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) μl; 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.

Adenosine stress CT can identify stress-induced myocardial perfusion defects with diagnostic accuracy comparable to SPECT, with similar radiation dose and with the advantage of providing information on coronary stenosis.

Objective In this study, the effects of traditional cardiac risk factors on coronary artery calcium (CAC) score and presence of plaque, including noncalcified plaque, measured by computed tomography coronary angiography, were compared among HIV-infected and non HIV-infected subjects, with respect to the presence of the metabolic syndrome (MS). Design and methods HIV-infected men recruited for the presence of the MS (HIV+MS, n=27) were compared to two control groups, HIV-infected men recruited without regard to metabolic criteria (HIV, n=87), and HIV-negative control men (C, n=40), also recruited without regard to any metabolic criterion. Results All three groups were similar in age, demographic parameters, and smoking. MS was seen in 100% of the HIV+MS group, compared to 28% in the HIV-infected control group and 11% in the HIV-negative controls. HIV+MS subjects had higher mean CAC score than HIV-infected controls (72±25 vs. 30±8, P=0.04, HIV+MS vs. HIV) and HIV-negative controls (72±25 vs. 18±7; P=0.02, HIV+MS vs. C). With respect to CAC, only the HIV+MS group had increased CAC compared to non HIV. In contrast, both HIV groups demonstrated an increased prevalence of plaque [63% vs. 38%, P=0.04 (HIV+MS vs. C) and 59% vs. 38%, P=0.02, (HIV vs. C)] and increased number of noncalcified plaque segments compared to the HIV-negative group [1.26±0.31 vs. 0.45±0.16, P=0.01 (HIV+MS vs. C); 1.02±0.18 vs. 0.45±0.16, P=0.04 (HIV vs. C)]. Plaque and noncalcified plaque did not differ significantly between the HIV groups. Conclusion Metabolic abnormalities in HIV patients are specifically associated with increased coronary artery calcification, whereas HIV itself or other factors may be associated with the development of noncalcified lesions.