4.4 Article

Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men

Journal

AIDS
Volume 24, Issue 2, Pages 243-253

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QAD.0b013e328333ea9e

Keywords

atherosclerosis; cardiovascular risk factors; coronary artery disease; coronary computed tomography angiography; HIV

Funding

  1. Bristol Myers Squibb, Inc
  2. NIH [K23 HL092792, K24 DK064545, F32 HL088991, T32 HL076136, M01 RR01066-25S1]
  3. NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR001066] Funding Source: NIH RePORTER
  4. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [F32HL088991, K23HL092792, T32HL076136] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [K24DK064545, P30DK040561] Funding Source: NIH RePORTER

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Objective: The degree of subclinical coronary atherosclerosis in HIV-infected patients is unknown. We investigated the degree of subclinical atherosclerosis and the relationship of traditional and nontraditional risk factors to early atherosclerotic disease using coronary computed tomography angiography. Design and methods: Seventy-eight HIV-infected men (age 46.5 +/- 6.5 years and duration of HIV 13.5 +/- 6.1 years, CD4 T lymphocytes 523 +/- 282; 81% undetectable viral load), and 32 HIV-negative men (age 45.4 +/- 7.2 years) with similar demographic and coronary artery disease (CAD) risk factors, without history or symptoms of CAD, were prospectively recruited. 64-slice multidetector row computed tomography coronary angiography was performed to determine prevalence of coronary atherosclerosis, coronary stenosis, and quantitative plaque burden. Results: HIV-infected men demonstrated higher prevalence of coronary atherosclerosis than non-HIV-infected men (59 vs. 34%; P=0.02), higher coronary plaque volume [55.9(0-207.7); median(IQR) vs. 0(0-80.5) mu l; P=0.02], greater number of coronary segments with plaque [1 (0-3) vs. 0 (0-1) segments; P=0.03], and higher prevalence of Agatston calcium score more than 0 (46 vs. 25%, P=0.04), despite similar Framingham 10-year risk for myocardial infarction, family history of CAD, and smoking status. Among HIV-infected patients, Framingham score, total cholesterol, low-density lipoprotein, CD4/CD8 ratio, and monocyte chemoattractant protein 1 were significantly associated with plaque burden. Duration of HIV infection was significantly associated with plaque volume (P=0.002) and segments with plaque (P=0.0009) and these relationships remained significant after adjustment for age, traditional risk factors, or duration of antiretroviral therapy. A total of 6.5%(95% confidence interval 2-15%) of our study population demonstrated angiographic evidence of obstructive CAD (>70% luminal narrowing) as compared with 0% in controls. Conclusion: Young, asymptomatic, HIV-infected men with long-standing HIV disease demonstrate an increased prevalence and degree of coronary atherosclerosis compared with non-HIV-infected patients. Both traditional and nontraditional risk factors contribute to atherosclerotic disease in HIV-infected patients. (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins

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