Abstract 15154: Therapeutic Effect of Optimal Medication on Biochemical Plaque Composition in Patients With Coronary Artery Disease as Serially Assessed by Intravascular Multi-Targeted Fluorescence Lifetime Imaging Fully Integrated With OCT

Abstract

Introduction: Fluorescence lifetime imaging (FLIm) is an emerging technique that can visualize detailed molecular properties of atherosclerosis. We conducted an in vivo serial molecular characterization of human coronary plaques using a fully-integrated, dual-modal, intravascular optical coherence tomography-FLIm (OCT-FLIm) system to explore the natural history of biochemical plaque composition. Methods: We prospectively enrolled patients with significant coronary artery disease those who underwent 6-month serial OCT-FLIm assessment for non-culprit/non-target lesions. A non-culprit/non-target lesion was defined as medically-treated angiographic mild-to-moderate stenosis diagnosed at index procedure. Biochemical plaque compositions were categorized by FLIm-derived parameters using a dedicated machine learning classifier. Each lesion was quantitatively assessed for the pre-specified plaque compositions and compared with the serial images. Results: Total 53 non-culprit/non-target lesions from 30 patients were enrolled. Angiography- and OCT-defined lesion severity showed no significant difference over the follow-up (p>0.05). Intriguingly, while the macrophage signal intensity decreased after 6 months (p=0.034), FLIm-based quantitative assessment revealed a worsened plaque compositional response by increased loose fibrous tissue (p=0.004) and decreased normal/fibrous tissue burden (p<0.001). These temporal changes in individual plaque components correlated well with the achieved LDL-cholesterol level at 6-month (p<0.05), whereas no correlation was found with hs-CRP (p>0.05). Conclusion: From this comprehensive serial assessment of human coronary atheroma by intravascular OCT-FLIm, optimal medical therapy alone was insufficient to effectively stabilize plaque composition, and additional therapeutic strategy should be explored to alter the natural course of atherosclerosis from a molecular perspective.