Patients with acute coronary syndromes had significantly higher PCAT attenuation at the culprit plaque level compared to those with stable angina pectoris (-67.5 vs -71.5 HU, P<0.001).
Observational (n=471)
Is pericoronary adipose tissue (PCAT) attenuation higher in patients with acute coronary syndromes compared to those with stable angina pectoris?
Vascular inflammation assessed by PCAT attenuation on computed tomography angiography is significantly higher in acute coronary syndromes compared to stable angina, highlighting its role in ACS pathogenesis.
Absolute Event Rate: -67.5% vs -71.5%
p-value: p=<0.001
Background: Vascular inflammation has been recognized as one of the key factors in the pathogenesis of acute coronary syndromes (ACS). Pericoronary adipose tissue (PCAT) attenuation by computed tomography angiography has emerged as a marker specific for coronary artery inflammation. We examined the relationship between clinical presentation and coronary artery inflammation assessed by PCAT attenuation and coronary plaque characteristics. Methods: Patients with ACS or stable angina pectoris (SAP) who underwent preintervention coronary computed tomography angiography and optical coherence tomography were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries. PCAT attenuation and optical coherence tomography findings were compared between patients with ACS versus SAP. Results: Among 471 patients (ACS: 198, SAP: 273), PCAT attenuation was higher in ACS patients than in SAP patients both at the culprit plaque level (−67.5±9.6 Hounsfield unit HU versus −71.5±11.0 HU, P< 0.001) and at the culprit vessel level (−68.3±7.7 HU versus −71.1±7.9 HU, P< 0.001). The mean PCAT attenuation of all 3 coronary arteries was also significantly higher in ACS patients than in SAP patients (−68.8±6.3 HU versus −70.5±7.1 HU, P =0.007). After adjusting patient characteristics, not only thin-cap fibroatheroma (OR: 3.41; 95% CI: 1.89–6.17) and macrophages (OR: 3.32; 95% CI: 1.76–6.26) but also PCAT attenuation around the culprit plaque (OR: 1.03; 95% CI: 1.00–1.05) was associated with the clinical presentation of ACS. Conclusions: PCAT attenuation at culprit plaque, culprit vessel, and pan-coronary levels was higher in ACS patients than in SAP patients. Vascular inflammation appears to play a crucial role in the development of ACS. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04523194
Araki et al. (Tue,) conducted a observational in Acute Coronary Syndromes and Stable Angina Pectoris (n=471). Acute Coronary Syndromes (ACS) vs. Stable Angina Pectoris (SAP) was evaluated on PCAT attenuation at the culprit plaque level (p=<0.001). Patients with acute coronary syndromes had significantly higher PCAT attenuation at the culprit plaque level compared to those with stable angina pectoris (-67.5 vs -71.5 HU, P<0.001).