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 wit...
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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.
There was no increased prevalence of patent foramen ovale in patients with myocardial infarction and normal coronary arteries. This suggests that paradoxical embolism through this intra-atrial passage is an uncommon c...
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There was no increased prevalence of patent foramen ovale in patients with myocardial infarction and normal coronary arteries. This suggests that paradoxical embolism through this intra-atrial passage is an uncommon cause for this syndrome.
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