Tailored therapy of ACE inhibitors in stable coronary artery disease: pharmacogenetic profiling of treatment benefit. (August 2010)

• Record Type: Journal Article
• Authors: Brugts, Jasper J; Boersma, Eric; Simoons, Maarten L
• Is Part Of: Pharmacogenomics. Volume 11:Number 8(2010)
• Page Start: 1115
• Page End: 1126
• Publication Date: 2010-08
• Subjects: ACE inhibitors -- coronary artery disease -- gene -- haplotype -- perindopril -- pharmacogenetics -- polymorphism -- secondary prevention; Pharmacogenomics -- Periodicals; 615.1
• DOI: 10.2217/pgs.10.103
• Languages: English
• ISSNs: 1462-2416

Abstract

Angiotensin-converting enzyme (ACE) inhibitors are among the most commonly used drugs in stable coronary artery disease as these agents have been proven to be effective for reducing the risk of cardiovascular morbidity and mortality. As with other drugs, individual variation in treatment benefit is likely. Such heterogeneity could be used to target ACE-inhibitor therapy to those patients most likely to benefit from treatment. However, prior attempts to target ACE-inhibitor therapy to those patients who are most likely to benefit of such prophylactic treatment in secondary prevention using clinical characteristics or the level of baseline risk appeared not to be useful. A new approach of 'tailored therapy' could be to integrate more patient-specific characteristics, such as the genetic information of patients. Pharmacogenetic research of ACE inhibitors in coronary artery disease patients is at a formative stage, and studies are limited. The Perindopril Genetic association (PERGENE) study is a large pharmacogenetic substudy of the randomized placebo-controlled European trial On Reduction of Cardiac Events with Perindopril in Patients with Stable Coronary Artery disease (EUROPA) trial, aimed to assess the feasibility of pharmacogenetic profiling of ACE-inhibitor therapy by perindopril. This article summarizes the recent findings of the PERGENE study and pharmacogenetic research of the treatment benefit of perindopril in stable coronary artery disease.