title: Comparison of Angiographic Burden of Coronary Artery Disease in Patients With Versus Without Hepatitis C Infection.
abstract: Hepatitis C virus (HCV) infection is thought to be associated with an increased risk of coronary heart disease (CHD) events, perhaps secondary to increased inflammation. We sought to examine the angiographic burden of coronary artery disease (CAD) in patients with HCV compared to HCV-negative patients. All consecutive HCV RNA-positive patients (n = 61) who underwent coronary angiography at the University of Arkansas for Medical Sciences from 2001 to 2013 were identified. A parallel group of HCV-negative controls (n = 61), matched for age, gender, and indication for coronary angiography served as control. Angiographic burden of CAD was assessed by computing Gensini scores. Statistical analysis was performed using SPSS 21.0. Patients with HCV had significantly lower levels of total and low-density lipoprotein cholesterol. Preangiographic use of aspirin and statin was significantly lower in the HCV cohort. Number of patients with obstructive CAD was less in HCV group (23% vs 39%, p <0.05). However, angiographic Gensini score was similar in both groups. There was no correlation between HCV RNA titers and Gensini score (p = 0.9, analysis of variance). In conclusion, patients with active HCV infection have similar angiographic CAD burden as HCV-negative patients. Furthermore, viral load does not appear to correlate with atherosclerosis burden. Patients with HCV have less-obstructive CAD and less-frequent use of aspirin and statins.
authors.affiliation: Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas. Electronic address: nvpothineni@uams.edu.
authors.forename: Naga V
authors.initials: NV
authors.lastname: Pothineni
authors.affiliation: Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
authors.forename: Yogita
authors.initials: Y
authors.lastname: Rochlani
authors.affiliation: Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
authors.forename: Srikanth
authors.initials: S
authors.lastname: Vallurupalli
authors.affiliation: Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
authors.forename: Swathi
authors.initials: S
authors.lastname: Kovelamudi
authors.affiliation: Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
authors.forename: Zubair
authors.initials: Z
authors.lastname: Ahmed
authors.affiliation: Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
authors.forename: Abdul
authors.initials: A
authors.lastname: Hakeem
authors.affiliation: Division of Cardiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas.
authors.forename: Jawahar L
authors.initials: JL
authors.lastname: Mehta
mesh_terms: D001131:Arkansas / Q000453:epidemiology; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000453:epidemiology / Q000209:etiology; D005260:Female; D005500:Follow-Up Studies; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology; D018937:Hepatitis C Antibodies / Q000032:analysis; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000821:virology; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000032:analysis; D012189:Retrospective Studies; D012307:Risk Factors
chemical_list: D018937:Hepatitis C Antibodies; D012367:RNA, Viral