Angiotensin converting enzyme gene polymorphisms and coronary risk in a Portuguese population

2004 
Background: A family history of coronary heart disease (CHD) is a strong risk marker for the disease, independently of classical risk factors. It could be decoded by recognizing the polymorphisms associated with increasedrisk. Renin-angiotensin system genes are candidate genes in CHD and the deletion allyle of the augioteusin converting enzyme (ACE) has been reported as deleterious. However, there is disagreement as to the role of the insertion/deletion polymorphism of the ACE gene in coronary risk. Aim: To evaluate whether ACE gene polymorphisms constitute a CHD risk factor. Methods: We conducted a population-based case-control study of 301 subjects with a history of myocardial infarction or angiographie evidence of coronary heart disease and 510 age- and gender-matched coutrols, without CHD, living in a region with high CHD mortality rates. Blood samples were taken, DNA extracted and genotypes determined by the polymerase chain reaction (PCR). Amplification products were identified by agarose gel electrophoresis. Statistical analysis: The Data were evaluated by SPSS for Windows, using the Student's t test, the chi-square test, odds ratios and 95 % confidence intervals. Results: The prevalence of the DD, ID and II genotype was 41.2%, 46.3 %, 12.5 % in the cases and 28.1 %, 55.2 % and 16.7 % in the control group. The frequency of the DD genotype was significantly higher in the cases than in the controls (41.2% vs. 28.1 %, odds ratio 1.79, 95% CI 1.31 to 2.4, p<0.0001) By contrast, the ID and II genotypes' prevalence was higher in the control group (55.2 % vs. 46.3 %, p = 0.002 and 16.7 vs. 12.5 %, p = NS, respectively) compared to the case group. Conclusions: This study clearly shows that the ACE DD polymorphism is strongly linked to CHD, and if our data are confirmed in a larger population sample, more aggressive vascular prevention could be justified in patients carrying the DD genotype.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    0
    References
    4
    Citations
    NaN
    KQI
    []