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Circulation, Vol 88, 472-480, Copyright © 1993 by American Heart Association
EM Gilbert, A Sandoval, P Larrabee, DG Renlund, JB O'Connell and MR Bristow
BACKGROUND. In subjects with heart failure, angiotensin converting enzyme
inhibitors exhibit mild systemic antiadrenergic effects, as deduced from
treatment-related lowering of systemic venous norepinephrine levels. The
effects of angiotensin converting enzyme inhibitors on cardiac adrenergic
drive in subjects with heart failure has not previously been investigated.
METHODS AND RESULTS. In a placebo- controlled, double-blind crossover study
of 14 patients, we measured cardiac and systemic adrenergic drive,
myocardial and lymphocyte beta- adrenergic receptors, and hemodynamic
changes at baseline and after 12 weeks of therapy. Relative to placebo,
lisinopril therapy was associated with only minimal, statistically
insignificant changes in hemodynamics, a significant increase in myocardial
beta-receptor density, no significant (P < .05) changes in cardiac or
systemic adrenergic drive, and no detectable change in lymphocyte
beta-receptor density. When subjects were rank ordered into groups with the
highest and lowest coronary sinus norepinephrine levels, those with the
highest norepinephrine levels exhibited significant decreases in central
venous norepinephrine, coronary sinus norepinephrine, and an increase in
myocardial beta-receptor density relative to changes in placebo or relative
to baseline values. Subjects with lower cardiac adrenergic drive exhibited
no significant changes in coronary sinus or systemic norepinephrine levels
or in myocardial beta-receptor density. CONCLUSIONS. The angiotensin
converting enzyme inhibitor lisinopril lowered cardiac adrenergic drive and
increased beta-receptor density in subjects with increased cardiac
adrenergic drive but had no effects on these parameters in subjects with
normal cardiac adrenergic drive. These data suggest that cardiac
antiadrenergic properties contribute to the efficacy of angiotensin
converting enzyme inhibitor in subjects with heart failure.
ARTICLES
Lisinopril lowers cardiac adrenergic drive and increases beta-receptor density in the failing human heart
Division of Cardiology, University of Utah School of Medicine, Salt Lake City.
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