Background No studies have yet assessed the ability of statin treatment to reduce arterial inflammation and achieve regression of coronary atherosclerosis in HIV-infected patients, a population with elevated risk of myocardial infarction. Methods In a randomized, double-blind, placebo-controlled trial, 40 HIV-infected participants with subclinical coronary atherosclerosis, evidence of arterial inflammation in the aorta by fluorodeoxyglucose positron emission tomography (FDG-PET) and low density lipoprotein(LDL)-cholesterol <3·37mmol/L(130mg/dL) were randomized to one year of treatment with atorvastatin (n=19) or placebo (n=21). Randomization was carried out by the MGH Clinical Research Pharmacy using a permuted-block algorithm, stratified by gender with a fixed block size of four, with 1:1 allocation to atorvastatin or identical matching placebo. Study codes were available only to the MGH Research Pharmacy and not to study investigators or participants. The prespecified primary endpoint was arterial inflammation, as assessed by FDG-PET of the aorta. Additional prespecified endpoints included coronary atherosclerotic plaque as assessed by coronary computed tomography angiography. We quantitatively assessed non-calcified and calcified plaque and high risk plaque features. Analysis was performed using intention-to-treat principle, using all available data, without imputation for missing data. Findings Thirty seven out of forty (92·5%) subjects completed the study, with equivalent discontinuation rates in both groups. Baseline parameters were similar between groups. After 12 months, change in FDG-PET uptake of the most diseased segment of the aorta was not different between atorvastatin and placebo, but technically adequate results comparing longitudinal changes in identical regions could only be assessed in a subset of patients (atorvastatin Δ −0·03 [95% CI: −0·17, 0·12] vs. placebo Δ −0·06 [−0·25, 0·13], p=0·77, n=21). Change in plaque could be assessed in all subjects completing the study. Atorvastatin reduced noncalcified coronary plaque volume compared to placebo (−19·4%(IQR: −39·2%, 9·3%) vs. +20·4%(−7·1%, 94·4%), p=0·009, n=37). In addition, the number of high risk plaques was significantly reduced by atorvastatin compared to placebo (change in number of low attenuation plaques −0·2[95% CI: −0·6, 0·2] vs. 0·4[0·0, 0·7], p=0·03, n=37 and change in number of positively remodeled plaques −0·2[95% CI −0·4, 0·1] vs. 0·4[−0·1, 0·8], p=0·04, n=37). Direct LDL-cholesterol (−1·00[95% CI −1·38, 0·61] vs. 0·30[0·04, 0·55] mmol/L, p<0·0001) and lipoprotein-associated phospholipase A2 (−52·2[95% CI −70·4, −34·0] vs. −13·3[−32·8, 6·2] ng/mL, p=0·005, n=37) significantly decreased with atorvastatin compared to placebo. Statin therapy was well-tolerated, with low incidence of clinical adverse events. Interpretation Compared to placebo, statin therapy reduces noncalcified plaque volume and high risk plaque features in HIV-infected patients with subclinical coronary atherosclerosis. Significant effects of statin therapy...

Background Mechanisms predisposing HIV-infected patients to increased CVD risk remain unclear. Objective To determine the interrelationship between arterial inflammation and high-risk coronary plaque morphology in HIV-infected patients with subclinical coronary atherosclerosis. Methods 41 HIV-infected patients on stable ART without known CVD but with atherosclerotic plaque on coronary CT angiography were evaluated with 18F-FDG-PET. Patients were stratified into two groups based on relative degree of arterial inflammation (aortic target-to-background-ratio, or TBR). High-risk coronary atherosclerotic plaque morphology features were compared between groups. Results HIV-infected patients with higher and lower TBR’s were similar with respect to traditional CVD risk parameters. Among HIV-infected patients with higher TBR, an increased percentage of patients demonstrated at least one low attenuation coronary atherosclerotic plaque (40% vs. 10%, p = 0.02) and at least one coronary atherosclerotic plaque with both low attenuation and positive remodeling (35% vs. 10%, p = 0.04). Moreover, in the higher TBR group, both the number of low attenuation plaques (LAP’s) per patient (p = 0.02) and the number of vulnerability features in the most vulnerable plaque (p = 0.02) were increased. TBR grouping remained significantly related to the number of LAP’s/subject (β=0.35, p = 0.004), controlling for age, gender, LDL, duration HIV, and CD4. Conclusion These data demonstrate a relationship between arterial inflammation on 18F-FDG-PET and high-risk coronary atherosclerotic plaque features among HIV-infected patients with sublclinical coronary atherosclerosis. Further studies are needed to determine whether arterial inflammation and related high-risk coronary morphology increase the risk of clinical CVD events in the HIV population.

The BVAVF is a viable alternative to the AVG in patients with inadequate superficial venous anatomy, especially in access-naïve patients. The decision to perform BVAVF must be weighed against the delay in functional maturation expected compared with AVG.