Lei Xing1, Takumi Higuma2, Zhao Wang3, Aaron D Aguirre2, Kyoichi Mizuno4, Masamichi Takano5, Harold L Dauerman6, Seung-Jung Park7, Yangsoo Jang8, Chong-Jin Kim9, Soo-Joong Kim9, So-Yeon Choi10, Tomonori Itoh11, Shiro Uemura12, Harry Lowe13, Darren L Walters14, Peter Barlis15, Stephen Lee16, Amir Lerman17, Catalin Toma18, Jack Wei Chieh Tan19, Erika Yamamoto2, Krzysztof Bryniarski2, Jiannan Dai2, Thomas Zanchin2, Shaosong Zhang20, Bo Yu21, Hang Lee22, James Fujimoto3, Valentin Fuster23, Ik-Kyung Jang24. 1. Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, and the Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China; Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 2. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 3. The Research Laboratory of Electronics, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts. 4. Department of Cardiovascular Medicine, Nippon Medical School, Tokyo, Japan. 5. Division of Cardiology, Nippon Medical School Chiba-Hokusoh Hospital, Chiba, Japan. 6. Department of Medicine, University of Vermont College of Medicine, Burlington, Vermont. 7. Department of Cardiology, Heart Institute, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea. 8. Division of Cardiology, Department of Internal Medicine, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea. 9. Division of Cardiology, Department of Internal Medicine, KyungHee University Hospital, Seoul, Republic of Korea. 10. Department of Cardiology, Ajou University School of Medicine, Suwon, Republic of Korea. 11. Division of Cardiology, Department of Internal Medicine, Iwate Medical University School of Medicine, Morioka, Japan. 12. Department of Cardiology, Kawasaki Medical School, Matsushima, Japan. 13. Cardiology Department, Concord Repatriation General Hospital, University of Sydney, Sydney, New South Wales, Australia. 14. Department of Cardiology, Prince Charles Hospital, University of Queensland, Brisbane, Queensland, Australia. 15. Cardiology Department, Northern Hospital and Department of Medicine, Faculty of Medicine, Dentistry and Health Sciences, University of Melbourne, Parkville, Victoria, Australia. 16. Department of Medicine, Queen Mary Hospital, Hong Kong University, Hong Kong, China. 17. Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic and College of Medicine, Rochester, Minnesota. 18. Heart and Vascular Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. 19. Department of Cardiology, National Heart Centre Singapore, Singapore. 20. Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, and the Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China. 21. Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, and the Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China. Electronic address: yubodr@163.com. 22. Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 23. Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. 24. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Division of Cardiology, Department of Internal Medicine, KyungHee University Hospital, Seoul, Republic of Korea. Electronic address: ijang@mgh.harvard.edu.
Abstract
BACKGROUND: Lipid-rich plaque (LRP) is thought to be a precursor to cardiac events. However, its clinical significance in coronary arteries has never been systematically investigated. OBJECTIVES: This study investigated the prevalence and clinical significance of LRP in the nonculprit region of the target vessel in patients undergoing percutaneous coronary intervention (PCI). METHODS: The study included 1,474 patients from 20 sites across 6 countries undergoing PCI, who had optical coherence tomography (OCT) imaging of the target vessel. Major adverse cardiac events (MACE) were defined as a composite of cardiac death, acute myocardial infarction, and ischemia-driven revascularization. Patients were followed for up to 4 years (median of 2 years). RESULTS: Lipid-rich plaque was detected in nonculprit regions of the target vessel in 33.6% of patients. The cumulative rate of nonculprit lesion-related MACE (NC-MACE) over 48 months in patients with LRP was higher than in those without LRP (7.2% vs. 2.6%, respectively; p = 0.033). Acute coronary syndrome at index presentation (risk ratio: 2.538; 95% confidence interval [CI]: 1.246 to 5.173; p = 0.010), interruption of statin use ≥1 year (risk ratio: 4.517; 95% CI: 1.923 to 10.610; p = 0.001), and LRP in nonculprit regions (risk ratio: 2.061; 95% CI: 1.050 to 4.044; p = 0.036) were independently associated with increased NC-MACE. Optical coherence tomography findings revealed that LRP in patients with NC-MACE had longer lipid lengths (p < 0.001), wider maximal lipid arcs (p = 0.023), and smaller minimal lumen areas (p = 0.003) than LRPs in patients without MACE. CONCLUSIONS: Presence of LRP in the nonculprit regions of the target vessel by OCT predicts increased risk for future NC-MACE, which is primarily driven by revascularization for recurrent ischemia. Lipid-rich plaque with longer lipid length, wider lipid arc, and higher degree of stenosis identified patients at higher risk of future cardiac events. (The Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538).
BACKGROUND:Lipid-rich plaque (LRP) is thought to be a precursor to cardiac events. However, its clinical significance in coronary arteries has never been systematically investigated. OBJECTIVES: This study investigated the prevalence and clinical significance of LRP in the nonculprit region of the target vessel in patients undergoing percutaneous coronary intervention (PCI). METHODS: The study included 1,474 patients from 20 sites across 6 countries undergoing PCI, who had optical coherence tomography (OCT) imaging of the target vessel. Major adverse cardiac events (MACE) were defined as a composite of cardiac death, acute myocardial infarction, and ischemia-driven revascularization. Patients were followed for up to 4 years (median of 2 years). RESULTS:Lipid-rich plaque was detected in nonculprit regions of the target vessel in 33.6% of patients. The cumulative rate of nonculprit lesion-related MACE (NC-MACE) over 48 months in patients with LRP was higher than in those without LRP (7.2% vs. 2.6%, respectively; p = 0.033). Acute coronary syndrome at index presentation (risk ratio: 2.538; 95% confidence interval [CI]: 1.246 to 5.173; p = 0.010), interruption of statin use ≥1 year (risk ratio: 4.517; 95% CI: 1.923 to 10.610; p = 0.001), and LRP in nonculprit regions (risk ratio: 2.061; 95% CI: 1.050 to 4.044; p = 0.036) were independently associated with increased NC-MACE. Optical coherence tomography findings revealed that LRP in patients with NC-MACE had longer lipid lengths (p < 0.001), wider maximal lipid arcs (p = 0.023), and smaller minimal lumen areas (p = 0.003) than LRPs in patients without MACE. CONCLUSIONS: Presence of LRP in the nonculprit regions of the target vessel by OCT predicts increased risk for future NC-MACE, which is primarily driven by revascularization for recurrent ischemia. Lipid-rich plaque with longer lipid length, wider lipid arc, and higher degree of stenosis identified patients at higher risk of future cardiac events. (The Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538).
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