ABSTRACT
Early restenosis in up to 30% of cases limits the benefits of percutaneous transluminal coronary angioplasty [PTCA]. The mechanisms that underlie restenosis are uncertain, although experimental evidence suggests that the renin-angiotensin system is involved in the vascular response to angioplasty. The ACE gene is one of the major genes of the renin-angiotensin and kallikrein-kinin systems and is a candidate gene for several cardiovascular diseases for which a genetic predisposition has been established. The ACE gene contains a common insertion deletion polymorphism termed I and D, respectively. The three possible genotypes are DD, ID and II, and the plasma level of ACE is highest with the DD genotype. This work aimed to investigate whether ACE gene polymorphism influences the risk of restenosis after PTCA to explore a relation between the total ACE level and restenosis and to compare the ACE genotypes of the patients of the study with those of a control group of healthy subjects. This study included 53 patients with CAD, 48 males and 5 females, their age ranged from 36 to 63 years. All patients were compared to 46 control subjects with age and sex matched. The patients were divided into two groups: group [A][40 patients with no restenosis] and group [B][13 patients with restenosis]. All patients were subjected to: full history and clinical examination, laboratory investigations which include estimation of serum angiotensin converting enzyme levels and detection of genotypes of the ACE gene I/D polymorphism, 12-lead electrocardiogram, treadmill exercise stress testing, coronary angiography and PTCA. The distribution of ACE genotype [DD] was not significantly different in-group B patients with restenosis compared with group A patients with no restenosis [8 out of 13, versus 15 out of 40 respectively, P> 0.05]. Plasma ACE levels did not differ between patients and control subjects [P value > 0.05]. Although plasma ACE levels were significantly higher in relation to ACE genotypes [P value < 0.05], plasma ACE levels were insignificant in relation to restenosis [P value > 0.05]. Since there was no evidence that variation at the ACE gene defined by the I/D polymorphism influences the extent of restenosis, it could be concluded that determination of ACE I/D genotypes is unlikely to be useful in identifying patients at higher risk of restenosis after PTCA and continued studies with clinically different subsets of patients is warranted