Insulin-resistance HCV infection-related affects vascular stiffness in normotensives. Issue 1 (January 2015)

• Record Type: Journal Article
• Authors: Perticone, Maria; Maio, Raffaele; Tassone, Eliezer Joseph; Tripepi, Giovanni; Di Cello, Serena; Miceli, Sofia; Caroleo, Benedetto; Sciacqua, Angela; Licata, Anna; Sesti, Giorgio; Perticone, Francesco
• Is Part Of: Atherosclerosis. Volume 238:Issue 1(2015)
• Page Start: 108
• Page End: 112
• Publication Date: 2015-01
• Subjects: Arteriosclerosis -- Periodicals; Electronic journals; 616.136
• DOI: 10.1016/j.atherosclerosis.2014.11.025
• Languages: English
• ISSNs: 0021-9150

Abstract

<abstract xml:lang="en" abstract-type="author" id="abs0010"> <title id="sectitle0010">Abstract</title> <sec> <p id="abspara0010"> <bold>Background and Aims</bold>. Arterial stiffness evaluated as pulse wave velocity, is an early marker of vascular damage and an independent predictor for cardiovascular events. We investigated if the insulin resistance/hyperinsulinemia chronic hepatitis C virus infection-related could influence arterial stiffness. <bold>Methods</bold>. We enrolled 260 outpatients matched for age, body mass index, gender, ethnicity: 52 with never-treated uncomplicated chronic hepatitis C virus infection (HCV<sup>+</sup>), 104 never-treated hypertensives (HT) and 104 healthy subjects (NT). Pulse wave velocity was evaluated by a validated system employing high-fidelity applanation tonometry. We also measured: fasting plasma glucose and insulin, total, LDL- and HDL-cholesterol, triglyceride, creatinine, e-GFR-EPI, HOMA, quantitative HCV-RNA. <bold>Results</bold>. HCV<sup>+</sup> patients with respect to NT had an increased pulse wave velocity (7.9 ± 2.1 vs 6.4 ± 2.1 m/s; <italic>P</italic> < 0.0001), similar to that observed in HT group (8.8 ± 3.2 m/s). HCV<sup>+</sup> patients, in comparison with NT, had higher triglyceride, creatinine, fasting insulin and HOMA (3.2 ± 1.3 vs 2.5 ± 1.0; <italic>P</italic> < 0.0001). At linear regression analysis, the correlation between pulse wave velocity and HOMA was similar in HT (<italic>r</italic> = 0.380, <italic>P</italic> < 0.0001) and HCV<sup>+</sup> (<italic>r</italic> = 0.369, <italic>P</italic> = 0.004) groups. At multiple regression analysis, HOMA resulted the major determinant of pulse wave velocity in all groups, explaining respectively 11.8%, 14.4% and 13.6% of its variation in NT, HT and HCV<sup>+</sup>. At correlational analysis hepatitis C virus-RNA and HOMA demonstrated a strong and linear relationship between them, explaining the 72.4% of their variation (<italic>P</italic> = 0.022). <bold>Conclusions</bold>. We demonstrated a significant and direct correlation between HOMA and pulse wave velocity in HCV<sup>+</sup> patients, similar to that observed in hypertensives.</p> </sec> </abstract>