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 journalArticle

82 Citations (Scopus)

Abstract

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
JournalCirculation
Volume88
Issue number4
StatePublished - Oct 1993
Externally publishedYes

Fingerprint

Heart Failure
Adrenergic Agents
Left Ventricular Function
Metoprolol
Therapeutics
Ventricular Pressure
Propranolol
Intravenous Administration
Myocardium
Down-Regulation
Hemodynamics
Blood Pressure
Lung

Keywords

  • β-adrenergic receptors
  • Cardiomyopathies
  • Elastance

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Haber, H. L., Simek, C. L., Gimple, L. W., Bergin, J. D., Subbiah, K., Jayaweera, A. R., ... Feldman, M. D. (1993). Why do patients with congestive heart failure tolerate the initiation of β-blocker therapy? Circulation, 88(4), 1610-1619.

Why do patients with congestive heart failure tolerate the initiation of β-blocker therapy? / Haber, Howard L.; Simek, Christopher L.; Gimple, Lawrence W.; Bergin, James D.; Subbiah, Komathi; Jayaweera, Ananda R.; Powers, Eric R.; Feldman, Marc D.

In: Circulation, Vol. 88, No. 4, 10.1993, p. 1610-1619.

Research output: Contribution to journalArticle

Haber, HL, Simek, CL, Gimple, LW, Bergin, JD, Subbiah, K, Jayaweera, AR, Powers, ER & Feldman, MD 1993, 'Why do patients with congestive heart failure tolerate the initiation of β-blocker therapy?', Circulation, vol. 88, no. 4, pp. 1610-1619.
Haber HL, Simek CL, Gimple LW, Bergin JD, Subbiah K, Jayaweera AR et al. Why do patients with congestive heart failure tolerate the initiation of β-blocker therapy? Circulation. 1993 Oct;88(4):1610-1619.
Haber, Howard L. ; Simek, Christopher L. ; Gimple, Lawrence W. ; Bergin, James D. ; Subbiah, Komathi ; Jayaweera, Ananda R. ; Powers, Eric R. ; Feldman, Marc D. / Why do patients with congestive heart failure tolerate the initiation of β-blocker therapy?. In: Circulation. 1993 ; Vol. 88, No. 4. pp. 1610-1619.
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abstract = "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.",
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AU - Haber, Howard L.

AU - Simek, Christopher L.

AU - Gimple, Lawrence W.

AU - Bergin, James D.

AU - Subbiah, Komathi

AU - Jayaweera, Ananda R.

AU - Powers, Eric R.

AU - Feldman, Marc D

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N2 - 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.

AB - 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.

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