Eruptive Calcified Nodules as a Potential Mechanism of Acute Coronary Thrombosis and Sudden Death.

Autor:	Torii S; CVPath Institute, Gaithersburg, Maryland, USA., Sato Y; CVPath Institute, Gaithersburg, Maryland, USA., Otsuka F; CVPath Institute, Gaithersburg, Maryland, USA; National Cerebral and Cardiovascular Center, Department of Cardiovascular Medicine, Osaka, Japan., Kolodgie FD; CVPath Institute, Gaithersburg, Maryland, USA., Jinnouchi H; CVPath Institute, Gaithersburg, Maryland, USA., Sakamoto A; CVPath Institute, Gaithersburg, Maryland, USA., Park J; CVPath Institute, Gaithersburg, Maryland, USA., Yahagi K; CVPath Institute, Gaithersburg, Maryland, USA., Sakakura K; CVPath Institute, Gaithersburg, Maryland, USA., Cornelissen A; CVPath Institute, Gaithersburg, Maryland, USA., Kawakami R; CVPath Institute, Gaithersburg, Maryland, USA., Mori M; CVPath Institute, Gaithersburg, Maryland, USA., Kawai K; CVPath Institute, Gaithersburg, Maryland, USA., Amoa F; CVPath Institute, Gaithersburg, Maryland, USA., Guo L; CVPath Institute, Gaithersburg, Maryland, USA., Kutyna M; CVPath Institute, Gaithersburg, Maryland, USA., Fernandez R; CVPath Institute, Gaithersburg, Maryland, USA., Romero ME; CVPath Institute, Gaithersburg, Maryland, USA., Fowler D; Office of the Chief Medical Examiner, Baltimore, Maryland, USA., Finn AV; CVPath Institute, Gaithersburg, Maryland, USA; University of Maryland, School of Medicine, Baltimore, Maryland, USA., Virmani R; CVPath Institute, Gaithersburg, Maryland, USA. Electronic address: rvirmani@cvpath.org.
Jazyk:	angličtina
Zdroj:	Journal of the American College of Cardiology [J Am Coll Cardiol] 2021 Apr 06; Vol. 77 (13), pp. 1599-1611.
DOI:	10.1016/j.jacc.2021.02.016
Abstrakt:	Background: Calcified nodule (CN) has a unique plaque morphology, in which an area of nodular calcification causes disruption of the fibrous cap with overlying luminal thrombus. CN is reported to be the least frequent cause of acute coronary thrombosis, and the pathogenesis of CN has not been well studied. Objectives: The purpose of this study is to provide a comprehensive morphologic assessment of the CN in addition to providing an evolutionary perspective as to how CN causes acute coronary thrombosis in patients with acute coronary syndromes. Methods: A total of 26 consecutive CN lesions from 25 subjects from our autopsy registry were evaluated. Detailed morphometric analysis was performed to understand the plaque characteristics of CN and nodular calcification. Results: The mean age was 70 years, with a high prevalence of diabetes and chronic kidney disease. CNs were equally distributed between men and women, with 61.5% of CNs found in the right coronary artery (n = 16), mainly within its mid-portion (56%). All CNs demonstrated surface nonocclusive luminal thrombus, consisting of multiple nodular fragments of calcification, protruding and disrupting the overlying fibrous cap, with evidence of endothelial cell loss. The degree of circumferential sheet calcification was significantly less in the culprit section (89° [interquartile range: 54° to 177°]) than in the adjacent proximal (206° [interquartile range: 157° to 269°], p = 0.0034) and distal (240° [interquartile range: 178° to 333°], p = 0.0004) sections. Polarized picrosirius red staining showed the presence of necrotic core calcium at culprit sites of CNs, whereas collagen calcium was more prevalent at the proximal and distal regions of CNs. Conclusions: Our study suggests that fibrous cap disruption in CN with overlying thrombosis is initiated through the fragmentation of necrotic core calcifications, which is flanked-proximally and distally-by hard, collagen-rich calcification in coronary arteries, which are susceptible to mechanical stress. Competing Interests: Funding Support and Author Disclosures Dr.Torii has received research grants from Sunrise Laboratories. CVPath Institute has received institutional research support from NIH-HL141425, Leducq Foundation Grant, 480 Biomedical, 4C Medical, 4Tech,Abbott, Accumedical, Amgen, Biosensors, Boston Scientific, Canon USA, Cardiac Implants, Celonova, Claret Medical, Concept Medical, Cook, CSI, DuNing, Inc, Edwards LifeSciences, Emboline, Endotronix, Envision Scientific, Lutonix/Bard, Gateway, Lifetech, Limflo, MedAlliance, Medtronic, Mercator, Merill, Microport Medical, Microvention, Mitraalign, Mitra Assist, NAMSA, Nanova, Neovasc, NIPRO, Novogate, Occulotech, OrbusNeich Medical, Phenox, Profusa, Protembis, Qool, ReCor Medical, Senseonics, Shockwave, Sinomed, Spectranetics, Surmodics, Symic, Vesper, W.L. Gore, and Xeltis. Dr. Finn has received honoraria from Abbott Vascular, Biosensors Boston Scientific, Celonova, Cook Medical, CSI, Lutonix Bard, Sinomed, and Terumo Corporation; and is a consultant to Amgen, Abbott Vascular, Boston Scientific, Celonova, Cook Medical, Lutonix Bard, and Sinomed. Dr. Cornelissen has received research grants from University Hospital RWTH Aachen. Dr. Virmani has received honoraria from Abbott Vascular, Biosensors, Boston Scientific, Celonova, Cook Medical, Cordis, CSI, Lutonix Bard, Medtronic, OrbusNeich Medical, CeloNova, SINO Medical Technology, ReCor, Terumo Corporation, W. L. Gore, and Spectranetics; and has served as a consultant to Abbott Vascular, Boston Scientific, Celonova, Cook Medical, Cordis, CSI, Edwards Lifesciences, Lutonix Bard, Medtronic, OrbusNeich Medical, ReCor Medical, Sinomededical Technology, Spectranetics, Surmodics, Terumo Corporation, W. L. Gore, and Xeltis. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. (Copyright © 2021 American College of Cardiology Foundation. All rights reserved.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu