Abstract 1973: Coronary Plaque Characterization of Culprit Lesions Assessed by in vivo Intracoronary Ultrasound Radiofrequency Data Analysis can Predict Angiographic No-reflow/Slow-flow Phenomenon during Coronary Intervention
Background: Although the mechanisms responsible for the development of no reflow/slow flow phenomenon are not fully understood, theoretical causes include microembolic effects leading to microcirculatory dysfunction. Recently, spectral analysis of intravascular ultrasound (IVUS) radiofrequency (IVUS-Virtual Histology [VH]) data demonstrated a potential to provide detailed quantitative information on plaque composition and morphology. We assessed the hypothesis that the assessment of coronary plaque characterization using IVUS-VH was clinically effective in predicting no-reflow/slow-flow phenomenon during percutaneous coronary intervention (PCI).
Methods and Results: Preintervention IVUS was performed prospectively in 64 culprit lesions (28 acute coronary syndrome [ACS] lesions and 36 non-ACS lesions) with coronary stenosis ≥ 90% in consecutive 53 patients. Patients with no-reflow/slow-flow phenomenon had plaque morphological differences compared with those without phenomenon (Table⇓). Multivariate analyses revealed that external elastic membrane (EEM)-cross sectional area (CSA) (p = 0.035), plaque plus media (PPM)-CSA (p = 0.032), fibro-fatty area (FFA) (p = 0.009) and composition (%FFA) (p = 0.044) were independent predictors of no-reflow/slow-flow phenomenon. Based on a receiver operating characteristic curve, the best cutoff levels of EEM-CSA, PPM-CSA, FFA (%FFA) were 16.6 mm2, 12.9 mm2 and 2.0 mm2 (20%), respectively. The hazard ratio of patients who had more than the best cutoff levels of all predictors was 8.5 compared with those who had less than the levels, after adjusting for fasting blood glucose, which were closely associated with no-reflow/slow-flow phenomenon. (p = 0.010).
Conclusions: Conventional IVUS and IVUS-VH data may help to predict no-reflow/slow-flow phenomenon. Positive remodeling with rich fibro-fatty plaque has a potential for the development of impaired coronary microcirculation caused by PCI.