Non-calcified Plaque Burden Research Articles

Abstract 4120670: Pericoronary Adipose Tissue Inflammation as a Marker of Increased Coronary Plaque Burden in Patients With Chronic Coronary Artery Disease With Zero Calcium Score

Background: Dysfunctional or excess adiposity plays pivotal role in the development of coronary atherosclerosis. It remains unclear whether pericoroanry adipose tissue (PCAT) inflammation is associated with increased coronary plaque burden in its early stage of atherosclerosis, independent of traditional coronary risks or cardiovascular-kidney metabolic health. Purpose: To investigate the association of PCAT inflammation with coronary plaque burden in patients with newly suspected with chronic coronary artery disease (CAD) and zero calcium score who underwent coronary computed tomography angiography (CCTA). Methods: This retrospective CCTA study consists of 294 chronic CAD patients with zero calcium score (59 years, male 51 %). Chronic CAD was defined as stable condition with presence of increased non-calcified plaque burden on CCTA (Figure 1A-D). PCAT attenuation (PCATA) was assessed by fat attenuation index in the major three coronary arteries (right coronary artery, RCA; left anterior descending artery; LAD, and left circumflex coronary artery, LCX)(Figure 1C and D). Multivariable analysis using linear regression model was performed to determine independent predictors of increased %PV by adjusting for traditional coronary risks, metabolic risks, and chronic kidney disease (CKD). Hisayama Risk Score (HRS) was calculated to estimate 10-year cardiovascular risks. Results: Mean %plaque volume (PV) and PCATA-RCA was 44±4.0％ and -77±8.8 HU. %PV was correlated with age (p<0.05), systolic blood pressure (p<0.05), non-HDL cholesterol (p<0.05), Hisayama risk score (p<0.05, Figure 2), PCATA-RCA (p<0.001, Figure 3), PCATA-LAD (p<0.001), and LCX-PCATA (p<0.001). In a multivariable linear regression model adjusting for age, sex, hypertension, diabetes, dyslipidemia, and current smoking (model 1), PCATA-RCA was independently associated with %PV [beta, 0.17; 95% confidential interval (CI) 0.115-0.217, p < 0.001]. In a model adjusting for age, sex, metabolic syndrome, body mass index ≥23kg/mm 2 , and CKD (model 2), PCATA-RCA (beta, 0.18; 95% CI 0.128-0.232, p<0.001) and high-risk HRS (beta, 3.1; 95% CI 1.35−4.87, p<0.001) were independently associated with %PV. Similarly, independent associations of PCATA in LAD and LCX with %PV was observed. Conclusion: This study demonstrates that PCATA is a robust marker related to increased burden of coronary atherosclerosis even in the early stage of atherosclerosis as defined by zero coronary artery calcium score.

Association of sodium-glucose cotransporter-2 inhibitor with regression of coronary plaque burden

Abstract Background Sodium-glucose cotransporter-2 inhibitor (SGLT2i), as a novel oral hypoglycemic therapy of type 2 diabetes mellitus (T2DM), has been proved to benefit cardiac function. However, it remains unknown whether SGLT2i has an impact on coronary plaque characteristics. Purpose The aim of this study was to investigate whether SGLT2i was able to improve coronary plaque composition, burden and inflammation [i.e., fat attenuation index (FAI)] using series coronary computed tomography angiography (CCTA) images among T2DM patients with angina pectoris. Methods T2DM patients presenting with angina pectoris admitted at our center were screened. Eligible patients were those underwent first CCTA within 3 months prior to initiating SGLT2i therapy, and repeated CCTA beyond 6 months after the first CCTA. Those patients not treated with SGLT2i underwent likewise longitudinal CCTA tests were propensity score matching in a 1:1 ratio using age, sex and CCTA time interval. Routine CCTA images were assessed for coronary plaque characteristics using dedicated softwares. Paired or unpaired Student’s t test or Mann–Whitney U test were used for comparing coronary plaque characteristics between series CCTA and patients with or without SGLT2i. The relationships between SGLT2i and changes of plaque characteristics was examined using logistic regression analysis. Results After propensity score matching, a total of 196 T2DM patients with angina pectoris were included (mean age, 60.4±9.2 years; male, 69.9%; SGLT2i treatment, 50%). Time interval between baseline and the last CCTA examinations was 400 (343,496) days. In the SGLT2i group, the non-calcified plaque burden [(39.86±14.30)% vs. (36.84±13.86)%, p=0.002)] and low attenuation non-calcified plaque burden (6.62 [4.11,10.13]% vs. 5.78 [3.40,9.28]%, p=0.042) were significantly decreased between two CCTA images. Whereas, in the non-SGLT2i group, there was no difference with regard to non-calcified and low attenuation non-calcified plaque burden between two CCTA images (all p>0.05). Moreover, changes of total plaque burden and non-calcified plaque burden were higher in the SGLT2i group than the non-SGLT2i group (all p<0.05). Importantly, SGLT2i was associated with total plaque volume (odd ratio=0.594, p=0.024) and non-calcified plaque volume regression (odd ratio=0.619, p=0.042) after adjusting for confounding factors. Conclusion SGLT2i significantly regresses coronary plaque burden, in particularly non-calcified plaque. These findings might explain the observed cardio-protective effect of SGLT2i in large trials.

