Journal Article10.1038/359641A0
Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction.
François Cambien,Odette Poirier,Laure Lecerf,Alun Evans,Jean-Pierre Cambou,Dominique Arveiler,Gérald Luc,Jean-Marie Bard,L Bara,Sylvain Ricard +9 more
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TL;DR: It is reported that the DD genotype, which is associated with higher levels of circulating ACE than the ID and II genotypes, is significantly more frequent in patients with myocardial infarction than in controls, especially among subjects with low body-mass index and low plasma levels of ApoB.
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Abstract: Factors involved in the pathogenesis of atherosclerosis, thrombosis and vasoconstriction contribute to the development of coronary heart disease. In a study comparing patients after myocardial infarction with controls, we have explored a possible association between coronary heart disease and a variation found in the gene encoding angiotensin-converting enzyme (ACE). The polymorphism ACE/ID is strongly associated with the level of circulating enzyme. This enzyme plays a key role in the production of angiotensin II and in the catabolism of bradykinin, two peptides involved in the modulation of vascular tone and in the proliferation of smooth muscle cells. Here we report that the DD genotype, which is associated with higher levels of circulating ACE than the ID and II genotypes, is significantly more frequent in patients with myocardial infarction (n = 610) than in controls (n = 733) (P = 0.007), especially among subjects with low body-mass index and low plasma levels of ApoB (P < 0.0001). The ACE/ID polymorphism seems to be a potent risk factor of coronary heart disease in subjects formerly considered to be at low risk according to common criteria.
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References
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TL;DR: The insertion/deletion polymorphism accounted for 47% of the total phenotypic variance of serum ACE, showing that the ACE gene locus is the major locus that determines serum ACE concentration.
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•Journal Article
Evidence, from combined segregation and linkage analysis, that a variant of the angiotensin I-converting enzyme (ACE) gene controls plasma ACE levels.
Laurence Tiret,B Rigat,Sophie Visvikis,C Breda,Pierre Corvol,François Cambien,Florent Soubrier +6 more
TL;DR: A combined segregation and linkage analysis provided evidence that the major-gene effect was due to a variant of the ACE gene, in strong linkage disequilibrium with the I/D polymorphism.
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