-blockade with nebivolol for prevention of acute ischaemic events in elderly patients with heart failure

Ambrosio, Giuseppe; Flather, Marcus; Böhm, Michael; Cohen‐Solal, Alain; Murrone, Adriano; Mascagni, Flavio; Spinucci, Giulio; Conti, M.; Veldhuisen, Dirk J. van; Tavazzi, Luigi; Coats, Andrew J.S.

doi:10.1136/hrt.2010.207365

Cited by 38 publications

(30 citation statements)

References 34 publications

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“…The observation that dl-nebivolol reduced significantly all-cause mortality in elderly patients with congestive heart failure of ischemic etiology, whereas first-generation antihypertensive β-blockers do not prevent ischemic cardiovascular events when compared with other antihypertensive interventions, 50 suggests that increased platelet-derived NO production in vivo may confer enhanced cardiovascular protection.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Platelet Nitric Oxide Production by Nebivolol Prevents Thrombosis

Momi

Caracchini

Falcinelli

et al. 2014

ATVB

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H ypertension is associated with an increased risk of arterial thrombotic events, such as stroke and myocardial infarction, 1 in which platelets are deeply involved. Previous studies have shown that β-adrenoceptor blockers reduce platelet activation and aggregation, 2 but this does not seem to be a class effect because not all β-blockers share this property. 3 dl-Nebivolol (a racemic mixture of d-and l-nebivolol) is a third-generation β 1 adrenoceptor-selective antagonist that, besides its β-blockade-mediated hypotensive effect, possesses direct vasodilatory properties through a mechanism involving the l-arginine/nitric oxide (NO) pathway. 4,5 Of the 2 enantiomers forming the racemic mixture of dl-nebivolol, d-nebivolol, which has an ≈200-fold greater affinity for β 1 -adrenoceptors than that of l-nebivolol, seems to be mainly responsible of selective β-blockade, 6 whereas the l-form is the main effector of the endothelium-dependent vasorelaxant effect. 7,8 dl-Nebivolol exerts its vasodilatory action by activating endothelial nitric oxide synthase (eNOS) and by preventing eNOS uncoupling, thus enhancing NO production. 9 Endothelium-derived NO is a powerful inhibitor of platelet activation and an antithrombotic agent. 10,11 Besides endothelium, eNOS is present in other cells, including platelets, [12][13][14] and several in vitro and in vivo observations in animals and in humans suggest that platelet-derived NO plays a significant anti-inflammatory and antithrombotic role. [15][16][17][18][19] dl-Nebivolol was previously reported to inhibit ADP-and collagen-induced aggregation of human platelets in vitro, 20 an effect prevented by the previous exposure of platelets to a NOS inhibitor, such as L-NG-nitroarginine methyl ester, and enhanced by preincubation with l-arginine, the substrate of NOS, suggesting that the antiplatelet effect of dl-nebivolol is mediated by an enhanced release of NO from platelets. 4 © 2014 American Heart Association, Inc. Objective-dl-Nebivolol, a selective β1-adrenergic receptor antagonist, besides its hypotensive activity exerts vasodilatory and platelet inhibitory effects in vitro by a mechanism involving nitric oxide (NO). Our aim was to evaluate whether nebivolol exerts in vivo antithrombotic effects, to unravel the mechanism of this action and to clarify the relative roles of its 2 enantiomers: d-and l-nebivolol. Methods and Results-In wild-type mice, dl-nebivolol, l-nebivolol, and d-nebivolol, but not bisoprolol, reduced mortality consequent to platelet pulmonary thromboembolism induced by the intravenous injection of collagen plus epinephrine (−44%, −45%, −29%, respectively; P<0.05), whereas in eNOS −/− mice only dl-nebivolol and d-nebivolol were effective. dl-Nebivolol, l-and d-nebivolol reduced photochemical damage-induced femoral artery thrombosis in wild-type mice, whereas in eNOS −/− mice only dl-nebivolol and d-nebivolol were active. Moreover, dl-nebivolol and l-nebivolol increased plasma, urinary-, and platelet-derived nitrites and nitrates (NOx), NO degradation products, in ...

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Section: Discussionmentioning

confidence: 99%

Stimulation of Platelet Nitric Oxide Production by Nebivolol Prevents Thrombosis

Momi

Caracchini

Falcinelli

et al. 2014

ATVB

View full text Add to dashboard Cite

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“…Recently, the fixed dose combination of nebivolol and valsartan was found effective and safe in a large clinical trial of more than 4,000 hypertensive patients [30]. Nebivolol use has been also tested and proven effective and tolerated in patients with heart failure [31][32][33][34].…”

Section: Discussion Nebivololmentioning

confidence: 99%

Erectile Function in Cardiovascular Disease and Hypertension: the Role of Nebivolol

Manolis¹,

Doumas²

2016

J Hypertens (Los Angel)

