Pericoronary Adipose Tissue Attenuation Research Articles

428 The Impact Of Virtual Monoenergetic Image Energy Levels On Pericoronary Adipose Tissue Attenuation Using Dual-source Photon-counting Detector Computed Tomography

Introduction: Increased pericoronary adipose tissue (PCAT) attenuation based on CT angiography (CTA) is a surrogate marker of perivascular inflammation and was shown to be associated with plaque development and vulnerability. The first-generation photon-counting detector CT (PCD-CT) has excellent temporal and spatial resolution and might allow for a more precise assessment of PCAT. PCD-CT allows tissue assessment in multiple energy ranges by providing virtual monoenergetic images (VMI). The aim of our study was to evaluate PCAT at different monoenergetic energy levels using a dual-source PCD-CT as compared with polychromatic images at 120 kV (T3D).

Prognostic value of pericoronary adipose tissue attenuation in patients with non-alcoholic fatty liver disease with suspected coronary artery disease

Pericoronary adipose tissue (PCAT) attenuation on coronary computed tomography angiography (CTA) has been emerged as a marker of pericoronary inflammation. We aimed to investigate the prognostic value of PCAT attenuation in patients with non-alcoholic fatty liver disease (NAFLD). We enrolled 232 NAFLD patients with suspected coronary artery disease and underwent coronary CTA. NAFLD was defined by abdominal CT as the ratio of hepatic attenuation to spleen attenuation less than 1.0. PCAT attenuation values were assessed by the crude analysis of mean CT attenuation value of the left anterior descending artery (LAD) and right coronary artery (RCA). As coronary CTA findings, luminal stenosis and high-risk plaque features were examined. Primary outcome was the composite of cardiovascular (CV) death, nonfatal acute coronary syndrome, and hospitalization for heart failure. During a median follow-up of 4.9years, 17 patients had CV events. LAD-PCAT attenuation in patients with CV events was higher than that without CV events (-66.9 ± 7.0 versus -70.5 ± 6.6; p = 0.032), while RCA-PCAT attenuation was not. LAD-PCAT attenuation and high-risk plaque features were independent predictors of CV events. The addition of LAD-PCAT attenuation to high-risk plaque features increased the C-statistics and global chi-square from 0.66 to 0.75 (p = 0.042) and 6.8 to 12.7 (p = 0.015), respectively. The net reclassification achieved by adding LAD-PCAT attenuation to high-risk plaque features was 0.494 (p = 0.041). High-LAD-PCAT attenuation was an independent predictor of CV events in NAFLD patients, regardless of CTA-verified high-risk plaque features. In addition, LAD-PCAT attenuation had an incremental prognostic value over high-risk plaque features.

Perivascular fat attenuation for predicting adverse cardiac events in stable patients undergoing invasive coronary angiography

BackgroundInflammation surrounding the coronary arteries can be non-invasively assessed using pericoronary adipose tissue attenuation (PCAT). While PCAT holds promise for further risk stratification of patients with low coronary artery disease (CAD) prevalence, its value in higher risk populations remains unknown. MethodsCORE320 enrolled patients referred for invasive coronary angiography with known or suspected CAD. Coronary computed tomography angiography (CCTA) images were collected for 381 patients for whom clinical outcomes were assessed 5 years after enrollment. Using semi-automated image analysis software, PCAT was obtained and normalized for the right coronary (RCA), left anterior descending (LAD), and left circumflex arteries (LCx). The association between PCAT and major adverse cardiovascular events (MACE) during follow up was assessed using Cox regression models. ResultsThirty-seven patients were excluded due to technical failure. For the remaining 344 patients, median age was 62 (interquartile range, 55–68) with 59% having ≥1 coronary artery stenosis of ≥50% by quantitative coronary angiography. Mean attenuation values for PCAT in RCA, LAD, and LCx were −74.9, −74.2, and −71.2, respectively. Hazard ratios and 95% confidence intervals (CI) for normalized PCAT in the RCA, LAD, and LCx for MACE were 0.96 (CI: 0.75–1.22, p ​= ​0.71), 1.31 (95% CI: 0.96–1.78, p ​= ​0.09), and 0.98 (95% CI: 0.78–1.22, p ​= ​0.84), respectively. For death, stroke, or myocardial infarction only, hazard ratios were 0.68 (0.44–1.07), 0.85 (0.56–1.29), and 0.57 (0.41–0.80), respectively. ConclusionsIn patients referred for invasive coronary angiography with suspected CAD, PCAT did not predict MACE during long term follow up. Further studies are needed to understand the relationship of PCAT with CAD risk.

