Abstract
BackgroundPatients with treated Human Immunodeficiency Virus-1 (HIV) infection are at increased risk of cardiovascular events. Traditionally much of this risk has been attributed to metabolic and anthropometric abnormalities associated with HIV, which are similar to the metabolic syndrome (MS), an established risk factor for cardiovascular mortality. It remains unclear whether treated HIV infection is itself associated with increased risk, via increase vascular stiffness.Methods226 subjects (90 with HIV) were divided into 4 groups based on HIV and MS status: 1) HIV-ve/MS-ve, 2) HIV-ve/MS + ve, 3) HIV + ve/MS-ve and 4)HIV + ve/MS + ve. CMR was used to determine aortic pulse wave velocity (PWV) and regional aortic distensibility (AD).ResultsPWV was 11% higher and regional AD up to 14% lower in the HIV + ve/MS-ve group when compared to HIV-ve/MS-ve (p < 0.01 all analyses). PWV and AD in the HIV + ve/MS-ve group was similar to that observed in the HIV-ve/MS + ve group (p > 0.99 all analyses). The HIV + ve/MS + ve group had 32% higher PWV and 30-34% lower AD than the HIV-ve/MS-ve group (all p < 0.001), and 19% higher PWV and up to 31% lower AD than HIV + ve/MS-ve subjects (all p < 0.05). On multivariable regression, age, systolic blood pressure and treated HIV infection were all independent predictors of both PWV and regional AD.ConclusionAcross multiple measures, treated HIV infection is associated with increased aortic stiffness and is also an independent predictor of both PWV and regional AD. The magnitude of the effect of treated HIV and MS are similar, with additive detrimental effects on central vascular elasticity.
Highlights
Patients with treated Human Immunodeficiency Virus-1 (HIV) infection are at increased risk of cardiovascular events
PWV was 11% higher in the HIV + ve/metabolic syndrome (MS)-ve group when compared to the HIV-ve/MS-ve group (6.2 ± 1.9 vs 5.6 ± 1.9 m/s, p = 0.008, Figure 2) and aortic distensibility reduced (PDA by 12%, AA by 14%, both p < 0.01, Figure 3)
We have shown that HIV and the metabolic syndrome are additive in their negative effects on PWV and aortic distensibility, suggesting that both are risk factors that act in different ways to impair vascular elasticity
Summary
Patients with treated Human Immunodeficiency Virus-1 (HIV) infection are at increased risk of cardiovascular events Much of this risk has been attributed to metabolic and anthropometric abnormalities associated with HIV, which are similar to the metabolic syndrome (MS), an established risk factor for cardiovascular mortality. Despite immunological modulation, aging with HIV is accompanied by an increased prevalence of metabolic abnormalities, atherosclerotic cardiovascular disease and higher all-cause mortality [1,2,3,4]. The pathogenesis of this accelerated atherosclerosis in HIV has not been fully elucidated. Whether viral factors amplify the atherogenic effect of traditional metabolic risk factors in HIV-infected individuals remains unclear
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