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Cardiovascular Complications: Risk Factors, Incidence, Prevalence, and Outcomes
Tuesday, 1:30 - 3:30 pm
Background: HIV-positive patients seem to have an increased risk of cardiovascular diseases, although the role of treatment with PI remains a controversial issue. In the present study we compared PI-treated patients (group A) with PI-naїve patients treated with a regimen including NNRTI (group B) and with patients treated with 2 NRTI or naїve to antiretroviral therapy (group C)
Methods: Group A included 105 patients, group B 120, group C 68. All treated patients had treatment for at least 12 months and were evaluated for familial history of cardiovascular disease, sedentary life, cigarette smoking, alcohol abuse, active drug addiction, and values for fasting glycemia, cholesterolemia, and triglyceridemia. Intima characteristics, pulsation and resistance indexes, and minimal, peak, and mean speed were evaluated using an AU5 ESAOTE color power Doppler. Atherosclerotic plaques were described.
Results: In group A, 55 patients (52.4%) demonstrated acquired lesions of the vascular wall including 25 patients with intima media thickness, 24 with intima media thickness plus atheromatous plaques, and 6 with plaques. In group B. 19 (15.2%) showed lesions, 10 of whom demonstrated intima media thickness, 3 plaques and 6 intima media thickness plus plaques. Of the 63 patients in group C, lesions were observed in 9 (14.3%) including 3 patients with intima media thickness, 4 with intima media thickness plus plaques, and 2 with plaques. The logistic regression model evidenced that the risk of vascular lesions is significantly correlated with type of therapy (Wald c2 = 44.24, p <0.0001), age (Wald c2 = 14.78, p = 0.0001), cigarette smoking (Wald c2 = 4.99, p = 0.025), and CD4+ cell count (Wald c2 = 6.88, p = 0.032), whereas the risk of lesions is significantly higher for patients with a CD4 cell count <200 x 106/L or between 200 and 500 x 106/L compared with those with a CD4 cell count >500 x 106/L. The Mantel-Haenszel test confirmed a strong relationship between vascular damage and use of PI during every stage of the disease (c2 = 33.89, p = 0.0002). Evaluating the interaction between the single risk factors and the presence of vascular damage, the only significant factor was the PI-based therapy (c2 = 46.65, p = 0.0001) When considering the presence of atheromasic plaques as a dependent variable in the logistic regression model, the predictive risk factors were, once again, the PI-based therapy and age.
Conclusions: These data in our ongoing study show a higher prevalence of acquired carotid lesions even when compared with patients treated with NNRTI-including regimens.
Keywords: vascular lesions; protease inhibitors; ultrasonography