Circulation, Vol 88, 1610-1619, Copyright © 1993 by American Heart Association
HL Haber, CL Simek, LW Gimple, JD Bergin, K Subbiah, AR Jayaweera, ER Powers and MD Feldman
BACKGROUND. Despite its negative inotropic effects, the initiation of
beta-adrenergic blockade is tolerated by patients with congestive heart
failure (CHF). Accordingly, we examined the acute hemodynamic effects of
beta-adrenergic blockade on systolic and diastolic left ventricular (LV)
function and ventriculo-arterial coupling. In addition, isolated myocardium
from patients with CHF shows selective beta 1-receptor downregulation,
implying a greater role for the beta 2-receptor in maintaining in vivo LV
contractility. As a secondary aim, we hypothesized that nonselective
beta-adrenergic blockade would have greater negative inotropic effect than
beta 1-blockade in patients with CHF. METHODS AND RESULTS. Patients with
clinical CHF (n = 24) and control patients without CHF (n = 24) were given
either the nonselective beta-blocker propranolol or the beta 1-selective
blocker metoprolol. LV pressure-volume relations were obtained before and
after the administration of intravenous beta-blocker, and measures of LV
systolic and diastolic function were examined. Patients with CHF had a
deterioration in LV systolic function with a fall in LV systolic pressure
(139 +/- 6 to 125 +/- 6 mm Hg), cardiac index (2.56 +/- 0.11 to 2.20 +/-
0.11 mL.min-1 x M-1), dP/dtmax (1173 +/- 63 to 897 +/- 50 mm Hg/s), and
end-systolic elastance (0.88 +/- 0.10 to 0.64 +/- 0.10 mm Hg/mL), P <
.05 for all. Although there was deterioration of active LV relaxation
(isovolumetric relaxation 63 +/- 2 to 73 +/- 3 milliseconds, peak filling
rate 543 +/- 33 to 464 +/- 28 mL/s, P < .05 for both), there was no
change in passive LV diastolic function (pulmonary capillary wedge, 24 +/-
2 to 24 +/- 1 mm Hg; chamber stiffness, 0.0154 +/- 0.0005 to 0.0163 +/-
0.0005 mL-1, P = NS for both), and a decrease in afterload (arterial
elastance 3.85 +/- 0.31 to 3.38 +/- 0.24 mm Hg/mL, P < .05). Control
patients had no change in these parameters other than a prolongation of
isovolumetric relaxation (48 +/- 1 to 55 +/- 2 milliseconds, P < .05).
The effects of propranolol (n = 12) versus metoprolol (n = 12) on these
parameters in patients with CHF were similar. CONCLUSIONS. These data do
not support a greater in vivo physiological role of the myocardial beta
2-receptor in CHF. The preservation of passive diastolic function and
ventriculo-arterial coupling provide possible explanations of why
beta-adrenergic blockade is tolerated by patients with CHF.
ARTICLES
Why do patients with congestive heart failure tolerate the initiation of beta-blocker therapy?
Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville 22908.
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