Increased levels of uric acid (UA) have been shown to be correlated with many clinical conditions. Uric acid may adversely affect the insulin signalling pathway inducing insulin resistance (IR). Several studies report the association between arterial stiffness (AS), an early indicator of atherosclerosis, and UA. The purpose of the present study was to evaluate the association between UA and AS, considering the potential role of IR. We enrolled 1114 newly diagnosed, never-treated hypertensive patients. Insulin resistance was assessed by the homeostatic model assessment (HOMA) index. Arterial stiffness was evaluated as the measurement of the carotid–femoral pulse wave velocity (PWV). The study cohort was divided into subgroups, according to increasing tertiles of UA. The mean values of UA were 5.2 ± 1.6 mg/dL in the overall population. Pulse wave velocity was linearly correlated with UA (p < 0.0001), HOMA (p < 0.0001), high sensitivity C-reactive protein (p < 0.0001), systolic blood pressure (p < 0.0001) and LDL cholesterol (p = 0.005). Uric acid was the strongest predictor of PWV and was associated with the highest risk for increased AS. The interaction analysis showed that the joint effect of increased UA and HOMA was significantly higher than that expected in the absence of interaction under the additive model, indicating that the two biomarkers synergically interacted for promoting vascular damage. Our data showed that UA interacted with IR to increase AS in a large cohort of newly diagnosed, never-treated hypertensive patients.
Vitamin D deficiency is linked to cardiac dysfunction, vascular remodeling, metabolic syndrome and insulin resistance (IR). The aim of the present study was to evaluate the association between vitamin D levels and cardiovascular (CV) organ damage in a large cohort of newly diagnosed treatment-naïve hypertensive patients, and the role of IR in this context. We enrolled 500 Caucasian individuals, without CV or renal complications. Subjects underwent a complete evaluation and measurements of vitamin D, standard laboratory determinations and instrumental examination, including echocardiography and applanation tonometry. Linear regression analyses were performed to assess the correlation between pulse wave velocity (PWV) and left ventricular mass index (LVMI) with different covariates. PWV was significantly correlated with age (p < 0.0001), LDL cholesterol (p < 0.0001), BMI (p = 0.001), pulse pressure (PP) (p = 0.005) and high sensitivity C-reactive protein (hs-CRP) (p = 0.006), while an inverse correlation was observed with vitamin D levels (p < 0.0001), Matsuda index (p < 0.0001) and estimated glomerular filtration ratio (e-GFR) (p = 0.006). LVMI significantly correlated with PP (p < 0.0001), hs-CRP (p < 0, 0001) and age (p = 0.001), while an inverse relationship was observed with vitamin D levels (p < 0.0001), Matsuda’s insulin sensitivity index (ISI) (p < 0.0001) and e-GFR (p < 0.0001). Vitamin D was the strongest predictor of PWV and LVMI, explaining, respectively, 28.3% and 19.1% of their variation. Our study suggests that low vitamin D might be a biomarker of end-organ damage.
Aim Heart failure (HF) is associated to endothelial dysfunction, a pathological condition characterized by imbalance between the production of vasoconstrictor and vasodilator factors, increase in the production of cytokines, down-regulation of eNOS, platelets activation and increased oxidative stress. Furthermore, endothelial dysfunction promotes the increase of arterial stiffness, augmenting myocardial damage. Sacubitril/Valsartan (sac/val) is used in the treatment of HF reduced ejection fraction (HFrEF) and has been proven effective in reducing CV disease progression and all-cause mortality in HFrEF patients. The aim of the study was to evaluate the effect of sac/val on endothelial dysfunction and arterial stiffness in patients with HFrEF, at baseline and after 6 months of treatment. Moreover, we evaluated the effects of sac/val on oxidative stress levels and platelets activation. Materials Methods We enrolled 46 Caucasian patients (mean age 70.1±7.1), suffering from HFrEF. Inclusion criteria were LVEF<35, functional class NYHA II or III. All clinical evaluation and laboratory tests were performed at baseline and after 6 months of treatment. The serum values of the markers of oxidative stress (8-isoprostane, NOX-2) and platelets activation (Sp-selectin, GPVI) were assessed with ELISA sandwich. Endothelial function was estimated with the measurement of the reactive hyperemia index (RHI); arterial stiffness (AS) was evaluated with the measurement of carotid-femoral pulse wave velocity (PWV), augmentation pressure (AP) and augmentation index (AI). Results The mean dose of sac/val was 180.5±110 mg without serious adverse events. At 6 months, data showed a significant improvement in in hemodynamic and clinical parameters such as heart rate (HR) (p<0.0001), NT-ProBNP (p<0.0001), fasting plasma glucose (FPG) (p<0.0001). Furthermore, there was a significant reduction in oxidative stress, platelets activation and inflammatory indices. We observed a significant improvement in PWV (p<0.0001), AI (p<0.0001), AP (p<0.0001) and RHI (p<0.0001). A linear correlation analysis was performed to assess the association between vascular parameters and different covariates expressed as Δ variation between baseline and follow-up. ΔPWV was directly correlated with ΔHOMA (p=0.037), ΔIL-6 (p=0.034), ΔTNF-α (p=0.001), Δ8-isoprostane (p=0.016), ΔNox-2 (p=0.01), ΔGP6 (p=0.018), ΔSp-selectin (p=0.023); ΔRHI was inversely correlated with ΔHOMA (p=0.003), ΔIL-6 (p=0.004), ΔTNF-α (p=0.023), ΔCRP (p=0.011), Δ8-isoprostane (p=0.012), ΔNox-2 (p=0.01), ΔGP6 (p=0.014), ΔSp-selectin (p=0.015). From stepwise multivariate linear regression model, ΔTNF-α was the stronger predictor of ΔPWV, justifying 48.5% of its variation and ΔSp-selectin was the major predictor of ΔRHI explaining 23.2% of its variation. Conclusion The treatment with sac/val improved endothelial dysfunction and arterial stiffness, due to reduced levels of oxidative stress, platelet activation and inflammation.
Systemic Sclerosis (SSc) is an autoimmune disorder characterized by organ and tissue fibrosis in which the incidence of atherosclerosis and cardiovascular events is increased, although the exact underlying mechanism remains unclear. Arterial stiffness is a marker of vascular damage that can predict cardiovascular events; therefore, this study aimed to assess the augmentation index (AIx) and pulse wave velocity (PWV), markers of stiffness, in a Systemic Sclerosis population and to detect potentially associated variables. Fourteen female Systemic Sclerosis patients and 14 age- and sex-matched controls were enrolled. Demographic, anthropometric, sero-hematological parameters and disease characteristics were collected for each participant. Arterial stiffness was evaluated using an applanation tonometry system. No differences were found between groups, except for BMI, fasting blood glucose, red blood cells count, hemoglobin, and treatment. Patients had increased augmentation index than the controls (p = 0.008). PWV was significantly decreased in SSc patients compared with the controls (p = 0.007). PWV was correlated with age (r = 0.462; p = 0.048) and BMI (r = 0.458; p = 0.050). Finally, patients with no specific auto-antibody pattern had greater AIx than those expressing anticentromere antibodies. Our study demonstrated that SSc patients had greater AIx, but lower PWV than the controls. In addition, few variables were correlated to arterial stiffness. Further studies are necessary to validate these findings and to establish medication’s role in modifying cardiovascular risk.
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