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Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review
Ahmed Babiker1, Jean Jeudy2, Seth Kligerman2
1Providence Hospital, Washington, DC, USA.
Insights
Hepatitis C virus (HCV) infection is linked to cardiovascular disease (CVD). Treating HCV may reduce the risk of developing or worsening CVD, improving patient outcomes.
Area of Science:
- Hepatology
- Cardiology
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) infection affects 170 million globally, causing chronic liver disease.
- HCV is a potential risk factor for cardiovascular disease (CVD), but its independent role is debated.
- Existing literature presents mixed findings on the association between HCV and CVD.
Purpose of the Study:
- To review the association between HCV infection and subclinical/clinical CVD.
- To explore potential mechanisms linking HCV to increased CVD risk.
- To evaluate the impact of HCV therapy on CVD outcomes.
Main Methods:
- Literature review of studies on HCV and CVD.
- Analysis of proposed pathophysiological mechanisms.
- Examination of evidence on HCV treatment efficacy for CVD.
Main Results:
- HCV infection, especially chronic cases, is consistently linked to increased subclinical CVD.
- Evidence suggests a potential increase in clinical CVD outcomes, morbidity, and mortality.
- Successful HCV treatment with sustained viral suppression correlates with improved CVD endpoints.
Conclusions:
- HCV infection contributes to increased CVD risk through inflammation, endothelial dysfunction, and arterial wall invasion.
- HCV treatment may mitigate CVD morbidity and mortality.
- New direct antiviral agents offer a feasible approach to HCV eradication, potentially reducing CVD burden.
Abstract:
Hepatitis C (HCV) infection has an estimated global prevalence of 2.5%, causing chronic liver disease in 170 million people worldwide. Recent data has identified HCV infection as a risk factor for subclinical and clinical cardiovascular disease (CVD), but these data have been mixed and whether HCV is an independent risk factor for development of CVD remains controversial. In this review, we present the literature regarding the association of HCV with subclinical and clinical CVD and the possible underlying mechanisms leading to increased CVD among those infected with HCV. HCV infection leads to increased CVD via direct and indirect mechanisms with chronic inflammation, endothelial dysfunction and direct invasion of the arterial wall cited as possible mechanisms. Our review showed that HCV infection, particularly chronic HCV infection, appears to lead to increased subclinical CVD most consistently and potentially also to increased clinical CVD outcomes, leading to increased morbidity and mortality. Furthermore, the majority of studies evaluating the impact of HCV therapy on CVD morbidity and mortality showed an improvement in subclinical and clinical CVD endpoints in patients who were successfully treated and achieved sustained viral suppression. These results are of particular interest following the development of new direct antiviral agents which have made HCV eradication simple and feasible for many more patients globally, and in doing so may possibly reduce CVD morbidity and mortality in those with chronic HCV infection.
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