Background: The introduction of highly active antiretroviral therapy reduced HIV-associated morbidity and mortality, at the cost of adverse metabolic effects that increase cardiovascular risk. The aim of this study was to evaluate the impact of exposure to protease inhibitors (PI) compared with exposure to non-nucleoside reverse transcriptase inhibitors (NNRTI) on carotid intima-media thickness (IMT) and blood flow velocity and to measure vascular involvement over a 2-year follow-up in HIV-infected patients treated with PI.
Methods: Thirty-five HIV-infected patients treated with PI (group I) and 15 patients treated with NNRTI (group II) underwent epiaortic vessel ultrasonography. The same evaluation was obtained in a group of 20 healthy subjects. After 20 +/- 2 months, 22 patients of group I were re-evaluated and the follow-up data were compared with those obtained at baseline.
Results: The ANOVA test showed a significant difference among the three groups for IMT and flow velocities. Bonferroni analyses showed significant differences in IMT and flow velocities in group I vs group II vs controls: IMT of the right common carotid artery was 0.742 +/- 0.135 mm in group I vs 0.642 +/- 0.131 mm in group II (p < 0.05) and 0.616 +/- 0.069 mm in controls (p = 0.002); IMT of left common carotid artery was 0.720 +/- 0.108 vs 0.659 +/- 0.066 mm (p < 0.05) and 0.640 +/- 0.081 mm (p < 0.01), respectively. There were no differences in group II vs healthy subjects. At follow-up examinations of group I, no significant differences were observed in both IMT and blood flow velocity when compared with baseline values.
Conclusions: The HIV-infected patients treated with PI show earlier vascular involvement as compared to those treated with NNRTI and to healthy subjects with similar distribution of cardiovascular risk factors. However, such damage seems to have no significant progression over a 2-year follow-up in HIV-infected patients treated with PI. These data emphasize the need for follow-up studies assessing whether these changes are predictive of adverse cardiac events.