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The association between chronic hepatitis C infection and cardiovascular risk
P Pateria1, G P Jeffrey1,2, G MacQuillan1,2
1Department of Gastroenterology and Hepatology, Sir Charles Gairdner Hospital.
Insights
Chronic hepatitis C (CHC) patients do not show increased subclinical vascular disease compared to controls. However, genotype 1 infection is linked to worse endothelial dysfunction and carotid intima-media thickness.
Area of Science:
- Cardiovascular Medicine
- Hepatology
- Virology
Background:
- Vascular disease is a significant cause of mortality in chronic hepatitis C (CHC) patients.
- The relationship between CHC infection and atherosclerosis remains incompletely understood.
- This study investigates subclinical vascular disease in CHC patients.
Purpose of the Study:
- To assess subclinical vascular disease in CHC patients compared to healthy controls.
- To determine if hepatitis C virus (HCV) genotype influences vascular disease risk.
- To evaluate the impact of antiviral treatment on vascular parameters in CHC patients.
Main Methods:
- Compared 50 CHC patients and 22 controls using clinical, biochemical, and vascular assessments.
- Measured arterial stiffness (pulse wave velocity), endothelial function (flow-mediated dilatation), and carotid intima-media thickness (CIMT).
- Reassessed vascular parameters in a subset of CHC patients after 18 months of antiviral therapy.
Main Results:
- No significant differences in baseline vascular risk factors or measures between CHC patients and controls.
- CHC patients with genotype 1 infection exhibited greater endothelial dysfunction and increased CIMT compared to non-genotype 1.
- Sustained virological response in treated CHC patients correlated with improved insulin resistance and arterial stiffness.
Conclusions:
- Subclinical vascular disease is not elevated in CHC patients overall compared to controls.
- Hepatitis C virus genotype 1 is associated with increased endothelial dysfunction and CIMT.
- Successful antiviral treatment leading to viral eradication may improve insulin resistance and arterial stiffness in CHC patients.
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.
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