Abstract
Introduction: While clinical predictors of plaque erosion (PE) in patients with acute coronary syndromes (ACS) were reported, PE was more frequently observed in the population with normal kidney function. On the other hand, earlier studies indicated that spotty calcification related to plaque rupture on the culprit site in ACS. However, the morphological features of coronary calcification on culprit site have not been investigated in relation to PE. Hypothesis: We assessed the hypothesis that the morphology of calcification on culprit site was associated with PE in ACS patients without chronic kidney disease (CKD). Methods: In the 166 ACS patients (66.9±10.7 years old, male 83 %), based on Optical Coherence Tomography/ Optical Frequency Domain Imaging, existence of PE on culprit site was investigated. In the morphological features of coronary calcification, the maximum thickness, maximum area, maximum angle, minimum depth from the lumen in axial sections, and the length in longitudinal image were determined. Results: There were the 73 patients with PE, 58 patients with calcification and 38 patients with CKD. A marginal significant difference in thickness (300 vs 190μm, p=0.07) and significant difference in angle (60 vs 23degree, p=0.001), area (0.89 vs 0.43mm 2 , p=0.001) and length (2.34 vs 1.12 mm, p=0.03) were observed between the patients with PE and the patients without PE. In the multiple regression analysis adjustment for age, gender, region location, maximum creatine phosphokinase, STEMI or not, diabetes mellitus, angiotensin receptor blockers use, statin use and systolic blood pressure on admission, angle (OR: 1.01, 95%CI: 1.002 to 1.013, p=0.005) and area (OR: 1.46, 95%CI: 1.02 to 2.1, p=0.04) each had significant associations with PE. Specifically, only in the patients without CKD, thickness (p=0.025), angle (p=0.003) and area (p=0.013) were significant indicators of PE. Conclusions: In conclusion, morphology of calcification on culprit site was a significant indicator of PE in the patients with ACS. Specifically, larger calcification might serve as a pathophysiology underlying in the phenotype of plaque vulnerability in ACS patients with normal kidney function.
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