High pericoronary adipose tissue attenuation on computed tomography angiography predicts cardiovascular events in patients with type 2 diabetes mellitus: post-hoc analysis from a prospective cohort study

BackgroundPericoronary adipose tissue (PCAT) attenuation on coronary computed tomography angiography (CTA) is a non-invasive biomarker for pericoronary inflammation. We aimed to investigate the prognostic value of PCAT attenuation in patients with type 2 diabetes mellitus (T2DM).MethodsWe included 333 T2DM patients (mean age, 66 years; male patients, 211; mean body mass index, 25 kg/m2) who underwent clinically indicated coronary CTA and examined their CT findings, coronary artery calcium score, pericardial fat volume, stenosis (> 50% luminal narrowing), high-risk plaque features of low-attenuation plaque and/or positive remodelling and/or spotty calcification, and PCAT attenuation. We assessed PCAT attenuation in Hounsfield units (HU) of proximal 40-mm segments of the left anterior descending artery (LAD) and right coronary artery (RCA). Cardiovascular events were defined as cardiac death, hospitalisation for acute coronary syndrome, late coronary revascularisation, and hospitalisation for heart failure.ResultsDuring a median follow-up of 4.0 years, we observed 31 cardiovascular events. LAD-PCAT attenuation was significantly higher in patients with cardiovascular events than in those without (− 68.5 ± 6.5 HU vs − 70.8 ± 6.1 HU, p = 0.045), whereas RCA-PCAT attenuation was not (p = 0.089). High LAD-PCAT attenuation (> − 70.7 HU; median value) was significantly associated with cardiovascular events in a model that included adverse CTA findings, such as significant stenosis and/or high-risk plaque (hazard ratio; 2.69, 95% confidence interval; 1.17–0.20, p = 0.020). After adding LAD-PCAT attenuation to the adverse CTA findings, the C-statistic and global chi-square values increased significantly from 0.65 to 0.70 (p = 0.037) and 10.9–15.0 (p = 0.043), respectively.ConclusionsIn T2DM patients undergoing clinically indicated coronary CTA, high LAD-PCAT attenuation could significantly predict cardiovascular events. This suggests that assessing LAD-PCAT attenuation can help physicians identify high-risk T2DM patients.

Clinical applications of cardiac computed tomography: a consensus paper of the European Association of Cardiovascular Imaging-part II.

Cardiac computed tomography (CT) was initially developed as a non-invasive diagnostic tool to detect and quantify coronary stenosis. Thanks to the rapid technological development, cardiac CT has become a comprehensive imaging modality which offers anatomical and functional information to guide patient management. This is the second of two complementary documents endorsed by the European Association of Cardiovascular Imaging aiming to give updated indications on the appropriate use of cardiac CT in different clinical scenarios. In this article, emerging CT technologies and biomarkers, such as CT-derived fractional flow reserve, perfusion imaging, and pericoronary adipose tissue attenuation, are described. In addition, the role of cardiac CT in the evaluation of atherosclerotic plaque, cardiomyopathies, structural heart disease, and congenital heart disease is revised.

Vascular inflammation in patients with obstructive sleep apnoea and coronary artery disease shown on coronary computed tomography angiography attenuation

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Obstructive sleep apnoea (OSA) is associated with increased plaque burden in coronary artery disease (CAD), but the role of vascular inflammation in this relationship is unclear. Coronary computed tomography angiography (CTA) enables surrogate assessment of systemic inflammation via subcutaneous adipose tissue attenuation (ScAT-a), and of coronary inflammation via epicardial adipose tissue volume and attenuation (EAT-v and EAT-a) and pericoronary adipose tissue attenuation (PCAT-a). Purpose To investigate whether vascular inflammation is increased in patients with severe OSA and high plaque burden. Methods Patients with clinically indicated polysomnography and coronary CTA were included. Severe OSA was classified as apnoea/hypopnoea index (AHI) >30. High plaque burden was defined as a CT-Leaman score (CT-LeSc) >8.3. Patients with both severe OSA and high plaque burden were defined as ‘Group 1’, all other patients were classified as ‘Group 2’. ScAT-a, EAT-a, EAT-v and PCAT-a were assessed on semi-automated software. Results A total of 91 patients were studied (59.3 ± 11.1 years). Severe OSA was associated with high plaque burden (p = 0.02). AHI correlated with CT-LeSc (r = 0.24, p = 0.023). Group 1 had lower EAT-a and PCAT-a compared to Group 2 (EAT-a: -87.6 vs. -84.0 HU, p = 0.01; PCAT-a: -90.4 vs. -83.4 HU, p < 0.01). However, among patients without high plaque burden, EAT-a was increased in patients with severe OSA versus mild-moderate OSA (-80.3 vs. -84.0 HU, p = 0.020). On multivariable analysis, EAT-a independently associated with severe OSA and high plaque burden (p < 0.02), and PCAT-a associated with severe OSA and high plaque burden, and hypertension (all p < 0.01). Conclusions EAT attenuation is decreased in patients with severe OSA and high plaque burden but increased in patients with severe OSA and low plaque burden. These divergent results suggest coronary inflammation may be increased in OSA independent of CAD, but larger studies are required to validate these findings.

