Abstract 3208: Comparison of Tissue Characteristics Between Acute Coronary Syndrome and Stable Angina Pectoris: An Integrated Backscatter Intravascular Ultrasound Analysis of Culprit and Non-Culprit Lesions
Background: Patients with acute coronary syndrome (ACS) have multiple complex coronary plaques associated with plaque vulnerability. However, limited data are available demonstrating tissue components of culprit and non-culprit lesions between ACS and stable angina pectoris (SAP) by use of intravascular ultrasound (IVUS). The present study assessed the tissue characteristics of coronary plaques between ACS and SAP of culprit and non-culprit lesions using integrated backscatter intravascular ultrasound (IB-IVUS).
Methods: IVUS was performed to 165 patients (40 patients with ACS) with 225 culprit (65 lesions in ACS) and 171 non-culprit lesions (42 lesions in ACS). And the segment with minimal luminal area in these lesions were measured by the conventional and IB-IVUS parameters using 40-MHz (motorized pullback 0.5mm/s) intravascular catheter. The percentage of fibrous area (fibrous area / plaque area, % FA) and the percentage of lipid area (lipid area / plaque area, % LA) were automatically calculated by IB-IVUS system.
Results: There were no significant differences in vessel area, plaque area and percentage of area stenosis of culprit and non-culprit lesions between ACS and SAP patients. Culprit and non-culprit lesions with ACS showed a significant increase in %LA (38 ± 18 vs. 30 ± 15 %, p=0.002, and 38 ± 21 vs. 32 ± 17 %, p=0.03, respectively) and a significant decrease in %FA (59 ± 15 vs. 63 ± 12 %, p=0.04, and 57 ± 18 vs. 62 ± 14 %, p<0.05, respectively) compared to those with SAP. On logistic regression analysis after adjusting for confounding and coronary risk factors, non-culprit lesions with ACS patients were significantly associated with the lipid-rich plaque (OR 3.55, 95% CI 1.40 –9.03, p=0.008).
Conclusions: Non-culprit coronary lesions with ACS patients are associated with the lipid-rich plaque, suggesting the extensive development of plaques instability in these patients.