Reduced inflammation assessed by pericoronary adipose tissue is associated with coronary plaque calcification

Abstract Introduction Pericoronary adipose tissue attenuation (PCAT) quantified from coronary computed tomography angiography (CCTA) is increasingly recognized as an inflammation marker in coronary artery disease (CAD). Inflamed PCAT has been linked to non-calcified plaque (NCP) and cardiovascular morbidity and mortality. Nevertheless, gaps remain in understanding how PCAT behaves during plaque stabilization. Purpose We investigated associations between coronary artery inflammation assessed by PCAT and the presence and type of coronary plaques, plaque burden, and coronary calcification. Methods An observational study involving 506 patients with suspected chronic coronary syndrome who underwent CCTA. PCAT was averaged across the proximal 40 mm segments of all three coronary vessels to represent the patient level. Plaque presence and types (calcified, mixed, and soft) were assessed. Total, NCP, and calcified plaque (CP) burdens were measured as normalized atheroma volumes. Coronary calcification was quantified using Agatson coronary artery calcification (CAC) score and categorized based on cut-offs of 0, 100, 400. Results The mean PCAT was -81.1 ±6.3 Hounsfield Unit (HU) without plaque and -79.7 ±6.0 HU with plaque (p= 0.01). PCAT differed between calcified (-81.8 HU), mixed (-79.8 HU), and soft (-77.0 HU) plaques (p<0.0001). Multivariate linear analysis (adjusted for clinical risk factors, cardiovascular medication, and tube voltage) showed PCAT positively associated with total plaque burden (estimate= 1.1 [95% CI: 0.3-1.8], p=0.004) and NCP burden (estimate= 2.4 [95% CI: 1.4-3.4]; p<0.0001), while the association with CP burden was negative, but not statistically significant (estimate= -1.7 [95%CI : -4.1-0.7], p=0.2). Multivariate linear analysis, which accounted for both calcified and non-calcified plaque, reaffirmed the positive association to NCP burden (estimate= 2.7 [95% CI: 1.7-3.7]; p<0.0001) and a significant negative association between CP burden (estimate= - 3.3 [95% CI: -5.8- -1.0]; p=0.007) and PCAT. No significant differences in PCAT levels were found among patients with a CAC score of 0 and those with CAC scores exceeding 400, or across different stages of CAC score categories (p>0.8). Conclusion PCAT increased with plaque presence, rising from calcified to mixed to soft plaques. Increased NCP burden associated with higher PCAT, while higher CP burden seemed to reduce PCAT, though not statistical significant. Interestingly, when NCP was absent, higher levels of CP burden were associated with reduced inflammation. This supports the hypothesis of plaque stabilization, proposing that calcification might stabilize the vessel and indirectly contribute to reducing inflammation.Figure 1 PCAT by plaque typesTable 1 PCAT & plaque burden

Artificial intelligence-based automated plaque quantification from CCTA to predict acute coronary syndrome on top of obstructive or ischemic coronary artery disease

Abstract Background Artificial intelligence (AI)-based quantitative computed tomography (AI-QCT) is a novel tool for automated plaque characterization and quantification from coronary computed tomography angiography (CCTA). The prognostic value of various AI-QCT plaque types on top of the presence of obstructive or ischemic coronary artery disease (CAD) is unknown. Purpose To investigate the added prognostic value for acute coronary syndrome (ACS) of AI-QCT total plaque burden (percent atheroma volume (PAV) %), and its subcomponents non-calcified plaque burden (NCPB), low-attenuation plaque burden (LAP), and calcified plaque burden (CPB) (%) on top of obstructive or ischemic CAD. Methods A cohort of 2007 symptomatic patients having undergone CCTA and selective downstream PET perfusion for suspected CAD was analyzed. Patients with prior or early elective revascularization within 6 months from CCTA were excluded. Obstructive CAD was defined as ≥1 vessel with >50% visual stenosis, and ischemic CAD as absolute hyperemic myocardial blood flow ≤2.3 ml/g/min in ≥2 adjacent segments on 15O-H2O PET. Multivariable Cox regressions adjusted for clinical confounders (age, sex hypertension, typical angina) including each plaque type separately (per 1.0%) on top of obstructive or ischemic CAD, respectively, were performed. The amount of LAP was <1% and therefore pooled together with NCPB. Results Throughout a median follow-up of 7 years, 72/2007 patients experienced ACS (50 myocardial infarction, 22 unstable angina). On top of obstructive CAD, all plaque types were independent predictors of ACS (Figure 1A), however according to the C-indexes (p-value vs. obstructive CAD), only PAV (C-index=0.814, p=0.010) and NCPB+LAP (C-index=0.818, p=0.014), but not CPB (C-index=0.800, p=0.066) significantly improved the prediction of ACS on top of obstructive CAD (C-index=0.790) (Figure 2A). On top of ischemic CAD (1967 patients, 66 events), all plaque types were also independent predictors of ACS (Figure 1B). But, similarly, according to the C-indexes (p-value vs. ischemic CAD), only PAV (C-index=0.818, p=0.003), and NCPB+LAP (C-index=0.818, p=0.005), but not CPB (C-index=0.798, p=0.054) significantly improved the prediction of ACS on top of ischemic CAD (C-index=0.776) (Figure 2B). NCPB+LAP alone performed similarly as PAV on top of obstructive (p=0.554) and ischemic CAD (p=0.991) (Figure 2). Conclusions Among patients with native coronary arteries treated medically, AI-based plaque quantification significantly improved the prediction of ACS on top of obstructive or ischemic CAD. The risk of ACS was largely related to NCPB+LAP, whereas CPB did not significantly improve risk stratification.Adjusted HR for ACS per plaque typeC-indexes for ACS

