Pericoronary Adipose Tissue Attenuation Research Articles

CORONARY INFLAMMATION ON CHEST COMPUTED TOMOGRAPHY AND COVID–19 MORTALITY

Abstract Aims The main factors associated with coronavirus disease–19 (COVID–19) mortality are age, comorbidities, pattern of inflammatory response and SARS–CoV–2 lineage involved in infection. However, the clinical course of the disease is extremely heterogeneous, and reliable biomarkers predicting adverse prognosis are lacking. Our aim was to elucidate the prognostic role of a novel marker of coronary artery disease inflammation, peri–coronary adipose tissue attenuation (PCAT), available from high–resolution chest computed tomography (HRCT), in COVID–19 patients with severe disease requiring hospitalization. Methods and Results Two distinct groups of patients, admitted to Parma University Hospital in Italy with COVID–19 in March 2020 and March 2021 (first and third wave peaks of COVID–19 pandemic in Italy, with prevalence of wild–type and B.1.1.7 SARS–CoV–2 lineage, respectively) were retrospectively enrolled. The primary endpoint was in–hospital mortality. Demographic, clinical, laboratory, HRCT data and coronary artery HRCT features (coronary calcium score and PCAT attenuation) were collected to establish which variables were associated with mortality. Among the 769 patients enrolled, 555 (72%) were discharged alive and 214 (28%) died. In multivariable logistic regression analysis age (p<0.001), number of chronic illnesses (p<0.001), smoking habit (p=0.006), P/F ratio (p=0.001), platelet count (p=0.002), blood creatinine (p<0.001), non–invasive mechanical ventilation (p<0.001), HRCT visual score (p<0.001) and PCAT (p<0.001), but not the calcium score, were independently associated with in–hospital mortality. Conclusion Coronary inflammation, measured with PCAT on HRCT, was independently associated with higher mortality in patients with severe COVID–19, while the pre–existent coronary atherosclerotic burden was not associated with adverse outcomes after adjustment for covariates.

Radiomics Analysis of Pericoronary Adipose Tissue From Baseline Coronary Computed Tomography Angiography Enables Prediction of Coronary Plaque Progression.

The relationship between plaque progression and pericoronary adipose tissue (PCAT) radiomics has not been comprehensively evaluated. We aim to predict plaque progression with PCAT radiomics features and evaluate their incremental value over quantitative plaque characteristics. Between January 2009 and December 2020, 500 patients with suspected or known coronary artery disease who underwent serial coronary computed tomography angiography (CCTA) ≥2 years apart were retrospectively analyzed and randomly stratified into a training and testing data set with a ratio of 7:3. Plaque progression was defined with annual change in plaque burden exceeding the median value in the entire cohort. Quantitative plaque characteristics and PCAT radiomics features were extracted from baseline CCTA. Then we built 3 models including quantitative plaque characteristics (model 1), PCAT radiomics features (model 2), and the combined model (model 3) to compare the prediction performance evaluated by area under the curve. The quantitative plaque characteristics of the training set showed the values of noncalcified plaque volume (NCPV), fibrous plaque volume, lesion length, and PCAT attenuation were larger in the plaque progression group than in the nonprogression group ( P < 0.05 for all). In multivariable logistic analysis, NCPV and PCAT attenuation were independent predictors of coronary plaque progression. PCAT radiomics exhibited significantly superior prediction over quantitative plaque characteristics both in the training (area under the curve: 0.814 vs 0.615, P < 0.001) and testing (0.736 vs 0.594, P = 0.007) data sets. NCPV and PCAT attenuation were independent predictors of coronary plaque progression. PCAT radiomics derived from baseline CCTA achieved significantly better prediction than quantitative plaque characteristics.

Layered plaque is associated with high levels of vascular inflammation and vulnerability in patients with stable angina pectoris.

Layered plaque, a signature of previous plaque destabilization and healing, is a known predictor for rapid plaque progression; however, the mechanism of which is unknown. The aim of the current study was to compare the level of vascular inflammation and plaque vulnerability in layered plaques to investigate possible mechanisms of rapid plaque progression. This is a retrospective, observational, single-center cohort study. Patients who underwent both coronary computed tomography angiography (CTA) and optical coherence tomography (OCT) for stable angina pectoris (SAP) were selected. Plaques were defined as any tissue (noncalcified, calcified, or mixed) within or adjacent to the lumen. Perivascular inflammation was measured by pericoronary adipose tissue (PCAT) attenuation at the plaque levels on CTA. Features of plaque vulnerability were assessed by OCT. Layered plaques were defined as plaques presenting one or more layers of different optical densities and a clear demarcation from underlying components on OCT. A total of 475 plaques from 195 patients who presented with SAP were included. Layered plaques (n = 241), compared with non-layered plaques (n = 234), had a higher level of vascular inflammation (-71.47 ± 10.74 HU vs. -73.69 ± 10.91 HU, P = 0.026) as well as a higher prevalence of the OCT features of plaque vulnerability, including lipid-rich plaque (83.8% vs. 66.7%, P < 0.001), thin-cap fibroatheroma (26.1% vs. 17.5%, P = 0.026), microvessels (61.8% vs. 34.6%, P < 0.001), and cholesterol crystals (38.6% vs. 25.6%, P = 0.003). Layered plaque was associated with a higher level of vascular inflammation and a higher prevalence of plaque vulnerability, which might play an important role in rapid plaque progression.Clinical trial registration: https://classic.clinicaltrials.gov/ct2/show/NCT04523194 .

