ArticleClinical Medicine Insights. Cardiology2011
Bucindolol: a pharmacogenomic perspective on its use in chronic heart failure.
Article in Clinical Medicine Insights. Cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Different forms of cardiomyocyte death in post-myocardial infarction ventricular remodeling: mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Novel target identification towards drug repurposing based on biological activity profiles.PloS one · 2025Article
- Understanding the Importance of Race/Ethnicity in the Care of the Hypertensive Patient.Current hypertension reports · 2015Review
- Contextualizing Genetics for Regional Heart Failure Care.Current cardiology reviewsReview
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bucindolol is a non-selective β-adrenergic receptor blocker with α-1 blocker properties and mild intrinsic sympatholytic activity. The Beta-Blocker Evaluation of Survival Trial (BEST), which is the largest clinical trial of bucindolol in patients with heart failure, was terminated prematurely and failed to show an overall mortality benefit. However, benefits on cardiac mortality and re-hospitalization rates were observed in the BEST trial. Bucindolol has not shown benefits in African Americans, those with significantly low ejection fraction and those in NYHA class IV heart failure. These observations could be due to the exaggerated sympatholytic response to bucindolol in these sub-groups that may be mediated by genetic polymorphisms or changes in gene regulation due to advanced heart failure. This paper provides a timely clinical update on the use of bucindolol in chronic heart failure.
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Registered trials
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