Coronary computed tomography angiography-based assessment of vascular inflammation in patients with obstructive sleep apnoea and coronary artery disease.

Obstructive sleep apnoea (OSA) is associated with increased coronary artery disease (CAD) plaque burden, but the role of vascular inflammation in this relationship is unclear. Coronary computed tomography angiography (CTA) enables surrogate assessment of systemic inflammation via subcutaneous adipose tissue attenuation (SCAT-a), and of coronary inflammation via epicardial adipose tissue volume and attenuation (EAT-v and EAT-a) and pericoronary adipose tissue attenuation (PCAT-a). We investigated whether patients with severe OSA and high plaque burden have increased vascular inflammation. Patients with overnight polysomnography within ≤12 months of coronary CTA were included. Severe OSA was classified as apnoea/hypopnoea index (AHI) >30. High plaque burden was defined as a CT-adapted Leaman score (CT-LeSc) ≥8.3. Patients with both severe OSA and high plaque burden were defined as 'Group 1', all other patients were classified as 'Group 2'. ScAT, PCAT and EAT attenuation and volume were assessed on semi-automated software. A total of 91 patients were studied (59.3±11.1 years). Severe OSA was associated with high plaque burden (P=0.02). AHI correlated with CT-LeSc (r=0.24, P=0.023). Group 1 had lower EAT-a and PCAT-a compared to Group 2 (EAT-a: -87.6 vs. -84.0 HU, P=0.011; PCAT-a: -90.4 vs. -83.4 HU, P<0.01). However, among patients with low plaque burden, EAT-a was higher in the presence of severe OSA versus mild-moderate OSA (-80.3 vs. -84.0 HU, P=0.020). On multivariable analysis, severe OSA and high plaque burden associated with EAT-a (P<0.02), and severe OSA and high plaque burden (P<0.01) and hypertension (P<0.01) associated with PCAT-a. EAT and PCAT attenuation are decreased in patients with severe OSA and high plaque burden, but EAT attenuation was increased in patients with severe OSA and low plaque burden. These divergent results suggest vascular inflammation may be increased in OSA independent of CAD, but larger studies are required to validate these findings.

Increased coronary pericoronary adipose tissue attenuation in diabetic patients compared to non-diabetic controls: A propensity score matching analysis

BackgroundPericoronary adipose tissue (PCAT) attenuation is an indicator of active inflammation of perivascular adipose tissue, which is supposed to increase in diabetic patients. We aimed to investigate the PCAT attenuation values and high-risk plaque (HRP) features in diabetic and non-diabetic subjects with different stenotic extents. MethodsConsecutive type 2 diabetes patients and non-diabetic patients with chest pain and intermediate pre-test probability of coronary artery disease (CAD) were prospectively enrolled and underwent coronary computed tomography angiography (CCTA). At per-patient level, PCAT attenuation values of three major epicardial coronary vessels, as well as HRP features were measured. PCAT attenuation values and HRP features were compared between diabetic and non-diabetic subjects according to the presence or absence of obstructive stenosis. Results1700 patients (mean age: 65.5 ​± ​11.7, 940 males) were divided into two groups according to presence of obstructive stenosis on CCTA. Propensity score matching was performed in further analysis. RCAPCAT was significantly higher in diabetic subjects than that in non-diabetic subjects, regardless of the presence of obstructive stenosis (−83.60 ​± ​9.51 HU vs. −88.58 ​± ​9.37 HU, p ​< ​0.001) or absence of obstructive stenosis (−83.70 ​± ​10.32 HU vs. −88.76 ​± ​8.28 HU, p ​< ​0.001). In contrast, HRP features were more commonly presented in diabetic patients with obstructive stenosis than in those without obstructive stenosis. According to subgroup analysis based on acquisition tube voltage, RCAPCAT was the only parameter showing consistent difference between diabetic and non-diabetic patients. ConclusionsRCAPCAT was significantly higher in diabetic patients than that in non-diabetic patients regardless of stenotic severity and plaque vulnerability.

