Hepatitis C and risk of coronary atherosclerosis – A systematic review

Olubamwo, Olubunmi; Aregbesola, Alex; Miettola, Juhani; Kauhanen, Jussi; Tuomainen, Tomi Pekka

doi:10.1016/j.puhe.2016.04.005

Cited by 20 publications

(21 citation statements)

References 26 publications

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“…Nonetheless, a meta-analysis by Olubamwo et al 66 concluded that HCV infection may increase the risk of occurrence and the severity of coronary atherosclerosis, which seems consistent with the results of the vast majority of studies evaluating the effect of HCV infection on severity of CAD.…”

Section: Hcv and Angiographic Cadsupporting

confidence: 63%

“…The preponderance of the data suggests an increased risk for the development of coronary artery atherosclerosis as well as an increase in the severity of CAD based on the majority of case-control studies in which HCV-infected patients underwent coronary angiography. 11 , 51 – 53 , 63 , 64 , 66 However, it is uncertain whether the likely increased risk of coronary atherosclerosis translates to an increased risk of MI among these patients since many studies were unable to demonstrate an association between HCV infection and rates of MI. For example in the study by Forde et al , 58 HCV infection did not increase the risk of MI but the mean follow-up period was only 3.2 years, which may have limited the ability to detect an association given the chronic nature of atherosclerosis and the cumulative risk that eventually leads to the sentinel clinical event of MI.…”

Section: Discussionmentioning

confidence: 99%

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Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review

Babiker

Jeudy

Kligerman

et al. 2017

Journal of Clinical and Translational Hepatology

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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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Section: Hcv and Angiographic Cadsupporting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review

Babiker

Jeudy

Kligerman

et al. 2017

Journal of Clinical and Translational Hepatology

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“…AS risk increases with age and therefore, presumably, duration of chronic viral infection. Current evidence indicates that the risk of a person with chronic hepatitis C developing coronary atherosclerosis is about triple the risk in uninfected persons (OR = 3.06, 95% CI = 1.99-4.72) (58). Virologic cure will be lead to improvements in some AS risk factors outlined above such as insulin resistance (37) In addition virologic cure will result in increases in serum cholesterol and LDL-C (60), creating a combination of circumstances that will aggravate early atherosclerotic lesions.…”

Section: Virologic Cure and Atherosclerosismentioning

confidence: 99%

Hepatitis C virus and atherosclerosis: A legacy after virologic cure?

Bassendine

Nielsen

Bridge

et al. 2017

Clinics and Research in Hepatology and Gastroenterology

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We discuss possible factors involved in the aetiopathogenesis of atherosclerosis in chronic HCV and hypothesise that an important mechanism underlying the development of AS is the presence of circulating low-density immune complexes that induce an inflammatory response.We suggest that HCV particles may be inducing an antibody response to lipoproteins present in the lipo-viral particles and sub-viral particles -a concept similar to the more general 'autoantibody' response to modified LDL.After virologic cure some AS risk factors will recede but an increase in serum cholesterol could result in progression of early atherosclerotic lesions, leaving a legacy from persistent HCV infection that has clinical and therapeutic implications.

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“…HCV primarily attacks hepatocytes causing necrosisespecially during acute infection marked by extremely high values of alanine aminotransferase (ALT) activity. In addition, hepatitis C infection triggers inflammation through stimulation of production of pro-inflammatory cytokines, which is associated with insulin resistance and hepatic steatosis [30] and has an association with atherosclerosis [31]. Furthermore, chronic HCV infection causes liver cirrhosis and hepatocellular carcinoma (HCC) in a relatively large proportion of infected individuals.…”

Section: Introductionmentioning

confidence: 99%

Markers of liver fibrosis and apoptosis in patients with HIV mono-infection and HIV/HCV co-infection

Vīksna¹,

Eksteina²,

Madelāne³

et al. 2019

HIV & AIDS Review

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Introduction: Human immunodeficiency virus (HIV)/hepatits C virus (HCV) co-infection has a significant impact on liver-related morbidity and mortality. Among many other pathogenic mechanisms leading to accelerated hepatic disease are liver fibrosis and hepatocyte apoptosis. Hence the objective of this investigator-initiated cross-sectional study was to analyse the plasma levels of hyaluronic acid, cytokeratin-18, and cytochrome c in order to assess their impact on progression of liver disease in patients with HIV/HCV co-infection comparing to those with HIV mono-infection. Material and methods: There were 80 patients with HIV infection included in the study. HCV co-infection was in 46 (57.5%) patients and HIV mono-infection in 34 patients. Blood levels of hyaluronic acid were tested using a Hyaluronic Acid test Kit, cytokeratin-18 neoepitope levels using M30-Apoptose ELISA test, and cytochrome c using human Cytochrome c ELISA test. Results: The levels of cytokeratin-18 and of hyaluronic acid were significantly higher in the group of patients with HIV/HCV co-infection. The differences in the level of cytochrome c were not significant. The analysis revealed that the main effect of HCV co-infection on the level of cytokeratin-18 is indirect. It is mediated by the level of hyaluronic acid. Conclusions: The progression of liver disease in patients with HIV/HCV co-infection is more pronounced compared to those with HIV mono-infection. It is shown by the higher plasma levels of hyaluronic acid, which is a relevant liver fibrosis marker and hepatocyte apoptosis marker cytokeratin-18 in patients with HIV/HCV co-infection. The hyaluronic acid level is important in assessing the impact of HCV co-infection on liver apoptosis.

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Hepatitis C and risk of coronary atherosclerosis – A systematic review

Cited by 20 publications

References 26 publications

Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review

Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review

Hepatitis C virus and atherosclerosis: A legacy after virologic cure?

Markers of liver fibrosis and apoptosis in patients with HIV mono-infection and HIV/HCV co-infection

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