Abstract 9668: Comprehensive Analysis of Intravascular Ultrasonic and Angiographic Morphology of Culprit Lesions Between ST-Segment Elevation Myocardial Infarction and Non-ST-Segment Elevation Acute Coronary Syndrome

Background: Rupture of vulnerable plaque is a major cause of acute coronary syndrome (ACS), with some clots being partially or totally occlusive. However, it is not clear why some plaque ruptures lead to ST-segment elevation myocardial infarction (STEMI), whereas others cause non-ST-segment elevation ACS (NSTEACS). Methods: A consecutive 158 ACS pts whose culprit lesions imaged by preintervention intravascular ultrasound (IVUS) were enrolled (STEMI=81; NSTEACS=77). IVUS and angiographic findings of culprit lesions, and clinical demographics were compared between the groups. Results: Pts’ characteristics were identical except lower rate of prior statin use in pts with STEMI (20% vs 44%, p=0.001). Angiographic complex Ambrose lesion and thrombus were more common in STEMI than in NSTEACS (83% vs 62%, p=0.002; 51% vs 5%, p<0.0001, respectively). In contrast, SYNTAX score was lower in STEMI (9±5 vs 12±7, p=0.01). In pts with STEMI, culprit echogenicity on IVUS was more hypoechoic (63% vs 40%, p=0.01), and the incidence of plaque rupture, attenuation and “microcalcification (granular calcification with attenuation)” were higher (53% vs 18%, p<0.0001; 86% vs 68%, p=0.01; 75% vs 61%, p=0.04, respectively). Further, the max area of ruptured cavity, echo lucent zone and arc of microcalcification were significantly greater in STEMI compared with NSTEACS (1.8±1.0mm 2 vs 1.1±0.9mm 2 , p=0.006; 1.5±0.7mm 2 vs 1.2±0.8mm 2 , p=0.004; 100±55° vs 77±51°, p=0.01, respectively). On quantitative and color-coded IVUS, vessel and plaque area were significantly larger at min lumen area (MLA) site in STEMI (16.6±5.4mm 2 vs 14.2±5.5mm 2 , p=0.003; 13.9±5.1mm 2 vs 11.6±5.2mm 2 , p=0.003, respectively) and at max vessel area site (20.2±5.4mm 2 vs 18.0±6.4mm 2 , p=0.007; 13.7±4.1mm 2 vs 12.2±5.6mm 2 , p=0.02, respectively), leading to larger necrotic (6.8±3.8mm 2 vs 4.8±3.9mm 2 , p=0.04) and lipidic (1.5±0.6mm 2 vs 1.1±0.6mm 2 , p=0.02) tissue area at MLA site in STEMI as well as fibrotic tissue (7.3±2.5mm 2 vs 5.7±2.2mm 2 , p=0.03). Conclusion: Morphological feature (outward vessel remodeling and IVUS vulnerability [e.g. greater ruptured cavity, larger necrotic and lipidic tissue, and microcalcification]) of culprit lesions might relate to clinical presentation of pts with ACS.