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20; 95% CI, 1.45�C7.02; P?=?0.004], but also low-grade RAS (covariate-adjusted OR, 2.97; 95% CI, 1.08�C8.12; P?=?0.032) independently predict CV events. A Kaplan�CMeier curve of event-free survival rates is shown in Fig.?2(c) (log-rank P?50% in women (HR 3.32 vs. 1.74) and in older (>50?years at baseline) subjects (HR 3.30 vs. 2.43). The HRs did not materially change in unadjusted and adjusted analysis when exclusion was performed for subjects with previous CVD, diabetes http://www.selleckchem.com/products/bay-57-1293.html mellitus or hypercholesterolaemia. Also, additional adjustment for pulse pressure and/or mean arterial pressure did not substantially change the results (Fig.?3). This was also true when http://www.selleck.cn/products/CAL-101.html omitting subjects radiographically classified by MRA instead of DSA or with exclusion of patients aged 50%) independently predicts adverse CV outcome [1, 16]. This study shows for the first time that in hypertensive patients CV risk is also considerably augmented in subjects with RAS http://www.selleckchem.com/products/gsk2126458.html pro-oxidant and procoagulant activities in experimental models and in humans, thereby aggravating the systemic atherosclerotic process [10]. Bearing this in mind, and the fact that angiotensin II concentrations increase predominantly in the early phases of RAS, we hypothesized that even low-grade renal arterial diameter reductions might in the long run translate into adverse CV outcome. In the analysis of a predefined MACE end-point, we demonstrated after full adjustment for confounding factors that in subjects with high-grade stenoses CV risk was increased by almost a factor of 3 (P?=?0.002), which is roughly in line with earlier studies addressing this topic [1, 16]. Interestingly, even a low-grade RAS showed a more than doubled risk (P?=?0.038) on CV events compared with the control group. One has to keep in mind, however, that from our data no cause�Ceffect relationships can and should be drawn.