Tomoyo Sugiyama1, Erika Yamamoto1, Francesco Fracassi1, Hang Lee2, Taishi Yonetsu3, Tsunekazu Kakuta4, Tsunenari Soeda5, Yoshihiko Saito5, Bryan P Yan6, Osamu Kurihara7, Masamichi Takano7, Giampaolo Niccoli8, Filippo Crea8, Takumi Higuma9, Shigeki Kimura10, Yoshiyasu Minami11, Junya Ako11, Tom Adriaenssens12, Niklas F Boeder13, Holger M Nef13, James G Fujimoto14, Valentin Fuster15, Aloke V Finn16, Erling Falk17, Ik-Kyung Jang18. 1. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 2. Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 3. Department of Interventional Cardiology, Tokyo Medical and Dental University, Tokyo, Japan. Electronic address: t-yonetsu.cvm@tmd.ac.jp. 4. Department of Cardiovascular Medicine, Tsuchiura Kyodo General Hospital, Tsuchiura, Japan. 5. Department of Cardiovascular Medicine, Nara Medical University, Kashihara, Japan. 6. Department of Medicine and Therapeutics, Chinese University of Hong Kong, Hong Kong, China. 7. Cardiovascular Center, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Japan. 8. Department of Cardiovascular and Thoracic Science, Catholic University of the Sacred Heart, Rome, Italy. 9. Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan. 10. Department of Cardiology, Kameda Medical Center, Kamogawa, Japan. 11. Department of Cardiovascular Medicine, Kitasato University School of Medicine, Sagamihara, Japan. 12. Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium. 13. Department of Cardiology, University of Giessen, Giessen, Germany. 14. Research Laboratory of Electronics, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts. 15. Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. 16. CVPath Institute, Gaithersburg, Maryland. 17. Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark. 18. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Division of Cardiology, Kyung Hee University Hospital, Seoul, Republic of Korea. Electronic address: ijang@mgh.harvard.edu.
Abstract
OBJECTIVES: This study conducted detailed analysis of calcified culprit plaques in patients with acute coronary syndromes (ACS). BACKGROUND: Calcified plaques as an underlying pathology in patients with ACS have not been systematically studied. METHODS: From 1,241 patients presenting with ACS who had undergone pre-intervention optical coherence tomography imaging, 157 (12.7%) patients were found to have a calcified plaque at the culprit lesion. Calcified plaque was defined as a plaque with superficial calcification at the culprit site without evidence of ruptured lipid plaque. RESULTS: Three distinct types were identified: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion (prevalence of 25.5%, 67.4%, and 7.1%, respectively). Eruptive calcified nodules were frequently located in the right coronary arteries (44.4%), whereas superficial calcific sheet was most frequently found in the left anterior descending coronary arteries (68.4%) (p = 0.012). Calcification index (mean calcification arc × calcification length) was greatest in eruptive calcified nodules, followed by superficial calcific sheet, and smallest in calcified protrusion (median 3,284.9 [interquartile range (IQR): 2,113.3 to 5,385.3] vs. 1,644.3 [IQR: 1,012.4 to 3,058.7] vs. 472.5 [IQR: 176.7 to 865.2]; p < 0.001). The superficial calcific sheet group had the highest peak post-intervention creatine kinase values among the groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 241 [IQR: 116 to 612] IU/l vs. 834 [IQR: 141 to 3,394] IU/l vs. 745 [IQR: 69 to 1,984] IU/l; p = 0.032). CONCLUSIONS: Three distinct types of calcified culprit plaques are identified in patients with ACS. Superficial calcific sheet, which is frequently located in the left anterior descending coronary artery, is the most prevalent type and is also associated with greatest post-intervention myocardial damage. (Identification of Predictors for Coronary Plaque Erosion in Patients With Acute Coronary Syndrome; NCT03479723).
OBJECTIVES: This study conducted detailed analysis of calcified culprit plaques in patients with acute coronary syndromes (ACS). BACKGROUND: Calcified plaques as an underlying pathology in patients with ACS have not been systematically studied. METHODS: From 1,241 patients presenting with ACS who had undergone pre-intervention optical coherence tomography imaging, 157 (12.7%) patients were found to have a calcified plaque at the culprit lesion. Calcified plaque was defined as a plaque with superficial calcification at the culprit site without evidence of ruptured lipid plaque. RESULTS: Three distinct types were identified: eruptive calcified nodules, superficial calcific sheet, and calcified protrusion (prevalence of 25.5%, 67.4%, and 7.1%, respectively). Eruptive calcified nodules were frequently located in the right coronary arteries (44.4%), whereas superficial calcific sheet was most frequently found in the left anterior descending coronary arteries (68.4%) (p = 0.012). Calcification index (mean calcification arc × calcification length) was greatest in eruptive calcified nodules, followed by superficial calcific sheet, and smallest in calcified protrusion (median 3,284.9 [interquartile range (IQR): 2,113.3 to 5,385.3] vs. 1,644.3 [IQR: 1,012.4 to 3,058.7] vs. 472.5 [IQR: 176.7 to 865.2]; p < 0.001). The superficial calcific sheet group had the highest peak post-intervention creatine kinase values among the groups (eruptive calcified nodules vs. superficial calcific sheet vs. calcified protrusion: 241 [IQR: 116 to 612] IU/l vs. 834 [IQR: 141 to 3,394] IU/l vs. 745 [IQR: 69 to 1,984] IU/l; p = 0.032). CONCLUSIONS: Three distinct types of calcified culprit plaques are identified in patients with ACS. Superficial calcific sheet, which is frequently located in the left anterior descending coronary artery, is the most prevalent type and is also associated with greatest post-intervention myocardial damage. (Identification of Predictors for Coronary Plaque Erosion in Patients With Acute Coronary Syndrome; NCT03479723).
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