Association of near-infrared spectroscopy-defined lipid rich plaque with lesion morphology and peri-coronary inflammation on computed tomography angiography

Background and aimsRecent studies have reported that the lipid-rich plaque (LRP) detected by near-infrared spectroscopy (NIRS) and the pericoronary adipose tissue attenuation (PCATA) evaluated by coronary computed tomography angiography (CCTA) are associated with worse outcomes. We sought to investigate the relationship between NIRS-defined LRP and PCATA or the incremental ability of PCATA for the prediction of the presence of NIRS-defined LRP when added to the CCTA-derived morphometric findings. MethodsA total of 101 de novo lesions of 101 patients with chronic coronary syndromes (CCS), who underwent pre-procedural CCTA and NIRS during percutaneous coronary intervention (PCI), were retrospectively studied. PCATA was assessed by the crude analysis of the mean CT attenuation value of the culprit vessel. NIRS-defined LRP was defined as a maximum lipid core burden index in 4 mm ≥ 400. Univariate and multivariate logistic regression analyses were performed to determine the predictors of NIRS-defined LRP. ResultsNIRS-defined LRP was observed in 37 patients and median PCATA was −72.71. A significant relationship was observed between LCBI and PCATA (r = 0.24, p = 0.001). PCATA (OR: 4.99; 95% CI: 1.48–16.82; p = 0.010) and CCTA-derived positive remodeling (OR: 12.53; 95% CI: 3.56–44.07; p < 0.001) were independent predictors of NIRS-defined LRP. Net reclassification and integrated discrimination improvement indices were both significantly improved when PCATA was added to the reference model including clinical characteristics and CCTA-derived morphometric findings. ConclusionsComprehensive assessment of CCTA including PCATA may provide reliable information to identify the presence of NIRS-defined LRP potentially leading to future adverse events after PCI.

Pericoronary Adipose Tissue Attenuation on Coronary Computed Tomography Angiography Associates With Male Sex and Indigenous Australian Ethnicity

Coronary artery disease (CAD) is a leading cause of mortality among Australian men and women. Indigenous Australians (IA) face higher rates of mortality due to coronary events and systemic vascular inflammation. Pericoronary adipose tissue attenuation is a surrogate imaging biomarker of coronary inflammation using routine coronary computed tomography angiography (CCTA). We aimed to elucidate if IA patients harbour higher coronary inflammation.

Predictive Utility of Pericoronary Adipose Tissue Attenuation for In-Stent Restenosis in Patients Undergoing Percutaneous Coronary Intervention

Predictive Utility of Pericoronary Adipose Tissue Attenuation for In-Stent Restenosis in Patients Undergoing Percutaneous Coronary Intervention

Computed Tomography-derived Characterization of Pericoronary, Epicardial, and Paracardial Adipose Tissue and Its Association With Myocardial Ischemia as Assessed by Computed Fractional Flow Reserve.

Increased pericoronary adipose tissue (PCAT) attenuation derived from coronary computed tomography (CT) angiography (CTA) relates to coronary inflammation and cardiac mortality. We aimed to investigate the association between CT-derived characterization of different cardiac fat compartments and myocardial ischemia as assessed by computed fractional flow reserve (FFRCT). In all, 133 patients (median 64 y, 74% male) with coronary artery disease (CAD) underwent CTA including FFRCT measurement followed by invasive FFR assessment (FFRINVASIVE). CT attenuation and volume of PCAT were quantified around the proximal right coronary artery (RCA), left anterior descending artery (LAD), and left circumflex artery (LCX). Epicardial adipose tissue (EAT) and paracardial adipose tissue (PAT; all intrathoracic adipose tissue outside the pericardium) were quantified in noncontrast cardiac CT datasets. Median FFRCT was 0.86 [0.79, 0.91] and median FFRINVASIVE was 0.87 [0.81, 0.93]. Subjects with the presence of myocardial ischemia (n=26) defined by an FFRCT-threshold of ≤0.75 showed significantly higher RCA PCAT attenuation than individuals without myocardial ischemia (n=107) (-75.1±10.8 vs. -81.1±10.6 HU, P=0.011). In multivariable analysis adjusted for age, body mass index, sex and risk factors, increased RCA PCAT attenuation remained a significant predictor of myocardial ischemia. Between individuals with myocardial ischemia compared with individuals without myocardial ischemia, there was no significant difference in the volume and CT attenuation of EAT and PAT or in the PCAT volume of RCA, LAD, and LCX. Increased RCA PCAT attenuation is associated with the presence of myocardial ischemia as assessed by FFR, while PCAT volume, EAT, and PAT are not.

