Prevalence, Features, and Prognosis of Artery-to-Artery Embolic ST-Segment-Elevation Myocardial Infarction: An Optical Coherence Tomography Study.
Aged
Aged, 80 and over
Case-Control Studies
Coronary Vessels
/ diagnostic imaging
Female
Humans
Male
Middle Aged
Myocardial Infarction
/ complications
Percutaneous Coronary Intervention
Plaque, Atherosclerotic
/ pathology
Prevalence
Prognosis
Retrospective Studies
Rupture, Spontaneous
/ complications
ST Elevation Myocardial Infarction
/ diagnosis
Thrombosis
/ complications
Tomography, Optical Coherence
/ methods
ST‐segment–elevation myocardial infarction
artery‐to‐artery embolic myocardial infarction
optical coherence tomography
plaque rupture
Journal
Journal of the American Heart Association
ISSN: 2047-9980
Titre abrégé: J Am Heart Assoc
Pays: England
ID NLM: 101580524
Informations de publication
Date de publication:
15 12 2020
15 12 2020
Historique:
pubmed:
1
12
2020
medline:
17
3
2021
entrez:
30
11
2020
Statut:
ppublish
Résumé
Background The major underlying mechanisms contributing to acute coronary syndrome are plaque rupture, plaque erosion, and calcified nodule. Artery-to-artery embolic myocardial infarction (AAEMI) was defined as ST-segment-elevation myocardial infarction caused by migrating thrombus formed at the proximal ruptured plaque. The aim of this study was to investigate the prevalence and clinical features of AAEMI by using optical coherence tomography. Methods and Results This study retrospectively enrolled 297 patients with ST-segment-elevation myocardial infarction who underwent optical coherence tomography before percutaneous coronary intervention. Patients were divided into 4 groups consisting of plaque rupture, plaque erosion, calcified nodule, and AAEMI according to optical coherence tomography findings. The prevalence of AAEMI was 3.4%. The culprit vessel in 60% of patients with AAEMI was right coronary artery. Minimum lumen area at the culprit site was larger in AAEMI compared with plaque rupture, plaque erosion, and calcified nodule (4.0 mm
Identifiants
pubmed: 33251922
doi: 10.1161/JAHA.120.017661
pmc: PMC7955389
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e017661Références
Int J Cardiol. 2016 Jan 15;203:766-74
pubmed: 26590891
Circ J. 2019 Apr 25;83(5):1085-1196
pubmed: 30930428
Neurology. 2000 Feb 8;54(3):674-8
pubmed: 10680802
JACC Cardiovasc Interv. 2018 Jan 22;11(2):172-180
pubmed: 29348012
J Am Coll Cardiol. 2018 Oct 30;72(18):2231-2264
pubmed: 30153967
Circulation. 2007 May 1;115(17):2344-51
pubmed: 17470709
Heart Vessels. 2013 Mar;28(2):166-72
pubmed: 22349692
Arterioscler Thromb Vasc Biol. 2000 May;20(5):1262-75
pubmed: 10807742
J Am Heart Assoc. 2019 Nov 5;8(21):e012322
pubmed: 31640466
J Comput Assist Tomogr. 1999 Jul-Aug;23(4):567-76
pubmed: 10433289
Stroke. 2018 Apr;49(4):905-911
pubmed: 29540606
Eur Heart J. 2015 Jun 7;36(22):1377-84
pubmed: 25713314
Atherosclerosis. 2014 Aug;235(2):532-7
pubmed: 24953494
Circ Cardiovasc Interv. 2017 Dec;10(12):
pubmed: 29246916
JACC Cardiovasc Interv. 2017 Dec 26;10(24):2473-2487
pubmed: 29268880
JACC Cardiovasc Interv. 2015 Aug 17;8(9):1166-1176
pubmed: 26117464
Circulation. 2015 Jul 28;132(4):241-50
pubmed: 26216084
EuroIntervention. 2018 Sep 20;14(7):806-814
pubmed: 29790478
Stroke. 2012 Dec;43(12):3313-8
pubmed: 23160885
J Am Coll Cardiol. 2002 Sep 4;40(5):904-10
pubmed: 12225714
JACC Cardiovasc Interv. 2011 Jan;4(1):76-82
pubmed: 21251632
J Am Coll Cardiol. 2013 Nov 5;62(19):1748-58
pubmed: 23810884
Ann Intern Med. 1978 Feb;88(2):155-61
pubmed: 626443