Key result
Silent plaque ruptures in non-infarct arteries occur in ~12% of AMI patients with greater atheroma volume.
Cohort (n=336)
Yes
Absolute Event Rate: 53.3% vs 49.5%
p-value: p=<0.001
Silent plaque ruptures in non-infarct-related arteries occur in approximately 10% of AMI patients, are associated with vulnerable plaque characteristics, and over half heal within one year.
Background/Introduction Plaque rupture is the predominant cause of acute myocardial infarction (AMI) and may also occur at non-obstructive lesions in non-infarct-related coronary arteries (non-IRAs) without inducing acute ischaemia (i.e. silent plaque rupture). Purpose The purpose of this study was to: (1) assess the frequency and characteristics of lesions with plaque rupture in non-IRAs among AMI patients; (2) evaluate morphological changes in plaque rupture over 52 weeks; and (3) investigate the baseline plaque morphology of new-onset silent plaque ruptures at 52 weeks. Methods This study analysed pooled data from the IBIS-4 and PACMAN-AMI trials. Patients presenting with AMI and non-obstructive lesions in non-IRAs underwent optical coherence tomography (OCT) and intravascular ultrasound (IVUS) imaging at baseline and after 52 weeks. Plaque rupture was defined as intimal disruption with a cavity on OCT. An IVUS-derived lesion was defined as a plaque burden of ≥40% with a longitudinal extension of ≥3 mm. To evaluate morphological changes at rupture sites, cross-section matching was manually performed using landmarks (e.g. side branches, calcifications) to align frames with rupture between OCT images at baseline and at the 52-week follow-up. Results Among 783 lesions from 336 patients evaluated by OCT at baseline, 46 rupture sites were identified in 41 lesions (5.2%) of 40 patients (11.9%). There was no significant difference in baseline patient characteristics or biochemical findings between patients with and without plaque rupture. Lesions with plaque rupture had a larger percentage atheroma volume (53.3±6.4% vs. 49.5±5.8%, P<0.001, Figure 1-A), a thinner minimum fibrous cap thickness (69±49 μm vs. 116±84 μm, P=0.010, Figure 1-B), a greater maximum lipid angle (210±96° vs. 146±63°, P<0.001), and a greater maximum 4-mm lipid core burden index (401±201 vs. 226±197, P<0.001, Figure 1-C) compared to those without (Figure 2). Although the minimum lumen area was comparable (5.5±2.3 mm² vs. 5.7±2.9 mm², P=0.690), the mean vessel area was larger in lesions with plaque rupture than in those without (20.5±4.8 mm² vs. 15.7±5.6 mm², P<0.001). Among 41 rupture sites in 38 lesions with serial intracoronary imaging, 21 (51.2%) healed at 52 weeks. At 52 weeks, 10 rupture sites in 10 lesions were newly detected, and thin-cap fibroatheroma (TCFA) was the most frequent baseline plaque morphology of new-onset plaque rupture. Conclusions OCT-detected plaque rupture in non-IRAs was observed in one in 10 AMI patients at the index event. Lesions with plaque rupture had a larger plaque burden, a thinner fibrous cap, and greater lipid accumulation. However, the minimum lumen area was comparable between lesions with and without plaque rupture. More than half of the plaque ruptures transitioned into a stabilised morphology, and TCFA was the most frequent underlying plaque morphology of new-onset silent plaque rupture during the one-year follow-up.Figure 1 Figure 2
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Kakizaki et al. (2025) conducted a cohort in Acute Myocardial Infarction (n=336). Silent plaque rupture vs. No silent plaque rupture was evaluated on Percentage atheroma volume (p=<0.001). Silent plaque ruptures in non-infarct-related arteries occurred in 11.9% of AMI patients and were associated with larger percentage atheroma volume (53.3% vs 49.5%, P<0.001).
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