Abstract 9530: Plaque Rupture, Compared to Plaque Erosion, is Associated With Higher Level of Pan-Coronary Inflammation, Measured by Peri-Coronary Adipose Tissue Attenuation on Coronary Computed Tomography Angiography

Introduction: Vascular inflammation plays a key role in plaque rupture, while the role of inflammation in plaque erosion remains less well defined. Peri-coronary adipose tissue attenuation (PCATA) has emerged as a marker specific for coronary artery inflammation. Direct comparison of the level of vascular inflammation between plaque rupture and plaque erosion has not been reported. Objectives: To compare the level of coronary inflammation between plaque rupture and plaque erosion using PCATA. Methods: Patients with non-ST-segment elevation acute coronary syndromes (NSTE-ACS) who underwent pre-intervention coronary computed tomography angiography and optical coherence tomography (OCT) culprit lesion imaging were enrolled. PCATA was measured in the culprit lesion and in the proximal 40mm segment of the coronary arteries. The relationship between OCT culprit plaque characteristics and PCATA was also examined. Results: Out of 198 patients, plaque rupture was the underlying mechanism in 107 patients (54.0%) and plaque erosion in 91 (46.0%) patients. Plaque rupture had higher PCATA than plaque erosion both at the culprit plaque level (-65.8 ± 7.5 vs. -69.5 ± 11.4 Hounsfield unit [HU], p = 0.010) and at the culprit vessel level (-67.1 ± 7.1 vs. -69.6 ± 8.2 HU, p = 0.024). The mean PCATA of all 3 coronary arteries was also significantly higher in plaque rupture than in plaque erosion indicating a higher level of inflammation (-67.9 ± 5.7 vs. -69.9 ± 6.8 HU, p = 0.030). In the multivariable analysis, plaque rupture was significantly associated with high PCATA at all 3 levels: culprit plaque, culprit vessel, and pan-coronary arteries. Conclusions: PCATA in culprit plaque, culprit vessel, and all 3 coronary arteries was higher in plaque rupture than in plaque erosion. The results indicate pan-coronary inflammation plays a more significant role in plaque rupture than in plaque erosion.

Plaque Rupture, Compared With Plaque Erosion, Is Associated With a Higher Level of Pancoronary Inflammation

ObjectivesThe aim of this study was to compare the level of coronary inflammation between plaque rupture and plaque erosion using pericoronary adipose tissue (PCAT) attenuation. BackgroundVascular inflammation plays a key role in plaque rupture, while the role of inflammation in plaque erosion remains less well defined. PCAT attenuation determined using computed tomography has emerged as a marker specific for coronary artery inflammation. MethodsPatients with non–ST-segment elevation acute coronary syndromes who underwent preintervention coronary computed tomographic angiography and optical coherence tomographic culprit lesion imaging were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries. ResultsAmong 198 patients, plaque rupture was the underlying mechanism in 107 (54.0%) and plaque erosion in 91 (46.0%). Plaque rupture had higher PCAT attenuation than plaque erosion both at the culprit plaque level (−65.8 ± 7.5 HU vs −69.5 ± 11.4 HU; P = 0.010) and at the culprit vessel level (−67.1 ± 7.1 HU vs −69.6 ± 8.2 HU; P = 0.024). The mean PCAT attenuation of all 3 coronary arteries was also significantly higher in patients with plaque rupture than in plaque erosion, indicating a higher level of inflammation (−67.9 ± 5.7 HU vs −69.9 ± 6.8 HU; P = 0.030). In multivariable analysis, plaque rupture was significantly associated with high PCAT attenuation. ConclusionsPCAT attenuation in culprit plaque, culprit vessel, and all 3 coronary arteries was higher in plaque rupture than in plaque erosion. The results suggest that pancoronary inflammation plays a more significant role in plaque rupture than in plaque erosion. (Massachusetts General Hospital and Tsuchiura Kyodo General Hospital Coronary Imaging Collaboration; NCT04523194)

Relationship Between Coronary Atheroma, Epicardial Adipose Tissue Inflammation, and Adipocyte Differentiation Across the Human Myocardial Bridge.

