Abstract 10602: The Relationship Between Layered Plaque and Plaque Volume in Patients With Acute Coronary Syndromes

Abstract

Introduction: Layered plaque is a signature of previous subclinical plaque destabilization and healing, which can be identified by optical coherence tomography (OCT). Silent plaque rupture or erosion with formation of a layer might contribute to rapid step-wise progression of plaque. We examined the relationship between layered plaques detected by OCT and plaque burden detected by intravascular ultrasound (IVUS) in patients with acute coronary syndromes (ACS). Methods: Patients presented with ACS who underwent preintervention OCT and IVUS were included in the analysis. Layered plaque was identified by OCT, and plaque burden was measured by IVUS around the culprit lesion. IVUS findings were compared between patients with layered plaque versus those without layered plaque. Results: Among 150 patients, total atheroma volume (TAV) (183.27 mm 3 [114.2 mm 3 to 275.0 mm 3 ] vs. 119.27 mm 3 [68.9 mm 3 to 185.5 mm 3 ], p=0.004), percent atheroma volume (PAV) (60.06 % [54.7 % to 60.1 %] vs. 53.69 % [46.8 % to 60.6 %], p=0.001), and plaque burden (PB) (86.51 % [81.7 % to 85.7 %] vs. 82.58 % [77.9 % to 85.4 %], p=0.001) were significantly higher in patients with layered plaques than non-layered plaques (Figure). When multi, single, and non-layered plaques were compared, TAV (188.69 mm 3 [122.1 mm 3 to 293.6 mm 3 ] vs. 137.85 mm 3 [100.1 mm 3 to 208.4 mm 3 ] vs. 119.27 mm 3 [68.9 mm 3 to 185.5 mm 3 ], p=0.021), PAV (62.12 % [56.8 % to 67.8 %] vs. 57.52 % [48.9 % to 60.1 %] vs. 53.69 % [46.8 % to 60.6 %] p<0.001), and PB (87.44 % [81.8 % to 89.3 %] vs. 84.7 % [77.9 % to 88.0 %] vs. 82.58 % [77.9 % to 85.4 %], p=0.018) were significantly greater in multi-layered plaques than others. Conclusions: This study demonstrates that layered plaques, compared to non-layered plaques, have significantly greater plaque burden in patients with ACS, indicating plaque disruption and healing process, rather than gradual smooth muscle proliferation, significantly contributes to plaque progression at the culprit lesion in patients with ACS.