Background: Epicardial adipose tissue ( EAT ) is hypothesized to alter atherosclerotic plaque composition, with potential development of high‐risk plaque ( HRP ). EAT can be measured by volumetric assessment ( EAT ‐v) or linear thickness ( EAT ‐t). We performed a systematic review and random‐effects meta‐analysis to assess the association of EAT with HRP and whether this association is dependent on the measurement method used. Methods and Results: Electronic databases were systematically searched up to October 2016. Studies reporting HRP by computed tomography or intracoronary imaging and studies measuring EAT ‐v or EAT ‐t were included. Odds ratios were extracted from multivariable models reporting the association of EAT with HRP and described as pooled estimates with 95% confidence intervals ( CIs ). Analysis was stratified by EAT measurement method. Nine studies (n=3772 patients) were included with 7 measuring EAT ‐v and 2 measuring EAT ‐t. Increasing EAT was significantly associated with the presence of HRP (odds ratio: 1.26 [95% CI, 1.11–1.43]; P <0.001). Patients with HRP had higher EAT ‐v than those without (weighted mean difference: 28.3 mL [95% CI, 18.8–37.8 mL]; P <0.001). EAT ‐v was associated with HRP (odds ratio: 1.19 [95% CI, 1.06–1.33]; P <0.001); however, EAT ‐t was not (odds ratio: 3.09 [95% CI, 0.56–17]; P =0.2). Estimates remained significant when adjusted for small‐study effect bias (odds ratio: 1.13 [95% CI, 1.03–1.28]; P =0.04). Conclusions: Increasing EAT is associated with the presence of HRP, and patients with HRP have higher quantified EAT ‐v. The association of EAT ‐v with HRP is significant compared with EAT ‐t; however, a larger scale study is still required, and further evaluation is needed to assess whether EAT may be a potential therapeutic target for novel pharmaceutical agents. Clinical Trial Registration: URL : https://www.crd.york.ac.uk/ . Unique identifier: CRD 42017055473.

FFRCT of 0.8 or less is a predictor of long-term clinical outcomes and is superior to clinically significant stenosis on coronary CT angiograms. A normal FFRCT is associated with favorable long-ter... BackgroundCoronary CT angiography with noninvasive fractional flow reserve (FFR) predicts lesion-specific ischemia when compared with invasive FFR. The longer term prognostic value of CT-derived FF...

Background: High-risk plaques (HRP) detected on coronary computed tomography angiography (CTA) confer an increased risk of acute coronary syndrome (ACS). Pericoronary adipose tissue attenuation (PCAT) is a novel biomarker of coronary inflammation. This study aimed to evaluate the association of PCAT with HRP and subsequent ACS development in patients with stable coronary artery disease (CAD). Methods: Patients with stable CAD who underwent coronary CTA from 2011 to 2016 and had available outcome data were included. We studied 41 patients with HRP propensity matched to 41 controls without HRP (60 ± 10 years, 67% males). PCAT was assessed using semi-automated software on a per-patient basis in the proximal right coronary artery (PCAT_RCA) and a per-lesion basis (PCAT_Lesion) around HRP in cases and the highest-grade stenosis lesions in controls. Results: PCAT_RCA and PCAT_Lesion were higher in HRP patients than controls (PCAT_RCA: −80.7 ± 6.50 HU vs. −84.2 ± 8.09 HU, p = 0.03; PCAT_Lesion: −79.6 ± 7.86 HU vs. −84.2 ± 10.3 HU, p = 0.04), and were also higher in men (PCAT_RCA: −80.5 ± 7.03 HU vs. −86.1 ± 7.08 HU, p < 0.001; PCAT_Lesion: −79.6 ± 9.06 HU vs. −85.2 ± 7.96 HU, p = 0.02). Median time to ACS was 1.9 years, within a median follow-up of 5.3 years. PCAT_RCA alone was higher in HRP patients who subsequently presented with ACS (−76.8 ± 5.69 HU vs. −82.0 ± 6.32 HU, p = 0.03). In time-dependent analysis, ACS was associated with HRP and PCAT_RCA. Conclusions: PCAT attenuation is increased in stable CAD patients with HRP and is associated with subsequent ACS development. Further investigation is required to determine the clinical implications of these findings.

Epicardial adipose tissue (EAT) is associated with cardiovascular risk. The longitudinal change in EAT volume (EATv) and density (EATd), and potential modulators of these parameters, has not been described. We prospectively recruited 90 patients with non-obstructive coronary atherosclerosis on baseline computed tomography coronary angiography (CTCA) performed for suspected coronary artery disease to undergo a repeat research CTCA. EATv in millilitres (mL) and EATd in Hounsfield units (HU) were analysed and multivariable regression analysis controlling for traditional cardiovascular risk factors (CVRF) performed to assess for any predictors of change. Secondary analysis was performed based on statin therapy. The median duration between CTCA was 4.3years. Mean EATv increased at follow-up (72 ± 33 mL to 89 ± 43 mL, p < 0.001) and mean EATd decreased (baseline −76 ± 6 HU vs. −86 ± 5 HU, p < 0.001). There were no associations between baseline variables of body mass index, age, sex, hypertension, hyperlipidaemia, diabetes or smoking on change in EATv or EATd. No difference in baseline, follow-up or delta EATv or EATd was seen in patients with (60%) or without baseline statin therapy. In this select group of patients, EATv consistently increased and EATd consistently decreased at long-term follow-up and these changes were independent of CVRF, age and statin use. Together with the knowledge of strong associations between EAT and cardiac disease, these findings may suggest that EAT is an independent parameter rather than a surrogate for cardiovascular risk.