A Multiomic Analysis to Identify Drivers of Subclinical Vascular Disease in Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) increases cardiovascular disease (CVD) risk, and this is not explained by traditional risk factors. Characterization of blood immunologic signatures that associate with subclinical CVD and predict its progression has been challenging and may help identify subgroups at risk. Patients with SLE (n = 77) and healthy controls (HCs) (n = 27) underwent assessments of arterial stiffness, vascular wall inflammation, and coronary atherosclerosis burden with cardio-ankle vascular index (CAVI); fluorodeoxyglucose-positron emission tomography/computed tomography (CT) (target-to-background ratio [TBR]); and coronary CT angiography. Whole blood bulk RNA sequencing was performed in a subset of study participants (HC n = 10, SLE n = 20). In a partially overlapping subset (HC n = 24, SLE n = 64), serum inflammatory protein biomarkers were quantified with an Olink platform. CAVI, TBR, and noncalcified coronary plaque burden (NCB) were increased in patients with SLE compared to HCs. When comparing patients with SLE with high CAVI scores to those with low CAVI scores or to HCs, there was a down-regulation of genes in pathways involved in the cell cycle and differentially regulated pathways related to metabolism. Distinct serum proteins associated with increased CAVI (CCL23, colony-stimulating factor 1, latency-activating peptide transforming growth factor β1, interleukin 33 [IL-33], CD8A, and IL-12B), NCB (monocyte chemotactic protein 4 and FMS-like tyrosine kinase 3 ligand [Flt3L]), and TBR (CD5, IL-1α, AXIN1, cystatin D [CST5], and tumor necrosis factor receptor superfamily 9; P < 0.05). Blood gene expression patterns and serum proteins that associate with worse vascular phenotypes suggest dysregulated immune and metabolic pathways linked to premature CVD. Cytokines and chemokines identified in associations with arterial stiffness, inflammation, and NCB in SLE may allow for characterization of new CVD biomarkers in lupus.

Non-Calcified Plaque Burden Is Associated With Increased Major Adverse Cardiovascular Events In A High Risk Appalachian Population With Low Coronary Artery Calcium Scores (0-100)

Non-Calcified Plaque Burden Is Associated With Increased Major Adverse Cardiovascular Events In A High Risk Appalachian Population With Low Coronary Artery Calcium Scores (0-100)

Mixed plaque on coronary CT angiography predicts atherosclerotic events in asymptomatic intermediate-risk individuals

ObjectiveCoronary CT angiography (CCTA) permits both qualitative and quantitative analysis of atherosclerotic plaque and may be a suitable risk modifier in assessing patients at intermediate risk of atherosclerotic cardiovascular disease....

Phenotyping coronary plaque by computed tomography in premature coronary artery disease

