Periodic fluctuations in the R-R interval have been used as noninvasive measures of cardiac autonomic tone. For example, a reduced heart rate variability has been shown to correlate with an increased mortality in patients recovering from myocardial infarction. The effects that physiologic perturbations such as exercise have on this heart rate variability have not been investigated. Therefore, heart rate variability was measured throughout a submaximal exercise test in 36 mongrel dogs with healed anterior myocardial infarctions. The amplitude of the respiratory component (0.24-1.04 Hz) was determined by time-series analysis techniques and was used as an index of cardiac vagal tone. On a subsequent day, a 2-minute coronary occlusion was initiated during the last minute of exercise. Twenty-two animals developed ventricular fibrillation (susceptible), whereas 14 animals did not (resistant). Exercise elicited a significantly greater increase in heart rate (resistant, 205.4 +/- 7.1; susceptible, 227.0 +/- 5.4 beats/min) in susceptible animals, which was accompanied by a greater reduction in the cardiac vagal tone index (resistant, 2.7 +/- 0.3; susceptible, 1.1 +/- 0.2 ln msec2) as compared with resistant animals. Conversely, atropine sulfate (50 micrograms/kg) given during exercise elicited a greater heart rate increase in the resistant dogs (heart rate change: resistant, 54.2 +/- 7.0; susceptible, 18.7 +/- 4.4 beats/min). Taken together, these data suggest that exercise elicited a greater reduction in cardiac vagal tone in animals known to be susceptible to ventricular fibrillation.

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There is increasing evidence that the use of cocaine can trigger lethal cardiac events, including ventricular fibrillation. The mechanism responsible for these lethal cardiac arrhythmias remains to be determined. Therefore, 13 mongrel dogs were instrumented so that heart rate, left ventricular pressure (LVP), and d(LVP)/dt could be measured. After a 3- to 4-wk recovery period, the left circumflex coronary artery was occluded for 2 min, beginning with the last minute of an exercise stress test and continuing for 1 min after the cessation of exercise. None of the dogs developed cardiac arrhythmias during the control exercise plus ischemia test. On a subsequent day, the test was repeated after the injection of cocaine HCl (1.0 mg/kg). Cocaine significantly (P less than 0.01) elevated heart rate, systolic LVP, and d(LVP)/dt, and it elicited cardiac arrhythmias in 12 of the 13 animals during the exercise plus test. In fact, 11 animals developed ventricular fibrillation. Verapamil, a calcium channel antagonist (250 micrograms/kg), attenuated the hemodynamic effects of cocaine and prevented the development of ventricular arrhythmias. These data suggest that cocaine can induce ventricular fibrillation during myocardial ischemia and that these lethal arrhythmias may be prevented by a calcium channel antagonist.

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