Presence Of Lipid-rich Plaque Research Articles

Abstract 10382: Large Lipid-Rich Plaque Predicts Intra-Stent Thrombus Formation After Primary Pci in Patients with Acute Coronary Syndrome: Insights from Near-infrared Spectroscopy and Optical Coherence Tomography Imaging Analysis

Backgrounds: The formation of intrastent thrombus is a PCI-related complication in subjects with ACS, which infrequently causes acute stent thrombosis. Given that lipid-rich plaque, a substrate for ACS, activates inflammation inducing prothrombotic state, the degree of lipidic plaque materials may associate with intrastent thrombus formation. Methods: Culprit lesions in 70 ACS subjects (=STEMI/NSTEMI/uAP=28/27/15) receiving newer-generation DES implantation were evaluated by both near-infrared spectroscopy (NIRS) and optical coherence tomography (OCT) imaging. NIRS-derived 4-mm maximum lipid-core-burden index (maxLCBI 4mm ) at culprit lesion was measured prior to PCI. OCT-derived intrastent thrombus-burden index (ITBI) after stent implantation were calculated as follows: [Σ(every 1-mm cross sectional thrombus-arc score: 1=1-90°,2=91-180°,3=181-270°,4=271-360°)/analyzed length]x(averaged longitudinal length). ITBI was compared between subjects with maxLCBI 4mm <400 and ≥400. Result: The averaged maxLCBI 4mm was 525±236, and dual-antiplatelet therapy with aspirin and clopidogrel, and aspirin and prasugrel was used in 43 and 56%, respectively. On OCT imaging analysis, maxLCBI 4mm was significantly associated with ITBI (r=0.55, p <0.001, Figure), whereas there were no significant relationships of minimum stent area (MSA) (r=0.18, p=0.13) and stent malapposition diameter with ITBI (r=0.00. p=0.97). Multivariate analysis demonstrated maxLCBI 4mm as an independent predictor of higher ITBI even after adjusting MSA, stent malapposition and other clinical characteristics (Table). Conclusions: The presence of lipid-rich plaque was associated with intrastent thrombus formation in the setting of ACS. Our findings suggest the potential importance to modulate activated prothrombotic cascade by using more potent antiplatelet agent in ACS patients exhibiting lipid-rich plaques.

Abstract 10822: Lower EPA/AA Ratio is Associated with a Higher Prevalence of Vulnerable Characteristics in Non-Culprit Coronary Plaques in Statin-Treated Patients with Coronary Artery Disease

Introduction: Low eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio is associated with an increased risk of cardiovascular events in patients with coronary artery disease (CAD). However, the association between EPA/AA ratio and the characteristics of non-culprit coronary plaque in statin-treated patients with CAD remains to be elucidated. Hypothesis: Lower EPA/AA ratio is associated with a higher prevalence of vulnerable characteristics in non-culprit coronary plaque in statin-treated patients with CAD. Methods: A total of 367 consecutive stain-treated patients with stable coronary disease, who underwent percutaneous coronary intervention for the culprit lesion and optical coherence tomography (OCT) imaging of a non-culprit plaque in a culprit vessel were included. The characteristics of non-culprit plaque assessed by OCT were compared between the lower EPA/AA group (EPA/AA <0.4, n=255) and the higher EPA/AA group (EPA/AA ≥0.4, n=112). Results: The prevalence of lipid-rich plaque (58.8 vs. 42.0%, p=0.004) and plaque with macrophage (56.1 vs. 32.1%, p<0.001) was significantly higher in the lower EPA/AA group than in the higher EPA/AA group (Panel A). The lower EPA/AA was independently associated with the presence of lipid-rich plaque (Odds ratio [OR], 1.837; 95% confidence interval [CI]: 1.130-3.004, p=0.015) and plaque with macrophage (OR, 2.764; 95% CI: 1.672-4.639, p<0.001) (Panel B). Conclusions: Lower EPA/AA ratio was associated with a higher prevalence of vulnerable characteristics in non-culprit plaque. The present results may partly explain the impact of low EPA/AA ratio on the increased incidence of recurrent events in patients with CAD.