Abstract Background Premature coronary artery disease (CAD) is an aggressive chronic disease with multiple recurrences mostly related to the progression or complication of new coronary lesions. Purpose To compare coronary plaque characteristics of individuals with premature CAD with those of incidental plaques found in matched individuals free of overt cardiovascular disease, using coronary computed tomography angiography (CCTA). Methods 106 individuals with premature CAD were matched by age, sex, smoking status, family history of CAD, and dyslipidemia with 106 controls free of overt cardiovascular disease. CCTA were standardly analyzed for CAD-RADS score, plaque composition (calcified, partially or non-calcified), and the following four high-risk plaque (HRP) features : spotty calcification, positive remodeling, napkin-ring sign, and low-attenuation plaque. Results At least one coronary plaque was found in 85% of individuals with premature CAD vs. 62% of matched controls. The prevalence of non-calcified plaques was higher among individuals with premature CAD (65.1% vs. 30.2%, p&amp;lt;0,001), as well as spotty calcification (42.5% vs. 17.9%, p&amp;lt;0.001), positive remodeling (41.5% vs. 9.4%, p&amp;lt;0.001), low-attenuation plaques (24.5% vs. 3.8%, p&amp;lt;0.001) and napkin-ring sign (1.9% vs. 0.0%) (Figure 1). Individuals with premature CAD exhibited an average of 2.2 (±2.7) HRP features per person, while the control group displayed 0.4 (±0.8) HRP per person (p&amp;lt;0.001). Within a median follow-up of 24 [16,34] months, 24 ischemic recurrent events occurred in 24 individuals, all in the in premature CAD group. Individuals with premature CAD and recurrent ischemic event had more high-risk plaque features (4.3±3.9) than those without ischemic recurrence (1.5±1.9). They displayed more frequently non-calcified plaques (91.7% vs. 57.3%) with positive remodeling (75.0% vs. 31.7%) and low-attenuation plaques (45.8% vs. 18.3%) as compared to those without ischemic recurrence (Figure 2). Conclusions Coronary atherosclerosis in individuals with premature CAD is characterized by a high and predominant burden of non-calcified plaque and unusual high prevalence of high-risk plaque features, contributing to disease progression with multiple recurrences in this setting.HRP features in study populationHRP according to ischemic recurrence

Computed tomography plaque analysis identifies residual inflammation in recent acute myocardial infarction patients

Abstract Introduction Residual inflammatory risk (RIR) following acute myocardial infarction (AMI) patients is associated with recurrent major adverse cardiovascular events. Atherosclerotic plaque quantification using computed tomographic coronary angiography (CTCA) can specifically identify inflamed plaque characteristics. We compared plaque burden and tissue composition in AMI patients with those of stable coronary artery disease (CAD) patients to identify imaging markers of RIR. Purpose We aimed to identify signs of residual inflammation in recent AMI patients via CTCA atheroma quantification. We hypothesised that recent AMI patients have plaque characteristics suggestive of inflammation. Methods 108 patients recruited from multiple sites with AMI &amp;lt;1 month were propensity-matched via CAD risk factors (age, gender, diabetes, hypertension, hyperlipidaemia, smoking and family history of CAD) with stable CAD patients in a 1:1 ratio. Propensity matched recent AMI and stable CAD patient cohorts had similar profiles: age (60±9.7 vs 57±10.0 years), gender (91.7% vs 92.6% male), diabetes (13.9% vs 15.7%), hypertension (44.4% vs 50.9%) and hyperlipidaemia (50.9% vs 63.9%, p&amp;gt;0.05 for all). Total plaque burden (total lesion volume/total vessel volume) and plaque composition (fibrous fatty [fibrofatty, FF, 31 – 130 HU], necrotic core [NC, -30 – 30 HU], fibrous [131 – 350 HU] and calcium [&amp;gt; 350 HU]) were extracted from CTCA scans and aggregated per patient. Culprit lesions of recent AMI patients were excluded from the analysis due to the fact that coronary stents would affect plaque characterisation. Multivariate linear regression, corrected for CAD risk factors, was used to compare these parameters between the two cohorts. Results Recent AMI patients and stable CAD patients had similar total plaque burden (β=0.001±0.013, p=0.950, Figure 1a). Patients with recent AMI had higher non-calcified plaque volume ratio (β=0.071±0.026, p&amp;lt;0.05, Figure 1b) due to higher FF (β=0.094±0.019, Figure 1d) and NC (β=0.025 ± 0.005, Figure 1e) plaque volume (p&amp;lt;0.05 for all), but less fibrous plaque volume (β = -0.048±0.019, p&amp;lt;0.05, Figure 1c). Conclusions Recent AMI patients had a greater non-calcified plaque burden than stable CAD patients due to larger FF and NC plaque burden. Since FF and NC components indicate ongoing inflammation in the plaque, while fibrous content indicates resolved inflammation; increased NC and FF burden suggest increased coronary plaque inflammation in non-culprit lesions of recent AMI patients, supporting the presence of residual inflammation in recent AMI patients.Figure 1

Abstract 18209: The Association Between Lp(a) and Low-Density Plaque Volume is Not Modified by CRP

