Silent plaque ruptures in non-obstructive lesions of non–infarct-related arteries: a multimodality, serial intracoronary imaging study

European Heart Journal

9 March 2026
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ESC Journals CORONARY ARTERY DISEASE, ACUTE CORONARY SYNDROMES, ACUTE CARDIAC CARE Acute Coronary Syndromes IMAGING

Abstract

AbstractBackground and Aims

Plaque rupture can occur at non-obstructive lesions in non–infarct-related coronary arteries (non-IRAs) without inducing ischaemia. This study aimed to: (1) assess the frequency and lesion characteristics of plaque rupture in non-IRAs of acute myocardial infarction (AMI) patients, (2) evaluate morphological changes in rupture sites over 52 weeks, and (3) investigate the baseline morphology of new-onset ruptures.

Methods

This study analysed pooled data from the IBIS-4 and PACMAN-AMI trials. Patients presenting with AMI underwent multimodality intracoronary imaging of non-IRAs at baseline and after 52 weeks.

Results

Among 783 lesions from 336 patients evaluated at baseline, plaque rupture was observed in 41 lesions of 40 patients (12%). Biomarkers including lipid and inflammation markers were comparable between patients with and without rupture in non-IRAs. Lesions with rupture showed larger percent atheroma volume (53.3 ± 6.4 vs. 49.5 ± 5.8%, estimated difference 3.6[1.9 to 5.4]), larger external elastic membrane area (20.5 ± 4.8 vs. 15.7 ± 5.6 mm2, 4.1[2.5 to 5.7]), and smaller minimum fibrous cap thickness (69 ± 49 vs. 116 ± 84 μm, −43[−75 to −11]) compared to those without. Among 41 rupture sites assessed serially, 21 (51%) healed by 52 weeks. At follow-up, 10 rupture sites were newly identified, and thin-cap fibroatheroma was the most frequent baseline morphology of those.

Conclusions

Plaque rupture in non-obstructive lesions of non-IRAs was present in 12% of AMI patients. Larger plaque volume, positive remodeling, and thinner fibrous cap were associated with rupture. More than half of untreated ruptures transitioned into stable morphologies. Thin-cap fibroatheroma was the most frequent underlying morphology of new-onset rupture.

Contributors

Ryota Kakizaki
Ryota Kakizaki

Author

Kitasato University School of Medicine Sagamihara , Japan

Ernest Spitzer
Ernest Spitzer

Author

Erasmus University Medical Centre Rotterdam , Netherlands (The)

Robert-Jan van Geuns
Robert-Jan van Geuns

Author

University Medical Centre St Radboud (UMCN) Nijmegen , Netherlands (The)

Thomas Engstrøm
Thomas Engstrøm

Author

Rigshospitalet - Copenhagen University Hospital Copenhagen , Denmark

Lorenz Räber
Lorenz Räber

Author

Swiss Cardiovascular Center Bern , Switzerland