Teruo Noguchi1, Atsushi Tanaka2, Tomohiro Kawasaki3, Yoichi Goto4, Yoshiaki Morita5, Yasuhide Asaumi4, Kazuhiro Nakao4, Reiko Fujiwara4, Kunihiro Nishimura6, Yoshihiro Miyamoto6, Masaharu Ishihara7, Hisao Ogawa4, Nobuhiko Koga3, Jagat Narula8, Satoshi Yasuda4. 1. Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan. Electronic address: tnoguchi@hsp.ncvc.go.jp. 2. Department of Cardiovascular Medicine, Saga University, Saga, Japan. 3. Cardiovascular Center, Shin-Koga Hospital, Kurume, Japan. 4. Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan. 5. Department of Radiology, National Cerebral and Cardiovascular Center, Suita, Japan. 6. Preventive Medicine and Epidemiologic Informatics, Center for Cerebral and Cardiovascular Disease Information, National Cerebral and Cardiovascular Center, Suita, Japan. 7. Division of Coronary Artery Disease, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan. 8. Icahn School of Medicine at Mount Sinai, New York, New York.
Abstract
BACKGROUND: Coronary high-intensity plaques detected by noncontrast T1-weighted imaging may represent plaque instability. High-intensity plaques can be quantitatively assessed by a plaque-to-myocardium signal-intensity ratio (PMR). OBJECTIVES: This pilot, hypothesis-generating study sought to investigate whether intensive statin therapy would lower PMR. METHODS: Prospective serial noncontrast T1-weighted magnetic resonance imaging and computed tomography angiography were performed in 48 patients with coronary artery disease at baseline and after 12 months of intensive pitavastatin treatment with a target low-density lipoprotein cholesterol level <80 mg/dl. The control group consisted of coronary artery disease patients not treated with statins that were matched by propensity scoring (n = 48). The primary endpoint was the 12-month change in PMR. Changes in computed tomography angiography parameters and high-sensitivity C-reactive protein levels were analyzed. RESULTS: In the statin group, 12 months of statin therapy significantly improved low-density lipoprotein cholesterol levels (125 to 70 mg/dl; p < 0.001), PMR (1.38 to 1.11, an 18.9% reduction; p < 0.001), low-attenuation plaque volume, and the percentage of total atheroma volume on computed tomography. In the control group, the PMR increased significantly (from 1.22 to 1.49, a 19.2% increase; p < 0.001). Changes in PMR were correlated with changes in low-density lipoprotein cholesterol (r = 0.533; p < 0.001), high-sensitivity C-reactive protein (r = 0.347; p < 0.001), percentage of atheroma volume (r = 0.477; p < 0.001), and percentage of low-attenuation plaque volume (r = 0.416; p < 0.001). CONCLUSIONS: Statin treatment significantly reduced the PMR of high-intensity plaques. Noncontrast T1-weighted magnetic resonance imaging could become a useful technique for repeated quantitative assessment of plaque composition. (Attempts at Plaque Vulnerability Quantification with Magnetic Resonance Imaging Using Noncontrast T1-weighted Technique [AQUAMARINE]; UMIN000003567).
BACKGROUND: Coronary high-intensity plaques detected by noncontrast T1-weighted imaging may represent plaque instability. High-intensity plaques can be quantitatively assessed by a plaque-to-myocardium signal-intensity ratio (PMR). OBJECTIVES: This pilot, hypothesis-generating study sought to investigate whether intensive statin therapy would lower PMR. METHODS: Prospective serial noncontrast T1-weighted magnetic resonance imaging and computed tomography angiography were performed in 48 patients with coronary artery disease at baseline and after 12 months of intensive pitavastatin treatment with a target low-density lipoprotein cholesterol level <80 mg/dl. The control group consisted of coronary artery diseasepatients not treated with statins that were matched by propensity scoring (n = 48). The primary endpoint was the 12-month change in PMR. Changes in computed tomography angiography parameters and high-sensitivity C-reactive protein levels were analyzed. RESULTS: In the statin group, 12 months of statin therapy significantly improved low-density lipoprotein cholesterol levels (125 to 70 mg/dl; p < 0.001), PMR (1.38 to 1.11, an 18.9% reduction; p < 0.001), low-attenuation plaque volume, and the percentage of total atheroma volume on computed tomography. In the control group, the PMR increased significantly (from 1.22 to 1.49, a 19.2% increase; p < 0.001). Changes in PMR were correlated with changes in low-density lipoprotein cholesterol (r = 0.533; p < 0.001), high-sensitivity C-reactive protein (r = 0.347; p < 0.001), percentage of atheroma volume (r = 0.477; p < 0.001), and percentage of low-attenuation plaque volume (r = 0.416; p < 0.001). CONCLUSIONS: Statin treatment significantly reduced the PMR of high-intensity plaques. Noncontrast T1-weighted magnetic resonance imaging could become a useful technique for repeated quantitative assessment of plaque composition. (Attempts at Plaque Vulnerability Quantification with Magnetic Resonance Imaging Using Noncontrast T1-weighted Technique [AQUAMARINE]; UMIN000003567).
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