Key result
High OCT lipid index and IVUS plaque burden predict myocardial no-reflow after primary STEMI PCI.
Why the study?
Do morphological characteristics of culprit plaques assessed by OCT and IVUS predict myocardial no reflow after primary PCI in patients with STEMI caused by plaque rupture?
Observational (n=72)
Do morphological characteristics of culprit plaques assessed by OCT and IVUS predict myocardial no reflow after primary PCI in patients with STEMI caused by plaque rupture?
Effect estimate: AUC 0.77 (lipid index) and AUC 0.70 (plaque burden)
p-value: p=<0.001
Large lipid index and plaque burden assessed by intracoronary imaging are critical morphological predictors of no reflow after primary PCI in STEMI caused by plaque rupture.
These OCT/IVUS thresholds may stratify no-reflow risk in STEMI plaque rupture; hypothesis-generating and should not yet change practice.
AIMS: Myocardial no reflow after percutaneous coronary intervention (PCI) is associated with poor outcome. Patients with ST-segment elevation myocardial infarction (STEMI) caused by plaque rupture are at high risk for no reflow. However, specific morphologic characteristics associated with no reflow are unknown in this population. The aim of this study is to identify the morphological characteristics of culprit plaques associated with no reflow in patients with STEMI caused by plaque rupture using both optical coherence tomography (OCT) and intravascular ultrasound (IVUS). METHODS AND RESULTS: We enrolled 145 patients with STEMI who underwent both OCT and IVUS within 12 h of symptom onset. Among these patients, we excluded those with plaque erosion and calcified nodule and included 72 patients who had plaque rupture as an underlying mechanism for STEMI. Myocardial no reflow, defined as Thrombolysis in Myocardial Infarction flow grade 0-2 and/or myocardial blush grade 0-1 after PCI, was observed in 28 patients (38.9%). Onset to recanalization time was similar between the groups with and without no reflow. Receiver-operating curve analysis revealed OCT-derived lipid index > 3500 [area under curve (AUC) 0.77, P < 0.001] and IVUS-derived plaque burden > 81.5% (AUC 0.70, P = 0.002) were the best discriminators for myocardial no reflow. CONCLUSION: No reflow occurred in nearly 40% of patients with STEMI caused by plaque rupture. Large lipid index and plaque burden were critical morphological discriminators between no reflow and normal flow.
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Soeda et al. (2016) conducted an observational in ST-segment elevation myocardial infarction (STEMI) caused by plaque rupture (n=72). Optical coherence tomography (OCT) and intravascular ultrasound (IVUS) morphological assessment was evaluated on Myocardial no reflow (TIMI flow grade 0-2 and/or myocardial blush grade 0-1 after PCI) (AUC 0.77 (lipid index) and AUC 0.70 (plaque burden), p=<0.001). An OCT-derived lipid index >3500 (AUC 0.77, P<0.001) and IVUS-derived plaque burden >81.5% (AUC 0.70, P=0.002) were the best discriminators for myocardial no reflow after primary PCI in STEMI.
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