Association of Hepatitis C Virus Seropositivity With Inflammatory Markers and Heart Failure in Persons With Coronary Heart Disease: Data From the Heart and Soul Study

Section of General Internal Medicine, Department of Medicine, Boston University School of Medicine/Boston Medical Center, Boston, MA 02118, USA.
Journal of cardiac failure (Impact Factor: 3.05). 06/2009; 15(5):451-6. DOI: 10.1016/j.cardfail.2008.12.003
Source: PubMed


How hepatitis C virus (HCV) affects coronary heart disease (CHD) risk factors and outcomes is largely unknown.
Among a cohort of patients with stable CHD, we examined the association between HCV seropositivity and levels of inflammatory markers (C-reactive protein [CRP], fibrinogen, interleukin-6, and tumor necrosis factor [TNF]-alpha) and risk for the following outcomes: death, cardiovascular (CV) events, and heart failure events. A total of 84 (8.6%) participants were found to be seropositive for HCV. HCV-seropositive patients were found to have significantly lower adjusted mean levels of CRP (2.6 vs. 4.4; P < .01) and fibrinogen (340 vs. 398; P < .01), but higher levels of TNF-alpha (7.1 vs. 4.8; P < .01). Age-adjusted rates for HCV seropositive vs. seronegative were as follows: death 93 vs. 42/1,000p-y (P < .01), CV events 62 vs. 40 (P=.13), and heart failure 76 vs. 29 (P < .01). After adjustment for demographic and clinical factors, HCV remained significantly associated with an increased risk for heart failure events (HR=2.13; 95% CI: 1.19-3.80).
In this cohort with CHD, HCV seropositive participants had higher rates of death, CV events, and heart failure hospitalizations during follow-up. After adjustment for CV risk factors, HCV seropositivity remained independently associated with risk for heart failure events.

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Available from: Alexander Monto, Mar 27, 2014
    • "Of these, five of the studies were eliminated either because the objective and design of the study were inappropriate, the quality was judged to be poor or there was no risk estimate (Bilora et al., 2002; Bilora et al., 2008; Boddi et al., 2010; Miyajima et al., 2013; Petta et al., 2012). Four of the studies were eliminated because the outcome was not proven to be strictly atherosclerosis related (Butt et al., 2009; Tsui et al., 2009; Lee et al., 2010; Liao et al., 2012). "
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    • "Synthesis and catabolism of APR is regulated by interleukin (IL-1, IL-6, IL-11), tumor necrosis factor (TNF), leukemia inhibitor factor, and oncostatin M. Tissue damage is associated with acceleration of positive APR (ceruloplasmin, C3, A1AG, A2MG, alpha-1 antitrypsin, alpha-1 antichymotrypsin, fibrinogen, haptoglobulin, CRP, and serum amyloid A protein) or deceleration of negative APR (prealbumin, albumin, transferrin, and alpha-2 glycoprotein) synthesis.14 Tsui et al.15 found HCV seropositivity to be associated with lower lipids, CRP and fibrinogen levels, and higher levels of IL-6 and TNF-α. "
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