title: Both hepatitis C virus and Chlamydia pneumoniae infection are related to the progression of carotid atherosclerosis in patients undergoing lipid lowering therapy.
abstract: Recent experimental and epidemiological findings suggest that infectious agents may play a role in the development and progression of atherosclerosis. We previously reported that Chlamydia pneumoniae (C. pneumoniae) infection reduces the effectiveness of lipid-lowering therapy for carotid atherosclerosis and that this micro-organism may play a role in the progression of atherosclerosis. In this study, we investigated the possible association between hepatitis C virus (HCV) infection and carotid arteriosclerosis. A total of 165 asymptomatic hypercholesterolemic patients were randomized to receive probucol (500 mg/day, n=82) or pravastatin (10 mg/day, n=83) and were followed for 2 years. The 2-year change of the maximum common carotid artery intima-media thickness (Max-IMT) was the primary endpoint, while the Max-IMT and the incidence of major cardiovascular events were secondary endpoint. All serum samples were tested for antibody to HCV (anti-HCV) by enzyme-linked immunosorbent assay (ELISA), and all anti-HCV-positive samples were assayed for HCV RNA. Patients without HCV infection (n=25) showed a significant reduction of Max-IMT (-10.9%) (p<0.0001), while a small decrease of Max-IMT was noted in the patients with HCV infection (n=25) (-0. 3%). Significant differences in the reduction of serum total cholesterol and LDL cholesterol were found between patients with and without HCV infection (both p<0.0001). No significant difference in therapeutic effect was noted between the probucol and the pravastatin groups. After adjustment for confounding risk factors, both C. pneumoniae infection and anti-HCV positivity were associated with a greater risk of an increase in Max-IMT (8.5635 [1.3738-15.7532], p<0.05, 9.5040 [0.2886-18.7194], p<0.05, respectively). These findings suggest that both chronic HCV infection and C. pneumoniae infection can reduce the effectiveness of lipid-lowering therapy for carotid atherosclerosis, and that the HCV may play a role in the progression of atherosclerosis in HCV infected patients.
authors.affiliation: Department of General Medicine, Kyushu University Hospital.
authors.forename: Yasunori
authors.initials: Y
authors.lastname: Sawayama
authors.forename: Kyoko
authors.initials: K
authors.lastname: Okada
authors.forename: Shinji
authors.initials: S
authors.lastname: Maeda
authors.forename: Hachiro
authors.initials: H
authors.lastname: Ohnishi
authors.forename: Norihiro
authors.initials: N
authors.lastname: Furusyo
authors.forename: Jun
authors.initials: J
authors.lastname: Hayashi
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D002340:Carotid Artery Diseases / Q000209:etiology* / Q000517:prevention & control*; D023521:Chlamydophila Infections / Q000150:complications*; D016993:Chlamydophila pneumoniae; D018450:Disease Progression; D005260:Female; D006526:Hepatitis C / Q000150:complications*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use*; D011341:Probucol / Q000627:therapeutic use*
chemical_list: D000924:Anticholesteremic Agents; D017035:Pravastatin; D011341:Probucol