Chronic beta-blocker treatment in patients with advanced heart failure

Teisman, Ard; Veldhuisen, Dirk J. van; Boomsma, Frans; Kam, P.J. de; Tjeerdsma, Geert; Pinto, Yigal M.; Zeeuw, Dick de; Gilst, Wiek H. van

doi:10.1016/s0167-5273(00)00172-8

Cited by 27 publications

(11 citation statements)

References 20 publications

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“…Moreover, elevated plasma angiotensin II levels were related to increased active renin protein and plasma angiotensin I levels. A previous study suggested that betablockers reduce the activity of the renin angiotensin system [18]. Our data support this suggestion (Fig.…”

Section: Discussionsupporting

confidence: 91%

Determinants of increased angiotensin II levels in severe chronic heart failure patients despite ACE inhibition

Wal

Plokker

Lok

et al. 2006

International Journal of Cardiology

120

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Section: Discussionsupporting

confidence: 91%

Determinants of increased angiotensin II levels in severe chronic heart failure patients despite ACE inhibition

Wal

Plokker

Lok

et al. 2006

International Journal of Cardiology

120

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“…Six‐months treatment with carvedilol in the present study clearly afforded a beneficial effect on symptoms, hospitalization rate and left ventricular remodeling, concommitent with a 50% reduction in active renin in the plasma, raising the possibility that a marked down‐regulation of the renin–angiotensin system may participate in the beneficial effect of this drug. A decrease in renin activity with betablockers in CHF patients has also been reported in other open‐label studies [7,8] and in the RESOLVD study [9].…”

Section: Discussionsupporting

confidence: 76%

Beneficial effects of carvedilol on angiotensin‐converting enzyme activity and renin plasma levels in patients with chronic heart failure

Solal

Jondeau

Beauvais

et al. 2004

European J of Heart Fail

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Objective: To assess the effects of carvedilol treatment on the renin-angiotensin system in patients with chronic heart failure (CHF). Background: Carvedilol improves survival of patients suffering from CHF but the effects of the drug on angiotensinconverting enzyme (ACE) activity, renin and aldosterone are not well characterized in patients receiving an ACE inhibitor. Methods: A randomized, multicenter, double-blind, 6-month, placebo-controlled study of carvedilol vs. placebo was conducted in 64 CHF patients. Circulating levels of ACE activity, active renin and aldosterone as well as left ventricular diameters and ejection fraction by echography were assessed. Results: During the study, left ventricular ejection fraction increased from 25"11% to 31"12% with carvedilol and from 27"12% to 28"12% with placebo (Ps0.03). This beneficial effect was associated with marked blunting of active renin secretion (y53% in the carvedilol group vs.y13% in the placebo group, Ps0.04). ACE activity was reduced by 30% in the carvedilol group (Ps0.07 vs. placebo). Aldosterone was not changed. Conclusion: Carvedilol markedly reduced the increase in active renin observed with time despite ACE-inhibitors and tended to decrease ACE activity. These findings may in part explain the beneficial actions of carvedilol and highlights the profound effect of betablockade on renin in patients already receiving ACE-inibitors.

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“…β‐blockers have a renin‐inhibiting effect and therefore inhibit the sympathetic system as well as the RAAS. Indeed, the suppression of angiotensin II by an ACE inhibitor is more effective in patients who are also treated with a β‐blocker, and the escape of angiotensin II from ACE inhibition is attenuated in patients treated with a β‐blocker [22,23]. There is evidence that the initiation of a β‐blocker prior to an ACE inhibitor prevents renal insufficiency as a side effect of the ACE inhibitor [24,25].…”

Section: Rationalementioning

confidence: 99%

Comparison of treatment initiation with bisoprolol vs. enalapril in chronic heart failure patients: rationale and design of CIBIS‐III

Willenheimer

Erdmann

Folláth

et al. 2004

European J of Heart Fail

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Background: Angiotensin-converting-enzyme (ACE) inhibitors and b-blockers are standard therapy for chronic heart failure (CHF). b-blockers are recommended to be initiated after ACE-inhibitors, but this order is not evidence based. The initiation order may be important since many, especially elderly CHF patients cannot tolerate target doses of both. Data suggest that b-blockers may be more important to CHF patients than ACE-inhibitors, especially in early stages of CHF. Aims: To compare the effect on combined death or hospitalisation of initial monotherapy with either bisoprolol or enalapril, followed by combination therapy. Methods: One-thousand CHF patients without ACE-inhibitor, b-blocker or angiotensin-receptor-blocker therapy will be randomised 1:1 to monotherapy with either enalapril or bisoprolol for 6 months, followed by combined therapy for 6-18 months. The primary objective is to show non-inferiority for bisoprolol-first vs. enalapril-first regarding combined death or hospitalisation. If that is shown, superiority for bisoprolol-first will be tested. Conclusions: If the trial shows non-inferiority for bisoprolol-first vs. enalaprilfirst, the first CHF therapy may be chosen based on individual judgement in each patient. If bisoprolol-first is superior to enalapril-first, a b-blocker should be given prior to an ACE-inhibitor in CHF, and the paradigm of testing CHF compounds against a background of ACE-inhibitor therapy will be challenged.

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Chronic beta-blocker treatment in patients with advanced heart failure

Cited by 27 publications

References 20 publications

Determinants of increased angiotensin II levels in severe chronic heart failure patients despite ACE inhibition

Determinants of increased angiotensin II levels in severe chronic heart failure patients despite ACE inhibition

Beneficial effects of carvedilol on angiotensin‐converting enzyme activity and renin plasma levels in patients with chronic heart failure

Comparison of treatment initiation with bisoprolol vs. enalapril in chronic heart failure patients: rationale and design of CIBIS‐III

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