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Journal Article
Multicenter Study
Observational Study
Effects of statin therapy on progression of mild noncalcified coronary plaque assessed by serial coronary computed tomography angiography: A multicenter prospective study.
American Heart Journal 2016 October
BACKGROUND: There are limited data assessing statin therapy in patients with nonobstructive coronary plaque on coronary computed tomography angiography (CCTA).
METHODS: Two hundred six consecutive patients with mild noncalcified plaque on CCTA were enrolled in this multicenter prospective observational study. Subjects were divided into 3 groups according to subsequent statin therapy: intensive statin therapy (n = 55), moderate statins (n = 85), and no statin (n = 66). Serial scans were performed after a median interval of 18 months. Low-attenuation plaque (LAP) volume, total plaque volume, and percent plaque volume were measured.
RESULTS: The LAP volume, total plaque volume, and percent plaque volume showed significant regression among intensive-statin compared with no-statin group (annualized changes: -7.1 ± 13.1 vs 0.9 ± 12.7 mm(3), P< .001; -16.4 ± 35.0 vs 12.3 ± 32.4 mm(3), P< .001; and -6.2% ± 11.8% vs 3.5% ± 12.1%, P< .001, respectively). Progression of LAP volume, total plaque volume, and percent plaque volume was retarded among moderate-statin compared with no-statin group (annualized changes: -2.8 ± 7.6 vs 0.9 ± 12.7 mm(3), P= .041; -0.1 ± 25.6 vs 12.3 ± 32.4 mm(3), P= .014; and -1.8% ± 11.2% vs 3.5% ± 12.1%, P= .006, respectively). On multivariable model predicting change in total plaque volume, higher baseline LAP volume, moderate statin therapy, and intensive statin therapy were each independent predictors of plaque regression (standardized coefficients: baseline LAP volume -0.36, P< .001; moderate statin -0.21, P= .004; intensive statin -0.36, P< .001, respectively).
CONCLUSIONS: This study suggests that statin treatment can retard progression and even induce regression of mild noncalcified coronary plaque. Patients with greater baseline LAP volume are more likely to benefit from statin therapy.
METHODS: Two hundred six consecutive patients with mild noncalcified plaque on CCTA were enrolled in this multicenter prospective observational study. Subjects were divided into 3 groups according to subsequent statin therapy: intensive statin therapy (n = 55), moderate statins (n = 85), and no statin (n = 66). Serial scans were performed after a median interval of 18 months. Low-attenuation plaque (LAP) volume, total plaque volume, and percent plaque volume were measured.
RESULTS: The LAP volume, total plaque volume, and percent plaque volume showed significant regression among intensive-statin compared with no-statin group (annualized changes: -7.1 ± 13.1 vs 0.9 ± 12.7 mm(3), P< .001; -16.4 ± 35.0 vs 12.3 ± 32.4 mm(3), P< .001; and -6.2% ± 11.8% vs 3.5% ± 12.1%, P< .001, respectively). Progression of LAP volume, total plaque volume, and percent plaque volume was retarded among moderate-statin compared with no-statin group (annualized changes: -2.8 ± 7.6 vs 0.9 ± 12.7 mm(3), P= .041; -0.1 ± 25.6 vs 12.3 ± 32.4 mm(3), P= .014; and -1.8% ± 11.2% vs 3.5% ± 12.1%, P= .006, respectively). On multivariable model predicting change in total plaque volume, higher baseline LAP volume, moderate statin therapy, and intensive statin therapy were each independent predictors of plaque regression (standardized coefficients: baseline LAP volume -0.36, P< .001; moderate statin -0.21, P= .004; intensive statin -0.36, P< .001, respectively).
CONCLUSIONS: This study suggests that statin treatment can retard progression and even induce regression of mild noncalcified coronary plaque. Patients with greater baseline LAP volume are more likely to benefit from statin therapy.
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