Coronary inflammation based on pericoronary adipose tissue attenuation in type 2 diabetic mellitus: effect of diabetes management

BackgroundCoronary inflammation plays crucial role in type 2 diabetes mellitus (T2DM) induced cardiovascular complications. Both glucose-lowering drug interventions (GLDIS) and glycemic control (GC) status potentially correlate coronary inflammation, as indicated by changes in pericoronary adipose tissue (PCAT) attenuation, and thus influence cardiovascular risk. This study evaluated the impact of GLDIS and GC status on PCAT attenuation in T2DM patients.MethodsThis retrospective study collected clinical data and coronary computed tomography angiography (CCTA) images of 1,342 patients, including 547 T2DM patients and 795 non-T2DM patients in two tertiary hospitals. T2DM patients were subgroup based on two criteria: (1) GC status: well: HbA1c < 7%, moderate: 7 ≤ HbA1c ≤ 9%, and poor: HbA1c > 9%; (2) GLDIS and non-GLDIS. PCAT attenuations of the left anterior descending artery (LAD-PCAT), left circumflex artery (LCX-PCAT), and right coronary artery (RCA-PCAT) were measured. Propensity matching (PSM) was used to cross compare PCAT attenuation of non-T2DM and all subgroups of T2DM patients. Linear regressions were conducted to evaluate the impact of GC status and GLDIS on PCAT attenuation in T2DM patients.ResultsSignificant differences were observed in RCA-PCAT and LCX-PCAT between poor GC-T2DM and non-T2DM patients (LCX: − 68.75 ± 7.59 HU vs. – 71.93 ± 7.25 HU, p = 0.008; RCA: − 74.37 ± 8.44 HU vs. − 77.2 ± 7.42 HU, p = 0.026). Higher PCAT attenuation was observed in LAD-PCAT, LCX-PCAT, and RCA-PCAT in non-GLDIS T2DM patients compared with GLDIS T2DM patients (LAD: − 78.11 ± 8.01 HU vs. − 75.04 ± 8.26 HU, p = 0.022; LCX: − 71.10 ± 8.13 HU vs. − 68.31 ± 7.90 HU, p = 0.037; RCA: − 78.17 ± 8.64 HU vs. − 73.35 ± 9.32 HU, p = 0.001). In the linear regression, other than sex and duration of diabetes, both metformin and acarbose were found to be significantly associated with lower LAD-PCAT (metformin: β coefficient = − 2.476, p=0.021; acarbose: β coefficient = − 1.841, p = 0.031).ConclusionInadequate diabetes management, including poor GC and lack of GLDIS, may be associated with increased coronary artery inflammation in T2DM patients, as indicated by PCAT attenuation on CCTA, leading to increased cardiovascular risk. This finding could help healthcare providers identify T2DM patients with increased cardiovascular risk, develop improved cardiovascular management programs, and reduce subsequent cardiovascular related mortality.

Evaluation of peri-plaque pericoronary adipose tissue attenuation in coronary atherosclerosis using a dual-layer spectral detector CT.

This study aimed to evaluate the differences between pericoronary adipose tissue (PCAT) attenuation at different measured locations in evaluating coronary atherosclerosis using spectral computed tomography (CT) and to explore valuable imaging indicators. A total of 330 patients with suspicious coronary atherosclerosis were enrolled and underwent coronary CT angiography with dual-layer spectral detector CT (SDCT). Proximal and peri-plaque fat attenuation index (FAI) of stenosis coronary arteries were measured using both conventional images (CIs) and virtual monoenergetic images (VMIs) ranging from 40 keV to 100 keV. The slopes of the spectral attenuation curve (λ) of proximal and peri-plaque PCAT at three different monoenergetic intervals were calculated. Additionally, peri-plaque FAI on CI and virtual non-contrast images, and effective atomic number were measured manually. A total of 231 coronary arteries with plaques and lumen stenosis were finally enrolled. Peri-plaque FAICI and FAIVMI were significantly higher in severe stenosis than in mild and moderate stenosis (p < 0.05), while peri-plaque λ, proximal FAI, and proximal λ were not statistically different. Proximal FAI, peri-plaque FAI, and peri-plaque λ were significantly higher in low-density non-calcified plaque (LD-NCP) and non-calcified plaque (NCP) than in calcified plaque (p < 0.01). Peri-plaque FAI was the highest in the LD-NCP group, while proximal FAI was the highest in the NCP group. In severe stenosis and in LD-NCP, peri-plaque FAI was significantly higher than proximal FAI (p < 0.05). The manually measured parameters related to peri-plaque PCAT attenuation had a positive correlation with the results of peri-plaque FAI measured automatically. Peri-plaque PCAT has more value in assessing coronary atherosclerosis than proximal PCAT. Peri-plaque PCAT attenuation is expected to be used as a standard biomarker for evaluating plaque vulnerability and hemodynamic characteristics.

