Objective To analyze the relationship between polymorphism at the Apolipoprotein AI (Apo AI) gene and the risk for coronary artery disease. Methods A total of 107 patients (mean age 56 ± 11 years) diagnosed as having stable angina pectoris (SAP) (23 cases), unstable angina pectoris (UAP)(23 cases) or myocardial infarction (MI) (61 cases)were prospectively evaluated. DNA was obtained from the 107 patients and 50 controls. In order to determine the Apo AI genotypes at two polymorphic sites (G/A at -75 bp, and C/T at +83 bp), DNA was PCR amplified and digested with MspI. Results The frequency of carriers of the rare allele at the - 75 bp site (M1-) was 0.49 in cases and 0.30 in controls ( P＜ 0.05). The frequencies of the M 1 - allele among patients with SAP, UAP, MI and controls were 0. 37 (vs. Controls, P ＞ 0.05), 0. 54 (vs. Controls, P ＜0.05), 0.52 (vs. Controls, P＜ 0.05) and 0.30, respectively. The frequencies for carriers of the rare allele at the + 83bp polymorphism (M2) were observed among patients with SAP (0.09, vs. Controls, P ＞0.05), UAP (0. 11, vs. Controls, P ＞ 0.05) or MI (0.12, vs. Controls, P ＞ 0.05) and controls (0. 12).There was an slightly increase in the frequency of the M1 - allele in patients with SAP to UAP or MI (0.37vs. 0.54 vs. 0.52; all P ＞ 0.05) and M1 polymorphism as a risk factor for CAD (OR=3.74, P ＜0.05). In the + 83bp polymorphism there was no difference in the allelelic frequencies in cases and controls (0. 11 vs. 0. 12; P ＞ 0.05). There was no significant difference in the frequency of the M2- allele in patients with SAP to UAP or MI (0.09 vs. 0.11 vs.0. 12; all P ＞ 0. 05) and M2 polymorphism not as a factor for CAD ( OR = 0. 80, P ＞ 0. 05) Plasma lipoprotein values in patients with the allele M1 - and M2 - had no different levels than those homozygous for the M1+ andM2+ (P＞ 0.05). Conclusion M1polymorphism (M1 - ) may be as a risk factor for CAD and M2 polymorphism (M2 - ) not as a factor for CAD in Chinese Xinjiang Uygur and Han population.

Ojbective To find the independent predictors for restenosis after coronary stenting.Methods Quantitative angiography was performed on 60 cases (67 successfully dilated lesions) after angioplasty over 6-months follow-up, and both univariate and multivariate logistic regression analysis were done to identify the correlations of restenosis with clinical factors. Results The total restenosis rate was 31.3％(21 of 67 lesions), and according to univariate analysis the patients who underwent coronary stenting ≥3.5mm had a lower rate of restenosis ( P ＜ 0. 01).Collateral circulation to the obstruction site, high maximal inflation pressure, smoking and the less minimal lumen diameter after PTCA made the rate of restenosis higherower ( P ＜ 0.05) . Multivariate logistic regression analysis showed that coronary stenting ≥ 3.5mm had a low rate of restenosis, but high maximal inflation pressure and smoking made the restenosis rate higher. Conclusion Coronary stent size, maximal inflation pressure and. smoking were independent predictors for restenosis.