Purpose: We aimed to investigate the relationship between high-risk plaque characteristics determined by coronary CT angiography (coronary CTA) and CT attenuation in pericoronary adipose tissue (PCAT) - a surrogate measure of coronary inflammation - in patients with acute coronary syndrome (ACS) and matched controls with stable coronary artery disease (CAD).

Materials and Methods: We analyzed CTA (performed before invasive coronary angiography) in consecutive patients who experienced their first non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina (n=19) and CTA in age- and gender-matched controls (n=16) with stable chest pain who also underwent invasive angiography after CTA. Culprit lesions were independently identified in ACS patients. Semi-automated software was used to quantify calcified plaque (CP), noncalcified plaque (NCP), low-density (LD) NCP, stenosis and contrast density difference. We further divided NCP into low- [-30 to 30 Hounsfield Units (HU)], intermediate- (31-130 HU) and high-attenuation NCP (131-350 HU) volumes, and corresponding burden (plaque volume x100%/vessel volume). CT attenuation of PCAT (HU) was measured in coronary CTA data sets around culprit- and non-culprit lesions in three-dimensional cylindrical layers. Assessment of coronary plaque characteristics and PCAT attenuation quantification was performed in 19 culprit lesions and 105 non-culprit lesions.  

Results: Low-attenuation and intermediate-attenuation NCP burden were higher in culprit (n=19) vs non-culprit (n=55) lesions of ACS patients (12.6% vs 3.6%, p<0.001; 38.4% vs 19.4%, p<0.001); high-attenuation NCP burden (131-350 HU) was similar in both groups (17.4 vs 18.5 %, p=0.72). Low-attenuation and intermediate-attenuation NCP burden were higher in culprit vs highest-grade stenosis lesion of matched control patients (12.6% vs 5.6%, p=0.002; 38.4% vs 22.1%, p<0.001). High-attenuation NCP burden was not significantly different (17.4% vs 22.7 %, p=0.09).

Culprit lesions also had higher NCP and LD-NCP burdens (NCP: 68.3% vs 50.5%, p<0.001; LD-NCP: 10.2% vs 5.5%, p=0.019), higher maximal stenosis (87.1% vs 65.6%; p=0.001) and contrast density differences (42.1% vs 21.8%; p=0.069) compared to the highest-grade stenosis lesion of matched control patients with stable CAD.

PCAT attenuation in CT was significantly higher around culprit lesions (n=19) compared to non-culprit lesions (n=55) of ACS patients (-69.1 HU vs -74.8 HU, p=0.014) as well as compared to the highest-grade stenosis lesions (n=16) of matched control patients (-69.1 HU vs -76.4 HU, p=0.013). Around culprit lesions, there was a significantly higher frequency of high PCAT CT attenuation ≥-68.2 HU compared to non-culprit lesions of ACS patients (47.8% vs. 15.7%, p=0.003).

PCAT attenuation in CT correlated significantly with only intermediate-attenuation NCP burden (r=0.45, p=0.007) but not the other NCP components.