Level of vascular inflammation is higher in acute coronary syndromes compared to chronic coronary disease

Abstract

Abstract Background Vascular inflammation has been recognized as one of the key factors in the pathogenesis of acute coronary syndromes (ACS). Peri-coronary adipose tissue (PCAT) attenuation by computed tomography angiography (CTA) 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 pre-intervention coronary CTA and optical coherence tomography (OCT) were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries. PCAT attenuation and OCT 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] vs. −71.5±11.0 HU, p<0.001) and the culprit vessel level (−68.3±7.7 HU vs. −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 vs. −70.5±7.1 HU, p=0.007). After adjusting patient characteristics, not only thin-cap fibroatheroma (OR: 2.44; 95% CI: 1.63–3.65) and macrophages (OR: 2.07; 95% CI: 1.34–3.21) but also PCAT attenuation in the culprit plaque (OR: 1.04; 95% CI: 1.02–1.06) 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. Funding Acknowledgement Type of funding sources: None.