Abstract
The angiotensin converting enzyme (ACE) is a strong candidate gene for myocardial infarction (MI). Insertion-deletion dimorphism in intron 16 of this gene has been inconclusively found to be associated with it. Several new polymorphisms in the ACE gene have been identified and among these, a dimorphism in exon 17, ACE G2350A, has a significant effect on plasma ACE concentrations. To assess the value of genotyping the ACE G2350A dimorphism in a genetically homogeneous population, we carried out a case-control study of dimorphism G2350A for a putative association with MI among Pakistani nationals. We investigated a sample population of 370 Pakistanis, comprising 163 controls, and 207 patients with clinical diagnosis of acute MI (AMI). ACE G2350A alleles were visualized by assays based on polymerase chain reaction and restriction endonuclease analysis. Frequencies of G alleles were 0.68 among controls and 0.72 among AMI patients. The ACE G2350A dimorphism showed no significant association with MI (chi2 = 0.90, 2 df, P = 0.64), plasma levels of homocysteine (P = 0.52) or with serum levels of folate (P = 0.299). The results indicate that ACE G2350A polymorphism is not associated with risk of myocardial infarction in the Pakistani population investigated here.
Highlights
Angiotensin converting enzyme (ACE) is a dipeptidyl carboxypeptidase I, (EC. 3.4.15.1) that activates angiotensin I through cleavage of the carboxyterminal dipeptide into the potent vasoconstrictor angiotensin II and inactivates the vasodilator peptide bradykinin (Erdös and Skidgel, 1987)
Experimental data suggest that the presence of high levels of plasma ACE could result in the thickening of the vascular wall eventually leading to the development of vascular disease (Erdös and Skidgel, 1987; Ehlers and Riordan, 1989)
The ACE gene is viewed as a quantitative trait locus (QTL) that modulates circulating ACE levels, and the ACE I/D dimorphism is a marker that is thought to be in linkage disequilibrium (LD) with functional variants located in the ACE gene (Cambian et al, 1992; Tiret et al, 1992; Arca et al, 1998) that are implicated in cardiovascular disease (CVD)
Summary
Angiotensin converting enzyme (ACE) is a dipeptidyl carboxypeptidase I, (EC. 3.4.15.1) that activates angiotensin I through cleavage of the carboxyterminal dipeptide into the potent vasoconstrictor angiotensin II and inactivates the vasodilator peptide bradykinin (Erdös and Skidgel, 1987). The ACE gene is viewed as a quantitative trait locus (QTL) that modulates circulating ACE levels, and the ACE I/D dimorphism is a marker that is thought to be in linkage disequilibrium (LD) with functional variants located in the ACE gene (Cambian et al, 1992; Tiret et al, 1992; Arca et al, 1998) that are implicated in CVDs. Several studies on the association of ACE I/D polymorphism and the risk for myocardial infarction (MI) (Bohn et al, 1993; Cambien et al, 1994; Evans et al, 1994; Soubrier and Cambien, 1994; Cambian and Evans, 1995; Lindpainter et al, 1995; Villard and Soubrier, 1996; Ferrieres et al, 1999; O’ Mally et al, 1999; Keavney et al, 2000), have generated inconsistent information. Our study is aimed at establishing whether the ACE G2350A dimorphism is a genetic marker and an independent risk factor for MI
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