Circulation, Vol 90, 976-982, Copyright © 1994 by American Heart Association
PB Adamson, MH Huang, E Vanoli, RD Foreman, PJ Schwartz and SS Hull Jr
BACKGROUND: Heart rate (HR) variability is a marker of tonic cardiac
autonomic activity and contributes in assessing risk for sudden death after
myocardial infarction. Recent clinical observations have indicated that
attenuation of HR variability, which occurs after myocardial infarction,
may be transient. This study addresses the issue of whether autonomic
control of heart rate recovers at different rates after myocardial
infarction in subjects at high and low risk for ventricular fibrillation
(VF). METHODS AND RESULTS: Thirty dogs, 22 with myocardial infarction and 8
sham-prepared animals, completed the study. Changes and recovery in cardiac
autonomic activity after myocardial infarction were examined by measuring
HR variability before and at defined intervals during the first 30 days
after infarction. Each HR variability measurement was made before and after
beta-blockade in dogs at high (n = 10) and low (n = 12) risk for VF.
Arrhythmia risk was determined on the basis of development of VF during
exercise and transient myocardial ischemia 30 days after infarction. No
sham- prepared animals developed VF. Preinfarction measurements of HR
variability were not different between the groups before beta-blockade, but
HR variability increased much more in response to beta-blockade in animals
destined to be resistant compared with susceptible animals (289 +/- 26 to
369 +/- 35 msec, delta 27.7%, versus 270 +/- 36 to 283 +/- 34 milliseconds,
delta 4.8%, respectively, P < .01). Immediately after infarction, HR
variability was significantly attenuated in all dogs, but in the resistant
dogs it recovered to pre-myocardial infarction levels within 10 days. After
the infarction, beta-blockade did not increase HR variability in either
group of animals. Postoperative increases in HR variability from
beta-blockade were preserved in the sham group. Susceptible animals were
characterized by a persistent attenuation of HR variability throughout the
30 days. CONCLUSIONS: The depression in HR variability produced by
myocardial infarction has a clearly different temporal recovery pattern
between low- and high-risk animals. After myocardial infarction,
beta-adrenergic blockade does not alter HR variability, thus preserving its
predictive value. Before myocardial infarction, however, beta-blockade
increases HR variability only in the animals destined to be at low risk for
lethal arrhythmias after the infarction. The recovery pattern of HR
variability after myocardial infarction may contribute to the early
recognition of individuals at high risk for sudden death.
ARTICLES
Unexpected interaction between beta-adrenergic blockade and heart rate variability before and after myocardial infarction. A longitudinal study in dogs at high and low risk for sudden death
Department of Internal Medicine, University of Oklahoma, HSC, Oklahoma City.
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