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Beta blockers are used for the management of arterial hypertension and are gold standard treatment for coronary artery disease and heart failure, medical conditions that affect large numbers of older patients and are associated with very high morbidity and mortality rates.Lifelong therapy in primary and secondary prevention (without and with established cardiovascular disease, respectively) is limited by low adherence to drugs which is accompanied by increased mortality. Drug adverse events and impaired quality of life are among the main causes of poor adherence to therapy. Erectile dysfunction is the 'prima ballerina' of drug-induced life quality impairment. Beta blockers exert detrimental effects on erectile function. In contrast, nebivolol (a third generation beta blocker with vasodilating properties and proven efficacy in patients with hypertension and heart failure) does not share the unfavourable effects of other beta blockers on erectile function due to increased nitric oxide bioavailability.Therefore, Nebivolol represents an attractive option for patients with hypertension, heart failure, and other related diseases who need to be treated with beta blockers.

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“…W grupie leczonej nebiwololem stwierdzono istotną (p = 0,008) redukcję incydentów niedokrwiennych (15,9%) w porównaniu z grupą kontrolną (10,7%). Jak przedstawiono na rycinie 4, zmniejszenie częstości incydentów sercowo-naczyniowych u chorych leczonych nebiwololem stwierdzono niezależnie od płci, wieku, wielkości frakcji wyrzucania lewej komory i obecności cukrzycy [39].…”

Section: Dy Of Effects Of Nebivolol Intervention On Outcomes and Rehounclassified

Protective effect of nebivolol to prevent target organ damage in hypertension

Widecka

2018

Arterial Hypertension

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StreszczeniePowikłania sercowo-naczyniowe (przerost lewej komory, migotanie przedsionków, niewydolność serca, incydenty wieńcowe, starzenie się naczyń i przyspieszona miażdżyca) są główną przyczyną zgonów u chorych z nadciśnieniem tętniczym. Stres oksydacyjny i aortalne ciśnienie centralne odgrywają kluczową rolę w patofizjologii systemu sercowo-naczyniowego oraz powikłań sercowo-naczyniowych. Leki przeciwnadciśnieniowe, nawet w obrębie tej samej klasy, wywierają różny wpływ na wskaźniki sztywności tętnic i funkcję śródbłonka. Nebiwolol jest b-adrenolitykiem trzeciej generacji o działaniu wazodylatacyjnym. W jego funkcji rozszerzającej naczynia pośredniczy szlak śródbłonkowej L-argininy/ /tlenku azotu (NO). Nebiwolol zwiększa biodostępność tlenku azotu. W ostatnich badaniach wykazano, że nebiwolol poprawia elastyczność naczyń w stopniu większym niż konwencjonalne b-adrenolityki (atenolol, metoprolol). Według wytycznych ESH/ESC 2013 niektóre b-adrenolityki o działaniu rozszerzającym naczynia, takie jak celiprolol, karwedilol i nebiwolol, zmniejszają ciśnienie centralne tętna i sztywność tętnic lepiej niż atenolol i metoprolol. Słowa kluczowe: nebiwolol, nadciśnienie, uszkodzenia narządowe, ciśnienie centralne Arterial Hypertens. 2018, vol. 22, no. 1, pages: 1-8 Abstract Clinical organ damage in the cardiovascular (left ventricular hypertrophy, atrial fibrillation, heart failure, coronary events, increased stiffness and atherosclerotic changes) are the major cause of death among patients with hypertension. Oxidative stress and aortic central pressure plays a key role in the pathophysiology of the cardiovascular system and cardiovascular outcome. Antihypertensive agents may, even within the same class, exert variable effects on arterial stiffness variables and endothelial function. Nebivolol is a third-generation b-blocker with vasodilator activity. Its vasodilatory function is mediated by the endothelial L-arginine/NO pathway. Nebivolol increases the bioavailability of NO in the vasculare. In recent studies, nebivolol was demonstrated to improve artery stiffness to a greater extent than impact than conventional b-adrenolitics (atenolol, metoprolol). According to guidelines ESH/ESC some of the vasodilatating b-adrenolitics, such as celiprolol, carvedilol and nebivolol, are reducing central pulse pressure and aortic stiffness better than atenolol or metoprolol.

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-blockade with nebivolol for prevention of acute ischaemic events in elderly patients with heart failure

Abstract: Nebivolol was effective in reducing cardiac ischaemic events in patients with HF of ischaemic aetiology. The prevention of ischaemic events can be an additional beneficial effect of β-blockade in HF patients with underlying CAD.

Cited by 38 publications

References 34 publications

Stimulation of Platelet Nitric Oxide Production by Nebivolol Prevents Thrombosis

Stimulation of Platelet Nitric Oxide Production by Nebivolol Prevents Thrombosis

Erectile Function in Cardiovascular Disease and Hypertension: the Role of Nebivolol

Protective effect of nebivolol to prevent target organ damage in hypertension

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