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. 2021 Apr 6;77(13):1599-1611.
doi: 10.1016/j.jacc.2021.02.016.

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

Sho Torii  1 , Yu Sato  1 , Fumiyuki Otsuka  2 , Frank D Kolodgie  1 , Hiroyuki Jinnouchi  1 , Atsushi Sakamoto  1 , Joohyung Park  1 , Kazuyuki Yahagi  1 , Kenichi Sakakura  1 , Anne Cornelissen  1 , Rika Kawakami  1 , Masayuki Mori  1 , Kenji Kawai  1 , Falone Amoa  1 , Liang Guo  1 , Matthew Kutyna  1 , Raquel Fernandez  1 , Maria E Romero  1 , David Fowler  3 , Aloke V Finn  4 , Renu Virmani  5
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Free article

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

Sho Torii et al. J Am Coll Cardiol. .
Free article

Abstract

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.

Keywords: acute myocardial infarction; calcified nodule; sudden coronary death.

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Conflict of interest statement

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.

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