Association between metformin treatment and coronary artery inflammation based on pericoronary adipose tissue attenuation in type 2 diabetes mellitus patients.

Cardiovascular disease (CVD) is the leading cause of mortality in type 2 diabetes mellitus (T2DM) patients. The role of metformin in reducing cardiovascular events is well-established, but its effect on coronary artery inflammation in T2DM patients is still unclear. In this study, we evaluated 547 T2DM patients who underwent coronary computed tomography angiography (CCTA) at Wuhan Central Hospital. Using propensity score matching, we compared the attenuation of pericoronary adipose tissue (PCAT), an imaging marker of coronary artery inflammation, between patients treated with and without metformin. Multiple linear regression models were used to analyze the influence of metformin on PCAT attenuation. The results of the propensity-matched analysis showed that patients on metformin therapy had significantly lower PCAT attenuation, indicating reduced coronary inflammation. Specifically, the PCAT attenuation in the left anterior descending artery (LAD) and right coronary artery (RCA) was lower in the metformin group compared to the non-metformin group. Metformin use was independently associated with decreased LAD-PCAT attenuation in the multivariate regression analysis. The association of metformin with PCAT attenuation differed significantly in populations analyzed in subgroups of patients with obesity and chronic kidney disease. In conclusion, our study shows a preliminary signal that metformin therapy may be associated with decreased coronary artery inflammation in T2DM patients, as indicated by PCAT attenuation on CCTA. And this correlation may vary depending on the patient population. This initial finding suggests that PCAT attenuation could be potentially used as an imaging biomarker to monitor the anti-inflammatory effects of medication.

Insulin resistance and coronary inflammation in patients with coronary artery disease: a cross-sectional study

BackgroundInsulin resistance (IR) is associated with coronary artery disease (CAD) severity. However, its underlying mechanisms are not fully understood. Therefore, our study aimed to explore the relationship between IR and coronary inflammation and investigate the synergistic and mediating effects of coronary inflammation on the association between IR and CAD severity.MethodsConsecutive patients with CAD who underwent coronary angiography and coronary computed tomography angiography between April 2018 and March 2023 were enrolled. The triglyceride–glucose index (TyG index) and peri-coronary adipose tissue (PCAT) attenuation around the proximal right coronary artery (RCA) were used to evaluate IR and coronary inflammation, respectively. The correlation between the TyG index and PCAT attenuation was analyzed using linear regression models. Logistic regression models were further used for investigating the correlation of the TyG index and PCAT attenuation with CAD severity. A mediation analysis assessed the correlation between IR and CAD severity mediated by coronary inflammation.ResultsA total of 569 participants (mean age, 62 ± 11 years; 67.8% men) were included in the study. PCAT attenuation was positively associated with the TyG index (r = 0.166; P < 0.001). After adjusting for potential confounders, the per standard deviation increment in the TyG index was associated with a 1.791 Hounsfield unit (HU) increase (95% confidence interval [CI], 0.920–2.662 HU; P < 0.001) in the PCAT attenuation. In total, 382 (67.1%) patients had multivessel CAD. The patients in the high-TyG index/high PCAT attenuation group had approximately 3.2 times the odds of multivessel CAD compared with those in the low-TyG index/low PCAT attenuation group (odds ratio, 3.199; 95%CI, 1.826–5.607; P < 0.001). Mediation analysis indicated that PCAT attenuation mediated 31.66% of the correlation between the TyG index and multivessel CAD.ConclusionsThe TyG index positively correlated with PCAT attenuation in patients with CAD. The TyG index and PCAT attenuation showed a synergistic correlation with multivessel CAD. Furthermore, PCAT attenuation partially mediated the relationship between the TyG index and CAD severity. Controlling inflammation in patients with high IR and coronary inflammation may provide additional benefits.

Impact of Pericoronary Adipose Tissue Attenuation on Periprocedural Myocardial Injury in Patients With Chronic Coronary Syndrome.

Perivascular inflammation contributes to the development of atherosclerosis and microcirculatory dysfunction. Pericoronary adipose tissue (PCAT) attenuation, measured by coronary computed tomography angiography, is a potential indicator of coronary inflammation. However, the relationship between PCAT attenuation, microcirculatory dysfunction, and periprocedural myocardial injury (PMI) remains unclear. Patients with chronic coronary syndrome who underwent coronary computed tomography angiography before percutaneous coronary intervention were retrospectively identified. PCAT attenuation and adverse plaque characteristics were assessed using coronary computed tomography angiography. The extent of microcirculatory dysfunction was evaluated using the angio-based index of microcirculatory resistance before and after percutaneous coronary intervention. Overall, 125 consecutive patients were included, with 50 experiencing PMI (PMI group) and 75 without PMI (non-PMI group). Multivariable analysis showed that older age, higher angio-based index of microcirculatory resistance, presence of adverse plaque characteristics, and higher lesion-based PCAT attenuation were independently associated with PMI occurrence (odds ratio [OR], 1.07 [95% CI, 1.01-1.13]; P=0.02; OR, 1.06 [95% CI, 1.00-1.12]; P=0.04; OR, 6.62 [95% CI, 2.13-20.6]; P=0.001; and OR, 2.89 [95% CI, 1.63-5.11]; P<0.001, respectively). High PCAT attenuation was correlated with microcirculatory dysfunction before and after percutaneous coronary intervention and its exacerbation during percutaneous coronary intervention. Adding lesion-based PCAT attenuation to the presence of adverse plaque characteristics improved the discriminatory and reclassification ability in predicting PMI. Adding PCAT attenuation at the culprit lesion level to coronary computed tomography angiography-derived adverse plaque characteristics may provide incremental benefit in identifying patients at risk of PMI. Our results highlight the importance of microcirculatory dysfunction in PMI development, particularly in the presence of lesions with high PCAT attenuation. URL: https://center6.umin.ac.jp/cgi-open-bin/ctr/ctr_view.cgi?recptno=R000057722; Unique identifier: UMIN000050662.

