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Higher Lipids Raise Acute MI Risk 22% to 64% in
Untreated HCV RNA+ Veterans
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CROI 2014, March 3-6, 2014, Boston
Mark Mascolini
Higher total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides boosted the risk of acute myocardial infarction (MI) more than 20% in a 6000-person analysis of untreated HCV RNA-positive veterans without HIV infection. These associations were not seen in HCV antibody-positive veterans without detectable HCV RNA.
University of Pittsburgh researchers and colleagues noted that prior work links HCV infection to a higher risk of coronary artery disease. But understanding the impact of HCV infection on cardiovascular disease is complicated by multiple risk factors in people with HCV infection and by the impact of HCV infection on lipids, which fall as HCV infection gets worse.
To address these issues, the investigators assessed the impact of lipid levels on acute MI in the Electronically Retrieved Cohort of HCV-Infected Veterans (ERCHIVES), a national cohort of HCV-positive veterans and matched HCV-negative controls. This analysis included veterans with a positive HCV antibody test at some point from 2001 through 2008. For each antibody-positive veteran, the researchers matched antibody-negative veterans by year, age, race, gender, and geographical location. The study excluded women, people with at least 4 weeks of HCV therapy, those with HIV infection, smokers, and people with a diagnosis of cardiovascular disease, hypertension, stage 3 or worse chronic kidney disease, diabetes, or chronic obstructive pulmonary disease. The investigators divided lipid levels into brackets based on National Cholesterol Education Program guidelines.
The study included 35,457 HCV antibody-positive and 45,299 antibody-negative veterans. Age averaged 51.4 in the HCV group and 51.3 in the HCV-negative group; 55% in both groups were white and one quarter black. Average body mass index was significantly lower in the HCV-positive group (27 versus 29 kg/m(2), P < 0.0001). The HCV group included a lower proportion with total cholesterol above 200 mg/dL (30% versus 47%), LDL cholesterol above 130 mg/dL (27% versus 42%), and triglycerides above 150 mg/dL (27% versus 37%) (P < 0.0001 for all lipid differences). Similar proportions of HCV positive and negative veterans had high-density lipoprotein (HDL) cholesterol below 40 mg/dL (37% and 35%).
The researchers determined acute MI risk in 5979 antibody-positive veterans also positive for HCV RNA and 167 antibody-positive veterans not positive for HCV RNA. Among HCV RNA-negative veterans, Cox regression analysis adjusting for age, race, body mass index, and other lipids determined that LDL cholesterol at or above 190 mg/dL versus below 100 mg/dL raised MI risk, but the association fell short of statistical significance (hazard ratio [HR] 13.36, 95% confidence interval [CI] 0.81 to 220.16, P = 0.07). No other lipid level predicted acute MI in HCV antibody-positive but RNA-negative veterans.
In contrast, among HCV RNA-positive veterans, adjusted analysis linked six lipid levels to MI risk when compared with ideal levels:
Raised risk of acute MI:
Total cholesterol above 240: HR 1.22, 95% CI 1.06 to 1.40, P = 0.01
LDL cholesterol at or above 190: HR 1.64, 95% CI 1.30 to 2.07, P < 0.01
Triglycerides 150 to 199: HR 1.25, 95% CI 1.09 to 1.43, P < 0.01
Triglycerides 200 to 499: HR 1.28, 95% CI 1.12 to 1.45, P < 0.01
Lowered risk of acute MI:
HDL cholesterol 40 to 59: HR 0.73, 95% CI 0.65 to 0.81, P < 0.01
HDL cholesterol at or above 60: HR 0.63, 95% CI 0.53 to 0.74, P < 0.01
The researchers concluded that higher lipid levels boost acute MI risk in HCV RNA-positive male veterans. HCV viremic participants with high LDL cholesterol had a 64% higher MI risk when compared with viremic veterans with ideal LDL levels. Further analysis determined that lipid-lowering therapy eliminated MI risk. Lack of an MI association in antibody-positive but RNA-negative veterans, the researchers suggested, could reflect the low number of such veterans in the analysis.
The investigators proposed that "optimizing lipid levels and eliminating HCV viral replication are potential strategies to consider in lowering the risk of acute MI in HCV-infected persons."
Reference
1. Butt AA, Chew KW, Corey K, et al. HCV viremia and the risk of acute myocardial infarction at various lipid levels. CROI 2014. Conference on Retroviruses and Opportunistic Infections. March 3-6, 2014. Boston. Abstract 685.
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