1. THE AUTONOMIC NERVOUS SYSTEM AND EXPERIMENTAL CARDIAC ARRHYTHMIAS
The Sympathetic Nervous System and Cardiac Arrhythmias
A number of studies have indicated that spectral analysis of RR variability provides a robust method for measuring vagal modulation of RR intervals in man and animals. Under special circumstances, spectral analysis of RR variability can provide insight into the activity of the sympathetic nervous system as well. There is a large body of evidence that indicates that the sympathetic nervous system plays a significant role in the genesis of cardiac arrhythmias, including malignant ventricular arrhythmias, such as ventricular tachycardia and v'entricular fibrillation (2-7).
The parasympathetic Nervous System and Cardiac Arrhythmias: A Model of Sudden Cardiac Death.
The parasympathetic nervous system plays a protective role, decreasing the likelihood of malignant ventricular arrhythmias. Some of the most impressive studies on vagal protection from malignant ventricular arrhythmias were done by Schwartz, Stone and their colleagues in a dog model of sudden cardiac death. Anterior myocardial infarction was produced in the dogs by open chest ligation of the anterior descending coronary artery. During the same operation, an occluder was placed around the circumflex cororiary artery. The dogs were allowed to recover. After recovery. dogs were exercised on a treadmill to near maximal heart rates, about 200 per minute, at which time the circumflex coronary was occluded. The sudden coronary occlusion produced myocardial ischemia in the setting of decreased vagal activity and increased sympathetic activity. Under these circumstances, about 55% of the dogs developed ventricular fibrillation (VF). The binary response to the test situation was quite reproducible, susceptible dogs developed VF epeatedly while non- susceptible dogs did not.
Billman et al. (11) showed that VF in response to the exercise-ischemia challenge could be predicted by measuring baroreflex sensitivity. baroreflex sensitivity was measured as the change in RR interval as a function of the increase in systolic blood pressure after an intravenous injection of phenylephrine. Dogs with low baroreflex sensitivity were susceptible to ventricular fibrillation when challenged with the exercise-ischemia test whereas dogs with high baroreflex sensitivity were not (see Figure I). The baroreflex sensitivity dropped after myocardial infarction, about 7070 of dogs showed a substantial drop from pre-infarction values. However, baroreflex sensitivity tended to aintain its rank order after infarction, i.e., the dogs with the lowest pre-infarction baroreflex sensitivity tended to have the lowest baroreflex sensitivity after infarction and, thus, be susceptible to ventricular fibrillation during the exercise-ischemia challenge. Thus, risk to ventricular fibrillation during myocardial Ischemia can be predicted by baroreflex sensitivity measured in normal dogs before experimental myocardial infarction is induced. Furthermore, susceptible dogs could be converted to non-susceptible status by exercise training, which Increased baroreflex sensitivity ( 12).
A smaller set of experiments in the same model of sudden death has shown that RR variability drops after myocardial infarction in the dog (1-3). Also, dogs with lower values for vagal measures of RR variability after infarction have a greater chance of developing ventricular fibrillation during the exercise-ischemia challenge (13). However, pre-infarction values for RR variability did not predict post infarction values or the response to the exercise-ischemia challenge (14).
