Baroreflex sensitivity and electrophysiological correlates in patients after acute myocardial infarction.

TG Farrell, V Paul, TR Cripps, M Malik, ED Bennett… - Circulation, 1991 - Am Heart Assoc
TG Farrell, V Paul, TR Cripps, M Malik, ED Bennett, D Ward, AJ Camm
Circulation, 1991Am Heart Assoc
BACKGROUND Several studies have identified transient disturbances of autonomic function
during the acute and recovery phases of myocardial infarction, and it has recently been
suggested that survivors of acute myocardial infarction with depressed vagal tone may be at
increased risk of sudden or arrhythmic death. METHODS AND RESULTS To investigate this
hypothesis, parasympathetic function was assessed by arterial baroreflex sensitivity (BRS)
testing (using the phenylephrine method) and by heart rate variability (HRV) analysis from …
BACKGROUND
Several studies have identified transient disturbances of autonomic function during the acute and recovery phases of myocardial infarction, and it has recently been suggested that survivors of acute myocardial infarction with depressed vagal tone may be at increased risk of sudden or arrhythmic death.
METHODS AND RESULTS
To investigate this hypothesis, parasympathetic function was assessed by arterial baroreflex sensitivity (BRS) testing (using the phenylephrine method) and by heart rate variability (HRV) analysis from 24-hour Holter recording in 68 patients at day 7-10 after infarction. The relation between autonomic tone and markers of arrhythmic propensity, including programmed ventricular stimulation (PVS) and late potentials in addition to other clinical variables, was examined. BRS for the whole group was 7.0 +/- 4.7 msec/mm Hg and was inversely correlated with age (r = 0.53, p less than 0.001) but not with left ventricular ejection fraction (r = 0.035, p = NS). In those patients in whom sustained monomorphic ventricular tachycardia (SMVT) was induced, BRS was significantly reduced (p = 0.001) as was HRV (p = 0.007) and left ventricular ejection fraction (p = 0.022). The strongest association between any variable (including HRV, BRS, late potentials, left ventricular ejection fraction, exercise testing, Q waves, and infarct site) and the induction of sustained monomorphic ventricular tachycardia was depressed BRS with a relative risk of 36.28 (95% confidence interval, 5-266).
CONCLUSIONS
This study confirms that depressed BRS identifies a subgroup at high risk for arrhythmic events after myocardial infarction and that programmed ventricular stimulation may be safely limited to this group without any loss of predictive accuracy.
Am Heart Assoc