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The association between chronic hepatitis C infection and cardiovascular risk
Author(s) -
Pateria P.,
Jeffrey G. P.,
MacQuillan G.,
Speers D.,
Ching H.,
Chinnaratha M. A.,
Watts G. F.,
Adams L. A.
Publication year - 2016
Publication title -
internal medicine journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 1444-0903
DOI - 10.1111/imj.12936
Subject(s) - medicine , pulse wave velocity , arterial stiffness , insulin resistance , endothelial dysfunction , subclinical infection , cardiology , brachial artery , intima media thickness , vascular resistance , vascular disease , gastroenterology , insulin , blood pressure , carotid arteries
Background Vascular disease is a common cause of death in patients with chronic hepatitis C (CHC) infection; however, the association between CHC and atherosclerosis is unclear. Aims To determine whether patients with CHC have increased subclinical vascular disease and whether genotype or antiviral treatment modifies this risk. Methods Fifty CHC patients and 22 age‐matched and sex‐matched healthy controls underwent clinical and biochemical assessment for vascular risk factors. In addition, vascular risk was assessed by measuring arterial stiffness (aortic augmentation index and carotid‐femoral pulse wave velocity (PWV)), endothelial dysfunction (brachial artery flow‐mediated dilatation (FMD) and dilatation post‐glycerol trinitrate administration) and carotid intima‐media thickness (CIMT). Assessment was repeated in subset of CHC patients ( n = 12) undergoing antiviral treatment 18 months after initiation of treatment. Results Baseline vascular risk factors and measures of arterial stiffness, endothelial dysfunction and CIMT were not different between cases and controls ( P > 0.2 for all). Genotype 1 CHC patients had greater endothelial dysfunction with lower FMD (8.2 ± 3.5% vs 10.9 ± 5.2%, P = 0.03) and higher right CIMT (0.6 ± 0.1 mm vs 0.5 ± 0.07 mm, P = 0.04) compared with non‐genotype 1. Patients who achieved sustained virological response (7/12) showed significant improvement in insulin resistance (homeostasis model of assessment of insulin resistance 2.3 ± 1.2 vs 1.8 ± 0.8, P = 0.02) and arterial stiffness (PWV 7.4 ± 1.1 m/s vs 6.5 ± 0.6 m/s, P = 0.04). Conclusions Subclinical vascular disease is not greater in CHC subjects compared with controls. However, among CHC subjects, genotype 1 infection is associated with greater endothelial dysfunction and increased carotid‐intima medial thickness compared with non‐genotype 1 infection. Successful viral eradication may improve insulin resistance and arterial stiffness.