Evidence from Genetic Studies

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Preliminary evidence for the involvement of the renin-angiotensin system in ischemic events also has come from retrospective but not prospective epidemiological studies of the ACE gene in humans. A retrospective case-controlled study of small sample size by Cambien et al. (11) suggested a link between polymorphism of the ACE gene with increased risk of MI. This finding, however, was not supported by data of a larger sample size from the Physicians' Health Study studied by Lindpaintner et al. (12), who found no association between the presence of the ACE gene D-allele and an increased risk of ischemic heart disease or MI (12,13). This ACE gene polymorphism consists of an insertion (I) or deletion (D) of a 287-bp sequence of DNA. Individuals containing the D/D genotype exhibit plasma ACE levels twice that of individuals containing the I/I genotype (11). The D/D genotype also is more prevalent in middle-aged men with a prior history of MI when compared to age-matched controls (11). An increased incidence of the ACE D/D genotype has been identified in children of patients with a history of MI compared with controls (14). Additional disease states, which have been associated with the D/D genotype include LV hypertrophy (15), hypertrophic cardiomyopathy (16), restenosis after coronary angioplasty (17), and progressive ventricular dilatation following anterior MI (18). Subjects enrolled in the Captopril and Thrombolysis Study (CATS) (19) underwent quantitative echocardiography immediately following therapy with streptokinase. After a 1-yr follow-up, both end-systolic and end-diastolic volumes, as well as plasma norepinephrine levels, were greater in the D/D genotype group. Furthermore, these effects were attenuated in patients with the D/D genotype group by therapy with captopril. Also, in a study by Kohno et al. (20) ACE inhibitor therapy was administered for >2 yr to 54 patients with hypertension and moderate to severe LV hypertrophy. In 17 patients with the D/D genotype, mean regression in posterior wall thickness and LV mass index was significantly less than in the other patients with I/D or I/I genotypes.

Lindpaintner et al. (12) found no association between the presence of the ACE gene D-allele and an increased risk of ischemic heart disease or MI. Explanations advanced in attempt to reconcile the conflicting and variable experimental results hinge on the influences that multiple environmental factors may have on the expression of a particular disease process and variations of genetic backgrounds among differing populations being studied (12,13).

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