Abstract
BackgroundStatin therapy has shown to deplete atherosclerotic plaque lipid content and induce plaque regression. However, how early the plaque lipid depletion can occur with low-density lipoprotein cholesterol (LDL-C) lowering in humans in vivo has not been fully described.MethodsWe enrolled 43 lipid treatment naïve subjects with asymptomatic carotid atherosclerosis and LDL-C ≥ 100 and ≤ 250 mg/dl. Rosuvastatin 5–20 mg/day was used to lower LDL-C levels to < 80 mg/dl. Lipid profile and carotid MRI scans were obtained at baseline, 3, 12, and 24 months. Carotid plaque lipid-rich necrotic core (LRNC) and plaque burden were measured and compared between baseline and during treatment.ResultsAmong the 32 subjects who completed the study, at 3 months, an average dose of rosuvastatin of 11 mg/day lowered LDL-C levels by 47% (125.2 ± 24.4 mg/dl vs. 66.7 ± 17.3 mg/dl, p < 0.001). There were no statistically significant changes in total wall volume, percent wall volume or lumen volume. However, LRNC volume was significantly decreased by 7.9 mm3, a reduction of 7.3% (111.5 ± 104.2 mm3 vs. 103.6 ± 95.8 mm3, p = 0.044). Similarly, % LRNC was also significantly decreased from 18.9 ± 11.9% to 17.9 ± 11.5% (p = 0.02) at 3 months. Both LRNC volume and % LRNC continued to decrease moderately at 12 and 24 months, although this trend was not significant.ConclusionsAmong a small number of lipid treatment naïve subjects, rosuvastatin therapy may induce a rapid and lasting decrease in carotid plaque lipid content as assessed by MRI.Trial registrationClinicalTrials.Gov numbers NCT00885872
Highlights
Statin therapy has shown to deplete atherosclerotic plaque lipid content and induce plaque regression
Atherosclerosis alone is thought to be a relatively benign disease and progresses with aging; it is frequently complicated by acute thrombosis, usually triggered by the rupture or erosion of an atherosclerotic plaque which is determined by plaque morphologic characteristics, local composition and inflammation [1,2]
Numerous studies have shown that magnetic resonance imaging (MRI) creates high contrast for internal features of plaques and that the combined information from multiple contrast weightings is critical for distinguishing all plaque components [3]
Summary
Statin therapy has shown to deplete atherosclerotic plaque lipid content and induce plaque regression. Atherosclerosis alone is thought to be a relatively benign disease and progresses with aging; it is frequently complicated by acute thrombosis, usually triggered by the rupture or erosion of an atherosclerotic plaque which is determined by plaque morphologic characteristics, local composition and inflammation [1,2]. Plaque rupture or erosion can lead to major cardiovascular events such as acute coronary syndromes and strokes. Development of high-resolution magnetic resonance imaging (MRI) techniques in recent years has made it possible to directly assess plaque composition. Numerous studies have shown that MRI creates high contrast for internal features of plaques and that the combined information from multiple contrast weightings is critical for distinguishing all plaque components [3]. Carotid MRI can accurately assess plaque tissue contents
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