Background. Osteoprotegerin (OPG) is a marker and regulator of arterial calcification, and it is related to cardiovascular survival in haemodialysis patients. The link between OPG and aortic stiffening-a consequence of arterial calcification-has not been previously evaluated in this population, and it is not known whether OPG-related mortality risk is mediated by arterial stiffening. Methods. At baseline, OPG and aortic pulse wave velocity (PWV) were measured in 98 chronic haemodialysis patients who were followed for a median of 24 months. The relationship between OPG and PWV was assessed by multivariate linear regression. The role of PWV in mediating OPG related cardiovascular mortality was evaluated by including both OPG and PWV in the same survival model. Results. At baseline mean (standard deviation) PWV was 11.2 (3.3) m/s and median OPG (interquartile range) was 11.1 (7.5-15.9) pmol/L. There was a strong, positive, linear relationship between PWV and lnOPG (P = 0.009, model R 2 = 0.540) independent of covariates. During follow-up 23 patients died of cardiovascular causes. In separate univariate survival models both PWV and lnOPG were related to cardiovascular mortality [hazard ratios 1.31 (1.14-1.50) and 8.96 (3.07-26.16), respectively]. When both PWV and lnOPG were entered into the same model, only lnOPG remained significantly associated with cardiovascular mortality [hazard ratio 1.11 (0.93-1.33) and 7.18 (1.89-27.25), respectively). Conclusion. In haemodialysis patients OPG is strongly related to PWV and OPG related cardiovascular mortality risk is, in part, mediated by increased PWV.Correspondence and offprint requests to: Gabor Speer,

Background: Measuring arterial stiffness (augmentation index (AI), aortic pulse wave velocity (PWV)) in hemodialysis (HD) patients has prognostic significance. To assess its validity, the new oscillometric Arteriograph device (AI_A, PWV_A) was compared to the validated PulsePen tonometer (AI_P, PWV_P). Methods: AI and PWV were measured in 98 patients with both devices before HD. Validity was evaluated by Pearson’s correlation, Bland-Altman analysis, and by assessing the prognostic value of AI and PWV to predict cardiovascular (CV) mortality over 29 months. Results: Correlation between AI_P and AI_A was significant (R = 0.527, p < 0.001). The mean difference of AI values obtained by the two devices was –20.6%, and 30% of the paired AI differences fall outside the ±1 SD boundary of the mean between-device difference. There was no significant correlation between the PWV_P and PWV_A readings (R = 0.173, p = 0.097). The average difference of PWV values by the two devices was –1.2 m/s, and 20.6% of the paired PWV differences fall outside the ±1 SD boundary. In survival analyses, only PWV_P but not PWV_A was significantly related to CV mortality. Conclusion: Lack of correlation between PWV_P and PWV_A and lack of prognostic significance of PWV_A suggest limited validity of Arteriograph to determine PWV in patients on HD.

Background and aims The aim of this study was to develop an integrated central blood pressure–aortic stiffness (ICPS) risk score to predict cardiovascular events. Methods It was a retrospective cohort study. A total of 100 chronic kidney disease (CKD) patients on conservative therapy were included. Pulse wave velocity (PWV), central systolic blood pressure (cSBP), and central pulse pressure (cPP) were measured. A score was assigned to tertiles of PWV (0–2), cPP (0–2), and cSBP (0 to the first and second and 1 to the third tertile) based on each parameter’s ability to individually predict cardiovascular outcome. The sum of these scores and three ICPS risk categories as predictors were studied. Finally, we compared discrimination of the ICPS risk categories with PWV, cSBP, and cPP. Results Adjusted for age and sex, patients in high and very high ICPS risk categories had increased cardiovascular risk (HR: 3.52, 95% CI: 1.65–7.49; HR: 7.56, 95% CI: 3.20–17.85, respectively). High and very high ICPS risk categories remained independent predictors in a model adjusted for multiple CV risk factors (HR: 4.58, 95% CI: 1.65–7.49; HR: 8.56, 95% CI: 3.09–23.76, respectively). ICPS risk categories (Harrell’s C: 0.723, 95% CI: 0.652–0.795) showed better discrimination than PWV (Harrell’s C: 0.659, 95% CI: 0.586–0.732, p = 0.028) and cSBP (Harrell’s C: 0.660, 95% CI: 0.584–0.735, p = 0.008) and there has been a tendency of significance in case of cPP (Harrell’s C: 0.691, 95% CI: 0.621–0.761, p = 0.170). Conclusion The ICPS score may clinically importantly improve the identification of CKD patients with elevated cardiovascular risk.

Aortic stiffening and aortic calcification are risk factors for cardiovascular events in hemodialysis (HD) patients, and these 2 risk factors are interrelated. Sevelamer decreases aortic calcification but its effect on aortic stiffness has not been investigated previously. Thirteen HD patients commencing sevelamer treatment and 13 matched controls were followed for 11 months. Aortic pulse wave velocity (PWV), augmentation index (AIx), and levels of inhibitors of vascular calcification (fetuin-A, matrix-GLA-protein, osteoprotegerin/RANKL) were measured at baseline and at the end of follow-up, and the differences between the groups were compared. Determinants of the changes in PWV during follow-up were assessed by multivariate linear regression. At baseline, PWV was 9.93 (2.10) m/s in sevelamer-treated patients and 9.20 (2.84) m/s in control patients (p=0.464). By the end of follow-up, PWV decreased by 0.83 (2.3) m/s in sevelamer-treated patients while it increased by 0.93 (1.88) m/s in controls (p=0.042). The direction of changes in AIx were similar, but not statistically significant. There were no significant differences in the levels of inhibitors of calcification either at baseline or during follow-up. In multivariate linear regression sevelamer treatment, diabetes, heart rate, and C-reactive protein were related to the change in PWV. These data suggest that sevelamer treatment is associated with an improvement in aortic stiffness in HD patients, but it does not seem to affect serum levels of inhibitors of vascular calcification.

PWV calculated using suprasternal notch-to-femoral distance minus suprasternal notch-to-carotid distance provides the strongest relationship to cardiovascular mortality. Longer torso weakens the predictive value of PWV, possibly due to more tortuosity of the aorta hence, more error introduced when using surface tape measurements.