BACKGROUND: Inconsistent data have suggested an interaction between Lp(a) and hs-CRP levels, putting patients with concomitant elevation at the greatest risk for atherosclerotic cardiovascular events. To date, the association between Lp(a), systemic inflammation as measured by hs-CRP, and coronary plaque phenotype has not been unraveled. METHODS: Among consecutive asymptomatic patients evaluated for primary prevention of coronary artery disease, we explored the associations between Lp(a), hs-CRP and coronary atherosclerosis using atherosclerosis imaging-quantitative coronary CT angiography (AI-QCT; Cleerly Labs, Cleerly Inc., Denver,CO). The associations between Lp(a), hs-CRP and the AI-QCT outcomes defined as percent atheroma volume (PAV) as well as percent low-density non-calcified plaque volume (LD-NCPV) were assessed using multivariable linear regression adjusted for clinical risk factors. RESULTS: The mean age of the 373 included patients was 56.2 ± 8.9 years, 71.6% were male, and 54.2% was on statin therapy. Mean±SD LDL-C was 106 ± 41 mg/dl, median (IQR) Lp(a) was 31 (11, 89) nmol/L, while median hs-CRP levels were 0.8 (0.4, 1.8) mg/L. In the multivariable-adjusted analysis, Lp(a) levels were significantly associated with an increase in PAV (0.367 increase in PAV per 100 nmol/l increase in Lp(a), p=0.026) and percent LD-NCPV (0.018 increase in PAV per 100 nmol/l increase in Lp(a), p=0.031). However, there was no effect of adding hs-CRP to the models (p=0.446), and we observed no direct relationship between hs-CRP and PAV (p=0.446) or percent LD-NCPV (0.871). Table 1. CONCLUSIONS: Lp(a) is associated with low-density non-calcified plaque and total coronary plaque burden. The current study found no impact of hs-CRP on these associations, nor were hs-CRP levels associated with plaque burden.

Pericoronary adipose tissue attenuation is associated with non-calcified plaque burden in patients with chronic coronary syndromes

BackgroundPericoronary adipose tissue attenuation (PCAT) is a marker of inflammation of the pericoronary fat tissue, which can be assessed by coronary computed tomography angiography (CCTA). Its prognostic value was reported in previous studies. Nevertheless, the relationship between PCAT, plaque burden and coronary artery disease (CAD) severity, are not well defined. AimWe sought to evaluate the relationship between PCAT, CAD severity based on the CAD-RADS 2.0 score and plaque burden in patients with chronic coronary syndrome (CCS). MethodsConsecutive patients with a clinical indication for CCTA due to suspected or known CCS were included in our study. PCAT was measured in the proximal 4 ​cm of each of the right coronary artery (RCA), left anterior descending artery (LAD), and the left circumflex artery (LCX). The CAD-RADS 2.0 score was assessed in all patients and total, calcified, and non-calcified plaque burden was quantitatively measured. Results868 patients (median age of 67.0 (IQR ​= ​58.0–75.0)yrs., 400 (46.1%) female) underwent CCTA between September 2020 and August 2022 due to CCS. Weak correlations were found between PCAT and the total plaque burden, as well as with the Agatston score, whereas no correlations were found between PCAT and CAD-RADS 2.0 score. Associations were also observed between the PCAT of the LAD, RCA and LCX with non-calcified plaque burden (Odds ratios of 1.22 (95%CI ​= ​1.15–1.29), 1.11 (95%CI ​= ​1.07–1.17) and 1.14 (95%CI ​= ​1.08–1.14), respectively, p ​< ​0.001 for all) which were independent of age, the Agatston score, and the CAD-RADS 2.0 score). In addition, higher PCAT were noticed with increasing number of plaques, exhibiting high-risk features per patient (p ​< ​0.05 by ANOVA for all). ConclusionPCAT exhibits significant associations with non-calcified plaque burden and plaques with high-risk features in patients undergoing CCTA for CCS. Thus, PCAT may identify high-risk patients who could benefit from more aggressive preventive therapy, which merits further investigation in future studies.

Cardiometabolic predictors of high-risk CCTA phenotype in a diverse patient population

IntroductionLow-attenuation non-calcified plaque (LAP) burden and vascular inflammation by pericoronary adipose tissue (PCAT) measured from coronary CT angiography (CCTA) have shown to be predictors of cardiovascular outcomes. We aimed to investigate the relationships of cardiometabolic risk factors including lipoprotein(a) and epicardial adipose tissue (EAT) with CCTA high-risk imaging biomarkers, LAP and vascular inflammation. MethodsThe patient population consisted of consecutive patients who underwent CCTA for stable chest pain and had a complete cardiometabolic panel including lipoprotein(a). Plaque, PCAT and EAT were measured from CT using semiautomated software. Elevated LAP burden and PCAT attenuation were defined as ≥4% and ≥70.5 HU, respectively. The primary clinical end-point was a composite of myocardial infarction, revascularization or cardiovascular death. ResultsA total of 364 consecutive patients were included (median age 56 years, 64% female); the majority of patients were of Hispanic (60%), and the rest were of non-Hispanic Black (21%), non-Hispanic White (6%) and non-Hispanic Asian (4%) race/ethnicity. The prevalence of elevated LAP burden and PCAT attenuation was 31 and 18%, respectively, while only 8% had obstructive stenosis. There were significant differences in plaque characteristics among different racial/ethnic groups (p<0.001). Lipoprotein(a) correlated with LAP burden in Hispanic patients. Patients with elevated LAP were older, more likely to be have diabetes, hypertension, hyperlipidemia and smoke with higher CAC and EAT volume (all P<0.05). Patients with elevated LAP were more likely to develop the primary clinical outcome (p<0.001) but those with elevated PCAT were not (p=0.797). ConclusionThe prevalence of LAP and PCAT attenuation were 31 and 18%, respectively. Lipoprotein(a) levels correlated with LAP burden in Hispanic patients. Age, male sex, hypertension and hyperlipidemia increased the odds of elevated LAP, which showed prognostic significance.