Coronary inflammation on chest computed tomography and COVID-19 mortality.

The main factors associated with coronavirus disease-19 (COVID-19) mortality are age, comorbidities, pattern of inflammatory response, and SARS-CoV-2 lineage involved in infection. However, the clinical course of the disease is extremely heterogeneous, and reliable biomarkers predicting adverse prognosis are lacking. Our aim was to elucidate the prognostic role of a novel marker of coronary artery disease inflammation, peri-coronary adipose tissue attenuation (PCAT), available from high-resolution chest computed tomography (HRCT) in COVID-19 patients with severe disease requiring hospitalization. Two distinct groups of patients were admitted to Parma University Hospital in Italy with COVID-19 in March 2020 and March 2021 (first- and third-wave peaks of the COVID-19 pandemic in Italy, with the prevalence of wild-type and B.1.1.7 SARS-CoV-2 lineage, respectively) were retrospectively enrolled. The primary endpoint was in-hospital mortality. Demographic, clinical, laboratory, HRCT data, and coronary artery HRCT features (coronary calcium score and PCAT attenuation) were collected to show which variables were associated with mortality. Among the 769 patients enrolled, 555 (72%) were discharged alive, and 214 (28%) died. In multivariable logistic regression analysis age (p< 0.001), number of chronic illnesses (p< 0.001), smoking habit (p= 0.006), P/F ratio (p= 0.001), platelet count (p= 0.002), blood creatinine (p< 0.001), non-invasive mechanical ventilation (p< 0.001), HRCT visual score (p< 0.001), and PCAT (p <0.001), but not the calcium score, were independently associated with in-hospital mortality. Coronary inflammation, measured with PCAT on non-triggered HRCT, appeared to be independently associated with higher mortality in patients with severe COVID-19, while the pre-existent coronary atherosclerotic burden was not associated with adverse outcomes after adjustment for covariates. The current study demonstrates that a relatively simple measurement, peri-coronary adipose tissue attenuation (PCAT), available ex-post from standard high-resolution computed tomography, is strongly and independently associated with in-hospital mortality. • Coronary inflammation can be measured by the attenuation of peri-coronary adipose tissue (PCAT) on high-resolution CT (HRCT) without contrast media. • PCAT is strongly and independently associated with in-hospital mortality in SARS-CoV-2 patients. • PCAT might be considered an independent prognostic marker in COVID-19 patients if confirmed in other studies.

Higher Noncalcified Plaque Volume Is Associated With Increased Plaque Vulnerability and Vascular Inflammation.

Recently, it was reported that noncalcified plaque (NCP) volume was an independent predictor for cardiac events. Pericoronary adipose tissue (PCAT) attenuation is a marker of vascular inflammation and has been associated with increased cardiac mortality. The aim of this study was to evaluate the relationships between NCP volume, plaque vulnerability, and PCAT attenuation. Patients who underwent preintervention coronary computed tomography angiography and optical coherence tomography were enrolled. Plaque volume was measured by computed tomography angiography, plaque vulnerability by optical coherence tomography, and the level of coronary inflammation by PCAT attenuation. The plaques were divided into 2 groups of high or low NCP volume based on the median NCP volume. Among 704 plaques in 454 patients, the group with high NCP volume had a higher prevalence of lipid-rich plaque (87.2% versus 75.9%; P<0.001), thin-cap fibroatheroma (38.1% versus 20.7%; P<0.001), macrophage (77.8% versus 63.4%; P<0.001), microvessel (58.2% versus 42.9%; P<0.001), and cholesterol crystal (42.0% versus 26.7%; P<0.001) than the group with low NCP plaque volume. The group with high NCP volume also had higher PCAT attenuation than the group with low NCP volume (-69.6±10.0 versus -73.5±10.6 Hounsfield unit; P<0.001). In multivariable analysis, NCP volume was significantly associated with thin-cap fibroatheroma and high PCAT attenuation. In the analysis of the combination of PCAT attenuation and NCP volume, the prevalence of thin-cap fibroatheroma was the highest in the high PCAT attenuation and high NCP volume group and the lowest in the low PCAT attenuation and low NCP volume group. Higher NCP volume was associated with higher plaque vulnerability and vascular inflammation. The combination of PCAT attenuation and NCP volume may help identify plaque vulnerability noninvasively. URL: https://www.clinicaltrials.gov; Unique identifier: NCT04523194.

