The angiotensinogen gene 235T variant is associated with an increased riskof restenosis after percutaneous transluminal coronary angioplasty

The therapeutic benefit of percutaneous transluminal coronary angioplasty ( PTCA) is limited by restenosis in 30-40% of patients. The underlying mechan isms are currently not well understood. Besides clinical and angiographic v ariables, genetic factors may be involved. In the present study, we investi gated the associations between the angiotensinogen T174M and M235T, the ang iotensin I-converting enzyme (ACE) I/D and the angiotensin II type I recept or A1166C gene polymorphisms and restenosis in 511 patients who had undergo ne successful PTCA (without stenting) and follow-up angiography. Clinical a nd angiographic variables were also considered as possible predictors of re stenosis. Stenosis severity was estimated by visual inspection of the angio grams. Altogether, 160 patients had restenosis, as defined by a greater tha n 50% reduction in the diameter of the dilated segment at follow-up angiogr aphy compared with the findings immediately following angioplasty. There we re significantly more carriers of the angiotensinogen 235T allele and more patients with the ACE DD genotype in the restenosis group than in the no re stenosis group, but only the angiotensinogen 235T allele land not the ACE D D genotype) remained significantly associated with restenosis following mul tifactorial analyses. No differences between the two groups were found with respect to the other gene polymorphisms. Patients who subsequently develop ed restenosis had a higher degree of stenosis and more severe lesions befor e PTCA, as well as less residual stenosis immediately after PTCA. We conclu de that the angiotensinogen M235T gene polymorphism may be an independent p redictor of restenosis after PTCA.