Dataset Information

Clinical Significance of the Presence or Absence of Lipid-Rich Plaque Underneath Intact Fibrous Cap Plaque in Acute Coronary Syndrome.

ABSTRACT: Background Although most coronary thromboses occur on the surface of lipid-rich plaque ( LRP ) with plaque rupture ( PR ), previous pathological and optical coherence tomography studies demonstrated diversity in the morphological characteristics of culprit plaque underlying the thrombus, including lesions with intact fibrous cap ( IFC ). We investigated the clinical significance of IFC in relation to the presence or absence of LRP observed via optical coherence tomography in culprit lesions of acute coronary syndrome. Methods and Results We investigated 510 patients with acute coronary syndrome who underwent optical coherence tomography for the culprit lesion. Optical coherence tomography analysis included the presence or absence of PR , which were categorized into the PR group and the IFC group, respectively. The IFC group was further categorized on the basis of the presence of LRP . Incidence of major adverse cardiac events ( MACEs ), including cardiac death, myocardial infarction, and clinically driven remote revascularizations, was compared. Culprit lesions were categorized into 328 PR s and 182 IFC s. MACEs occurred in 85 patients (16.7%) during the median follow-up duration of 621 days. LRP was detected in 325 lesions (99%) with PR , whereas 60 (33.0%) of the lesions with IFC did not show LRP . Kaplan-Meier analysis revealed significantly lower MACEs in the IFC group compared with the PR group. Furthermore, the IFC group without LRP showed significantly lower MACEs compared with the IFC group with LRP . Multivariate Cox proportional hazards analysis demonstrated that IFC without LRP was an independent predictor of better prognosis. Conclusions Exclusion of LRP underneath IFC culprit lesions in acute coronary syndrome may predict a lower risk of future MACEs .

SUBMITTER: Hoshino M

PROVIDER: S-EPMC6512119 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Clinical Significance of the Presence or Absence of Lipid-Rich Plaque Underneath Intact Fibrous Cap Plaque in Acute Coronary Syndrome.

Hoshino Masahiro M Yonetsu Taishi T Usui Eisuke E Kanaji Yoshihisa Y Ohya Hiroaki H Sumino Yohei Y Yamaguchi Masao M Hada Masahiro M Hamaya Rikuta R Kanno Yoshinori Y Murai Tadashi T Lee Tetsumin T Kakuta Tsunekazu T

Journal of the American Heart Association 20190501 9

Background Although most coronary thromboses occur on the surface of lipid-rich plaque ( LRP ) with plaque rupture ( PR ), previous pathological and optical coherence tomography studies demonstrated diversity in the morphological characteristics of culprit plaque underlying the thrombus, including lesions with intact fibrous cap ( IFC ). We investigated the clinical significance of IFC in relation to the presence or absence of LRP observed via optical coherence tomography in culprit lesions of a ...[more]

PMID: 31057022

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Project description:Thin-cap fibroatheroma (TCFA) and plaque rupture have been recognized as the most frequent risk factor for thrombosis and acute coronary syndrome. Intravascular optical coherence tomography (IVOCT) can identify TCFA and assess cap thickness, which provides an opportunity to assess plaque vulnerability. We developed an automated method that can detect lipidous plaque and assess fibrous cap thickness in IVOCT images. This study analyzed a total of 4360 IVOCT image frames of 77 lesions among 41 patients. Expert cardiologists manually labeled lipidous plaque based on established criteria. To improve segmentation performance, preprocessing included lumen segmentation, pixel-shifting, and noise filtering on the raw polar (r, θ) IVOCT images. We used the DeepLab-v3 plus deep learning model to classify lipidous plaque pixels. After lipid detection, we automatically detected the outer border of the fibrous cap using a special dynamic programming algorithm and assessed the cap thickness. Our method provided excellent discriminability of lipid plaque with a sensitivity of 85.8% and A-line Dice coefficient of 0.837. By comparing lipid angle measurements between two analysts following editing of our automated software, we found good agreement by Bland-Altman analysis (difference 6.7° ± 17°; mean ~ 196°). Our method accurately detected the fibrous cap from the detected lipid plaque. Automated analysis required a significant modification for only 5.5% frames. Furthermore, our method showed a good agreement of fibrous cap thickness between two analysts with Bland-Altman analysis (4.2 ± 14.6 µm; mean ~ 175 µm), indicating little bias between users and good reproducibility of the measurement. We developed a fully automated method for fibrous cap quantification in IVOCT images, resulting in good agreement with determinations by analysts. The method has great potential to enable highly automated, repeatable, and comprehensive evaluations of TCFAs.