BackgroundInflammation in epicardial adipose tissue (EAT) may contribute to coronary atherosclerosis. Myocardial bridge is a congenital anomaly in which the left anterior descending coronary artery takes a “tunneled” course under a bridge of myocardium: while atherosclerosis develops in the proximal left anterior descending coronary artery, the bridged portion is spared, highlighting the possibility that geographic separation from inflamed EAT is protective. We tested the hypothesis that inflammation in EAT was related to atherosclerosis by comparing EAT from proximal and bridge depots in individuals with myocardial bridge and varying degrees of atherosclerotic plaque.Methods and ResultsMaximal plaque burden was quantified by intravascular ultrasound, and inflammation was quantified by pericoronary EAT signal attenuation (pericoronary adipose tissue attenuation) from cardiac computed tomography scans. EAT overlying the proximal left anterior descending coronary artery and myocardial bridge was harvested for measurement of mRNA and microRNA (miRNA) using custom chips by Nanostring; inflammatory cytokines were measured in tissue culture supernatants. Pericoronary adipose tissue attenuation was increased, indicating inflammation, in proximal versus bridge EAT, in proportion to atherosclerotic plaque. Individuals with moderate‐high versus low plaque burden exhibited greater expression of inflammation and hypoxia genes, and lower expression of adipogenesis genes. Comparison of gene expression in proximal versus bridge depots revealed differences only in participants with moderate‐high plaque: inflammation was higher in proximal and adipogenesis lower in bridge EAT. Secreted inflammatory cytokines tended to be higher in proximal EAT. Hypoxia‐inducible factor 1a was highly associated with inflammatory gene expression. Seven miRNAs were differentially expressed by depot: 3192‐5P, 518D‐3P, and 532‐5P were upregulated in proximal EAT, whereas miR 630, 575, 16‐5P, and 320E were upregulated in bridge EAT. miR 630 correlated directly with plaque burden and inversely with adipogenesis genes. miR 3192‐5P, 518D‐3P, and 532‐5P correlated inversely with hypoxia/oxidative stress, peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PCG1a), adipogenesis, and angiogenesis genes.ConclusionsInflammation is specifically elevated in EAT overlying atherosclerotic plaque, suggesting that EAT inflammation is caused by atherogenic molecular signals, including hypoxia‐inducible factor 1a and/or miRNAs in an “inside‐to‐out” relationship. Adipogenesis was suppressed in the bridge EAT, but only in the presence of atherosclerotic plaque, supporting cross talk between the vasculature and EAT. miR 630 in EAT, expressed differentially according to burden of atherosclerotic plaque, and 3 other miRNAs appear to inhibit key genes related to adipogenesis, angiogenesis, hypoxia/oxidative stress, and thermogenesis in EAT, highlighting a role for miRNA in mediating cross talk between the coronary vasculature and EAT.

High peri-coronary inflammation assessed by coronary CT angiography predicts cardiovascular events in type 2 diabetes mellitus patients

Abstract Background Type 2 diabetes mellitus (T2DM) is associated with an increased risk of cardiovascular (CV) events, therefore there is a need to identify T2DM patients at higher risk. A novel imaging biomarker, the peri-coronary adipose tissue (PCAT) attenuation on coronary CT angiography (CTA), reflects peri-coronary inflammation. We hypothesized that the assessment of PCAT attenuation is useful for risk stratification in T2DM patients. Purpose We aimed to investigate whether high PCAT attenuation is related to increased risk of CV events in T2DM patients. Methods This study is a post-hoc analysis of the prospective cohort study consist of T2DM patients who underwent clinically indicated coronary CTA at a Japanese University Hospital. As CT findings, coronary artery calcium score, epicardial adipose tissue volume, high-risk plaque features (positive remodeling, low density plaque, spotty calcification), significant stenosis (&amp;gt;50% luminal narrowing), and PCAT attenuation were examined. PCAT attenuation was assessed in Hounsfield units (HU) of proximal 40-mm segments of the left anterior descending artery. CV events was defined as CV death, acute coronary syndrome, and hospitalization for heart failure. Results In a total of 333 T2DM patients (63% male, age 66±11 years), the mean PCAT attenuation was −70.6±6.1 HU. During the follow-up period of 4.2 years, 20 CV events (2 cases of CV death, 14 of acute coronary syndrome, 4 of heart failure) were confirmed. Patients with CV events had higher PCAT attenuation than those without CV events (−67.4 vs −70.8 HU, p=0.013). Multivariate linear regression analysis revealed that the independent determinants of PCAT attenuation were male (p&amp;lt;0.001) and statin use (p=0.024). In univariate Cox regression analyses, high-risk plaque features (HR 4.837, 95% CI 1.120–20.895, p=0.035), significant stenosis (HR 2.852, 95% CI 1.159–7.015, p=0.022), and PCAT attenuation (HR 1.119, 95% CI 1.34–1.212, p=0.005) were significantly associated with CV events. On the other hand, coronary artery calcium score (p=0.055) and epicardial adipose tissue volume (p=0.449) were not significantly associated with CV events. In multivariate Cox regression analysis, PCAT attenuation was independently associated with CV events after adjustment for coronary CTA findings and traditional CV risk factors (HR 1.105, 95% CI 1.017–1.200, p=0.018). Receiver operating characteristic curve analysis showed the optimal cut-off value of PCAT attenuation to predict CV events was −69.3 HU (sensitivity 58.5%, specificity 65.0%). Kaplan-Meier analysis showed that patients with high PCAT attenuation (≥−69.3 HU) had more CV events than those with low PCAT attenuation (p=0.013, log-rank test). Conclusion High PCAT attenuation was a strong predictor of CV events in T2DM patients independent of coronary CTA findings and traditional risk factors. Our study suggested that assessment of PCAT attenuation could be a valuable tool for risk stratification in T2DM patients. Funding Acknowledgement Type of funding sources: None. Figure 1. Representative casesFigure 2. Kaplan-Meier curves