Phenotyping coronary plaque by computed tomography in premature coronary artery disease.

Premature coronary artery disease (CAD) is an aggressive disease with multiple recurrences mostly related to new coronary lesions. This study aimed to compare coronary plaque characteristics of individuals with premature CAD with those of incidental plaques found in matched individuals free of overt cardiovascular disease, using coronary computed tomography angiography (CCTA). Of 1552 consecutive individuals who underwent CCTA, 106 individuals with history of acute or stable obstructive CAD ≤45 years were matched by age, sex, smoking status, cardiovascular heredity, and dyslipidaemia with 106 controls. CCTA were analysed for Coronary Artery Disease Reporting and Data System score, plaque composition, and high-risk plaque (HRP) features, including spotty calcification, positive remodelling, low attenuation, and napkin-ring sign. The characteristics of 348 premature CAD plaques were compared with those of 167 incidental coronary plaques of matched controls. The prevalence of non-calcified plaques was higher among individuals with premature CAD (65.1 vs. 30.2%, P < 0.001), as well as spotty calcification (42.5 vs. 17.9%, P < 0.001), positive remodelling (41.5 vs. 9.4%, P < 0.001), low attenuation (24.5 vs. 3.8%, P < 0.001), and napkin-ring sign (1.9 vs. 0.0%). They exhibited an average of 2.2 (2.7) HRP, while the control group displayed 0.4 (0.8) HRP (P < 0.001). Within a median follow-up of 24 (16, 34) months, individuals with premature CAD and ischaemic recurrence (n = 24) had more HRP [4.3 (3.9)] than those without ischaemic recurrence [1.5 (1.9)], mostly non-calcified with low attenuation and positive remodelling. Coronary atherosclerosis in individuals with premature CAD is characterized by a high and predominant burden of non-calcified plaque and unusual high prevalence of HRP, contributing to disease progression with multiple recurrences. A comprehensive qualitative CCTA assessment of plaque characteristics may further risk stratify our patients, beyond cardiovascular risk factors.

Relationship between impaired myocardial blood flow by positron emission tomography and low-attenuation plaque burden and pericoronary adipose tissue attenuation from coronary computed tomography: From the prospective PACIFIC trial

BackgroundPositron emission tomography (PET) is the clinical gold standard for quantifying myocardial blood flow (MBF). Pericoronary adipose tissue (PCAT) attenuation may detect vascular inflammation indirectly. We examined the relationship between MBF by PET and plaque burden and PCAT on coronary CT angiography (CCTA). MethodsThis post hoc analysis of the PACIFIC trial included 208 patients with suspected coronary artery disease (CAD) who underwent [15O]H2O PET and CCTA. Low-attenuation plaque (LAP, < 30HU), non-calcified plaque (NCP), and PCAT attenuation were measured by CCTA. ResultsIn 582 vessels, 211 (36.3%) had impaired per-vessel hyperemic MBF (≤ 2.30 mL/min/g). In multivariable analysis, LAP burden was independently and consistently associated with impaired hyperemic MBF (P = 0.016); over NCP burden (P = 0.997). Addition of LAP burden improved predictive performance for impaired hyperemic MBF from a model with CAD severity and calcified plaque burden (P < 0.001). There was no correlation between PCAT attenuation and hyperemic MBF (r = − 0.11), and PCAT attenuation was not associated with impaired hyperemic MBF in univariable or multivariable analysis of all vessels (P > 0.1). ConclusionIn patients with stable CAD, LAP burden was independently associated with impaired hyperemic MBF and a stronger predictor of impaired hyperemic MBF than NCP burden. There was no association between PCAT attenuation and hyperemic MBF.

Interplay Between Zero CAC, Quantitative Plaque Analysis, and Adverse Events in a Diverse Patient Cohort.