Pericoronary adipose tissue attenuation in patients with acute aortic dissection based on coronary computed tomography angiography.

Periaortic fat is associated with coronary disease. Thus, it was hypothesized that the inflammation associated with acute aortic dissection (AAD) spreads to pericoronary adipose tissue (PCAT) via thoracic periaortic fat. Pericoronary adipose tissue attenuation (PCATa) serves as a marker for inflammation of perivascular adipose tissue (PVAT). This study sought to examine PCATa in individuals diagnosed with AAD. Consecutive patients with chest pain from May 2020 to September 2022 were prospectively enrolled in this study and underwent coronary computed tomography angiography (CCTA) and/or aorta computed tomography angiography (CTA). Based on the results of the CTA, the patients were divided into the following two groups: (I) the AAD group; and (II) the non-AAD group. PCATa of the right coronary angiography (RCA), left anterior descending (LAD), and left circumflex (LCx) was quantified for each patient using semi-automated software. The PCATa values were compared between the AAD and non-AAD patients according to the atherosclerosis of the coronary arteries. Similarly, the PCATa values of the AAD patients were compared between the preoperative and postoperative steady states. A total of 136 patients (42 female, 94 male; mean age: 63.3±11.9 years) were divided into the two groups according to the presence of aortic dissection on CTA. The RCAPCATa, LADPCATa, and LCxPCATa values were significantly higher in the AAD subjects than the non-AAD subjects, regardless of the presence or absence of atherosclerosis in the coronary arteries [-85.1±9.3 vs. -92.9±10.0 Hounsfield unit (HU); -83.2±7.4 vs. -89.9±9.1 HU; -77.5±8.4 vs. -85.6±7.9 HU, all P<0.001). The preoperative RCAPCATa, LADPCATa, and LCxPCATa values were higher in the AAD patients than the postoperative steady-state patients (-82.9±8.7 vs. -97.6±8.8 HU; -79.8±7.6 vs. -92.8±6.8 HU; -74.6±7.1 vs. -87.7±6.9 HU, all P<0.001). According to the multivariable logistic regression analysis, high RCAPCATa and LADPCATa values were associated with AAD regardless of the degree of stenosis [odds ratio (OR) =0.014; 95% confidence interval (CI): 0.001-0.177; P=0.001 and OR =0.010; 95% CI: 0.001-0.189; P=0.002]. PCATa on computed tomography was increased in patients with AAD regardless of the presence or absence of coronary artery disease (CAD). This suggests that vascular inflammation is present in AAD independent of CAD. Further research should be conducted to investigate the potential of this imaging biomarker to predict AAD and monitor patients' responses to therapies for AAD.

Association of mean pericoronary adipose tissue attenuation with different demographic factors in a subgroup of patients without coronary artery disease stratified by sex, body mass index, and age.

In patients without coronary artery disease (CAD), few studies have evaluated the association between mean pericoronary adipose tissue attenuation (PCATMA) and patient-based demographic factors, for example, age or sex. Therefore, the purpose of this study is to investigate the association between PCATMA and various demographic factors in patients without CAD. In this case-control study, the 806 patients who underwent coronary computed tomography angiography and were not diagnosed with CAD between July 2020 and July 2022 were retrospectively enrolled. Their PCATMA values of the proximal right coronary artery were measured automatically. Patients without CAD were stratified according to sex, body mass index (BMI), and age, and the relationship between PCATMA and different clinical characteristics was explored using Fisher's exact test or Chi-squared test and independent t-tests or Wilcoxon Mann-Whitney U tests. Compared to non-smoking women [-88.00 (-95.00, -81.00) HU], women who smoked [-84.00 (-94.00, -78.00) HU, P=0.037] had higher PCATMA values and a positive correlation with PCATMA (rs=0.101, P=0.036). Compared to non-hypertensive patients with BMI ≥24.91 kg/m2 [-87.00 (-95.00, -81.00) HU], hypertensive patients with BMI ≥24.91 kg/m2 [-84.00 (-92.00, -78.00) HU, P=0.004] had higher PCATMA values, and a positive correlation with PCATMA (rs=0.144, P=0.004). In a subgroup of patients without CAD stratified by sex, BMI, and age, PCATMA values were all higher in patients with dyslipidemia (women, men, BMI ≥24.91 kg/m2, BMI <24.91 kg/m2, age ≥55 years, and age <55 years: -82.00, -82.00, -81.50, -82.00, -81.00 and -83.50 HU, respectively) than in those without dyslipidemia (-89.00, -89.00, -89.00, -90.00, -90.00 and -88.00 HU, respectively; all P<0.001) and showed a positive relationship (rs=0.328, 0.339, 0.342, 0.326, 0.367, and 0.298, respectively; all P<0.001). Higher PCATMA attenuation values were observed in patients with dyslipidemia, smoking women, and hypertensive patients with BMI ≥24.91 kg/m2, suggesting that PCATMA values can be used to detect patients at high risk for future events with CAD even if they do not currently have atherosclerosis.

