Myocardial Infarction, Stroke, and Mortality in cART-Treated HIV Patients on Statins.

Despite combination antiretroviral therapy (cART), people living with HIV (PLWH) continue to have more systemic inflammation and metabolic disturbances than the general population. These risk factors for atherosclerosis and organ dysfunction may be ameliorated by statins. We retrospectively analyzed 438 cART treated PLWH from the Nutrition For Healthy Living (NFHL) cohort to determine the association between statins and myocardial infarction (MI), stroke, and all-cause mortality as a composite. We used Cox proportional hazards regression as our main analysis. The average age was 44 years, 32% were women, and 67 of the 438 subjects used statins. There was no association between statins and our composite endpoint in two separate models [1.26 (0.57-2.79) in statin history model and 0.93 (0.65-1.32) per year in statin duration model]. The composite outcome was significantly associated with CD4 count, age, and smoking status in both models. CD4 count remained significant even after exclusion of mortality from the composite (HR=0.88, p=0.02). Confounding control via propensity scoring and multiple imputations did not change the results. Statins did not have an effect on MI, stroke, and mortality. Interestingly, CD4 count appears to be an important predictor of these outcomes, even after exclusion of death from the composite.

Short communication: effects of omega-3 fatty acids on triglycerides and high-density lipoprotein subprofiles in HIV-infected persons with hypertriglyceridemia.

Hypertriglyceridemia and low high-density lipoprotein (HDL)-cholesterol (HDL-C) may contribute to a presumed accelerated risk for cardiovascular disease in HIV-infected individuals. We evaluated the effect of omega-3 fatty acid treatment on triglycerides, low-density lipoprotein (LDL)-C, HDL-C, and HDL subpopulations. Forty-one HIV-seropositive subjects with hypertriglyceridemia (≥150 mg/dl) on active antiretroviral therapy were enrolled in this placebo-controlled, double-blind, randomized, crossover trial comparing the effects of omega-3 fatty acid treatment (1.9 g EPA and 1.5 g DHA) on triglycerides, LDL-C, HDL-C, and HDL subpopulations. An independent sample t-test was used to assess the study start to posttreatment change for all components. After omega-3 fatty acid treatment, triglyceride levels decreased 63.2±86.9 mg/dl (p<0.001). No significant changes in total cholesterol, LDL-C, or HDL-C were found. Within HDL subpopulations, significant changes were seen in the most atheroprotective HDL particles, α-1, which increased by 2.5±5.6 mg/dl (p<0.05), and preα-1, which increased by 0.6±1.0 mg/dl (p<0.001). Preα-3, a presumably atherogenic HDL particle, decreased by 0.5±0.9 mg/dl (p<0.01). Omega-3 fatty acid treatment significantly lowered triglyceride levels in HIV-positive patients with moderate hypertriglyceridemia. While no study-wide improvements in LDL-C or HDL-C were detected, the HDL subpopulation profile changed in a beneficial way suggesting more cardioprotection after treatment.

Progression of carotid intima-media thickness and coronary artery calcium over 6 years in an HIV-infected cohort.

OBJECTIVE: To evaluate changes in cardiovascular disease risk surrogate markers in a longitudinal cohort of HIV-infected adults over 6 years. DESIGN: Internal carotid artery (ICA) and common carotid artery (CCA) intima-media thickness (IMT), coronary artery calcium (CAC), vascular, and HIV risk factors were prospectively examined over 6 years in HIV-infected adults from 2002 to 2010. SETTING: Longitudinal cohort study with participants from urban center and surrounding communities. SUBJECTS/PARTICIPANTS: Three hundred forty-five HIV-infected participants were recruited from a longitudinal cohort study. Two hundred eleven participants completed the study and were included in this analysis. MAIN OUTCOME MEASURES: Total and yearly ICA and CCA IMT change; CAC score progression. RESULTS: Participants were 27% female and 49% nonwhite; mean age at start was 45 ± 7 years. The median change in ICA and CCA over 6 years was 0.15 mm (0.08, 0.28) and 0.12 mm (0.09, 0.15), respectively. Age, baseline triglycerides ≥150 mg/dL, and pack-years smoking were associated with ICA IMT change; age, cholesterol, nadir CD4 count, and protease inhibitor use were associated with CCA IMT change. Diabetes, HIV viral load, and highly active antiretroviral therapy duration were associated with CAC progression. CONCLUSIONS: Carotid IMT and CAC progressed in this HIV-infected cohort. Some HIV-specific characteristics were associated with surrogate marker changes, but the majority of risk factors continue to be traditional. Aggressive identification and management of modifiable risk factors may reduce progression of cardiovascular disease risk in this population.

