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Effects of hepatitis C virus on cardiovascular risk in infected patients: a comparative study
C P M S Oliveira1, C R Kappel, E R Siqueira
1Department of Gastroenterology, University of Sao Paulo School of Medicine, Sao Paulo, Brazil.
Insights
Hepatitis C virus (HCV) infection is linked to intermediate cardiovascular risk and elevated pro-inflammatory cytokines, suggesting a potential role in atherosclerosis development. Further research is needed to clarify this association.
Area of Science:
- Hepatology
- Cardiology
- Immunology
Background:
- The association between Hepatitis C virus (HCV) infection and cardiovascular disease pathogenesis remains incompletely understood.
- HCV may influence cardiovascular risk through inflammatory pathways.
Purpose of the Study:
- To assess the direct impact of HCV on cardiovascular risk.
- To correlate cardiovascular risk with pro-inflammatory and anti-inflammatory cytokine levels in HCV patients.
Main Methods:
- Study included 62 treatment-naive, non-obese, non-diabetic HCV genotype 1 patients and compared them to healthy blood donors.
- Evaluated cardiovascular risk using the Framingham score, serum cytokines (IL-6, IL-10, TNF-α), and traditional cardiovascular risk factors.
- Excluded patients with pre-existing cardiovascular diseases, hypertension, renal failure, cancer, or on specific medications.
Main Results:
- HCV patients exhibited an intermediate cardiovascular risk (Framingham score median 12%) and significantly higher levels of pro-inflammatory cytokines (IL-6, TNF-α) compared to controls.
- The Framingham score directly correlated with total cholesterol and diastolic blood pressure, and inversely with HDL-C.
- Ratios of pro-inflammatory to anti-inflammatory cytokines (TNF-α/IL-10, IL-6/IL-10) were elevated in HCV patients.
Conclusions:
- HCV monoinfection, in non-obese, non-diabetic, treatment-naive individuals, is associated with intermediate cardiovascular risk.
- Elevated pro-inflammatory cytokines (IL-6, TNF-α) are characteristic of HCV infection and may contribute to increased cardiovascular risk.
Abstract:
The role of hepatitis C virus (HCV) in the pathogenesis of atherosclerosis and cardiovascular events is unclear. The aim of this study was to evaluate the direct effect of HCV on cardiovascular risk and correlate it with pro and anti-inflammatory cytokines in patients with HCV. HCV monoinfected patients, genotype 1, naive, non-obese (BMI<30) and non-diabetics were included and compared to controls (blood donors). Patients with prior diagnosis of cardiovascular diseases, hypertension, chronic renal failure, cancer and chronic use of lipid-lowering drugs or immunosuppressants were excluded. Age, BMI, systolic blood pressure (SBP) and diastolic (DBP), fasting glucose and lipid levels were determined. Serum cytokines (IL-6, IL-10 and TNF-α) and Framingham score were also evaluated. 62 HCV patients, 34 (54.8%) were males and none of them was smoking. The Framingham scores (median and 25th and 75th percentiles) were 12% (6.5-14%), showing an intermediate cardiovascular risk in patients with HCV. There was significant direct correlation between Framingham and total cholesterol (p=0.043) and DBP (p=0.007). HDL-C (p=0.002) was inversely correlated with the Framingham score. HCV patients had higher levels of proinflammatory cytokines (IL-6 and TNF-α) compared to controls (p<0.0001) and the relation of proinflammatory/anti-inflammatory TNF-α/IL10 and IL-6/IL10 were higher in HCV patients (p<0.01). The Framingham score was directly correlated to IL-6 and TNF-α, but differences were not statistically significant. Patients with HCV monoinfected, nonobese, naïve and non diabetic have an intermediate cardiovascular risk, as measured by the Framingham score and high levels of proinflammatory cytokines (IL-6 and TNF).
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