Influence of beta-blockers on endothelial function: A meta-analysis of randomized controlled trials

Peller, Michał; Ozierański, Krzysztof; Balsam, Paweł; Grabowski, Marcin; Filipiak‬, Krzysztof J.; Opolski, Grzegorz

doi:10.5603/cj.a2015.0042

Cited by 48 publications

(30 citation statements)

References 33 publications

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“…123 Indeed, a recent meta-analysis of 1,273 patients from 16 studies by Peller et al on the effects of beta-blockers on endothelial function in various groups of patients did shown some benefit, however the study did include somewhat homogenous groups of patients. 124 The authors did find, consistent with studies in hypertension, that the best improvement in endothelial function was seen with 3 rd generation beta-blockers such as nebivolol.…”

Section: Diuretics and Beta-blockerssupporting

confidence: 77%

Endothelial dysfunction in human essential hypertension

Mordi

Delles

et al. 2016

Journal of Hypertension

120

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Abstract:Although the endothelium has a number of important functions, the term endothelial dysfunction is commonly used to describe impairment in its vasodilatory capacity. It is increasingly recognised that this is related to hypertension, although whether it predates hypertension or is a consequence of it is still unknown. In this review we explore the mechanisms of endothelial dysfunction in hypertension, its prognostic significance and methods of pharmacological reversal. Powered by Editorial Manager® and ProduXion Manager® from Aries Systems Corporation CONDENSED ABSTRACTEndothelial dysfunction is prevalent in hypertension and has a recognised association with the condition. In this article we review the pathophysiology of endothelial dysfunction in human hypertension, its prognostic significance and methods of pharmacological reversal. We appreciate the opportunity to revise this manuscript again and particularly would like to thank Reviewer whose constructive criticism has certainly improved the manuscript. We have addressed the minor comments suggested as attached to this letter.We are extremely grateful once again to the reviewers and the editors for their detailed critique which has undoubtedly improved the quality of the manuscript.We thank you once again for the opportunity to resubmit our manuscript and look forward to your decision. Yours sincerely Dr Ify Mordi Submission letterReviewer #2:I thank you the author for their last revision: the paper improved quite a lot! Just few points should be still addressed:We thank the reviewer for their positive appraisal of our revised manuscript -we agree that the comments provided have substantially improved the review. We agree with the reviewer that this sentence is out of place. Given the length of the review and the fact that this is covered elsewhere we have now deleted the sentence.-Please move the description of micromyography to the invasive methods as tissue biopsies are necessary.We thank the reviewer for pointing out this error. We have now moved the description of myography to the invasive methods section (page 5). We have no conflict of interest. Endothelial Dysfunction in Human Essential Hypertension Manuscript 2 ABSTRACTAlthough the endothelium has a number of important functions, the term endothelial

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Section: Diuretics and Beta-blockerssupporting

confidence: 77%

Endothelial dysfunction in human essential hypertension

Mordi

Delles

et al. 2016

Journal of Hypertension

120

View full text Add to dashboard Cite

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“…It is well established that the activated sympathetic nervous system (SNS) becomes a -culprit‖ in the development of HF and knowledge of the underlying cardiac neural pathophysiological mechanisms has led to the introduction of β-blockers as a therapy. Some studies have shown that β-blocker treatment can improve endothelial function [37]. In our results, there was an increased tendency for FMD values to increase after three months of β-blocker therapy but the differences failed to reach statistical significance.…”

Section: Accepted Manuscriptcontrasting

confidence: 80%

Peripheral endothelial function may predict the effectiveness of beta-blocker therapy in patients with idiopathic dilated cardiomyopathy

Xie

Chen

et al. 2016

International Journal of Cardiology

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“…27 Moreover, in vitro studies using human cell lines have documented the involvement of FGD5 as an important factor in the proangiogenic action of endothelial growth factor, 28 further highlighting the potential role of FGD5 in the development/progression of vasculature-related diseases including HTN. Studies have shown the positive effect of β-blockers on the endothelial dysfunction, 29 and several mechanistic studies indicate toward the involvement of the endothelial and vasculaturerelated mechanism of the BP-lowering effects of the β-blockers. 30 Further studies are needed to understand the functional underpinning of this SNP in the FGD5 gene in improved BP response to β-blockers.…”

Section: Discussionmentioning

confidence: 99%

Genomic Association Analysis Reveals Variants Associated With Blood Pressure Response to Beta‐Blockers in European Americans

Singh

Rouby

McDonough

et al. 2019

Clinical Translational Sci

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European Americans (EA) have a better antihypertensive response to β‐blockers when compared with African Americans, albeit with some variability. We undertook a genomewide association study to elucidate the underlying genetic determinants in EA contributing to this variability in blood pressure (BP) response. A discovery genomewide association study of change in BP post–metoprolol treatment was performed in EA participants (n = 201) from the Pharmacogenomic Evaluation of Antihypertensive Responses‐2 (PEAR‐2) study and tested for replication in the atenolol‐treated EA from the PEAR study (n = 233). Rs294610 in the FGD5, which encodes for FYVE, RhoGEF and PH Domain Containing 5, (expression quantitative trait loci for FGD5 in the small intestine) was significantly associated with increased diastolic BP response to β‐blockers in the PEAR‐2 study (P = 3.41 × 10−6, β = −2.70) and replicated (P = 0.01, β = −1.17) in the PEAR study. Post–meta‐analysis of these studies, an additional single nucleotide polymorphism rs45545233 in the SLC4A1, encoding for Solute Carrier Family 4 Member 1, (expression quantitative trait loci for dual specificity phosphatase 3 in the artery tibial) was identified that was significantly associated with a poor response to β‐blockers (P = 3.43 × 10−6, β = 4.57) and was replicated in the atenolol add‐on cohort (P = 0.007, β = 4.97). We identified variants in FGD5 and SLC4A1, which have been previously cited as candidate genes for hypertension, to be associated with a β‐blocker BP response in EA. Further elucidation is warranted of the underlying mechanisms of these variants and genes by which they influence the BP response to β‐blockers.

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Influence of beta-blockers on endothelial function: A meta-analysis of randomized controlled trials

Abstract: Background: Endothelial dysfunction (ED) frequently precedes cardiovascular diseases (CVD) and is a well-established ; p = 0.008) and higher than in the ivabradine group (1.6 ± 3.61 vs -0.3 ± 1.66; p = 0.02 (Cardiol J 2015; 22, 6: 708-716)

Cited by 48 publications

References 33 publications

Endothelial dysfunction in human essential hypertension

Endothelial dysfunction in human essential hypertension

Peripheral endothelial function may predict the effectiveness of beta-blocker therapy in patients with idiopathic dilated cardiomyopathy

Genomic Association Analysis Reveals Variants Associated With Blood Pressure Response to Beta‐Blockers in European Americans

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