Abstract 16645: Atorvastatin Reduces Ascending Aortic Plaque Volume on CT in HIV: Correlation With Coronary Plaque Volume and Serum Oxidized LDL
Introduction: HIV is associated with excess aortic inflammation and serum oxidized LDL (oxLDL); oxLDL is associated with atherosclerosis.
Hypothesis: Atorvastatin reduces ascending aortic plaque volume on CT in HIV, and these changes correlate with oxLDL.
Methods: Forty persons with subclinical coronary atherosclerosis, LDL cholesterol <130 mg/dL, and treated HIV participated in a 12-month randomized, double blind trial of atorvastatin vs. placebo. Participants had ECG-gated CT angiography (CTA) of the ascending thoracic aorta/coronary arteries and serum oxLDL at enrollment and 12 months. The primary outcome was change in volume of ascending aortic plaque including aortic wall thickening, quantified by an independent reader blinded to treatment allocation. Change in plaque volume was compared between statin and placebo arms with the Wilcoxon rank sum test. We previously reported atorvastatin decreases coronary plaque volume and oxLDL - correlation with aortic plaque volume was assessed with Spearman’s correlation coefficient.
Results: Thirty-seven completed the trial (17 atorvastatin, 20 placebo). Twelve months of atorvastatin reduced aortic plaque volume relative to placebo: median change in aortic plaque volume was -107.0 mm3 [-441.0, 177.5] for statin vs. +151 mm3 [-34.3, 551.5] for placebo (p=0.015). The percent change in aortic plaque volume was -4.1% [-16.7, 7.9] for statin vs. +7.9% [-3.8, 17.6] for placebo (p=0.026). Excellent intra-reader reliability was found for aortic plaque volume (ICC: 0.90). There was not significant correlation between change in aortic and coronary plaque (rs 0.14, p=0.42). Change in aortic plaque correlated with oxLDL (0.41, p=0.013).
Conclusions: In persons with HIV and subclinical atherosclerosis, 12 months of atorvastatin reduced ascending aortic plaque with correlation to oxLDL. Absent correlation between change in ascending aortic and coronary plaque suggests distinct underlying pathophysiology.
Author Disclosures: M.T. Lu: None. B. Szilveszter: None. K.V. Fitch: None. U. Hoffmann: Research Grant; Significant; HeartFlow, Siemens Healthcare. Consultant/Advisory Board; Significant; HeartFlow. S.K. Grinspoon: Consultant/Advisory Board; Modest; Navidea, Theratechnologies, Bristol Meyers Squibb, Merck, Gilead. J. Lo: None.
- © 2016 by American Heart Association, Inc.