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Evidence for association between hepatitis C virus seropositivity and coronary artery disease

For the full text see.....





Hepatitis C Is a Risk Factor for Heart Disease

February 2, 2010

February is American Heart Month. Since Hepatitis C has been proven to be a risk factor for coronary artery disease, the usual ways to reduce heart disease risk is insufficient for those with the virus.

For the full tesxt see.........


.Association between hepatitis C virus seropositivity, carotid-artery plaque, and intima-media thickening.



We investigated the relation between positivity for hepatitis C virus (HCV) and carotid-artery plaque and carotid intima-media thickening by analysing cross-sectional data of individuals undergoing a general health screening test. Of 4784 individuals enrolled, 104 (2.2%) were seropositive for HCV. After adjustment for confounding risk factors, HCV seropositivity was found to be associated with an increased risk of carotid-artery plaque (odds ratio 1.92 [95% CI 1.56-2.38], p=0.002) and carotid intima-media thickening (2.85 [2.28-3.57], p<0.0001). These findings suggest a possible role for chronic hepatitis C in the pathogenesis of carotid arteri


Circ J. 2008 Dec;72(12):1960-5. Epub 2008 Oct 29.

Hepatitis C infection is associated with increased coronary artery atherosclerosis defined by modified Reardon severity score system.


Department of Cardiology, Dicle University, Diyarbakir.



The link between arteriosclerotic disease in the carotid or coronary artery and chronic hepatitis Cvirus (HCV) infection has been shown in some studies although other studies have produced contrary results. However, the effect of chronic HCV infection on the extension or severity of coronary artery disease (CAD) has not been determined so the aim of the present study was to determine the effect of HCV infection on the severity of CAD.


The study group comprised 139 HCV seropositive and 225 HCV seronegative patients with angiographically documented CAD. A modified scoring system of Reardon et al was used. There were no significant differences between groups in terms of sex, age, hypertension, diabetes mellitus, smoking or family history. Levels of C-reactive protein and fibrinogen were significantly higher in the HCV seropositive group (p<0.001) and the Reardon severity score was higher (8.75+/-1.69 vs 6.01+/-1.80, p<0.001). After adjustment, HCV seropositivity still represented an independent predictor for severity of coronary atherosclerosis demonstrated by higher Reardon severity score with an odds ratio of 2.018 (95% confidence interval 1.575-2.579, p<0.001).


HCV infection is an independent predictor for increased coronary atherosclerosis, as demonstrated by higher Reardon severity score.


Gut. 2007 Aug;56(8):1105-10. Epub 2006 Sep 6.

Mnd cardiovascular risk profiles and hepatitis C virus infection in rural Egypt.etabolic a


Department of Community, Environmental and Occupational Medicine, Ain Shams University, Cairo, Egypt.



To investigate the relationship between lipid profiles and diabetes with past and chronic hepatitis C virus (HCV) infection among village residents of Egypt.


Fasting lipids and glucose profiles were compared among adults never infected with HCV (negative HCV antibodies), infected in the past (positive HCV antibodies and negative HCV RNA) and chronically infected (positive HCV antibodies and HCV RNA).


Of the 765 participants, 456 (59.6%) were female, and median age was 40 (range 25-88) years. Chronic HCV infection was present in 113 (14.8%) and past infection in 67 (8.8%). After adjustment for age and sex, participants with chronic HCV infection had lower plasma low density lipoproteins (LDL) cholesterol and triglyceride levels compared with those never infected (age and sex adjusted differences (95% CI) were -19.0 (-26.3 to -11.7) mg/dl and -26.2 (-39.0 to -13.3) mg/dl, respectively). In contrast, participants with cleared HCV infection had higher triglyceride levels compared with those never infected (age and sex adjusted difference (95% CI) was +16.0 (0.03 to 31.9) mg/dl). In multivariate analysis, participants with chronic HCV infection were more likely to have diabetes (OR 3.05, 95% CI 1.19 to 7.81) compared with those never infected, independent of LDL cholesterol levels.


In conclusion, this community based study has shown that in a single population, chronic HCV infection is associated with glucose intolerance and, despite that, a favourable lipid pattern. An intriguing finding was the high triglyceride levels observed among participants with past infection, suggesting that elevated triglycerides at the time of acute infection may facilitate viral clearance.






Stroke. 2010 Dec;41(12):2894-900. Epub 2010 Oct 21.