Association between near-infrared spectroscopy defined lipid rich plaque and pericoronary adipose tissue inflammation on computed tomography angiography

Abstract Background A recent study has shown that lipid-rich plaque (LRP) detected by near-infrared spectroscopy (NIRS) is a significant predictor of future adverse events. Pericoronary adipose tissue inflammation (FAI; fat attenuation index) evaluated by computed tomography angiography (CTA) has also been reported to be linked with cardiac events. The relationship between NIRS-defined LRP and FAI remains to be determined. Methods A total of 82 de novo culprit lesions in 82 patients with chronic coronary syndromes (CCS) who underwent perprocedural CTA and NIRS was retrospectively studied. FAI was assessed by the crude analysis of the mean CT attenuation value (−190 to −30 Hounsfield units; higher values indicating inflammation) of pericoronary adipose tissue. Plaque morphology was assessed by coronary CTA and grey-scale intravascular ultrasound (IVUS). NIRS-defined LRP was defined as a maximum lipid core burden index (LCBI) in 4 mm ≥400. Relationship between NIRS-defined LRP, CTA/grey-scale IVUS findings, and FAI was assessed. Univariate and multivariate logistic regression analyses were performed to determine the predictors for NIRS-derived LRP. Results NIRS-defined LRP was observed in 35 (42.6%) patients. Maximum LCBI showed modest correlations both with FAI (r=0.29, p-value=0.007) and CT-derived remodeling index (r=0.51, p<0.001). Receiver operating characteristic (ROC) curve analysis revealed that the best cut-off values of FAI and CT-derived remodeling index for predicting NIRS-defined LRP were −70.7 (AUC: 0.65, 95% CI: 0.53–0.71, P<0.05) and 1.11 (AUC: 0.74, 95% CI: 0.63–0.86, P<0.01), respectively. Multivariate logistic regression analysis showed FAI ≥−70.7 (odds ratio [OR]: 4.27; 95% CI: 1.28–14.3; p-value = 0.02) and CT-derived remodeling index (OR: 10.7; 95% CI: 2.99–32.2; p-value <0.001) were independent predictors of the presence of NIRS-defined LRP, whereas there was no statistically significant and independent predictor of IVUS-derived factors for NIRS-defined LRP. When stratified according to the presence or absence of FAI ≥−70.7 and CT-derived remodeling index ≥1.11, 93% of the lesions showed NIRS-derived LRP when both factors were present, and NIRS-derived LRP was safely ruled out (88%) when both factors were absent. Conclusions FAI of the culprit lesion in CCS was an independent predictor of NIRS-defined LRP, supporting the notion that local pericoronary adipose tissue inflammation may correlate to the presence of LRP. Comprehensive assessment of coronary CTA including FAI evaluation may provide a highly accurate information with high sensitivity and specificity for identifying high risk lesions potentially leading to future cardiac events. Funding Acknowledgement Type of funding source: None

Gender differences in plaque characteristics of nonculprit lesions in patients with coronary artery disease

BackgroundAlthough numerous reports suggest sex-related differences in atherosclerosis, limited data describing gender-associated differences in plaque morphology and composition are currently available. The aim of the present study was to compare coronary nonculprit plaque characteristics in women and men with coronary artery disease (CAD) by optical coherence tomography (OCT).MethodsThis was a retrospective study. A total of 187 nonculprit plaques were identified in 103 patients with CAD who underwent OCT imaging of all 3 coronary arteries. These patients included 77 (74.8%) men and 26 (25.2%) women.ResultsFemale patients were significantly older than males (mean age, 70.8 ± 7.3 vs 60.8 ± 9.8 years; P < 0.001) and less likely to be current smokers (P = 0.007). OCT analysis included the presence of lipid-rich plaque, maximum lipid arc, lipid-core length, lipid index (LI), fibrous cap thickness, and the incidence of thin-cap fibroatheroma (TCFA). Nonculprit plaques in men exhibited greater lipid-core length and LI compared with those of women (9.4 ± 4.5 vs. 7.3 ± 4.3 mm, P = 0.024; 1615.1 ± 893.8 vs. 1237.8 ± 859.8, P = 0.035, respectively). In the univariate linear regression model, sex and current smoker were all associated with a larger LI, whereas only use of statin was independent risk factor for a larger LI in multivariate analysis.ConclusionsCoronary nonculprit plaques in male patients with CAD contain larger lipid cores than those of female patients.

