Increased burden and severity of metabolic syndrome and arterial stiffness in treatment-naïve HIV+ patients from Cameroon

Background: Human immunodeficiency virus (HIV) and its therapy are associated with increased aortic stiffness and metabolic syndrome (MetS) phenotype in Caucasian patients. We hypothesized that, independently of antiretroviral therapy, HIV infection in native black African patients is associated with increased burden of cardiometabolic risk factors that may accelerate arterial structural damage and translate into increased aortic stiffness. Patients and methods: Ninety-six apparently healthy Cameroonian subjects (controls) were compared to 108 untreated Cameroonian HIV+ patients (HIV-UT) of similar age. In each participant, pulse wave velocity (Complior), aortic augmentation index (SphygmoCor), brachial blood pressure (Omron 705 IT), fasting plasma glucose (FPG), and lipids were recorded, as well as the prevalence and severity of MetS, based on the American Heart Association/National Heart, Lung, and Blood Institute score ≥3/5. Results: Prevalence of impaired fasting glucose (FPG 100-125 mg · dL-1) and of diabetes (FPG > 125 mg · dL-1) was higher in HIV-UT than in controls (47% versus 27%, and 26% versus 1%, respectively; both P < 0.01). Fasting triglycerides and the atherogenic dyslipidemia ratio were significantly higher in HIV-UT than in controls. Hypertension prevalence was high and comparable in both groups (41% versus 44%, respectively; not significant). HIV-UT patients exhibited a twice-higher prevalence of MetS than controls (47% versus 21%; P = 0.02). Age-and sex-adjusted pulse wave velocity was higher in HIV-UT than in controls (7.5 ± 2.2 m/s versus 6.9 ± 1.7 m/s, respectively; P = 0.02), whereas aortic augmentation index was significantly lower (6% ± 4% versus 8% ± 7%, respectively; P = 0.01). Conclusion: Similar to Caucasian populations, native Cameroonian HIV-UT patients showed a higher prevalence of MetS and its phenotype, associated with increased aortic stiffness, an early marker of atherosclerosis. © 2013 Ngatchou et al, publisher and licensee Dove Medical Press Ltd.