Abstract 10435: Phenotypes and Microstructural Plaque Characteristics in an Oct Analysis

IntroductionPostmortem studies suggest that thin-cap fibroatheroma (TFCA) is the main anatomic substrate for acute myocardial infarction. In vivo high resolution intravascular imaging such as optical coherence tomography (OCT) findings are scarce and subject of controversy associated with the debate...

Full description

Saved in:
Bibliographic Details
Published in:Circulation (New York, N.Y.) Vol. 138; no. Suppl_1 Suppl 1; p. A10435
Main Authors: S Gomes, Paula M P, Pedrini, Stella M, Freitas, Barbara P, Almeida, Breno O, M Campos, Carlos A H, Lemos, Pedro A, Junior, José M, Franken, Marcelo, Caixeta, Adriano
Format: Journal Article
Language:English
Published: by the American College of Cardiology Foundation and the American Heart Association, Inc 06-11-2018
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:IntroductionPostmortem studies suggest that thin-cap fibroatheroma (TFCA) is the main anatomic substrate for acute myocardial infarction. In vivo high resolution intravascular imaging such as optical coherence tomography (OCT) findings are scarce and subject of controversy associated with the debate regarding phenotypes and plaque characteristics in ACS pts.PurposeTo investigate culprit plaque phenotypes and composition in pts with ACS by applying a contemporary microstructural analysis and definition.MethodsBetween 2012 and 2017, 110 pts with ACS who underwent pre-intervention OCT imaging were retrospectively identified. OCT examination was performed using either C7-XR or LightLab Imaging Inc (Abbott Vascular, USA). OCT images were quantitatively and qualitative analyzed using the dedicated software QIVUS (3.0, Medis Medical Imaging Systems, the Netherlands version). TCFA was defined as plaque with the maximal lipid arc > 90 degree and thinnest fibrous thickness of 65 um or less. Plaques were described according to phenotypes (fibrotic, fibrocalcific, thick-layer fibroatheroma [ThCFA], and TCFA) and were also classified on 3 subgroupsrupture, erosion, and calcified nodule. Pts were gathered in 2 groupsunstable angina (UA)/non-STEMI and STEMI.ResultsAmong 110 lesions, 54 (49%) were UA, 31 (28) were non-STEMI) and 25 (23%) were STEMI. Compared with pts UA/Non-STEMI, those with STEMI had greater percentage of lipid arch, red thrombus, higher rate of rupture plaque and TFCA (Table). Independent predictors of plaque rupture were diabetes (OR 6.16; IC 1.33-28.58; p-value 0.02), and STEMI presentation (OR 9.35; IC 1.66- 52.61; p-value- 0.01). There was a trend toward a protective effect of prior statin use for plaque rupture (OR 0.38; IC 0.11- 1.29; p-value 0.12). Table1Morphological and Phenotypes Plaque Analysis in Patients with ACSConclusionIn this single-center study, culprit lesion of pts with STEMI had more necrotic core, red thrombus, and TFCA with plaque rupture; whereas pts with UA/Non-STEMI had more ThFCA and fibrotic/fibrocalcic plaques. Hence, clinical presentation may be driven by distinct pathophysiologic mechanisms in ACS pts. Independent predictor of plaque rupture were associated with clinical condition (diabetes), and presentation (STEMI). The use of statin prior hospitalization may be protective against plaque rupture.
ISSN:0009-7322
1524-4539