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Background:  Lipid abnormalities and insulin resistance induced by protease inhibitor-based HAART could increase the risk of premature atherosclerosis. Whether the treatment alone directly contributes to accelerating atherosclerosis has not been studied in depth. This study aimed to ascertain the relationship between subclinical atherosclerosis and HAART.

Methods:  We enrolled in a cross-sectional study 132 HIV-infected patients, 64 of whom were at low cardiovascular risk, 34 at moderate risk, and 34 at high risk. Subjects with known cardiovascular diseases or diabetes mellitus were excluded. High-resolution B-mode ultrasound imaging was used to examine femoral and carotid arteries; subclinical atherosclerosis was defined when plaques were observed in one or more sites. Cardiovascular risk was assessed by the Framingham risk score—sex, age, total cholesterol, HDL cholesterol, systolic blood pressure, and smoking—and was categorized as:  A: low risk (< 5%), B: moderate risk (5 to 10%), and C high risk (> 10%) of 10-year risk of coronary events. Univariate and multivariate logistic regression analyses were performed, with the presence of subclinical atherosclerosis being the depend variable.

Results:  Baseline characteristics of the 132 enrolled patients were:  mean age (SD) 43.1 years (10); 78% male; 50.8% current smokers; mean years (SD) of HIV infection 8.1 (4.8); mean years of antiretroviral therapy (SD) 7.7 (3.1). As for therapy, 39 were naive, 44 were currently on PI-based treatment, and 49 were currently on NRTI-based treatment. The prevalence of subclinical atherosclerosis in relation to the Framingham risk score group was:  group A 34.4%, group B 70.6%, and group C 94.1% (p: 0.0001); in relation to therapy: naives 23.1%, PI-based 75%; and NNRTI-based 73.5%. Prevalence in the group with low cardiovascular risk:  naives 4 (12.5%); PI-based 11 (68.8%); and NNRTI-based 7 (43.8%) (p = 0.0001). In multivariate analysis, independent variables associated with subclinical atherosclerosis (HR: 95% CI) were Framingham risk score group B (3.2, 1.2 to 8.4), Framingham risk score group C (16.9, 3.5 to 80.6); PI-based therapy (5.1, 1.7 to 15.2); NRTI-based therapy (4.4, 1.5 to 12.9). In low cardiovascular risk group, only age (per 10 years: 3.4, 1.2 to 9.6) and PI-based therapy (10, 2.1 to 47.7) were independent predictors of subclinical atherosclerosis.

Conclusions:  When adjusted for known cardiovascular risk factors, HAART, mainly PI-based, should be considered an independent and strong predictor of subclinical atherosclerosis.

Keywords: Atherosclerosis; Cardiovascular risk factors; Protease Inhibitor