Prognostic impact of arterial stiffness in patients with symptomatic peripheral arterial disease.

OBJECTIVES: Arterial stiffness (AS) is increasingly recognized as an independent risk factor in different high-risk populations. Whether changes in AS can predict prognosis in patients with symptomatic peripheral arterial disease (PAD) has never been investigated. The aim of the present study was to test the hypothesis that AS is an independent predictor of all-cause and cardiovascular disease (CVD) mortality in patients with symptomatic PAD. METHODS: A cohort of 117 symptomatic PAD patients (aged 62.3 ± 7.7 years) were prospectively recruited from the Department of Vascular Surgery, Tartu University Hospital, between 2002 and 2010. The AS was measured using pulse wave analysis and assessment of pulse wave velocity (PWV). RESULTS: During the follow-up period (mean 4.1 ± 2.2 years) there were 32 fatal events. Kaplan-Meier analysis showed that the probability of all-cause and CVD mortality decreased with increasing small artery elasticity (SAE), as estimated by the log-rank test (p = .004; p = .005, respectively). By contrast, large artery elasticity, augmentation index, and aortic and brachial PWV were not significantly related to mortality. In a Cox proportional hazard model, SAE above the median was associated with decreased all-cause and CVD mortality after adjustment for confounding factors: relative risk (RR), 0.37; 95% confidence interval (CI), 0.17-0.81; p = .01; RR, 0.11; 95% CI, 0.01-0.86; p = .04, respectively). CONCLUSIONS: This study provides the first evidence, obtained from an observational study, that decreased small artery elasticity is an independent predictor of all-cause and CVD mortality in patients with symptomatic PAD.

Aortic stiffness and vitamin D are independent markers of aortic calcification in patients with peripheral arterial disease and in healthy subjects.

OBJECTIVE: Arterial stiffness is a significant determinant of cardiovascular risk and is related to vascular calcification. Vitamin D may regulate arterial calcification and has been associated with cardiovascular survival benefits. However, data about the relationship between arterial stiffness, aortic calcification and vitamin D levels in patients with peripheral arterial disease (PAD) and in healthy subjects are limited. We examined the potential association between aortic calcification, arterial stiffness and vitamin D levels in patients with symptomatic PAD and in healthy individuals. METHODS: We studied 78 men with PAD (aged 63 ± 7 years) and 74 healthy men (aged 61 ± 10 years). Aortic pulse wave velocity (aPWV) was determined by applanation tonometry using the Sphygmocor device. Aortic calcification score (ACS) was quantified by computed tomography. Serum 25-hydroxyvitamin D (25(OH)D) levels were measured using a radioimmune assay. RESULTS: ACS (4.9(2.3-8.9) vs. 0.2(0.03-1.6) (cm³); p < 0.01), aPWV (9.8 ± 2.4 vs. 8.2 ± 1.6 (m s⁻¹; p < 0.01) and 25(OH)D (15.1 ± 5.4 vs. 19.0 ± 5.9 (ng ml⁻¹); p < 0.01) were different in the patients compared with the controls. In multivariate analysis, ACS was independently determined by 25(OH)D, aPWV, calcium and age in patients with PAD (R² = 0.49; p < 0.001) and by 25(OH)D, aPWV, cholesterol/high-density lipoprotein (HDL) and age in the control group (R² = 0.55; p < 0.001). Increased aPWV and lower levels of 25(OH)D were associated with decreased ankle-brachial pressure index (p = 0.03). CONCLUSION: These results indicate that calcification of the aorta is independently associated with aortic stiffness and serum 25(OH)D level in patients with PAD and in healthy subjects. Aortic stiffness and abnormal vitamin D level may contribute to vascular calcification and are related to higher severity grade of atherosclerotic disease.

Effects of a synbiotic product on blood antioxidative activity in subjects colonized with Helicobacter pylori.

AIM: To evaluate the impact of the consumption of a synbiotic product on the antioxidative activity markers of blood in asymptomatic H. pylori-colonized persons. METHODS AND RESULTS: Fifty-three healthy adult volunteers without gastric symptoms participated in a randomized, double-blind placebo-controlled study. The crossover consumption of the enterocoated capsules containing antioxidative Lactobacillusfermentum ME-3, Lact. paracasei 8700:2 and Bifidobacterium longum 46 with Raftilose P95 lasted for 3 weeks and did not change the H. pylori colonization. In H. pylori-positive subjects the sera values of total antioxidative status (TAS) were significantly lower compared to H. pylori-negative subjects (0.97 vs 1.05 mmol l(-1), P = 0.008). After the consumption of the synbiotic, TAS values (0.97 vs 1.03 mmol l(-1), P = 0.004) increased, while the ratio between oxidized and reduced glutathione (0.035 vs 0.030, P = 0.016) decreased in H. pylori-positive subjects. CONCLUSIONS: The consumption of a synbiotic containing an antioxidative probiotic strain improved the reduced systemic antioxidative activity in H. pylori-colonized asymptomatic subjects. SIGNIFICANCE AND IMPACT OF THE STUDY: A synbiotic product containing an antioxidative probiotic strain may be useful in the reduction of systemic oxidative stress in H. pylori infection.

Arterial elasticity is associated with endothelial vasodilatory function and asymmetric dimethylarginine level in healthy subjects.

Arterial stiffening may be linked to the reduced bioactivity of nitric oxide (NO) and increased plasma concentrations of the endogenous NO synthase inhibitor asymmetric dimethylarginine (ADMA). The aim of this study was to investigate whether large (C1) and small artery (C2) elasticity is associated with endothelial function index (EFI) and plasma concentration of ADMA. We included 63 healthy subjects, aged 19 to 70 years, in the study. EFI, C1 and C2 were assessed by pulse wave analysis (PWA) and ADMA level was measured using an enzyme-linked immunoassay. Linear regression analysis revealed significant positive correlation between EFI and both C1 and C2 (R = 0.29, p = 0.02; R = 0.38, p = 0.002, respectively). A significant inverse association occurred between ADMA and C1 as well as C2 (R = -0.32, p = 0.03; R = -0.37, p = 0.009, respectively). In multiple regression analysis, C2 was determined by EFI, ADMA, age and BMI, and C1 was correlated with EFI, age and BMI. These findings suggest that endothelial vasodilatory dysfunction and accumulation of ADMA may be important mechanisms underlying reduced arterial elasticity in healthy subjects.