Pharmacogenetic Effect of the Stromelysin (MMP3) Polymorphism on Stroke Risk in Relation to Antihypertensive Treatment | Zendy

Richard Sherva | Zendy; Charles E. Ford | Zendy; John H. Eckfeldt | Zendy; Barry R. Davis | Zendy; Eric Boerwinkle | Zendy; Donna K. Arnett | Zendy

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Pharmacogenetic Effect of the Stromelysin (MMP3) Polymorphism on Stroke Risk in Relation to Antihypertensive Treatment

Author(s) -

Richard Sherva,

Charles E. Ford,

John H. Eckfeldt,

Barry R. Davis,

Eric Boerwinkle,

Donna K. Arnett

Publication year - 2010

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.110.593798

Subject(s) - medicine , chlorthalidone , stroke (engine) , lisinopril , hazard ratio , mmp3 , amlodipine , pharmacogenetics , genotype , cardiology , blood pressure , angiotensin converting enzyme , confidence interval , genetics , mechanical engineering , gene expression , biology , gene , engineering

Atherothrombotic diseases including stroke share a common etiology of atherosclerosis, and susceptibility to atherosclerosis has a genetic component. Stromelysin-1 (matrix metalloproteinase-3 [MMP3]) regulates arterial matrix composition and is a candidate gene for atherothrombosis. A common polymorphism of MMP3 alters expression levels and affects atherosclerotic progression and plaque stability. As part of the Genetics of Hypertension Associated Treatment study, ancillary to the Antihypertensive and Lipid Lowering to Prevent Heart Attack Trial, we evaluated the 5A/6A polymorphism in MMP3 to determine its association with stroke and determine whether it modifies clinical outcome response to blood pressure-lowering drugs.

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