Circulation, Vol 80, 314-323, Copyright © 1989 by American Heart Association
WS Colucci, JP Ribeiro, MB Rocco, RJ Quigg, MA Creager, JD Marsh, DF Gauthier and LH Hartley
The mechanism responsible for the attenuated heart rate (HR) response to
exercise in patients with congestive heart failure (CHF) was investigated
in 46 normal subjects and 59 patients with CHF stratified by peak exercise
oxygen consumption (VO2). The peak exercise HR and the increment in HR from
rest to peak exercise were decreased in CHF patients, and both correlated
strongly with peak VO2 (r = 0.810, p less than 0.0001; r = 0.863, p less
than 0.0001, respectively). Peak exercise norepinephrine level (NE) and the
increment in NE from rest to peak exercise were not attenuated in CHF
patients. Resting NE was elevated in CHF patients and correlated inversely
with peak VO2 (r = - 0.595, p less than 0.001). However, no significant
correlation occurred between peak VO2 and either peak exercise NE or the
exercise increment in NE. The ratio of the exercise increments in HR and
NE, and indirect index of sinoatrial node sympathetic responsiveness, was
markedly reduced in CHF patients and was inversely related to the severity
of exercise impairment. Likewise, the HR response to a graded isoproterenol
infusion was markedly reduced in CHF patients. Age- matching of normal
subjects and CHF patients did not affect the foregoing observations.
Infusion of CHF patients with the phosphodiesterase inhibitor milrinone
caused a significant increase in the ratio of the exercise increments in HR
and NE. These data strongly suggest that the attenuated HR response to
exercise in CHF patients is due, at least in part, to postsynaptic
desensitization of the beta- adrenergic receptor pathway.
ARTICLES
Impaired chronotropic response to exercise in patients with congestive heart failure. Role of postsynaptic beta-adrenergic desensitization
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
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