Atherosclerosis. 2015 Jan;238(1):108-12.

Insulin-resistance HCV infection-related affects vascular stiffness in normotensives.

Perticone M1, Maio R2, Tassone EJ2, Tripepi G3, Di Cello S2, Miceli S2, Caroleo B2, Sciacqua A2, Licata A4, Sesti G2, Perticone F2.
  • 1Department of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Italy. Email: mariaperticone@hotmail.com.
  • 2Department of Medical and Surgical Sciences, University Magna Græcia of Catanzaro, Italy.
  • 3CNR-IBIM, National Research Council-Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension, Reggio Calabria, Italy.
  • 4Biomedical Department of Internal and Specialistic Medicine, University of Palermo, Italy.

 

Abstract

Background and Aims. 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. Methods. We enrolled 260 outpatients matched for age, body mass index, gender, ethnicity: 52 with never-treated uncomplicated chronic hepatitis C virus infection (HCV(+)), 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. Results. HCV(+) patients with respect to NT had an increased pulse wave velocity (7.9 ± 2.1 vs 6.4 ± 2.1 m/s; P < 0.0001), similar to that observed in HT group (8.8 ± 3.2 m/s). HCV(+) patients, in comparison with NT, had higher triglyceride, creatinine, fasting insulin and HOMA (3.2 ± 1.3 vs 2.5 ± 1.0; P < 0.0001). At linear regression analysis, the correlation between pulse wave velocity and HOMA was similar in HT (r = 0.380, P < 0.0001) and HCV(+) (r = 0.369, P = 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(+). At correlational analysis hepatitis C virus-RNA and HOMA demonstrated a strong and linear relationship between them, explaining the 72.4% of their variation (P = 0.022). Conclusions. We demonstrated a significant and direct correlation between HOMA and pulse wave velocity in HCV(+) patients, similar to that observed in hypertensives.

KEYWORDS: Arterial stiffness; Chronic hepatitis C virus infection; Insulin resistance

PMID: 25461736

 

Supplements:

In the last years growing evidences demonstrated that Hepatitis C Virus (HCV) infection is responsible not only of liver damage per se, but it generates both metabolic and haemodynamic alterations that, taken together, increase the cardiovascular risk of HCV+ patients. About that, our group has recently demonstrated that HCV+ patients show an increased cardiac mass, as well as an impaired metabolic profile, similarly to what observed in hypertensive patients (Perticone M, et al. Hepatology 2014). In particular, the aim of the present study was to investigate if insulin resistance (IR)/hyperinsulinemia, a common condition in HCV+ patients, could influence arterial stiffness. IR is a condition characterized by both an abnormal endogenous insulin production and a reduced tissues sensibility to this hormone; this induces, in turn, increased levels of plasma insulin and its enhanced activity growth factor-like in many organs and tissues (i.e. heart, muscles, etc.). This condition is very frequent in HCV+ patients, for both hepatic and extra-hepatic mechanisms. In particular, in the present study, we investigated if the condition of IR has some effects on arterial stiffness in normotensives HCV+ patients. Arterial stiffness, a physiologic condition increasing with age, is associated with traditional cardiovascular risk factors and its presence increases the risk of cardiovascular events. For this study, arterial stiffness was evaluated through a validated system that employs high-fidelity applanation tonometry (Sphygmocor™; AtCor Medical, Sydney, Australia). The results obtained by this technique can be considered an important surrogate for cardiovascular morbidity and mortality. Surprisingly, HCV+ normotensive patients, compared with healthy subjects, showed an increased arterial stiffness, similarly to what observed in hypertensive patients. Thus, this study demonstrates, for the first time, that the inflammatory process present in HCV infection, interferes with the structure of arterial wall, as well as with cardiac geometry. For this reason, it could be recommended to define the cardiovascular risk profile also in HCV+ patients.

 

MP FotoContact:

Maria Perticone, MD

Department of Experimental and Clinical Medicine

University Magna Graecia of Catanzaro, Italy.

Email: mariaperticone@hotmail.com

 

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