CAD-RADS score, vascular inflammation, and plaque vulnerability

Abstract Background Coronary artery disease reporting and data system (CAD-RADS), which is widely used to report the severity of coronary artery disease on coronary computed tomography angiography (CTA), predicts the risk of future cardiovascular events. However, the relationship between the CAD-RADS score and vascular inflammation and plaque vulnerability has not been investigated. Objective The aim of this study was to correlate the CAD-RADS score with vascular inflammation and plaque vulnerability. Methods This is an observational, single-center cohort study with prospective clinical follow-up. Patients who underwent both coronary CTA and optical coherence tomography (OCT) before coronary intervention were enrolled. All OCT and CTA images were analyzed at the core laboratory. Patients were categorized into two groups according to the CAD-RADS score (≤4a or 4b/5). All coronary arteries were analyzed for high-risk plaque features (positive remodeling, low-attenuation plaque, napkin-ring sign, and spotty calcification) and peri-coronary adipose tissue (PCAT) attenuation. PCAT attenuation was measured around the culprit lesion and in the proximal segment of all 3 coronary arteries. OCT features of plaque vulnerability were evaluated in culprit vessels. Major adverse cardiovascular and cerebrovascular events (MACCE) were defined as composite endpoints of unplanned target vessel revascularization, unplanned non-target vessel revascularization, nonfatal acute coronary syndrome, stroke, and cardiac death. Results Among 369 patients with 902 lesions, 104 (28.2%) were categorized in CAD-RADS 4b/5 and 265 (61.8%) in CAD-RADS ≤4a. Patients with CAD-RADS 4b/5 had higher PCAT attenuation than those with CAD-RADS ≤4a at all three levels (mean of 3 coronary vessels: -67.9 ± 6.9 HU vs. -70.2 ± 6.5, P=0.004; culprit vessel: -67.4 ± 7.9 vs. -70.2 ± 7.6, P=0.004; culprit plaque: -67.0 ± 9.3 vs. -69.9 ± 10.5, P=0.009; respectively) (Figure 1 A). Lipid-rich plaque and macrophage, as detected by OCT, were more prevalent in the culprit vessel in patients with CAD-RADS 4b/5 than in those with CAD-RADS ≤4a (89.0% vs. 78.5%, P=0.001; 76.6% vs. 64.9%, P=0.001; respectively) (Figure 1B). All HRP features, as detected by CTA, were more frequently observed in patients with CAD-RADS 4b/5 than those with CAD-RADS ≤4a (P for all &amp;lt;0.001) (Figure 2). The cumulative incidence of MACCE was higher in patients with CAD-RADS 4b/5 than in those with CAD-RADS ≤4a (15.0% vs. 5.8%, P=0.045). Conclusions Higher CAD-RADS score was associated with a higher level of pan-coronary vascular inflammation and plaque vulnerability.Figure 1Figure 2

Abstract 14643: Coronary Spotty Calcification is Associated With a Higher Level of Plaque Vulnerability and Vascular Inflammation in Patients With Stable Angina

Background: There is controversy on clinical implication of spotty calcification in the coronary arteries. Optical coherence tomography (OCT) enables detailed plaque characterization including features of plaque vulnerability. Pericoronary adipose tissue (PCAT) attenuation is a recently developed marker for perivascular inflammation. Methods: Patients with stable angina pectoris (SAP) who had both computed tomography angiography (CTA) and OCT prior to coronary intervention were included. They were classified into two groups: spotty calcification group (calcification arc &lt;90°, length &lt;4mm) and macro calcification group. Non-calcified plaques or plaques with mixed spotty and macro calcification were excluded. The OCT findings of the culprit lesion and PCAT attenuation of the culprit vessel were compared between the two groups. Results: Among 316 patients, 62 had spotty calcifications and 66 had macro calcification in the culprit lesion. The spotty calcification group showed a significantly higher prevalence of lipid rich plaque (91.9% vs. 74.2%, p=0.008; Figure A), greater mean lipid arc (183.1 vs. 150.5°, p=0.01), and a higher level of PCAT attenuation (-71.7 ± 7.68 vs. -74.9 ± 9.17 HU, p=0.03; Figure B), compared with the macro calcification group. Conclusion: Plaques with spotty calcification are associated with a higher prevalence of lipid-rich plaques and a higher level of perivascular inflammation, compared to those with macro calcification.

Abstract 13586: Sex-Specific Association Between Perivascular Inflammation and Plaque Vulnerability

