OBJECTIVES: Obesity and metabolic syndrome (MetS) are associated with structural and functional vascular abnormalities. MetS and its components may increase arterial stiffness and the risk of cardiovascular events. However, the relationship of MetS and its components, including obesity, with arterial stiffness is still not fully understood. SUBJECTS AND METHODS: In a group of 116 patients undergoing treatment for hypertension, we searched for the relationships between parameters of MetS and aortic stiffness expressed by pulse wave velocity (PWVAo). PWVAo was measured using an arteriograph working on the oscillometric principle, and pulse wave analysis (PWA) for noninvasive assessment of the parameters of central hemodynamics. RESULTS: From the cluster of parameters of MetS we found a signifi cant association between body mass index (BMI) and aortic stiffness, and between fasting plasma glucose/type 2 diabetes (FPG/T2DM) and aortic stiffness. We did not fi nd signifi cant relationships between other components of MetS (HDL cholesterol and triglycerides) and aortic stiffness, based on the infl uence of hypolipidemic therapy. Arterial stiffness increased with age and was higher in females. CONCLUSION: Arterial stiffness was associated with age, sex, and MetS components (BMI and FPG/T2DM). Surprisingly, the parameters of dyslipidemia do not infl uence stiffness parameters, which can be explained by hypolipidemic therapy. The infl uence of hypolipidemic therapy should therefore be borne in mind when evaluating arterial tree function (Tab. 7, Ref. 62).
Introduction: In the ODYSSEY OUTCOMES trial, alirocumab improved cardiovascular outcomes and reduced death after acute coronary syndrome (ACS). Median follow-up was 2.8 yrs (range 2-5). The effects of alirocumab on long-term survival are unknown. Objective: To calculate projected life span and potential survival gains with alirocumab vs placebo after ACS using validated nonparametric age-based methods. Methods: In ODYSSEY OUTCOMES (NCT01663402), 18,924 patients with recent ACS and elevated atherogenic lipoproteins despite high-intensity or maximum-tolerated statin therapy were randomized to alirocumab or placebo. All-cause death was a secondary trial outcome. Age-based estimates of projected survival and event-free (all-cause death, nonfatal myocardial infarction, nonfatal ischemic stroke) survival were calculated. In each treatment arm at every year of age, lifespan was estimated from area under the survival curve, to a maximum of 85 yrs. Differences in areas under the survival curves provide an estimate of the benefit of alirocumab on survival. Results: Mean (SD) baseline age was 58.5 (9.3) yrs. Mean survival benefits with alirocumab vs placebo ranged from 0.03 to 1.62 yrs, decreasing with age and becoming neutral at age 80-85 yrs. For example, at age 40, estimated survival was another 37.5 yrs with alirocumab and 35.9 yrs with placebo (difference 1.62 yrs [95% CI, 0.30-2.94]; P =0.016). At age 60, it was 20.5 vs 19.6 yrs (difference 0.88 [95% CI, 0.16-1.61]; P =0.017); at age 75 it was 8.8 vs 8.3 (difference 0.57 [0.09-1.05]; P =0.019); and at age 80, it was 4.5 vs 4.5 years (difference 0.03 [-0.28 to 0.35]; P =0.83). Mean event-free survival benefit similarly ranged from 1.85 to 0.0 yrs. Conclusions: Modeling suggests that long-term treatment with alirocumab may result in a meaningful increase in survival among patients less than 80 yrs of age. This analysis may facilitate shared decision-making with patients. Funding: Sanofi, Regeneron Pharmaceuticals
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