Abstract
Introduction: Vascular inflammation plays a key role in plaque rupture, while the role of inflammation in plaque erosion remains less well defined. Peri-coronary adipose tissue attenuation (PCATA) has emerged as a marker specific for coronary artery inflammation. Direct comparison of the level of vascular inflammation between plaque rupture and plaque erosion has not been reported. Objectives: To compare the level of coronary inflammation between plaque rupture and plaque erosion using PCATA. Methods: Patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS) who underwent pre-intervention coronary computed tomography angiography and optical coherence tomography (OCT) culprit lesion imaging were enrolled. PCATA was measured in the culprit lesion and in the proximal 40mm segment of the coronary arteries. The relationship between OCT culprit plaque characteristics and PCATA was also examined. Results: Out of 198 patients, plaque rupture was the underlying mechanism in 107 patients (54.0%) and plaque erosion in 91 (46.0%) patients. Plaque rupture had higher PCATA than plaque erosion both at the culprit plaque level (-65.8 ± 7.5 vs. -69.5 ± 11.4 Hounsfield unit [HU], p = 0.010) and at the culprit vessel level (-67.1 ± 7.1 vs. -69.6 ± 8.2 HU, p = 0.024). The mean PCATA of all 3 coronary arteries was also significantly higher in plaque rupture than in plaque erosion indicating a higher level of inflammation (-67.9 ± 5.7 vs. -69.9 ± 6.8 HU, p = 0.030). In the multivariable analysis, plaque rupture was significantly associated with high PCATA at all 3 levels: culprit plaque, culprit vessel, and pan-coronary arteries. Conclusions: PCATA in culprit plaque, culprit vessel, and all 3 coronary arteries was higher in plaque rupture than in plaque erosion. The results indicate pan-coronary inflammation plays a more significant role in plaque rupture than in plaque erosion.
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