4.6 Article

Level of Vascular Inflammation Is Higher in Acute Coronary Syndromes Compared with Chronic Coronary Disease

Journal

CIRCULATION-CARDIOVASCULAR IMAGING
Volume 15, Issue 11, Pages -

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCIMAGING.122.014191

Keywords

acute coronary syndrome; stable angina; computed tomography angiography; optical coherence tomography; pericoronary adipose tissue attenuation

Funding

  1. Al-lan Gray Fellowship Fund in Cardiology
  2. National Heart, Lung, and Blood Institute grants [1R01HL148787-01A1, 1R01HL151266]

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Vascular inflammation plays a crucial role in the development of ACS, and PCAT attenuation is higher in ACS patients compared to SAP patients.
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 (-6 8.8 +/- 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: 1.8 9-6.17) 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.

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