- This study evaluated the relationship between clinical presentation (acute coronary syndrome [ACS] or stable angina pectoris [SAP]) and coronary artery inflammation assessed based on pericoronary adipose tissue (PCAT) attenuation on CT angiography. coronary artery and optical coherence tomography. Among 471 patients (SCA, n = 198; SAP, n = 273), PCAT attenuation was greater in those with SCA than in those with SAP, both at the culprit plaque and culprit vessel levels. The mean PCAT attenuation in the three major coronary arteries was also significantly higher in patients with ACS.
- These findings suggest that inflammation may be a key factor in ACS and that PCAT attenuation may be useful in identifying patients at risk for ACS. More research is needed to validate PCAT attenuation as a surrogate marker of ACS risk.
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 specific marker for coronary artery inflammation.
We examined the relationship between clinical presentation and coronary artery inflammation assessed by PCAT attenuation and coronary plaque characteristics.
Patients with ACS or stable angina pectoris (SAP) who underwent coronary computed tomography angiography and optical coherence tomography before the intervention 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.
Among 471 patients (ACS: 198, SAP: 273), PCAT attenuation was greater in patients with ACS than in patients with SAP, both at the level of the culprit plaque (-67.5 ± 9.6 Hounsfield units [HU] versus -71.5 ± 11.0 HU, P < 0.001) and at the level of the culprit vessel (-68.3 ± 7.7 HU versus -71.1 ± 7.9 HU, P < 0.001).
The mean PCAT attenuation of the 3 coronary arteries was also significantly higher in patients with ACS than in patients with SAP (-68.8 ± 6.3 HU versus -70.5 ± 7.1 HU, P = 0.007).
After adjusting for patient characteristics, not only thin layer 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.
- Pericoronary adipose tissue (PCAT) attenuation at the culprit plaque, culprit vessel, and pancoronary levels was greater in ACS patients than in SAP patients.
- Vascular inflammation appears to play a crucial role in the development of ACS.
