ARGUE with the concept that sudden cardiac death is an important area about which much remains to be learned. Perhaps 90% of sudden deaths are associated with coronary artery disease and associated myocardial ischemia. Most sudden cardiac deaths involve rate and rhythm disturbances. The relationship between these functional determinants and the autonomic nervous system intuitively appears crucial but remains very poorly understood. Only two or three decades ago the cardiac nerves were known primarily as mechanisms whereby the heart might be accelerated or slowed. Almost all that is known beyond this has come out of research efforts over the past few years. Dramatically improved insights have emerged concerning the regulatory influence of cardiac innervation on cardiac impulse formation and conduction, patterns of depolarization and repolarization, myocardial contractility, matching of rates and rhythms to metabolic demands, and the delivery of gases and nutrients by way of precise control of the coronary vasculature. Still, real understanding of the neural link stands out as a critically significant deficit in our ability to come to closure concerning this cardiovascular problem. This task force addressed the following questions relevant to the role of the autonomic nervous system to the heart and the prevention of sudden cardiac death: (1) How can neural activity be assessed noninvasively? (2) Is the antifibrillatory effect of exercise mediated through changes in autonomic nervous system activity? (3) What is the current status of neurosurgical approaches to arrhythmia management? (4) To what extent can the pattern of autonomic activity be altered by behavioral training techniques? How can neural activity be assessed noninvasively? There are several methods available for the noninvasive measurement of neural activity in the heart; e.g., plasma catecholamine analysis, pharmacologic challenges, and analysis of heart rate variability. There was a consensus in the task force that some measures were clearly superior to others. Plasma levels of catecholamines are widely used as indicators of sympathetic activity. However, there is growing evidence that changes in catecholamine levels do not reflect well what happens at the cardiac level. ' Because of the high specificity of the autonomic nervous system, localized changes in cardiac sympathetic activity may not significantly modify the overall catecholamine plasma level. The analysis of baroreceptor reflexes may provide useful information. Infusion of the a-adrenergic agonist phenylephrine raises blood pressure and the attendant decrease in heart rate is an index of baroreflex sensitivity. A large increase in RR interval for a given blood pressure increase reflects a combination of powerful vagal reflexes and of relatively weak sympathetic reflexes. A small increase in the RR interval for the same blood pressure increase reflects a combination of weak vagal reflexes and of powerful sympathetic reflexes. These changes are the result of an algebraic summation of sympathetic and vagal reflexes, the latter being more important in determining the end-organ response at the sinus node level. Autonomic activity assessed through the analysis of baroreceptor reflexes has been demonstrated to be relevant to sudden cardiac death in experimental animals.2 The likelihood of the development of ventricular fibrillation in dogs with a healed myocardial infarction exposed to transient myocardial ischemia is greater in those animals with the most significant impairment in baroreflex sensitivity, i.e., with reduced vagal reflexes. Baroreceptor reflexes are depressed, although in a nonuniform manner, after myocardial infarction in dogs. Data from patients with myocardial infarction suggest that the same occurs in man. Furthermore, this reduction in baroreflex sensitivity after myocardial infarction is transient, as documented by its return, in the same patients, to normal values 1 year after infarction.4 Although this technique is rather easily applied to man, data should be interpreted with caution because several factors may influence the baroreceptor control of heart rate. Among these are ventricular function, levels of autonomic tone in the myocardium, and emotional state. Ongoing studies will determine if depressed baroreceptor reflexes are associated with an increased incidence of malignant arrhythmias.5 Should