Key result
Silent non-culprit plaque ruptures occur in ~12% of AMI patients, with most healing spontaneously.
Why the study?
Plaque rupture can occur at non-obstructive lesions in non-infarct-related coronary arteries without inducing ischaemia, but its frequency, characteristics, and morphological changes over time are not well defined.
What is the frequency, morphological characteristics, and 52-week evolution of silent plaque ruptures in non-obstructive lesions of non-infarct-related arteries in patients with acute myocardial infarction?
Observational (n=336)
Yes
What is the frequency, morphological characteristics, and 52-week evolution of silent plaque ruptures in non-obstructive lesions of non-infarct-related arteries in patients with acute myocardial infarction?
Answers are grounded in this paper and cite their sources.
Silent plaque ruptures in non-infarct-related arteries occur in 12% of AMI patients, are associated with larger plaque volume and thinner fibrous caps, and over half heal within 52 weeks.
BACKGROUND 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.
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Kakizaki et al. (2026) conducted an observational in Acute myocardial infarction (n=336). Plaque rupture vs. No plaque rupture was evaluated on Percent atheroma volume (MD 3.6, 95% CI 1.9 to 5.4). Plaque rupture in non-obstructive lesions of non-infarct-related arteries was present in 12% of AMI patients and was associated with larger percent atheroma volume (MD 3.6%; 95% CI 1.9-5.4).
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