Coronary artery calcium scoring (CAC) has garnered attention in the diagnostic approach to chest pain patients. However, little is known about the interplay between zero CAC, sex, race, ethnicity, and quantitative coronary plaque analysis. We conducted a retrospective analysis from our computed tomography registry of patients with stable angina without prior myocardial infarction or revascularization undergoing coronary computed tomography angiography at Montefiore Healthcare System. Follow-up end points collected included invasive angiography, type-1 myocardial infarction, coronary revascularization, cardiovascular and all-cause death. A total of 2249 patients were included (66% female). The median follow-up was 5.5 years. The median age of those without CAC was 52 years (interquartile range, 44-59) and 60 years (interquartile range, 53-68) in those with CAC. Most patients were Hispanic (58%), and the rest were non-Hispanic Black (28%), non-Hispanic White (10%), and non-Hispanic Asian (5%). The majority had CAC=0 (55%). The negative predictive value of CAC=0 was 92.8%, 99.9%, and 99.9% for any plaque, obstructive coronary artery stenosis, and the composite outcome of all-cause death, myocardial infarction, or coronary revascularization, respectively. Among patients without CAC (n=1237), 89 patients (7%) had evidence of plaque on their coronary computed tomography angiography with a median low-attenuation noncalcified plaque burden of 4% (2-7). There were no significant differences in the negative predictive value for CAC=0 by sex, race, or ethnicity. Patients with ≥2 risk factors had higher odds of having plaque with zero CAC. In summary, no sex, race, or ethnicity differences were demonstrated in the negative predictive value of a zero CAC; however, patients with ≥2 risk factors had a higher prevalence of plaque. A small percentage (7%) of symptomatic patients undergoing coronary computed tomography angiography with zero CAC had noncalcified coronary plaque, with the implication that caution is needed for downscaling of preventive treatment in patients with zero CAC, chest pain, and multiple risk factors.

Predicting coronary plaque progression with conventional plaque parameters and radiomics features derived from coronary CT angiography.

To determine the value of combining conventional plaque parameters and radiomics features derived from coronary computed tomography angiography (CCTA) for predicting coronary plaque progression. Clinical data and CCTA images of 400 patients who underwent at least two CCTA examinations between January 2009 and August 2020 were analyzed retrospectively. Diameter stenosis, total plaque volume and burden, calcified plaque volume and burden, noncalcified plaque volume and burden (NCPB), pericoronary fat attenuation index (FAI), and other conventional plaque parameters were recorded. The patients were assigned to a training cohort (n = 280) and a validation cohort (n = 120) in a 7:3 ratio using a stratified random splitting method. The area under the receiver operating characteristics curve (AUC) was used to evaluate the predictive abilities of conventional parameters (model 1), radiomics features (model 2), and their combination (model 3). FAI and NCPB were identified as independent risk factors for coronary plaque progression in the training cohort. Both model 2 (training cohort AUC: 0.814, p < 0.001; validation cohort AUC: 0.729, p = 0.288) and model 3 (training cohort AUC: 0.824, p < 0.001; validation cohort AUC: 0.758, p = 0.042) had better diagnostic performances in predicting plaque progression than model 1 (training cohort AUC: 0.646; validation cohort AUC: 0.654). Moreover, model 3 was slightly higher than model 2, although not statistically significant. The combination of conventional coronary plaque parameters and CCTA-derived radiomics features had a better ability to predict plaque progression than conventional parameters alone. The conventional coronary plaque characteristics such as noncalcified plaque burden, pericoronary fat attenuation index, and radiomics features derived from CCTA can identify plaques prone to progression, which is helpful for further clinical decision-making of coronary artery disease. • FAI and NCPB were identified as independent risk factors for predicting plaque progression. • Coronary plaque radiomics features were more advantageous than conventional parameters in predicting plaque progression. • The combination of conventional coronary plaque parameters and radiomics features could significantly improve the predictive ability of plaque progression over conventional parameters alone.

Low-density Non-calcified Plaque Burden Derived From Artificial Intelligence-guided CCTA Quantification Is Associated With 1-year Cardiovascular Outcomes

Low-density Non-calcified Plaque Burden Derived From Artificial Intelligence-guided CCTA Quantification Is Associated With 1-year Cardiovascular Outcomes

Body mass components affecting low-attenuation noncalcified coronary plaque burden

