Why do patients with congestive heart failure tolerate the initiation of β-blocker therapy?

Howard L. Haber, Christopher L. Simek, Lawrence W. Gimple, James D. Bergin, Komathi Subbiah, Ananda R. Jayaweera, Eric R. Powers, Marc D. Feldman

Research output: Contribution to journalArticlepeer-review

83 Scopus citations


Background. Despite its negative inotropic effects, the initiation of β-adrenergic blockade is tolerated by patients with congestive heart failure (CHF). Accordingly, we examined the acute hemodynamic effects of β-adrenergic blockade on systolic and diastolic left ventricular (LV) function and ventriculo-arterial coupling. In addition, isolated myocardium from patients with CHF shows selective β1-receptor downregulation, implying a greater role for the β2-receptor in maintaining in vivo LV contractility. As a secondary aim, we hypothesized that nonselective β-adrenergic blockade would have greater negative inotropic effect than β1-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 β-blocker propranolol or the β-selective blocker metoprolol. LV pressure-volume relations were obtained before and after the administration of intravenous β-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 · M-2), 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 β2-receptor in CHF. The preservation of passive diastolic function and ventriculo-arterial coupling provide possible explanations of why β-adrenergic blockade is tolerated by patients with CHF.

Original languageEnglish (US)
Pages (from-to)1610-1619
Number of pages10
Issue number4
StatePublished - Oct 1993
Externally publishedYes


  • Cardiomyopathies
  • Elastance
  • β-adrenergic receptors

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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