Postprandial Hyperchylomicronemia and Thin-Cap Fibroatheroma in Nonculprit Lesions.

Objective- Although postprandial hypertriglyceridemia can be a risk factor for coronary artery disease, the extent of its significance remains unknown. This study aimed to investigate the correlation between the postprandial lipid profiles rigorously estimated with the meal tolerance test and the presence of lipid-rich plaque, such as thin-cap fibroatheroma (TCFA), in the nonculprit lesion. Approach and Results- A total of 30 patients with stable coronary artery disease who underwent a multivessel examination using optical coherence tomography during catheter intervention for the culprit lesion were enrolled. Patients were divided into 2 groups: patients with TCFA (fibrous cap thickness ≤65 µm) in the nonculprit lesion and those without TCFA. Serum remnant-like particle-cholesterol and ApoB-48 (apolipoprotein B-48) levels were measured during the meal tolerance test. The value of remnant-like particle-cholesterol was significantly greater in the TCFA group than in the non-TCFA group ( P=0.045). Although the baseline ApoB-48 level was similar, the increase in the ApoB-48 level was significantly higher in the TCFA group than in the non-TCFA group ( P=0.028). In addition, the baseline apolipoprotein C-III levels was significantly greater in the TCFA group ( P=0.003). These indexes were independent predictors of the presence of TCFA (ΔApoB-48: odds ratio, 1.608; 95% confidence interval, 1.040-2.486; P=0.032; apolipoprotein C-III: odds ratio, 2.581; 95% confidence interval, 1.177-5.661; P=0.018). Conclusions- Postprandial hyperchylomicronemia correlates with the presence of TCFA in the nonculprit lesion and may be a residual risk factor for coronary artery disease.

An Optical Coherence Tomography Assessment of Stent Strut Apposition Based on the Presence of Lipid-Rich Plaque in the Carotid Artery

Purpose: To evaluate the rate of stent malapposition, plaque prolapse, and fibrous cap rupture detected by optical coherence tomography (OCT) after carotid artery stenting (CAS) based on the presence of lipid-rich plaque, which may be associated with acute stent thrombosis. Methods: A retrospective study was conducted involving 26 consecutive patients who underwent CAS with OCT imaging acquired before stent deployment and after stent dilation. Adequate imaging quality could not be obtained in 6 patients (out-of-screen images and residual blood), which left 20 patients (mean age 63 years; 13 men) for analysis. Plaque characteristics were determined from 500 selected OCT cross sections; a lipid-rich plaque was defined by lipid present in ≥2 quadrants. Cross-sectional OCT images within the stented segment were evaluated at 1-mm intervals for the presence of malapposition, plaque prolapse, and fibrous cap rupture. The data were compared between patients with and without lipid-rich plaques. The patients were examined at 6 months to determine the degree of in-stent restenosis (ISR). Results: Patients with lipid-rich plaque demonstrated a higher rate of embedded stent struts (29.4% vs 23.7%, p<0.001) and a lower rate of well apposed struts (54.6% vs 59.6%, p<0.001) compared to patients with non–lipid-rich plaque. Rates of plaque prolapse (65.5% vs 49.1%, p<0.001) and fibrous cap rupture (65.5% vs 49.1%, p<0.001) were significantly higher in patients with lipid-rich plaque. ISR ranged from none to 42% in 12 patients; malapposed stent struts and fibrous cap ruptures were not more frequent in the patients with obvious ISR. The 8 patients with no obvious restenosis still had malapposed struts, embedded struts, plaque prolapse, and fibrous cap rupture. Conclusion: Embedded stent struts, plaque prolapse, and fibrous cap rupture were more frequent and well-apposed stent struts were less frequent after CAS in patients with lipid-rich plaque.