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): National Institute of Cardiology in Warsaw, Poland Background Weight control is a major risk modifier for coronary artery disease. However, the effect exerted by individual body mass components on coronary plaque may not be uniform. Low-attenuation noncalcified plaque (LAP) has been recently identified as an independent predictor of cardiovascular outcomes [1]. Purpose To determine the relationship between changes in body mass composition and LAP burden. Methods 89 participants of Dietary Intervention to Stop Coronary Atherosclerosis in Computed Tomography (DISCO-CT) were enrolled into the analysis (40% women, mean age 60±7.7 years). Patients with non-obstructive (stenosis&amp;lt;70%) coronary atherosclerosis confirmed in coronary computed tomography angiography (CCTA) and qualified to conservative treatment were randomized (1:1) to intensive diet and lifestyle intervention atop optimal medical therapy (OMT) versus OMT alone over 66.8±13.7 months [2]. Body mass (BM) and body mass components including total body fat (TBF), skeletal muscle mass (SMM), visceral cell mass (VCM), and extracellular mass (ECM) were measured at baseline and follow-up (InBody S10 analyser, South Korea). LAP burden was defined as the volume of coronary plaque &amp;lt;30 Hounsfield units divided by the vessel volume, and expressed in %. Changes in body components were compared with changes in LAP measured in serial CCTA scans (QAngioCT, Medis Medical Imaging Systems, the Netherlands). Results Reduction in BM was significantly higher in the experimental (∆BM=-3.6±4.9 kg) vs control arm (∆BM=-1.4±2.9 kg; p = 0.016) and so was the reduction in TBF (∆TBF=-4.2±5.3 kg vs ∆TBF=0.2±4.3 kg, respectively; p&amp;lt;0.001). SMM increased by 0.4±2.6 kg in the experimental arm and decreased by 1.0±2.1 kg in the control arm (p = 0.006). No significant interarm differences were observed for changes in VCM and ECM. Reduction in LAP was higher in the experimental vs control arm (∆LAP=-0.42±1.4% vs ∆LAP=-0.03±0.45%, respectively; p = 0.078). In the entire study population, a significant positive correlation between LAP reduction and BM reduction was revealed (r=0.45, p&amp;lt;0.001). Multivariate regression model incorporating the investigated body mass components identified TBF as the only component associated with LAP reduction (table). Conclusions Body mass reduction may decrease LAP burden due to body fat reduction.

Predictive value of DEEPVESSEL-fractional flow reserve and quantitative plaque analysis based on coronary CT angiography for major adverse cardiac events

To investigate the predictive value of the combination of DEEPVESSEL-fractional flow reserve (DVFFR) and quantitative plaque analysis using coronary computed tomographic angiography (CCTA) for major adverse cardiac events (MACE). In this retrospective study, data from 69 vessels from 58 consecutive patients were collected. These patients who underwent coronary angiography (CAG) with DVFFR were divided into MACE-positive and MACE-negative groups. DVFFR measurements were obtained from CCTA images acquired before CAG, and an FFR or DVFFR value≤0.80 was considered haemodynamically significant. CCTA images were analysed quantitatively using automated software to obtain the following indices: total plaque volume (TPV) and burden (TPB), calcified plaque volume (CPV) and burden (CPB), non-calcified plaque volume (NCPV) and burden (NCPB), low-attenuation plaque (LAP), minimum lumen area (MLA), stenosis grade (SG) and lesion length (LL). Univariate and multivariate logistic regression, correlation, and receiver operating characteristic (ROC) analyses were used for statistical analysis. DVFFR was highly correlated with invasive FFR (R=0.728), and the Bland-Altman plot showed good agreement between DVFFR and FFR (95% CI: -0.109-0.087) on a per-vessel level. DVFFR showed a high diagnostic performance in identifying abnormal haemodynamic vessels, with an area under the ROC curve (AUC) of 0.984. In multivariate analysis, the following biomarkers were predictors of MACE: DVFFR ≤ 0.8, SG, TPB, NCPB, and LL values. The combination of the above independent risk factors yielded the most valuable prediction for MACE (AUC:0.888). DVFFR was highly correlated with FFR with satisfactory diagnostic accuracy. DVFFR, together with plaque analysis indices, yielded valuable predictions for MACE.

Gender Differences in Epicardial Adipose Tissue and Plaque Composition by Coronary CT Angiography: Association with Cardiovascular Outcome.

Background: To investigate gender differences in epicardial adipose tissue (EAT) and plaque composition by coronary CT angiography (CCTA) and the association with cardiovascular outcome. Methods: Data of 352 patients (64.2 ± 10.3 years, 38% female) with suspected coronary artery disease (CAD) who underwent CCTA were retrospectively analyzed. EAT volume and plaque composition from CCTA were compared between men and women. Major adverse cardiovascular events (MACE) were recorded from follow-up. Results: Men were more likely to have obstructive CAD, higher Agatston scores, and a larger total and non-calcified plaque burden. In addition, men displayed more adverse plaque characteristics and EAT volume compared to women (all p < 0.05). After a median follow-up of 5.1 years, MACE occurred in 8 women (6%) and 22 men (10%). In multivariable analysis, Agatston calcium score (HR 1.0008, p = 0.014), EAT volume (HR 1.067, p = 0.049), and low-attenuation plaque (HR 3.82, p = 0.036) were independent predictors for MACE in men, whereas only low-attenuation plaque (HR 2.42, p = 0.041) showed predictive value for events in women. Conclusion: Women demonstrated less overall plaque burden, fewer adverse plaque characteristics, and a smaller EAT volume compared to men. However, low-attenuation plaque is a predictor for MACE in both genders. Thus, a differentiated plaque analysis is warranted to understand gender differences of atherosclerosis to guide medical therapy and prevention strategies.