HIV-positive subjects on HAART and naive subjects had a higher prevalence of metabolic syndrome compared to healthy controls (19.4% and 13.8% vs 4.5%; P<0.001).
Cross-Sectional (n=332)
Does HIV infection and HAART increase the prevalence of metabolic syndrome and alter arterial structure and function compared to healthy controls?
HAART in HIV-positive subjects is associated with an increased prevalence of metabolic syndrome and greater arterial stiffness compared to healthy controls.
Absolute Event Rate: 19.4% vs 4.5%
p-value: p=<0.001
BACKGROUND: Human immunodeficiency virus (HIV) infection itself and highly active antiretroviral treatment (HAART) have been proposed to be associated with a higher prevalence of metabolic syndrome, but, to date, prevalence and phenotype of metabolic syndrome among HIV subjects and the related structural and functional vascular alterations are not conclusively defined. METHODS: We analyzed the data of 108 HIV-infected subjects without known cardiovascular risk factors: 72 were on HAART (group A, age 46.5±7.5 years, clinical blood pressure 125.7/74.9±11.6/7.8 mmHg) and there 36 in a naïve group (group B, age 40.7±7.9 years, blood pressure 126/75.8±9.8/7.7 mmHg). A total of 224 healthy subjects served as controls (group C, age 44.9±6.9 years, blood pressure 123.7/75.7±9.8/7.1 mmHg). Arterial stiffness was measured by aorto-femoral pulse wave velocity (PWV, sfigmocor), and carotid intima media thickness (IMT) was measured by a semiautomatic echotracking system (Esaote-WTS). RESULTS: Metabolic syndrome was more frequent in HIV-positive subjects than in controls (19.4%, 13.8%, 4.5% for groups A, B, and C; P<0.001), with no significant difference between HAART and naïve. In metabolic syndrome subjects, group A displayed lipid profile alterations more frequently (91%, 50%, 57% for groups A, B, and C; P<0.05), whereas others metabolic syndrome components were equally represented in the three groups. In metabolic syndrome subjects, IMT was similar 556±108, 542±164, and 564±110.4 μm for groups A, B, and C; P=not significant (NS), whereas PWV was significantly greater in HAART subjects when compared with controls (10.8±1.8, 9.±1.1, 9.3±1 cm/sec for groups A, B, and C; P=0.02 for A vs. C). Moreover, in this group (metabolic syndrome+HAART), PWV was higher than in subjects on HAART but without metabolic syndrome. CONCLUSIONS: HIV subjects showed a higher prevalence and a different pattern of metabolic syndrome components. HAART, more than HIV infection per se, appeared to be responsible for the increased prevalence of metabolic syndrome and arterial function derangement.
Maloberti et al. (Fri,) conducted a cross-sectional in HIV infection (n=332). HAART vs. Naive HIV subjects and healthy controls was evaluated on Prevalence of metabolic syndrome (p=<0.001). HIV-positive subjects on HAART and naive subjects had a higher prevalence of metabolic syndrome compared to healthy controls (19.4% and 13.8% vs 4.5%; P<0.001).