Hepatitis C virus infection and increased risk of cerebrovascular disease.


Graduate Institute of Epidemiology, College of Public Health, National Taiwan University, Taipei, Taiwan.



The association between hepatitis C virus (HCV) infection and cerebrovascular disease remains controversial. This study aimed to assess the risk of lethal cerebrovascular diseases associated with chronic HCV infection.


In this community-based prospective cohort study, 23 665 residents (aged 30 to 65 years) were enrolled in 1991 to 1992. They were personally interviewed using structured questionnaires and provided blood samples for various serological and biochemical tests at study entry. Serum HCV RNA level and HCV genotype were tested for participants seropositive for antibodies against HCV (anti-HCV). Deaths from cerebrovascular disease during follow-up were ascertained by computerized linkage with National Death Certification profiles from 1991 to 2008 (International Classification of Diseases, 9th Revision 430 to 438). Multivariate-adjusted hazard ratio with 95% CI was estimated for each risk predictor.


There were 255 cerebrovascular deaths during 382 011 person-years of follow-up. The cumulative risk of cerebrovascular deaths was 1.0% and 2.7% for seronegatives and seropositives of anti-HCV, respectively (P<0.001). The hazard ratio (95% CI) of cerebrovascular death was 2.18 (1.50 to 3.16) for anti-HCV seropositives after adjustment for several conventional risk factors of cerebrovascular disease. Compared with participants seronegative for anti-HCV as the referent, the multivariate-adjusted hazard ratio (95% CI) was 1.40 (0.62 to 3.16), 2.36 (1.42 to 3.93), and 2.82 (1.25 to 6.37), respectively, for anti-HCV-seropositive participants with undetectable, low, and high serum levels of HCV RNA (P<0.001 for trend). However, no significant association was observed between HCV genotype and cerebrovascular death.


Chronic HCV infection is an independent risk predictor of cerebrovascular deaths showing a biological gradient of cerebrovascular mortality with increasing serum HCV RNA level.






J Hepatol. 2012;56 Suppl 1:S56-65.

The interaction of metabolic factors with HCV infection: does it matter?


Department of Internal Medicine, University of Turin, Italy.


Given the pandemic spread of the hepatitis C virus (HCV) infection and the metabolic syndrome (MS), the burden of their interaction is a major public health issue, bound to increase in the near term. A better appreciation of the clinical consequences of the relationship between HCV and MS is needed, not only due to their potential synergism on liver disease severity, but also because of the multifaceted interactions between HCV and glucose and lipid metabolism. HCV infection per se does not carry an increased risk of MS, but is able to perturb glucose homeostasis through several direct and indirect mechanisms, leading to both hepatic and extrahepatic insulin resistance. This translates into accelerated liver disease progression (including the development of hepatocellular carcinoma), reduced response to antivirals and, in susceptible individuals, increased risk of developing full-blown type 2 diabetes. HCV may also cause hepatic steatosis, especially in patients infected with genotype 3, although the clinical impact of viral steatosis is debated. Possibly as a result of HCV-induced insulin resistance, and despite a paradoxically favourable lipid profile, the cardiovascular risk is moderately increased in chronic hepatitis C. In addition, the interaction with the MS further increases the risks of cirrhosis, hepatocellular carcinoma, diabetes, and cardiovascular events. Thus, targeted lifestyle and pharmacological measures are urgently warranted in chronichepatitis C with metabolic alterations.




Hepatology. 2011 Dec 2. doi: 10.1002/hep.25508. [Epub ahead of print]

Carotid atherosclerosis and chronic hepatitis C: A prospective study of risk associations.


Sezione di Gastroenterologia, Di.Bi.M.I.S, Universitŕ di Palermo, Italia.