Introduction: Females were reported to have lower levels of perivascular inflammation assessed by pericoronary adipose tissue (PCAT) attenuation than males. However, the sex-specific difference in the association between perivascular inflammation and plaque vulnerability is unknown. Objective: The aim of this study was to investigate the sex-specific association between perivascular inflammation and plaque vulnerability. Methods: Patients who underwent coronary computed tomography angiography (CTA) and optical coherence tomography (OCT) were enrolled. All images were analyzed at a core laboratory. The level of perivascular inflammation was assessed by PCAT attenuation on CTA and plaque vulnerability by OCT. Patients were divided into three groups according to the tertile range of PCAT attenuation (T1: ≤ -72.7 HU, T2: -72.8 - -66.9 HU, or T3: ≥ -67.0). Results: A total of 888 lesions in 363 patients were included; 176 lesions in 77 females (2.3 plaques per patient) and 712 lesions in 286 males (2.5 plaques per patient). Females were older (median [IQR] age: 71 [66-78] vs. 64 [56-72], P &lt;0.001) but had less severe coronary artery disease than males. Thin-cap fibroatheroma (TCFA) was more prevalent, and lipid index and macrophage grade were greater in T3 group than T1 group in females, but there was no difference among three groups in males (T3 vs. T2 vs. T1 in females: 45.5%* vs. 34.2% vs. 21.0; 1448 ± 1183* vs. 1140 ± 1000 vs. 942 ± 975; 14 ± 12* vs. 9 ± 14 vs. 7 ± 10; respectively; T3 vs. T2 vs. T1 in males: 32.0% vs. 27.1% vs. 25.0; 1273 ± 1140 vs. 1191 ± 1128 vs. 1060 ± 1138; 9 ± 12 vs. 8 ± 9 vs. 7 ± 10; respectively; * indicates P &lt;0.05 vs. T1) (Figure). Conclusions: A higher level of perivascular inflammation was associated with higher plaque vulnerability in females, but not in males.

Abstract 18432: Lipoprotein(a) is Associated With Long-Term Plaque Progression, Pericoronary Inflammation and High-Risk Plaque on Serial Coronary CT Angiography

Background This study investigated the effect of lipoprotein(a) (Lp[a]) on long-term plaque progression, high-risk plaque (HRP) and pericoronary adipose tissue attenuation (PCATa) in patients suspected of coronary artery disease. Methods: Per-protocol, patients from a coronary CT angiography (CCTA) cohort (Diemen et al., 2021) were invited for repeat CCTA imaging, regardless of symptoms. A total of 299 patients underwent follow-up CCTA imaging with a median scan interval of 10.2 [IQR 8.7-11.2] years. Patients who underwent coronary artery bypass grafting and vessels revascularized by percutaneous coronary intervention were excluded. Scans were analyzed using atherosclerosis-imaging quantitative CCTA (AI-QCT; Cleerly Inc.). The associations between high (Tertile 3; &gt;67 nmol/l) and low Lp(a) (Tertile 1 and 2; ≤67 nmol/l), baseline and follow-up plaque burden and characteristics were evaluated using multivariable regression adjusted for clinical risk factors, statin use and scanner settings. Results: In total, 274 patients were included, mean age was 57±7 years, 42% were women. Patients with high Lp(a) levels had higher volumes of percent atheroma volume (PAV) at baseline and follow-up and higher rate of plaque progression (Figure 1A). The difference in PAV caused by high Lp(a) versus low Lp(a) patients was similar to the effect of a 12-year age difference. At baseline, patients in the highest tertile of Lp(a) levels had a higher prevalence of both HRP (OR 2.24; p=0.009) and above-median right coronary artery PCATa (OR 1.76; p=0.049). Finally, patients with high Lp(a) levels had a twofold higher incidence of major adverse cardiovascular events (MACE; Figure 1B; p=0.044). Conclusion: Patients with high Lp(a) levels had increased coronary plaque burden, increased prevalence of high-risk plaque and pericoronary inflammation as well as increased plaque progression leading to an increased incidence of MACE throughout 10-year follow-up.

Abstract 15654: Layered Plaques and Plaque Vulnerability in Patients With Stable Angina Pectoris

Backgrounds: Layered plaque, a signature of previous plaque destabilization and healing, is one of the predictors for rapid plaque progression, the mechanism of which is unknown. Aims: To investigate the level of vascular inflammation and plaque vulnerability in layered plaques to elucidate possible mechanisms of rapid plaque progression. Methods: Patients who underwent both coronary computed tomography angiography (CTA) and optical coherence tomography (OCT) were selected. Plaques were defined as any tissue (noncalcified, calcified, or mixed) within or adjacent to the lumen. Pericoronary adipose tissue (PCAT) attenuation was measured at the plaque level on CTA. OCT features of plaque vulnerability were assessed at the corresponding site. Results: A total of 475 plaques from 195 patients presented with stable angina pectoris were included. Layered plaques (n=241), compared to non-layered plaques (n=234), had a higher level of vascular inflammation (-70.94 [-77.86, -64.66] HU vs. -73.52 [-80.83, -67.66] HU, P=0.014, Figure 1). Layered plaques also had a higher prevalence of the features of plaque vulnerability (Figure 2), including lipid-rich plaque (83.8% vs. 66.7%, P&lt;0.001), thin-cap fibroatheroma (TCFA) (26.1% vs. 17.5%, P=0.026), microchannel (61.8% vs. 34.6%, P&lt;0.001), and cholesterol crystal (38.6% vs. 25.6%, P=0.003). Conclusions: Layered plaque was associated with higher levels of vascular inflammation and plaque vulnerability, which might play an important role in plaque progression.

