ArticleAmerican heart journal2007
Absence of an interaction between the angiotensin-converting enzyme insertion-deletion polymorphism and pravastatin on cardiovascular disease in high-risk hypertensive patients: the Genetics of Hypertension-Associated Treatment (GenHAT) study.
Article in American heart journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00563901 (GenHAT - Genetics of Hypertension Associated Treatments - Ancillary to ALLHAT), which is not on this map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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.
GenHAT - Genetics of Hypertension Associated Treatments - Ancillary to ALLHAT
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- ACE (I/D) polymorphism and response to treatment in coronary artery disease: a comprehensive database and meta-analysis involving study quality evaluation.BMC medical genetics · 2009Pooled it
- Added value of pharmacogenetic testing in predicting statin response: results from the REGRESS trial.The pharmacogenomics journal · 2013Trial
- Associations between antihypertensive drug-related gene polymorphisms and cardiovascular outcomes in hypertensive patients: a gene-drug interaction study.Scientific reports · 2026Article
- Pharmacogenomic substudies of randomized controlled trials: consideration of safety outcomes.Therapeutic advances in drug safety · 2014Article
- Characteristics associated with informed consent for genetic studies in the ACCORD trial.Contemporary clinical trials · 2014Article
- Review of the cost effectiveness of pharmacogenetic-guided treatment of hypercholesterolaemia.PharmacoEconomics · 2013Review
- Gene-drug interaction in stroke.Stroke research and treatment · 2011Article
- Pharmacogenetics of cardiovascular drug therapy.Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases · 2009Article
- ACE genotype, risk and causal relationship to stroke: implications for treatment.Current treatment options in cardiovascular medicine · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundThe aim of this study was to determine whether the angiotensin-converting enzyme (ACE) insertion-deletion (ID) polymorphism interacts with pravastatin to modify the risk of coronary heart disease (CHD) and other cardiovascular end points in a large clinical trial.
methodsGenHAT is an ancillary study of the ALLHAT. The ACE ID genotyped population in the lipid-lowering arm of ALLHAT included 9467 participants randomly assigned to pravastatin (n = 4741) or to usual care (n = 4726). The efficacy of pravastatin in reducing the risk of primary outcome (all-cause mortality) and secondary outcomes (fatal CHD and nonfatal myocardial infarction, cardiovascular disease [CVD] mortality, CHD, stroke, other CVD, non-CVD mortality, stroke, and heart failure) was compared between the genotype strata (dominant model ID + II vs DD, additive model II vs ID vs DD), by examining an interaction term in a Cox proportional hazards model.
resultsThe relative risk of fatal CHD and nonfatal myocardial infarction among subjects randomized to pravastatin compared with subjects randomized to usual care was similar in subjects with the II genotype (hazard ratio [HR] 0.84, 95% CI 0.59-1.18), the ID genotype (HR 0.84, 95% CI 0.68-1.03), and the DD genotype (HR 0.99, 95% CI 0.77-1.27).
conclusionsWe found no evidence that the ACE ID genotype was a major modifier of the efficacy of pravastatin in reducing the risk of cardiovascular events.
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Registered trials
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