HIV infection and progression of carotid and coronary atherosclerosis: the CARE study.

BACKGROUND: Progression of carotid intima-media thickness (c-IMT) and coronary artery calcium (CAC) are increasingly used as surrogates for vascular risk. We assessed the predictors of c-IMT and CAC progression in a large longitudinal cohort of HIV-infected adults. METHODS: c-IMT, CAC scores, and vascular and HIV risk factors were evaluated at baseline and at 3-year follow-up in 255 HIV-infected adults. Multivariate regression was used to determine the predictors of atherosclerotic progression. RESULTS: The mean change in c-IMT per year of follow-up was 0.016 mm for the common and 0.020 mm for the internal. Significant predictors of yearly progression were age, systolic blood pressure, triglycerides, and insulin for common c-IMT and triglycerides >=150 mg/dL, glucose >126 mg/dL, use of glucose-lowering medications, quantitative insulin sensitivity check index, high waist circumference, and current smoking for internal c-IMT. Twenty-eight percent had CAC progression. Of those with zero CAC at baseline, 32% had detectable scores at follow-up. Of those with detectable CAC at baseline, 26% had progression at follow-up. For CAC score, quantitative insulin sensitivity check index, apolipoprotein B, and triglycerides predicted progression. Those with abnormal surrogate markers at baseline were more likely to have the metabolic syndrome reversed and be started on antihypertensive medications over the 3-year follow-up period than those who had no abnormalities at baseline. CONCLUSIONS: Although c-IMT and CAC progression rates in HIV-infected patients appear higher than expected for this age and risk groups, traditional cardiovascular risk factors remain the strongest determinants of carotid and coronary atherosclerotic disease progression in HIV-infected patients. Aggressive cardiovascular risk reduction is effective at slowing the atherosclerotic progression in those with preexisting disease.

Effect of a dietary intervention and n-3 fatty acid supplementation on measures of serum lipid and insulin sensitivity in persons with HIV.

BACKGROUND: Elevated serum triglyceride and low HDL-cholesterol concentrations have been reported in persons with HIV. OBJECTIVE: The effect of a dietary intervention plus n-3 (omega-3) fatty acid supplementation on serum triglycerides and markers of insulin sensitivity was investigated. DESIGN: Fifty-four persons with HIV and elevated serum triglycerides (>150 mg/dL) and/or abnormal Quantitative Insulin Sensitivity Check Index values (<0.35 but >0.30) were recruited for a dietary intervention in which total fat, type of fat, fiber, and glycemic load were controlled along with supplementation with n-3 fatty acids to achieve an intake of 6 g/d. The subjects were randomly assigned to an intervention or control group, and serum lipids, markers of insulin sensitivity, and serum phospholipid fatty acids were measured in both groups at baseline, 3 wk, and 13 wk. RESULTS: Triglycerides in the intervention group decreased from a median of 180 mg/dL (interquartile range: 141, 396) to 114 mg/dL (interquartile range: 84, 169) from baseline to 3 wk, whereas they remained stable in the control group (P = 0.003). Serum phospholipid fatty acids indicated a decrease in de novo lipogenesis and a decrease in arachidonic acid (% nmol; P