Project description:OBJECTIVES:The aim of this study was to investigate whether and what carotid plaque characteristics predict systemic cardiovascular outcomes in patients with clinically established atherosclerotic disease. BACKGROUND:Advancements in atherosclerosis imaging have allowed assessment of various plaque characteristics, some of which are more directly linked to the pathogenesis of acute cardiovascular events compared to plaque burden. METHODS:As part of the event-driven clinical trial AIM-HIGH (Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides: Impact on Global Health Outcomes), subjects with clinically established atherosclerotic disease underwent multicontrast carotid magnetic resonance imaging (MRI) to detect plaque tissue composition and high-risk features. Prospective associations between MRI measurements and the AIM-HIGH primary endpoint (fatal and nonfatal myocardial infarction, ischemic stroke, hospitalization for acute coronary syndrome, and symptom-driven revascularization) were analyzed using Cox proportional hazards survival models. RESULTS:Of the 232 subjects recruited, 214 (92.2%) with diagnostic image quality constituted the study population (82% male, mean age 61 ± 9 years, 94% statin use). During median follow-up of 35.1 months, 18 subjects (8.4%) reached the AIM-HIGH endpoint. High lipid content (hazard ratio [HR] per 1 SD increase in percent lipid core volume: 1.57; p = 0.002) and thin/ruptured fibrous cap (HR: 4.31; p = 0.003) in carotid plaques were strongly associated with the AIM-HIGH endpoint. Intraplaque hemorrhage had a low prevalence (8%) and was marginally associated with the AIM-HIGH endpoint (HR: 3.00; p = 0.053). High calcification content (HR per 1 SD increase in percent calcification volume: 0.66; p = 0.20), plaque burden metrics, and clinical risk factors were not significantly associated with the AIM-HIGH endpoint. The associations between carotid plaque characteristics and the AIM-HIGH endpoint changed little after adjusting for clinical risk factors, plaque burden, or AIM-HIGH randomized treatment assignment. CONCLUSIONS:Among patients with clinically established atherosclerotic disease, carotid plaque lipid content and fibrous cap status were strongly associated with systemic cardiovascular outcomes. Markers of carotid plaque vulnerability may serve as novel surrogate markers for systemic atherothrombotic risk.

Project description:Recent genome wide association studies have identified a number of genes that contribute to the risk for coronary heart disease. One such gene, TCF21, encodes a basic-helix-loop-helix transcription factor believed to serve a critical role in the development of epicardial progenitor cells that give rise to coronary artery smooth muscle cells (SMC) and cardiac fibroblasts. Using reporter gene and immunolocalization studies with mouse and human tissues we have found that vascular TCF21 expression in the adult is restricted primarily to adventitial cells associated with coronary arteries and also medial SMC in the proximal aorta of mouse. Genome wide RNA-Seq studies in human coronary artery SMC (HCASMC) with siRNA knockdown found a number of putative TCF21 downstream pathways identified by enrichment of terms related to CAD, including "vascular disease," "disorder of artery," and "occlusion of artery," as well as disease-related cellular functions including "cellular movement" and "cellular growth and proliferation." In vitro studies in HCASMC demonstrated that TCF21 expression promotes proliferation and migration and inhibits SMC lineage marker expression. Detailed in situ expression studies with reporter gene and lineage tracing revealed that vascular wall cells expressing Tcf21 before disease initiation migrate into vascular lesions of ApoE-/- and Ldlr-/- mice. While Tcf21 lineage traced cells are distributed throughout the early lesions, in mature lesions they contribute to the formation of a subcapsular layer of cells, and others become associated with the fibrous cap. The lineage traced fibrous cap cells activate expression of SMC markers and growth factor receptor genes. Taken together, these data suggest that TCF21 may have a role regulating the differentiation state of SMC precursor cells that migrate into vascular lesions and contribute to the fibrous cap and more broadly, in view of the association of this gene with human CAD, provide evidence that these processes may be a mechanism for CAD risk attributable to the vascular wall.

