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

Solal, Alain Cohen; Jondeau, Guillaume; Beauvais, Florence; Berdeaux, Alain

doi:10.1016/j.ejheart.2003.12.007

Cited by 26 publications

(2 citation statements)

References 14 publications

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“…Propranolol treatment reduced plasma renin activity, AT I, AT II, and AT 1–7 in the portal vein and periphery in cirrhotic patients compared with non-treated patients 80. Carvedilol inhibited basal and stimulated ACE production in human endothelial cells81 and exhibited beneficial effects on ACE activity and plasma renin activity levels in chronic heart failure patients 82. In addition, proliferating infantile hemangioma expressed two essential components of the RAS, namely ACE and the AT II receptor, that accounted for the propranolol-induced accelerated involution of large proliferating infantile hemangioma 83–85.…”

Section: Genetic Factors That Relate To β-Adrenergic Inhibition and Cmentioning

confidence: 98%

The roles of beta-adrenergic receptors in tumorigenesis and the possible use of beta-adrenergic blockers for cancer treatment: possible genetic and cell-signaling mechanisms

Lương

Nguyễn²

2012

CMAR

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Cancer is the leading cause of death in the USA, and the incidence of cancer increases dramatically with age. Beta-adrenergic blockers appear to have a beneficial clinical effect in cancer patients. In this paper, we review the evidence of an association between β-adrenergic blockade and cancer. Genetic studies have provided the opportunity to determine which proteins link β-adrenergic blockade to cancer pathology. In particular, this link involves the major histocompatibility complex class II molecules, the renin–angiotensin system, transcription factor nuclear factor-kappa-light-chain-enhancer of activated B cells, poly(ADP-ribose) polymerase-1, vascular endothelial growth factor, and the reduced form of nicotinamide adenine dinucleotide phosphate oxidase. Beta-adrenergic blockers also exert anticancer effects through non-genomic factors, including matrix metalloproteinase, mitogen-activated protein kinase pathways, prostaglandins, cyclooxygenase-2, oxidative stress, and nitric oxide synthase. In conclusion, β-adrenergic blockade may play a beneficial role in cancer treatment. Additional investigations that examine β-adrenergic blockers as cancer therapeutics are required to further elucidate this role.

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Section: Genetic Factors That Relate To β-Adrenergic Inhibition and Cmentioning

confidence: 98%

The roles of beta-adrenergic receptors in tumorigenesis and the possible use of beta-adrenergic blockers for cancer treatment: possible genetic and cell-signaling mechanisms

Lương

Nguyễn²

2012

CMAR

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“…77 Carvedilol inhibited basal and stimulated ACE production in human endothelial cells 78 and exhibited beneficial effects on ACE activity and PRA levels in patients with CHF . 79 In addition, proliferating infantile hemangiomas expressed 2 essential components of the RAS, namely ACE and the AT II receptor, which are responsible for the propranolol-induced accelerated involution of large proliferating infantile hemangiomas. [80][81][82] Taken together, the RAS is activated in AD and the impact of beta-adrenergic receptor blockade on this system will affect AD.…”

Section: Genetic Factors Associated With Beta-adrenergic Inhibition Amentioning

confidence: 99%

The Role of Beta-Adrenergic Receptor Blockers in Alzheimer’s Disease

Lương

Nguyễn

2013

Am J Alzheimers Dis Other Demen

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According to genetic studies, Alzheimer's disease (AD) is linked to beta-adrenergic receptor blockade through numerous factors, including human leukocyte antigen genes, the renin-angiotensin system, poly(adenosine diphosphate-ribose) polymerase 1, nerve growth factor, vascular endothelial growth factor, and the reduced form of nicotinamide adenine dinucleotide phosphate. Beta-adrenergic receptor blockade is also implicated in AD due to its effects on matrix metalloproteinases, mitogen-activated protein kinase pathways, prostaglandins, cyclooxygenase-2, and nitric oxide synthase. Beta-adrenergic receptor blockade may also have a significant role in AD, although the role is controversial. Behavioral symptoms, sex, or genetic factors, including Beta 2-adrenergic receptor variants, apolipoprotein E, and cytochrome P450 CYP2D6, may contribute to beta-adrenergic receptor blockade modulation in AD. Thus, the characterization of beta-adrenergic receptor blockade in patients with AD is needed.

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β‐Blockers in Heart Failure: Benefits of β‐Blockers According to Varying Male Proportions of Study Patients

Yang

Zhao

et al. 2012

Clinical Cardiology

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Background: In patients with heart failure (HF), b-blockers reduce mortality. It's not known whether the beneficial effects of the b-blockers were associated with the differing male proportions of study patients. It also remains to be clarified regarding the true beneficial effects of the 3 b-blockers recommended by the guideline on mortality in the real world. Hypothesis: The benefits of b-blockers in HF patients were sex-related different. Methods: Randomized, placebo controlled clinical trials were included if they evaluated the beneficial effects of the three b-blockers on mortality and on hospital admissions on an intention-to-treat basis, and lasted at least 3 months. Results: Twenty-eighty trials with 14,829 patients were included. The b-blockers significantly reduced all cause mortality by 29.6%, cardiac death by 29.8%, sudden death by 49.4%, respectively. The magnitude of benefits of b-blockers in HF patients was increased with the increased male proportion. A similar magnitude of reduction in all cause mortality was observed among the three b blockers. A trend toward to reduced cardiac death was observed among the three b blockers, but only in bisoprolol was this statistically different (RR, 0.72; 95%CI, [0.59-0.87]). Metoprolol was significantly superior to carvedilol (P = 0.008) or bisoprolol (P = 0.034) in reduced sudden death. Conclusions: In patients with HF, the 3 commonly used b-blockers significantly reduced mortality. Greater benefits of b-blockers were observed in the higher male proportion studies. The metoprolol was significantly superior to carvedilol or bisoprolol in reduced sudden death. Additional trials are required to determine whether the benefits of b-blockers will be observed in female HF patients. IntroductionCompelling evidence now exists that proves adrenergic blockade is at the center of neurohormonal antagonism in heart failure. β-Blocker treatment of heart failure will improve patients' symptoms, left ventricular function, and the rate of hospital admission.1,2 The most recently updated ACC/AHA practice guideline published in 2009 recommended that β-blockers should be used in all stable patients with current or prior symptoms of heart failure (HF) and reduced left ventricular ejection fraction (LVEF) unless contraindicated.3 To our knowledge, several high-quality meta-analyses of clinical randomized trials with β-blockers in HF patients were conducted and published from 1998 to 2005. 4 -7 It is legitimate, therefore, to question whether another meta-analysis article is necessary.

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

Cited by 26 publications

References 14 publications

The roles of beta-adrenergic receptors in tumorigenesis and the possible use of beta-adrenergic blockers for cancer treatment: possible genetic and cell-signaling mechanisms

The roles of beta-adrenergic receptors in tumorigenesis and the possible use of beta-adrenergic blockers for cancer treatment: possible genetic and cell-signaling mechanisms

The Role of Beta-Adrenergic Receptor Blockers in Alzheimer’s Disease

β‐Blockers in Heart Failure: Benefits of β‐Blockers According to Varying Male Proportions of Study Patients

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