Author/Authors :
Karl Stangl، نويسنده , , Ingolf Cascorbi، نويسنده , , Verena Stangl، نويسنده , , Michael Laule، نويسنده , , Przemyslaw M. Mrozikiewicz، نويسنده , , Michaela Schwarz، نويسنده , , Stephan B. Felix، نويسنده , , Heinz Theres، نويسنده , , Gert Baumann، نويسنده , , Ivar Roots، نويسنده ,
Abstract :
Background Contradictory reports exist concerning the role of the angiotensin II type 1 receptor A1166C polymorphism as a coronary risk factor. Moreover, it is unknown whether the A1166C polymorphism is associated with thrombotic complications after coronary catheter interventions. Methods We investigated the role of the A1166C polymorphism as a risk factor in 1000 patients with coronary artery disease (CAD) and in 1000 age- and sex-matched controls. A total of 649 patients receiving interventions (270 coronary angioplasty, 102 atherectomy, and 277 stenting) were investigated for a 30-day composite end point including target vessel revascularization, myocardial infarction, or death. Results The composite end point was reached by 42 patients (6.5%) without evidence that the C allele was associated with excess procedural risk (odds ratio 0.93; 95% confidence interval 0.79-1.75; P = .82). Further analyses by device failed to show linkage with adverse events complicating coronary angioplasty, atherectomy, and stenting. Moreover, in the entire CAD group (n = 1000), the polymorphism even showed a trend to underrepresentation (odds ratio 0.83; 95% confidence interval 0.69-1.004, P = .054). Conclusions These results indicate that the A1166C polymorphism neither represents a risk factor for adverse events complicating coronary interventions nor seems to have significant impact on further long-term processes such as development and severity of CAD. (Am Heart J 2000;140:170-5.)