BACKGROUND: The role of antiretroviral therapy in acceleration of atherosclerosis in patients with human immunodeficiency virus (HIV) infection is controversial. We hypothesized that aortic stiffness, an early marker of arteriosclerosis, may be increased in HIV patients treated with protease inhibitors. METHODS AND RESULTS: In 32 HIV-infected patients treated with protease inhibitors and 32 age-, sex-, and blood pressure-matched HIV-uninfected control subjects, we obtained aortic pulse wave velocity and central aortic pressure waveform, from which aortic augmentation was calculated. HIV patients had a higher aortic pulse wave velocity (7.6+/-1.1 versus 6.8+/-1.2 m x s(-1), P=0.015) and aortic augmentation (6.8+/-5 versus 4.6+/-4 mm Hg, P=0.037) than control subjects. Age and HIV infection (both P<0.05) independently predicted aortic pulse wave velocity when a consistent number of cardiovascular risk factors was simultaneously controlled for. The cumulative duration of treatment was a predictor of aortic pulse wave velocity, each 5 years of treatment duration being independently related to a 1.35 m x s(-1) increase in pulse wave velocity. CONCLUSIONS: Aortic stiffness is increased in HIV-positive individuals receiving antiretroviral therapy including a protease inhibitor. Pulse wave velocity increases with longer exposure to protease inhibitors. We hypothesize that arteriosclerosis is a side effect of antiretroviral treatment including a protease inhibitor.
BACKGROUND: The role of antiretroviral therapy in acceleration of atherosclerosis in patients with human immunodeficiency virus (HIV) infection is controversial. We hypothesized that aortic stiffness, an early marker of arteriosclerosis, may be increased in HIVpatients treated with protease inhibitors. METHODS AND RESULTS: In 32 HIV-infectedpatients treated with protease inhibitors and 32 age-, sex-, and blood pressure-matched HIV-uninfected control subjects, we obtained aortic pulse wave velocity and central aortic pressure waveform, from which aortic augmentation was calculated. HIVpatients had a higher aortic pulse wave velocity (7.6+/-1.1 versus 6.8+/-1.2 m x s(-1), P=0.015) and aortic augmentation (6.8+/-5 versus 4.6+/-4 mm Hg, P=0.037) than control subjects. Age and HIV infection (both P<0.05) independently predicted aortic pulse wave velocity when a consistent number of cardiovascular risk factors was simultaneously controlled for. The cumulative duration of treatment was a predictor of aortic pulse wave velocity, each 5 years of treatment duration being independently related to a 1.35 m x s(-1) increase in pulse wave velocity. CONCLUSIONS: Aortic stiffness is increased in HIV-positive individuals receiving antiretroviral therapy including a protease inhibitor. Pulse wave velocity increases with longer exposure to protease inhibitors. We hypothesize that arteriosclerosis is a side effect of antiretroviral treatment including a protease inhibitor.
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