Abstract 556: Type of Lipid Lowering Therapy Impacts Atherosclerosis Progression in Peripheral Arterial Disease as Assessed by MRI
Introduction: Lipid lowering improves exercise performance in peripheral arterial disease (PAD), but its effect on atherosclerotic plaque progression in PAD is unknown.
Hypothesis: We hypothesized that lowering LDL cholesterol in PAD would reduce superficial femoral artery (SFA) plaque burden assessed by magnetic resonance imaging (MRI).
Methods: Sixty eight patients with mild-to-moderate symptomatic PAD (mean age 63±10 years, ankle brachial index 0.71±0.23) had the first 15–20cm of the SFA in their most symptomatic leg imaged with black blood multi-slice turbo spin echo MRI before and 1 year after therapy. Statin-naïve patients were randomized to simvastatin 40 mg or simvastatin 40 mg/ezetimibe 10mg (R, n= 36). Those on a statin received open-label ezetimibe 10mg (Z, n= 32). Plaque volume (PV) defined as total vessel volume (TVV) minus lumen volume was measured. Changes in parameters between groups were compared by F-test and examined with Spearman correlation coefficient.
Results: R group designation remains blinded as 2-year follow-up is ongoing. LDL at baseline was higher in R (118±36 mg/dl) than Z (99±25 mg/dl, p< 0.02). The decrease in LDL at 1 year was greater in R (−41±36) than Z (−20±30, p<0.01), such that final LDL was similar (77±33 in R and 80±33 in Z). Total cholesterol changes were similar. No between group changes in HDL, triglycerides, CRP or lipoprotein (a) were seen. Plaque volume regressed in R while it progressed in Z (see table⇓). Total vessel volume followed the same trend (p<0.09). No correlation was found between change in lipids or CRP and plaque volume.
Conclusions: Statin-naïve patients with PAD begun on simvastatin with or without ezetimibe had regression of atherosclerosis in the SFA at 1 year when compared to those already on statins begun on ezetimibe despite similar final LDL. Thus, the degree and/or mechanism of LDL lowering or duration of statin use may be more important than the final LDL achieved in halting atherosclerotic plaque progression.