Neurovascular alterations in chronic hepatitis C: a case-control study

摘要

Introduction: Hepatitis C is a major health problem: approximately 170 million people are infected with the hepatitis C virus worldwide. It is unclear whether chronic hepatitis C affects atherosclerosis and whether it can cause endothelial and/or autonomic nervous system (ANS) dysfunction. Materials and methods: From April 2008 through April 2009, we studied 76 patients with biopsyconfirmed chronic hepatitis C and no evidence of cirrhosis, ascites, portal hypertension, encephalopathy, or hepatocellular carcinoma. The age-, sex-, BMI- and cardiovascular risk factor- matched control group comprised 76 healthy, HCV-negative individuals with no evidence of liver, autoimmune, or immunoproliferative diseases and no history of cardiovascular events. Twenty five of the hepatitis C patients were treatment-naive; the other 51 had been treated with interferon (but only 25 had persistent virological responses). Color Doppler sonography was used to measure the intima-media-thickness (IMT) of the common and internal carotid arteries. Endothelial function was assessed in the brachial artery with the flow-mediated-dilatation (FMD) test. The ANS was assessed with the tilt, laying to standing, Valsalva, hand grip, deep breath, and stroop tests. Results: The case group (mean age 52 + 13 years) had a significantly higher internal carotid IMT (0.86 + 0.3 vs 0.67 + 0.1 mmfor controls; p = 0.002). Chronic hepatitis C was also associated with an odds ratio for carotid plaque formation (reflected by an IMT > 1.3 mm) of 2.15. Cases also had significantly reduced FMD in the brachial artery (0.46 + 0.9 vs 0.76 + 0.7 for controls; p = 0.005) and significantly altered sympathetic and parasympathetic function (p = 0.001 vs controls in the Valsalva, hand grip, deep breath, and stroop tests). Within the case group, all alterations were more severe in patients with significant viremia. Discussion: Our findings suggest that chronic hepatitis C may be a nonclassic cardiovascular risk factor since it seems to influence the onset of pre-atherosclerotic lesions and to promote atherosclerotic plaque formation in patients with pre-existing increases in carotid IMT. It also seems to cause dysfunctions of the vascular endothelium and ANS. Conclusions: Chronic hepatitis C may increase cardiovascular risk and promote ANS dysfunctions, particularly when patients have experienced treatment failure and have persistent viremia. These patients may require cardiovascular and neurologic follow-up.