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Updated: Mar 7, 2026

Histological Quantification of Chronic Myocardial Infarct in Rats
Published on: December 11, 2016
Tissue characterization and phenotype classification in patients presenting with acute myocardial infarction:
Cristiano F Souza1, Akiko Maehara2,3, Gary S Mintz2
1Department of Interventional Cardiology, Federal University of São Paulo, São Paulo, Brazil.
Objectives:
We sought to assess a new modality of radiofrequency intravascular ultrasound (IVUS) called iMAP-IVUS (Boston Scientific, Santa Clara, California) during the evaluation of patients presenting with high-risk acute coronary syndromes.
Background:
There are limited data on plaque tissue characterization and phenotype classification using iMAP-IVUS.
Methods:
In the iWonder study patients presenting with ST-elevation myocardial infarction (STEMI) or non-STEMI underwent three-vessel grayscale IVUS and iMAP-IVUS tissue characterization prior to percutaneous intervention. In total 385 lesions from 100 patients were divided into culprit (n = 100) and nonculprit (n = 285) lesions. Lesion phenotype was classified as (i) thin-cap fibroatheroma (iMAP-derived TCFA); (ii) thick-cap fibroatheroma; (iii) pathological intimal thickening; (iv) fibrotic plaque; and (v) fibrocalcific plaque.
Results:
Culprit lesions had smaller minimum lumen cross-sectional area (MLA) with greater plaque burden compared to non-culprit lesions. Volumetric analysis showed that culprit lesions had longer length and larger vessel and plaque volumes compared to non-culprit lesions. iMAP-IVUS revealed that culprit lesions presented more NC and fibrofatty volume, both at lesion level and at the MLA site (all P < 0.001). Any fibroatheroma was more frequently identified in culprit lesions compared with non-culprit lesions (93% vs. 78.9%, P = 0.001), anywhere within the lesion 19.0%, P < 0.001) as well as at the MLA site (18.0% vs. 9.5%, P = 0.07).
Conclusions:
Three-vessel radiofrequency iMAP-IVUS demonstrated a greater plaque burden and higher prevalence of any fibroatheroma as well as iMAP-derived TCFAs in culprit versus non-culprit lesions in patients presenting with STEMI or non-STEMI undergoing percutaneous coronary intervention. © 2017 Wiley Periodicals, Inc.
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