Objective: To test the hypothesis that Human Immunodeficiency Virus (HIV) infection in Black patients is associated with increased cardiometabolic risk factors that may increase aortic stiffness assessed by pulse wave...Objective: To test the hypothesis that Human Immunodeficiency Virus (HIV) infection in Black patients is associated with increased cardiometabolic risk factors that may increase aortic stiffness assessed by pulse wave velocity (PWV). Methods: We matched 96 Cameroonian Controls to 238 (Un) treated HIV-positive patients [HIV] for age. In each participant, aortic PWV (ComplioR), blood pressures (BP), lipid profile and fasting blood glucose (FPG) were measured. Results: Waist circumference was lower in HIV than in Controls (both p g·dl-1), and of diabetes (FPG > 125 mg·dl-1) were higher in HIV than in the Controls (50% vs 27%, and 23% vs 1%, respectively;both p < 0.0001). HDL-C was lower in HIV as compared to the Control (p = 0.02). Fasting triglycerides (TG) and the atherogenic dyslipidemia ratio [log(TG)/HDL-C] were higher in HIV than in the Controls (both p < 0.05). Hypertension prevalence was high but comparable in the two groups (48% vs 44% respectively, p > 0.05). HIV patients exhibited a twice-higher prevalence of MetS (AHA/NHLBI score 33/5) than that of the Controls (41% vs 21%;p 0.01). Similarly, severity of MetS phenotype was higher in HIV as compared to the Controls (2.14% vs 1.59%;p < 0.0001). PWV adjusted for age, mean BP and gender was faster in HIV in comparison to the controls (7.33 m/s vs 6.86 m/s, respectively;p = 0.036). Conclusions: HIV infection is associated with higher prevalence of MetS and its phenotype in Black African patients that may induce increased aortic stiffness.展开更多
文摘Objective: To test the hypothesis that Human Immunodeficiency Virus (HIV) infection in Black patients is associated with increased cardiometabolic risk factors that may increase aortic stiffness assessed by pulse wave velocity (PWV). Methods: We matched 96 Cameroonian Controls to 238 (Un) treated HIV-positive patients [HIV] for age. In each participant, aortic PWV (ComplioR), blood pressures (BP), lipid profile and fasting blood glucose (FPG) were measured. Results: Waist circumference was lower in HIV than in Controls (both p g·dl-1), and of diabetes (FPG > 125 mg·dl-1) were higher in HIV than in the Controls (50% vs 27%, and 23% vs 1%, respectively;both p < 0.0001). HDL-C was lower in HIV as compared to the Control (p = 0.02). Fasting triglycerides (TG) and the atherogenic dyslipidemia ratio [log(TG)/HDL-C] were higher in HIV than in the Controls (both p < 0.05). Hypertension prevalence was high but comparable in the two groups (48% vs 44% respectively, p > 0.05). HIV patients exhibited a twice-higher prevalence of MetS (AHA/NHLBI score 33/5) than that of the Controls (41% vs 21%;p 0.01). Similarly, severity of MetS phenotype was higher in HIV as compared to the Controls (2.14% vs 1.59%;p < 0.0001). PWV adjusted for age, mean BP and gender was faster in HIV in comparison to the controls (7.33 m/s vs 6.86 m/s, respectively;p = 0.036). Conclusions: HIV infection is associated with higher prevalence of MetS and its phenotype in Black African patients that may induce increased aortic stiffness.