Pericoronary adipose tissue attenuation, low-attenuation plaque burden and 5-year risk of myocardial infarction

Abstract Introduction Pericoronary adipose tissue (PCAT) attenuation has emerged as a surrogate marker of pericoronary inflammation. To date, no studies have compared the impact of pericoronary adipose tissue (PCAT) attenuation and quantitative plaque burden on cardiac outcomes. Purpose We aimed to establish the relative merits of these approaches to risk prediction and hypothesised that the combination of PCAT attenuation and quantitative plaque burden measures could provide additive and improved prediction of myocardial infarction in patients with stable chest pain. Methods In a post-hoc analysis of a randomized controlled trial, we investigated the association between the future risk of fatal or non-fatal myocardial infarction and PCAT attenuation measured from CT coronary angiography using multivariable Cox regression models including plaque burden, obstructive coronary disease and cardiac risk score (incorporating age, sex, diabetes, smoking, hypertension, hyperlipidaemia and family history of cardiovascular disease). Results In 1697 evaluable participants (mean age 58±10 years), there were 37 myocardial infarctions after a median follow-up of 4.7 [interquartile interval, 4.0–5.7] years. Median low-attenuation plaque burden was 4.20 [0–6.86] % and mean PCAT −76±8 Hounsfield units (HU). PCAT attenuation of the right coronary artery (RCA) was predictive of myocardial infarction (hazard ratio [HR] 1.55, 95% CI 1.08–2.22; p=0.017, per 1 standard deviation increment) with an optimum threshold of −70.5 HU [Hazards ratio (HR) 2.45, 95% CI 1.2–4.9; p=0.01]. Univariable analysis also identified the burden of non-calcified, low-attenuation and calcified plaque as well as Agatston coronary calcium score, presence of obstructive coronary artery disease and cardiovascular risk score were predictors of myocardial infarction (Figure 1). In multivariable analysis, only the low-attenuation plaque burden (HR 1.80, 95% CI 1.16 to 2.81, p=0.011, per doubling) and PCAT-RCA (HR 1.47 95%1.02 to 2.13, p=0.040, per standard deviation increment) remained predictors of myocardial infarction (Figure 1). In multivariable analysis, adding PCAT-RCA ≥-70.5 HU to low-attenuation plaque burden &amp;gt;4% (optimum threshold for future myocardial infarction; HR = 4.87, 95% CI 2.03–11.78; p&amp;lt;0.0001) led to improved prediction of future myocardial infarction (HR 11.7, 95% CI 3.3–40.9; p&amp;lt;0.0001); Figure 2. In ROC analysis, integration of PCAT-RCA attenuation and LAP burden, increased the prediction for myocardial infarction compared to LAP alone (ΔAUC=0.04; p=0.01). Conclusion CT coronary angiography defined PCAT attenuation and low-attenuation plaque have marked and additive predictive value for the risk of fatal or non-fatal myocardial infarction. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): The Chief Scientist Office of the Scottish Government Health and Social Care Directorates, British Heart Foundation, National Institute of Health/National Heart, Lung, and Blood Institute grant

Pericoronary adipose tissue attenuation index (FAI) – a new imaging biomarker and its diagnostic and prognostic utility: a systematic review and meta-analysis

