In this issue of Angiology, Ticulescu et al assess the role of arterial stiffness in relation to established risk factors in predicting cardiovascular (CV) remodeling. They assessed left ventricular mass index (LVMi) and carotid intima media thickness (IMT) in patients with moderate renal impairment. Outpatients with stage III chronic kidney disease ([CKD] n 1⁄4 89) and with stage II CKD (n 1⁄4 52) underwent echocardiographic and supra-aortic trunk scanning; carotid IMT was measured 1 cm beneath the carotid bifurcation, whereas arterial stiffness was assessed at the right carotid as the b index. As Ticulescu et al point out, this echotracking estimation of arterial stiffness represents a useful and feasible technique that allows the evaluation of both heart and vessels during one examination. The 2 groups were similar for established CV risk factors (ie, age, gender, hypertension, hypercholesterolemia, diabetes mellitus [DM], and smoking) and relevant drug treatment. No significant differences were found in terms of blood pressure, biochemical parameters (except for creatinine clearance), IMT, LVMi, and presence of carotid plaques. After multivariate analysis, the b index of arterial stiffness was an independent predictor of IMT (along with age, DM, and hypercholesterolemia) in patients with stage III CKD; the most powerful predictor was DM, followed by age, b index, and hypercholesterolemia. In the stage II CKD group, DM was the only independent predictor of IMT. As discussed by Ticulescu et al, this finding could reflect the functional effect of arterial wall remodeling at different stages of CKD; the intimal layer plays a main role in atherogenesis during earlier stages of CKD, whereas in more advanced CKD, the atherosclerotic process mainly involves the medial layer. Chronic kidney disease is recognized as a CV risk factor, and these patients should be treated accordingly. On the other hand, arterial stiffness, regulated by numerous factors, such as mean arterial pressure, structural alterations of the arterial wall, endothelial dysfunction, and inflammation, may accelerate the atherosclerotic process. There are several different noninvasive methods for the assessment of arterial stiffness including pulse wave velocity (PWV), relating change in vessel diameter (or area) to distending pressure, arterial pulse waveform analysis, ambulatory arterial stiffness index, augmentation index, and b index; PWV is the most recognized and established index of arterial stiffness. Arterial stiffness and CKD are closely linked by shared risk factors and associated increased CV mortality. In a cohort of hemodialysis patients, both carotid IMT and b index of arterial stiffness were independently predictive of CV mortality even after adjustment for other relevant covariates, implicating the distinct roles of stiffness and thickness of arterial wall in the pathogenesis of CV disease. Furthermore, arterial stiffness assessed by aortofemoral PWV was the only arterial index (among carotid IMT, systemic arterial compliance, and carotid-derived augmentation index) independently associated with CV outcome in patients with stages IV and V CKD. It should be noted that arterial stiffness is a predictor for CV events not only in renal patients but also in the general population, in patients with hypertension, impaired glucose intolerance, and coronary artery disease. Furthermore, a recent meta-analysis showed that aortic PWV was a strong predictor of CV events and all-cause mortality in 15 877 individuals; the higher the baseline CV risk, the higher the predictive ability of arterial stiffness. Interestingly, aortic PWV was a stronger independent predictor (r 1⁄4 .48; P 1⁄4 .002) of a 25% decline in renal function or initiation of renal replacement therapy compared with systolic blood pressure (r 1⁄4 .17; P 1⁄4 .039) and urine-proteinto-creatinine ratio (r 1⁄4 .20; P 1⁄4 .021) in patients with stages III and IV CKD.
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