The 4G/5G promotor polymorphism of the plasminogen activator inhibitor-1 gene and late lumen loss after coronary stent placement in smoking and nonsmoking patients

Background: Instent restenosis remains a significant clinical problem. Iden tification of patients at risk for instent restenosis may allow selection o f individualized appropriate therapeutic approaches. Genetic polymorphisms have been suggested to be associated with the risk of instent restenosis. S moking is known to influence hemostatic parameters. Hypothesis: This study investigated the influence of the 4G/5G promotor pol ymorphism of the plasminogen activator inhibitor type 1 (PAI-1) gene on ins tent restenosis in smoking and nonsmoking patients, Methods: In all, 300 consecutive patients (133 nonsmoking; 167 smoking) wit h elective coronary stent placement and 6-month angiographic follow-up were studied. Quantitative coronary angiography and genotyping with polymerase chain reaction analysis were performing in all patients. Results: Nonsmoking PAI-1 4G/4G carriers showed a significantly greater lat e lumen loss (n = 38; 0.54 +/- 0.53 mm) compared with nonsmoking PAI-1 4G/5 G (n = 68; 0.38 +/- 0.45 mm) or 5G/5G (n = 27; 0.19 +/- 0.23 mm) carriers, analysis of variance (ANOVA) p <0.001. Smoking patients with the genotypes 4G/4G (n = 46; 0.53 +/- 0.54 mm.) and 4G/5G (n = 79; 0.37 +/- 0.41 mm) had alate loss similar to that of nonsmoking patients. Smoking 5G/5G carriers h ad the highest late loss of all smoking patients (n = 42; 0.63 +/- 0.50); A NOVA p <0.05; nonsmoking 5G/5Gvs. smoking 5G/5G p < 0.001. Conclusion: The promotor polymorphism. of the PAI-1 gene has a significant influence on instent restenosis after coronary stent implantation. The 5G/5 G genotype, predisposes nonsmoking gene carriers to less late lumen loss, w hereas in smoking gene carriers this genotype is associated with the greate st late lurnen loss. TIfis might be explained by an altered expression patt ern of hemostatic parameters.