Circulation, Vol 83, 945-952, Copyright © 1991 by American Heart Association
TG Farrell, V Paul, TR Cripps, M Malik, ED Bennett, D Ward and AJ Camm
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.
ARTICLES
Baroreflex sensitivity and electrophysiological correlates in patients after acute myocardial infarction
Department of Cardiological Sciences, St. George's Hospital, London, UK.
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