There are contrasting results in studies of cardiovascular risk in patients with genotype 1 chronic hepatitis C (G1 CHC). We evaluated the prevalence of carotid atherosclerosis compared with a control population in order to assess the potential association between atherosclerosis, host and viral factors, and liver histological features. In all, 174 consecutive biopsy-proven G1 CHC patients were evaluated by anthropometric and metabolic measurements and 174 patients attending an outpatient cardiology unit were used as controls. Intima-media thickness (IMT) and carotid plaques, defined as focal thickening of >1.3 mm at the level of common carotid, were evaluated using ultrasonography. All G1 CHC biopsies were scored by one pathologist for staging and grading, and graded for steatosis. Carotid plaques were found in 73 (41.9%) G1 CHC patients compared with 40 (22.9%) control patients (P < 0.001). Similarly, G1 CHC patients had a greater IMT compared with control patients (1.04 ± 0.21 versus 0.90 ± 0.16; P < 0.001). Multivariate logistic regression analysis showed that older age (odds ratio [OR] 1.047, 95% confidence interval [CI]: 1.014-1.082, P = 0.005), and severe hepatic fibrosis (OR 2.177, 95% CI: 1.043-4.542, P = 0.03),were independently linked to the presence of carotid plaques. In patients ≤55 years, 15/6 7 cases with F0-F2 fibrosis (22.3%) had carotid plaques, compared with 11/21 (52.3%) with F3-F4 fibrosis (P = 0.008). By contrast, in patients >55 years the prevalence of carotid plaques was similar in those with or without severe fibrosis (25/43, 58.1% versus 22/43, 51.1%; P = 0.51). Conclusion: Severe hepatic fibrosis is associated with a high risk of early carotid atherosclerosis in G1 CHC patients.



J Clin Virol. 2010 Jan;47(1):72-5. Epub 2009 Nov 5.

Hepatitis C virus RNA localization in human carotid plaques.


Clinica Medica Generale e Cardiologia, Department of Medical and Surgical Critical Care, University of Florence, Italy.



Hepatitis C virus (HCV) infection has certain characteristics that enable it to play an important role in atherosclerosis. Some studies report its association with an increased risk of carotid artery plaque.


The aim of this study was to evaluate the presence of HCV genomic sequences and replicative intermediates in plaque tissues.


A cohort of consecutive, prospectively recruited patients with HCV infection and chronic ischemic heart disease from the Cardiology, Vascular Surgery and Hepatology Units of a University Hospital in Florence, Italy, were studied.


Positive-strand HCV RNA was detected in seven carotid plaque tissues from anti-HCV-positive patients and was not detected in the nine carotid plaque tissues obtained from anti-HCV-negative patients. In three patients, HCV RNA was found in carotid plaque and not in serum. HCV replicative intermediates were detected in three plaque samples. Direct sequencing of HCV RNA from the plaque and serum showed HCV genotypes 2 (five cases) and 1 (two cases).


The novel finding of HCV RNA sequences in plaque tissue strongly suggests an active local infection. This in turn makes it conceivable that t




Dig Liver Dis. 2007 Sep;39 Suppl 1:S55-60.

HCV infection facilitates asymptomatic carotid atherosclerosis: preliminary report of HCV RNA localization in human carotid plaques.


Clinica Medica Generale e Cardiologia, Department of Medical and Surgical Critical Care, University of Florence, Florence, Italy.



Clinical and experimental evidence suggests that hepatitis C virus (HCV) infection shows peculiar characteristics that strongly support a role in the development of atherosclerosis. We aimed to investigate whether (a) HCV infection can facilitate asymptomatic carotid lesions and (b) the presence of HCV RNA sequences can be shown in plaque tissues.


The status of carotid arteries, studied as intima-media thickness (IMT) in carotid bifurcation and prevalence and severity of plaques in internal carotid artery, was investigated by high-resolution B-mode ultrasonography in 31 HCV seropositive (HCV+) and in 120 age-matched HCV seronegative (HCV-) subjects evaluated for cardiovascular risk factors. The atherosclerotic risk profile, inflammation markers and main liver function tests were also studied in all patients. HCV RNA sequences were investigated by highly sensitive reverse transcriptase-polymerase chain reaction (RT-PCR) in plaque tissues and serum of 2 HCV+ patients who underwent carotid revascularization.


Genomic and antigenomic HCV RNA strands were evidenced within both the carotid plaque tissues examined. The prevalence of an IMT > 1 mm, but not the prevalence and severity of internal carotid plaques, was significantly higher (P < 0.001) in HCV+ than in HCV patients. The atherosclerotic risk profile for traditional and inflammatory factors did not differ between the HCV+ and HCV- groups. Main liver function tests did not differ between the two groups. HCV positivity was significantly associated with >1 mm IMT (P < 0.01) according to univariate analysis, and this association remained significant in multivariate regression analysis.

Conclusions: The novel finding of HCV RNA sequences within carotid plaques suggests a local pro-atherogenetic action of the virus inside the plaque. On the whole our data strongly support that HCV infection facilitates the occurrence of carotid atherosclerotic lesions.







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