Pericoronary adipose tissue attenuation predicts outcome of percutaneous intervention for chronic total occlusion

To investigate the association between pericoronary adipose tissue (PCAT) attenuation (PCATA) and outcomes of chronic total occlusion (CTO) after percutaneous coronary intervention (PCI), and to establish a clinical model that can be easily generalised to predict the outcomes of PCI-CTO. Between September 2015 and September 2019, patients from two centres were enrolled retrospectively. The primary endpoint was a procedural success (defined as achieving residual stenosis of <30% and a grade 3 thrombolysis in myocardial infarction [TIMI] flow). The new predictive model was generated by factors that were determined by multivariate analysis. The PCATA of CTO (PCATA-CTO) score was developed by assigning 1 point for each independent predictor, and then summing all points accrued. In addition, the predictive efficacy and interobserver and intraobserver agreement of PCATA-CTO and other scoring systems based on coronary computed tomography angiography (CCTA) were compared. A total of 201 patients (mean age 58.9±10.8 years, 85% male) were enrolled. The PCI success was achieved in 76% of the lesions. PCAT was higher in the PCI success group (-72.44±10.45HU versus -76.76±10.54 HU, p<0.05). Multivariable analysis yielded severe calcification, lesion length ≥15 mm, and perivascular fat attenuation index (FAI) ≤-69.5HU as independent negative predictors for procedural success. The area under the receiver operating characteristic curves for the PCATA-CTO score was 0.72. Comparing the PCATA-CTO score with other predictive scores, the PCATA-CTO score showed the highest interobserver (kappa=0.74) and intraobserver agreement (kappa=0.90, all p<0.01). FAI ≤-69.5HU is an independent negative predictor of procedural success. The PCATA-CTO score improved the reliability of the prediction model. Its potential for clinical implementation requires evaluation.

Low-attenuation coronary plaque burden and troponin release in chronic coronary syndrome: A mediation analysis

BackgroundCoronary low-attenuation plaque (LAP) burden is a strong predictor of myocardial infarction in patients with stable chest pain. We aimed to assess the relationship between LAP burden and circulating levels of high-sensitivity cardiac troponin T (hs-cTnT), and to explore the potential underlying etiology in patients undergoing clinically indicated coronary CT angiography (CCTA). MethodsA comprehensive metabolic and lipid panel, as well as C-reactive protein (CRP) and hs-cTnT tests were obtained from consecutive patients with stable chest pain at the time of CCTA. Qualitative and quantitative coronary plaque analysis, CT-derived fractional flow reserve (FFR) calculation, and pericoronary adipose tissue (PCAT) attenuation measurement around the right coronary artery were performed on CCTA images. Linear regression analyses were performed to identify independent associations with hs-cTnT concentration and mediation analysis was used to assess whether ischemia or markers of inflammation mediate hs-cTnT elevation. ResultsIn total, 114 patients (56.3 ​± ​10.6 years, 44.7 ​% female) were enrolled. In multivariable analysis, age (β ​= ​0.04 [95%CI: 0.02; 0.06], p ​< ​0.001), female sex (β ​= ​−0.77 [95%CI: −1.20; 0.33], p ​< ​0.001), and LAP burden (β ​= ​0.03 [95%CI: 0.001; 0.06], p ​= ​0.04) were independently associated with hs-cTnT levels. Mediation analysis, on the other hand, did not identify a significant mediating effect of lesion-specific ischemia based on CT-FFR, circulating CRP levels, or PCAT values between LAP burden and hs-cTnT levels (all p ​> ​0.05). ConclusionAlthough ischemia and inflammation have previously been proposed to mediate the association between LAP burden and hs-cTnT levels, our results did not confirm the role of these pathophysiological pathways in patients with stable chest pain.

Coronary artery disease reporting and data system (CAD-RADS), vascular inflammation and plaque vulnerability

BackgroundCoronary artery disease reporting and data system (CAD-RADS) predicts future cardiovascular events in patients with coronary artery disease (CAD). However, information on vascular inflammation and vulnerability remains scarce. MethodsPatients who underwent coronary computed tomography angiography (CTA) and optical coherence tomography (OCT) prior to coronary intervention were enrolled. All three coronary arteries were evaluated for CAD-RADS score and pericoronary adipose tissue (PCAT) attenuation, while the culprit vessel was analyzed for plaque vulnerability by OCT. ResultsA total of 385 patients with 915 lesions were divided into two groups based on CAD-RADS score: 103 (26.8%) were categorized as CAD-RADS 4b/5 and 282 (73.2%) as CAD-RADS ≤4a. Patients with CAD-RADS 4b/5 had a higher level of PCAT attenuation (mean of 3 coronary arteries) than those with CAD-RADS ≤4a (−68.4 ​± ​6.7 HU vs. −70.1 ​± ​6.5, P ​= ​0.022). The prevalence of macrophage was higher, and lipid index was greater in patients with CAD-RADS 4b/5 than CAD-RADS ≤4a (94.2% vs. 83.0%, P ​= ​0.004, 1845 vs. 1477; P ​= ​0.003). These associations were significant in the culprit vessels of patients with chronic coronary syndrome but not in those with acute coronary syndromes. ConclusionsHigher CAD-RADS score was associated with higher levels of vascular inflammation and plaque vulnerability.