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There are clinic and genetic polymorphism differences in coronary artery disease (CHD). Percutaneous coronary intervention (PCI), clinic, angiographic, procedure technique may influence the evolution, major events (death, AMI, revascularization) and clinical restenosis. This study aims to evaluate if there are genetic polymorphism differences between patients with and without CHD and if it would influence in long-term follow-up after PCI.
Method and Results
It was studied two groups: the coronary disease group (CDG) with 182 patients of a closed health system with CHD that were submitted to PCI from 2001 and 2007 and to genetic follow-up evaluation until 12/31/2008; the control group (CG) with 36 patients, were angiographically normal and were also submitted to genetic evaluation. The polymorphisms evaluated were the ACE I/D and A166C (AT1R). In this period 221 procedures were performed in 182 patients of CDG. Qui square, Fisher exact and Student t test were used. Cox multivariate regression analysis were not performed because only three clinical characteristics and A166C had p<0.10 in univariable analysis.
The CG and CDG patients were: female 20 (55.6%) and 49 (26.9%), (P=0.0007); age 55.9±11.1 and 60.8±10.5 (P=0.0100); tobacco smokers 5 (13.9%) and 67 (36.8%), (P=0.0132); diabetes 4 (11.1%) and 48 (26.4%), (P=0.0802); hypertension 29 (80.6%) and 146 (80.2%), (P=0.9631); dyslipidemia 14 (38.9%) and 112 (61.5%), (P=0.0119); family history 12 (33.3%) and 60 (33.0%), (P=0.9659); obesity 9 (25.0%) and 60 (33.0%), (P=0.3476); ACE polymorphism DD 16 (44.5%), DI 17 (47.2%), II 3 (8.3%) and DD 81 (44.5%), DI 70 (38.5%), II 31 (17.0%), (P=0.3612); A166C polymorphism AA 36 (100.0), AC 0 (0.0%), CC 0 (0.0%) and AA 135 (74.2%), 42 (23.1%), 5 (2.7%), (P=0.0026). In CDG there were no difference: between ACE and A166C polymorphism at one, two or three vessel disease; between majors events, deaths, AMI and revascularization; and between restenosis and the mean vessel diameter, lesion extension and bare metal or drug eluting stents.
It was demonstrated that CDG were genetically A166C polymorphism different from normal CG who did not have CC and AC. CDG were older with more males gender, smokers and dyslipidemia in contrast with CG. There were no differences between the studied variables, illness extension, major events and restenosis in the CDG. Cox multivariable analysis were not performed as in univariable analysis only three variables have shown p<0.10.