Circulation, Vol 84, 1040-1048, Copyright © 1991 by American Heart Association
JD Parker, JS Landzberg, JA Bittl, I Mirsky and WS Colucci
BACKGROUND. We tested the hypothesis that beta-adrenergic receptor-
stimulated acceleration of left ventricular (LV) isovolumic relaxation
(i.e., positive lusitropic response) is attenuated in patients with severe
congestive heart failure (CHF) compared with patients without LV
dysfunction or CHF. METHODS AND RESULTS. The beta-adrenergic agonist
dobutamine was infused by the intracoronary route in 14 subjects (normal
group, six; CHF patients, eight) and by the intravenous route in a second
group of 14 subjects (normal group, four; CHF patients, 10). The positive
inotropic response to intracoronary or intravenous dobutamine was
substantially and significantly reduced in the patients with CHF. LV
isovolumic relaxation rate was determined by the methods of Weiss (TL),
Mirsky (T1/2), and by a nonlinear regression technique (TNL). LV isovolumic
relaxation assessed by all three methods was significantly prolonged in CHF
patients compared with normal subjects. Intracoronary and intravenous
infusions of dobutamine caused significant acceleration of LV isovolumic
relaxation in both normal subjects and patients with CHF. The magnitude of
the dobutamine- stimulated acceleration of isovolumic relaxation in
patients with CHF was comparable with that in normal subjects. CONCLUSIONS.
These data demonstrate that beta-adrenergic receptor stimulation causes
significant acceleration of LV isovolumic relaxation in both normal
subjects and patients with severe CHF. Coronary to our hypothesis, the
lusitropic response to beta-adrenergic stimulation is well preserved in
patients with severe CHF despite substantial attenuation of the beta-
adrenergic positive inotropic response. These findings have potentially
important implications regarding the physiology and pharmacology of
adrenergically mediated LV relaxation in humans.
ARTICLES
Effects of beta-adrenergic stimulation with dobutamine on isovolumic relaxation in the normal and failing human left ventricle
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
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