Kenichi Tsujita1, Kenshi Yamanaga2, Naohiro Komura2, Kenji Sakamoto2, Seigo Sugiyama3, Hitoshi Sumida4, Hideki Shimomura5, Takuro Yamashita6, Hideki Oka7, Koichi Nakao8, Sunao Nakamura9, Masaharu Ishihara10, Kunihiko Matsui11, Naritsugu Sakaino12, Natsuki Nakamura13, Nobuyasu Yamamoto14, Shunichi Koide15, Toshiyuki Matsumura16, Kazuteru Fujimoto17, Ryusuke Tsunoda18, Yasuhiro Morikami19, Koushi Matsuyama6, Shuichi Oshima4, Koichi Kaikita2, Seiji Hokimoto2, Hisao Ogawa20. 1. Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. Electronic address: tsujita@kumamoto-u.ac.jp. 2. Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. 3. Jinnouchi Hospital, Kumamoto, Japan. 4. Division of Cardiology, Kumamoto Central Hospital, Kumamoto, Japan. 5. Department of Cardiovascular Medicine, Fukuoka Tokushukai Medical Center, Kasuga, Japan. 6. Division of Cardiology, Social Insurance Omuta Tenryo Hospital, Omuta, Japan. 7. Division of Cardiology, Health Insurance Hitoyoshi General Hospital, Hitoyoshi, Japan. 8. Division of Cardiology, Saiseikai Kumamoto Hospital Cardiovascular Center, Kumamoto, Japan. 9. Interventional Cardiology Unit, New Tokyo Hospital, Matsudo, Japan. 10. Division of Coronary Artery Disease, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan. 11. Department of Community Medicine, Kumamoto University, Kumamoto, Japan. 12. Division of Cardiology, Amakusa Medical Center, Amakusa, Japan. 13. Division of Cardiology, Shin-Beppu Hospital, Beppu, Japan. 14. Division of Cardiology, Miyazaki Prefectural Nobeoka Hospital, Nobeoka, Japan. 15. Division of Cardiology, Health Insurance Kumamoto General Hospital, Yatsushiro, Japan. 16. Division of Cardiology, Japan Labor Health and Welfare Organization Kumamoto Rosai Hospital, Yatsushiro, Japan. 17. National Hospital Organization Kumamoto Medical Center, Kumamoto, Japan. 18. Japanese Red Cross Kumamoto Hospital, Kumamoto, Japan. 19. Division of Cardiology, Kumamoto City Hospital, Kumamoto, Japan. 20. Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan; Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Japan.
Abstract
BACKGROUND AND AIMS: Although dual low-density lipoprotein cholesterol (LDL-C)-lowering therapy (DLLT) with statin-ezetimibe combination showed clinical benefit in patients with acute coronary syndrome (ACS) confirming "the lower, the better," the underlying mechanisms of DLLT are still unknown. METHODS: PRECISE-IVUS trial evaluated the effects of DLLT on IVUS-derived coronary atherosclerosis and lipid profile, compared with atorvastatin monotherapy, quantifying the coronary plaque response in 100 ACS patients. We explored the potential predictors of plaque regression. RESULTS:Lower total cholesterol, LDL-C, triglyceride, remnant-like particles cholesterol, and stronger reduction of small dense LDL-C and cholesterol absorption markers were observed in patients with plaque regression compared to those with progression. Multivariate analysis revealed that achieved LDL-C was the strongest predictor for coronary plaque regression (95% CI: 0.944-1.000, p = 0.05), followed by age (95% CI: 0.994-1.096, p = 0.09). CONCLUSIONS: Incremental LDL-C lowering by DLLT was associated with stronger coronary plaque regression, reconfirming that lowering LDL-C to levels below previous targets provided additional clinical benefit.
RCT Entities:
BACKGROUND AND AIMS: Although dual low-density lipoprotein cholesterol (LDL-C)-lowering therapy (DLLT) with statin-ezetimibe combination showed clinical benefit in patients with acute coronary syndrome (ACS) confirming "the lower, the better," the underlying mechanisms of DLLT are still unknown. METHODS: PRECISE-IVUS trial evaluated the effects of DLLT on IVUS-derived coronary atherosclerosis and lipid profile, compared with atorvastatin monotherapy, quantifying the coronary plaque response in 100 ACS patients. We explored the potential predictors of plaque regression. RESULTS: Lower total cholesterol, LDL-C, triglyceride, remnant-like particles cholesterol, and stronger reduction of small dense LDL-C and cholesterol absorption markers were observed in patients with plaque regression compared to those with progression. Multivariate analysis revealed that achieved LDL-C was the strongest predictor for coronary plaque regression (95% CI: 0.944-1.000, p = 0.05), followed by age (95% CI: 0.994-1.096, p = 0.09). CONCLUSIONS: Incremental LDL-C lowering by DLLT was associated with stronger coronary plaque regression, reconfirming that lowering LDL-C to levels below previous targets provided additional clinical benefit.
Authors: Walter Masson; Martin Lobo; Daniel Siniawski; Graciela Molinero; Gerardo Masson; Melina Huerín; Juan Patricio Nogueira Journal: Lipids Health Dis Date: 2020-05-27 Impact factor: 3.876