Cardiovascular events in chronic hepatitis C

Abstract

In chronic hepatitis C, initial stiffness of at least 7 kPa was associated with cardiovascular events. Rapid progression of liver stiffness does not seem to be associated with these events.

Hepatitis C virus eradication by direct-acting antiviral agents improves carotid atherosclerosis in patients with severe liver fibrosis

“…This issue could stem by the fact that, in a short-medium term scenario, IMT could be more sensitive that a stable plaque to changes in inflammatory and fibrogenic mediators related to HCV infection. HCV in fact can lead to increased cardiovascular risk by leading to insulin resistance [45], by inducing a systemic inflammatory status via NK and TH1-mediated responses [46], via increase in TNFalpha and IL-6 levels [47,48] and reduction in adiponectin levels [49], and via endothelial damage directly related to the HCV infection [50,51]. However, we cannot exclude a potential effect of virological eradication on carotid plaques in a longer follow-up.…”

The Effect of Viral Clearance Achieved by Direct-Acting Antiviral Agents on Hepatitis C Virus Positive Patients with Type 2 Diabetes Mellitus: A Word of Caution after the Initial Enthusiasm

“…These data suggest that the improvement of extrahepatic manifestations of HCV infection (in particular, cardiovasculopathies and nephropathies) coinciding with the most frequent complications of diabetic disease may improve after viral clearance due not only to glycometabolic control amelioration, but also to other mechanisms yet to be established. In the case of nephropathy, it is likely that HCV eradication may lead to an improvement in vasculitis-cryoglobulinemic damage [56,57]; the beneficial effect of viral eradication on cardiovascular diseases may be derived from the disappearance of the systemic inflammatory status [58], the decrease in TNF-α and IL-6 levels [59,60], and the increase in adiponectin levels [61].…”

Hepatitis C virus and cardiovascular: A review

“…Hepatic steatosis and visceral obesity could contribute to this inflammatory status by prompting production of reactive oxygen species and inflammatory cytokines [18] . Along this line, endothelial damage directly related to the HCV infection [58] , [59] , or expression of a vasculitis due to mixed cryoglobulinemia [60] could further contribute to the link between HCV infection and higher cardiovascular risk.…”