TY - JOUR
T1 - Risk of cardiovascular disease due to chronic hepatitis C infection
T2 - A review
AU - Babiker, Ahmed
AU - Jeudy, Jean
AU - Kligerman, Seth
AU - Khambaty, Miriam
AU - Shah, Anoop
AU - Bagchi, Shashwatee
N1 - Publisher Copyright:
© 2017 Authors.
PY - 2017
Y1 - 2017
N2 - 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 regard-ing 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 in-vasion 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.
AB - 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 regard-ing 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 in-vasion 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.
KW - Atherosclerosis
KW - Cardiovascular disease
KW - Cerebrovascular disease
KW - Coronary heart disease
KW - Hepatitis C
UR - http://www.scopus.com/inward/record.url?scp=85047568929&partnerID=8YFLogxK
U2 - 10.14218/JCTH.2017.00021
DO - 10.14218/JCTH.2017.00021
M3 - Review article
AN - SCOPUS:85047568929
SN - 2225-0719
VL - 5
SP - 343
EP - 362
JO - Journal of Clinical and Translational Hepatology
JF - Journal of Clinical and Translational Hepatology
IS - 4
ER -