Article

Effects of nebivolol on left ventricular function in elderly patients with chronic heart failure: results of the ENECA study.

Institute of Cardiology, University of Debrecen, 4004 Debrecen, P.O.B.: 1, Hungary.
European Journal of Heart Failure (Impact Factor: 5.25). 06/2005; 7(4):631-9. DOI: 10.1016/j.ejheart.2004.10.015
Source: PubMed

ABSTRACT To examine the effect of the beta(1)-selective beta-blocker nebivolol, administered as add-on therapy, on left ventricular function in 260 elderly patients (>65 years) with chronic heart failure (CHF).
The principal inclusion criteria were (1) NYHA class II-IV CHF and (2) a left ventricular ejection fraction (LVEF) <= 35%. The primary end-point was the change in LVEF in response to nebivolol treatment for 8 months.
Baseline LVEF values in the two groups were as follows: nebivolol 25.41+/-7.09% and control 26.41+/-5.55%. LVEF improved significantly (p=0.027) more in the nebivolol group (6.51+/-9.15%) than in the control group (3.97+/-9.20%), the relative improvement (percentage increase in the initial value) being 35.70+/-57.62% in the nebivolol group and 19.19+/-40.96% (p=0.008) in the placebo group. Examination of different subgroups did not reveal any heterogeneity in the effects of nebivolol treatment vs. placebo treatment. There were no significant differences between the nebivolol and placebo groups as concerns the changes in clinical status, quality of life, or safety parameters.
The findings of the ENECA study confirmed that nebivolol significantly improved cardiac function and proved to be safe and well tolerated in elderly patients with signs of CHF and an impaired LVEF.

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    ABSTRACT: The use of β-blockers (BB) in heart failure (HF) has been considered a contradiction for many years. Considering HF simply as a state of inadequate systolic function, BB were contraindicated because of their negative effects on myocardial contractility. Nevertheless, evidence collected in the past years have suggested that additional mechanisms, such as compensatory neuro-humoral hyperactivation or inflammation, could participate in the pathogenesis of this complex disease. Indeed, chronic activation of the sympathetic nervous system, although initially compensating the reduced cardiac output from the failing heart, increases myocardial oxygen demand, ischemia and oxidative stress; moreover, high catecholamine levels induce peripheral vasoconstriction and increase both cardiac pre- and after-load, thus determining additional stress to the cardiac muscle (1). As a consequence of such a different view of the pathogenic mechanisms of HF, the efficacy of BB in the treatment of HF has been investigated in numerous clinical trials. Results from these trials highlighted BB as valid therapeutic tools in HF, providing rational basis for their inclusion in many HF treatment guidelines. However, controversy still exists about their use, in particular with regards to the selection of specific molecules, since BB differ in terms of adrenergic β-receptors selectivity, adjunctive effects on α-receptors, and effects on reactive oxygen species and inflammatory cytokines production. Further concerns about the heterogeneity in the response to BB, as well as the use in specific patients, are matter of debate among clinicians. In this review, we will recapitulate the pharmacological properties and the classification of BB, and the alteration of the adrenergic system occurring during HF that provide a rationale for their use; we will also focus on the possible molecular mechanisms, such as genetic polymorphisms, underlying the different efficacy of molecules belonging to this class.
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