Project description:ObjectivesTo investigate the association of pericoronary adipose tissue mean attenuation (PCATMA) with coronary artery disease (CAD) characteristics on coronary computed tomography angiography (CCTA).MethodsWe retrospectively investigated 165 symptomatic patients who underwent third-generation dual-source CCTA at 70kVp: 93 with and 72 without CAD (204 arteries with plaque, 291 without plaque). CCTA was evaluated for presence and characteristics of CAD per artery. PCATMA was measured proximally and across the most severe stenosis. Patient-level, proximal PCATMA was defined as the mean of the proximal PCATMA of the three main coronary arteries. Analyses were performed on patient and vessel level.ResultsMean proximal PCATMA was -96.2 ± 7.1 HU and -95.6 ± 7.8HU for patients with and without CAD (p = 0.644). In arteries with plaque, proximal and lesion-specific PCATMA was similar (-96.1 ± 9.6 HU, -95.9 ± 11.2 HU, p = 0.608). Lesion-specific PCATMA of arteries with plaque (-94.7 HU) differed from proximal PCATMA of arteries without plaque (-97.2 HU, p = 0.015). Minimal stenosis showed higher lesion-specific PCATMA (-94.0 HU) than severe stenosis (-98.5 HU, p = 0.030). Lesion-specific PCATMA of non-calcified, mixed, and calcified plaque was -96.5 HU, -94.6 HU, and -89.9 HU (p = 0.004). Vessel-based total plaque, lipid-rich necrotic core, and calcified plaque burden showed a very weak to moderate correlation with proximal PCATMA.ConclusionsLesion-specific PCATMA was higher in arteries with plaque than proximal PCATMA in arteries without plaque. Lesion-specific PCATMA was higher in non-calcified and mixed plaques compared to calcified plaques, and in minimal stenosis compared to severe; proximal PCATMA did not show these relationships. This suggests that lesion-specific PCATMA is related to plaque development and vulnerability.Key points• In symptomatic patients undergoing CCTA at 70 kVp, PCATMA was higher in coronary arteries with plaque than those without plaque. • PCATMA was higher for non-calcified and mixed plaques compared to calcified plaques, and for minimal stenosis compared to severe stenosis. • In contrast to PCATMA measurement of the proximal vessels, lesion-specific PCATMA showed clear relationships with plaque presence and stenosis degree.

Project description:Recent genome wide association studies have identified a number of genes that contribute to the risk for coronary heart disease. One such gene, TCF21, encodes a basic-helix-loop-helix transcription factor believed to serve a critical role in the development of epicardial progenitor cells that give rise to coronary artery smooth muscle cells (SMC) and cardiac fibroblasts. Using reporter gene and immunolocalization studies with mouse and human tissues we have found that vascular TCF21 expression in the adult is restricted primarily to adventitial cells associated with coronary arteries and also medial SMC in the proximal aorta of mouse. Genome wide RNA-Seq studies in human coronary artery SMC (HCASMC) with siRNA knockdown found a number of putative TCF21 downstream pathways identified by enrichment of terms related to CAD, including “vascular disease,” “disorder of artery,” and “occlusion of artery” as well as disease-related cellular functions including “cellular movement,” and “cellular growth and proliferation.” In vitro studies in HCASMC demonstrated that TCF21 expression promotes proliferation and migration and inhibits SMC lineage marker expression. Detailed in situ expression studies with reporter gene and lineage tracing revealed that vascular wall cells expressing Tcf21 before disease initiation migrate into vascular lesions of ApoE-/- and Ldlr-/- mice. While Tcf21 lineage traced cells are distributed throughout the early lesions, in mature lesions they contribute to the formation of a subcapsular layer of cells, and others become associated with the fibrous cap. The lineage traced fibrous cap cells activate expression of SMC markers and growth factor receptor genes. Taken together, these data suggest that TCF21 may have a role regulating the differentiation state of SMC precursor cells that migrate into vascular lesions and contribute to the fibrous cap and more broadly, in view of the association of this gene with human CAD, provide evidence that these processes may be a mechanism for CAD risk attributable to the vascular wall.

Dataset Information

Clinical Significance of the Presence or Absence of Lipid-Rich Plaque Underneath Intact Fibrous Cap Plaque in Acute Coronary Syndrome.

Publications

Clinical Significance of the Presence or Absence of Lipid-Rich Plaque Underneath Intact Fibrous Cap Plaque in Acute Coronary Syndrome.

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