Abstract Background Pericoronary fat attenuation index (FAI) on coronary computed tomography angiography (CCTA) imaging has been proposed as a sensitive marker of coronary vascular inflammation with prognostic value for major cardiovascular events. To date though there is no systematic review of the published literature and no meta-analyzed data of previously published results. Methods We performed a systematic review and meta-analysis according to the PRISMA guidelines. We systematically explored published literature in MEDLINE (Pubmed) before February 1, 2021 for studies assessing FAI in both diagnostic and prognostic clinical settings in patients with or without cardiovascular disease. The primary outcome was the mean difference in FAI attenuation between stable and unstable coronary plaques. The secondary outcome was the hazard ratio of high FAI values for future cardiovascular events. We calculated I2 to test heterogeneity. We used random effects modelling for the meta-analyses to assess the primary and secondary outcome. Results In total, 16 studies and 6,944 patients were included in this meta-analysis. FAI was significantly higher in unstable compared to stable plaques with a mean difference of 4.07 HU (95% CI: 1.10–7.89, I2=88%). Higher FAI values offered incremental prognostic value for major cardiovascular events (MACE) in studies with prospective follow-up (HR=3.29, 95% CI= 1.88–5.76, I2=75%). Conclusion FAI is a promising imaging biomarker that may be successfully be used for detection of coronary inflammation, discrimination between stable and unstable plaques and prognosis of future MACE. There is undeniable need of further studies to establish the utility of this biomarker in clinical practice in order to improve coronary plaque discrimination and cardiovascular risk prognostication. Funding Acknowledgement Type of funding sources: None.

Association between pericoronary adipose tissue attenuation and outcome after second-generation cryoballoon ablation for atrial fibrillation.

Previous studies reported the association between inflammation and atrial fibrillation (AF). Pericoronary adipose tissue (PCAT) attenuation, PCATA, on cardiac CT angiography (CTA) reflects pericoronary inflammation. We hypothesized that the PCATA predicts AF recurrence after cryoballoon ablation (CBA) for paroxysmal and persistent AF. We studied 364 patients (median age, 65 years) with persistent (n = 41) and paroxysmal (n = 323) AF undergoing successful first-session second-generation CBA with pre-ablation cardiac CTA. Three-vessel (3V)-PCATA was defined as the mean CT attenuation value of PCAT of all three major coronary arteries. Predictors of AF recurrence during follow-up were evaluated. AF recurrence after the 3-month blanking period was detected in 90 patients (24.7%) during the median follow-up of 26 (interquartile range, 19-42) months. AF recurrence was associated with prior stroke and statin use, NT-proBNP and high-sensitivity cardiac troponin-I levels, left ventricular dimension, left atrial volume index (LAVI), 3V-PCATA, and early AF recurrence during the blanking period. On multivariable Cox proportional hazard analysis, prior stroke (hazard ratio [HR], 2.208, 95% confidence interval [CI], 1.166-4.180, p = 0.015), LAVI (HR, 1.030, 95% CI, 1.010-1.051, p = 0.003), 3V-PCATA (HR, 1.034, 95% CI, 1.001-1.069, p = 0.046), and early AF recurrence (HR, 2.858, 95% CI, 1.855-4.405, p < 0.001) remained statistically significant. Pre-ablation CTA-derived 3V-PCATA, representing pericoronary inflammation, was an independent predictor of recurrence after first-session AF ablation using a second-generation cryoballoon. Assessment of 3V-PCATA may identify patients at high risk of AF recurrence after CBA for AF.

Association between higher pericoronary adipose tissue attenuation measured by coronary computed tomography angiography and nonalcoholic fatty liver disease: A matched case-control study.

Non-alcoholic fatty liver disease (NAFLD) is a risk factor for cardiac mortality. Pericoronary adipose tissue (PCAT) attenuation, expressed by the fat attenuation index on coronary computed tomography angiography, reflects pericoronary inflammation. We aimed to investigate the association between PCAT attenuation and NAFLD.This is a single-center cohort study comprising of patients who underwent coronary computed tomography angiography for suspected stable coronary artery disease between January and December 2020. Patient characteristics and coronary computed tomography angiography findings were analyzed between patients with NAFLD (n = 78) and a propensity score-matched cohort of patients without NAFLD (n = 78). PCAT attenuation was assessed in Hounsfield units (HU) of proximal 40-mm segments of the left anterior descending artery (LAD) and right coronary artery.The mean PCAT attenuation in LAD and right coronary artery were significantly higher in patients with NAFLD than those without NAFLD. When patients were divided into 2 groups using the median LAD-PCAT attenuation of −72.5 HU, the high PCAT attenuation group had more males (82% vs 67%, P = .028) and NAFLD patients (63% vs 37%, P = .001) compared to the low PCAT attenuation group. No differences in age, body mass index, conventional cardiovascular risk factors, or the presence of high-risk plaque were observed between the 2 groups. In the multivariate logistic analysis, NAFLD was independently associated with high PCAT attenuation (odds ratio 2.912, 95% confidence interval 1.386 to 6.118, P = .005).NAFLD is associated with high PCAT attenuation on coronary computed tomography angiography. This finding suggests that pericoronary inflammation is involved in the increased cardiac mortality in NAFLD patients.