Key result
Nonruptured plaques occur in ~31% of STEMIs and contain less lipidic plaque than ruptured lesions.
Why the study?
The study sought to evaluate the incidence of ruptured plaques and nonruptured plaques and compare patient characteristics and plaque morphology between the two culprit types in STEMI using OCT.
What are the differences in patient characteristics and plaque morphology between ruptured and nonruptured plaques in STEMI patients assessed by OCT?
Observational (n=75)
What are the differences in patient characteristics and plaque morphology between ruptured and nonruptured plaques in STEMI patients assessed by OCT?
Absolute Event Rate: 30.7% vs 69.3%
Nearly one-third of STEMI patients have nonruptured plaques as the culprit lesion, which occur in younger, more often smoking patients and exhibit less vulnerable plaque features on OCT compared to ruptured plaques.
Nonruptured culprit plaques in STEMI may reflect distinct mechanisms; leaves open whether OCT phenotyping should inform targeted therapies.
AIMS: This study sought to evaluate the incidence of ruptured plaques and nonruptured plaques (NRP) and to compare patient characteristics and detailed plaque morphology features between the two culprit types in ST-segment elevation myocardial infarction (STEMI) patients, using optical coherence tomography (OCT). METHODS AND RESULTS: Using OCT, the culprit lesions in patients with STEMI were assessed prior to stent implantation. The culprit lesion was categorized as ruptured plaques or NRP, and the plaque components were evaluated. Fifty-two patients (69.3%) presented with ruptured plaques and 23 (30.7%) with NRP. Patients with NRP were younger (58.0 ± 10.4 vs 64.7 ± 9.9 years, P = 0.01) and more often smokers (72.7% vs 37.1%, P = 0.001), compared to ruptured plaques. NRP contained significantly more fibrotic plaque (20.0% [interquartile range (IQR) 13.7-29.8] vs 11.3% [IQR 6.9-18.1], P = 0.005), but less lipidic plaque (44.0% ± 13.7 vs 59.3% ± 13.6, P < 0.001), less superficial [5.0% (IQR 2.8-7.5) vs 8.1% (IQR 5.7-11.0), P = 0.005] and profound macrophages [0.9% (IQR 0.0-1.7) vs 2.2% (IQR 0.9-4.7), P = 0.003]. The prevalence, numbers and lengths of thin-cap fibroatheroma (TCFA) were significantly lower in NRP, compared to ruptured plaques [47.8% vs 88.5%, 0 (IQR 0-1) vs 1 (IQR 1-2) and 0 mm (IQR 0-2.7) vs 4.5 mm (IQR 2.3-7.7), P < 0.001]. CONCLUSIONS: One-third of STEMI patients had culprit lesions without an OCT-detectable ruptured plaque. Culprit lesions with NRP contained less vulnerable plaque components, such as lipid plaque, TCFAs and macrophages compared to ruptured plaques.
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Hansen et al. (2020) conducted an observational in ST-segment elevation myocardial infarction (STEMI) (n=75). Nonruptured plaques (NRP) vs. Ruptured plaques was evaluated on Incidence of ruptured plaques and nonruptured plaques (NRP). Nonruptured plaques were found in 30.7% of STEMI patients and contained significantly less lipidic plaque (44.0% vs 59.3%, P<0.001) and thin-cap fibroatheroma compared to ruptured plaques.
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