Baroreceptor reflex control of heart rate: a predictor of sudden cardiac death.

Abstract

To explore the possibility that the analysis of autonomic reflexes could identify subgroups at high risk of ventricular fibrillation, we studied chronically instrumented mongrel dogs randomly divided into two groups.Twelve dogs served as controls and 17 were studied 3-4 weeks after anterior wall myocar- dial infarction (MI).After recovery, the dogs were given bolus i.v.injections of phenylephrine, 10 .tg/kg,and nitroprusside, 100 ptg/kg, to raise or lower systolic arterial pressure 30-50 mm Hg.The RR intervals were plotted against the systolic pressure during the preceding beats, and the slope (baroreflex slope) was determined by least-squares-fit linear regression.On a subsequent day, the left circumflex coronary artery was occluded for 2 minutes, beginning with the last minute of an exercise stress test and continuing for 1 minute after the cessation of exercise (MI group only).The dogs could be divided into two groups based on their response to this test; 11 dogs (65%) had ventricular fibrillation (susceptible), whereas six dogs (35%) did not (resistant).The baroreflex slope (control 20.49 ± 8.59; resistant 10.95 ± 4.68; susceptible 4.60 + 1.77 msec/mm Hg) and the heart rate response to a 30-mm Hg increase in arterial pressure (control -56.5 + 14.8; resistant -40.0 ± 12.2; susceptible -12.9 ± 5.0 beats/min) for the susceptible dogs were signifi- cantly different from those of the control and resistant dogs.This may indicate that the resistant dogs have a greater capability to activate strong vagal reflexes, which reduce vulnerability to ventricular fibrillation.We conclude that anterior wall MI significantly attenuates the baroreceptor reflex control of heart rate and that analysis of the heart rate response to arterial pressure increases allows identification of subgroups of dogs at higher risk for ventricular fibrillation.A prospective study in patients with MI is warranted.EARLY IDENTIFICATION of patients with ischemic heart disease at high risk for sudden death is a prerequisite for the use of aggressive preventive measures.Conversely, a more conservative approach may be used in low-risk patients.Important progress has been made in the risk stratification for both sudden and nonsudden cardiovascular deaths.'However, identi- fying patients at a high risk for ventricular fibrillation remains elusive.Some of these patients have been identified,4' but the underlying mechanisms, whether persistent electrical instability or major hemodynamic impairment, have not been clarified.A large body of evidence indicates that the autonomic nervous system plays a critical role in triggering ventricular fibrillation."'0In particular, vagal activa- tion is generally viewed as protective, ' while in- creased sympathetic activity predisposes the heart to ventricular fibrillation.12 3 Conversely, both pharma- cologic'4 and surgical'5 16 antiadrenergic interventions protect against sudden death due to ventricular fibrillation.Surprisingly, there has been no attempt to use auto- nomic reflex changes to discriminate among patients at high or low risk for sudden death.Changes in heart rate mediated by baroreceptor reflex can provide a mean- ingful way to assess autonomic neural control of the heart.Takeshita et al.'7 found that myocardial ische- mia attenuates baroreflex control of heart rate in re- sponse to arterial pressure increases.Clinical studies