Atherosclerotic Plaque Angiogenesis as a Mechanism of Intraplaque Hemorrhage and Acute Coronary Rupture

2010 ◽  
pp. 213-236
Author(s):  
Frank D. Kolodgie ◽  
Aloke V. Finn ◽  
Jagat Narula ◽  
Renu Virmani
Keyword(s):  
Atherosclerotic Plaque ◽  
Intraplaque Hemorrhage

scholarly journals Association Between Carotid Atherosclerotic Plaque Calcification and Intraplaque Hemorrhage

2017 ◽  
Vol 37 (6) ◽  
pp. 1228-1233 ◽  
Author(s):  
Ruolan Lin ◽  
Shuo Chen ◽  
Gaifen Liu ◽  
Yunjing Xue ◽  
Xihai Zhao
Keyword(s):  
Atherosclerotic Plaque ◽  
Intraplaque Hemorrhage ◽  
Carotid Atherosclerotic Plaque

Platelets enter atherosclerotic plaque via intraplaque microvascular leakage and intraplaque hemorrhage: A histopathological study in carotid plaques

2012 ◽  
Vol 222 (2) ◽  
pp. 355-359 ◽  
Author(s):  
Guus W. van Lammeren ◽  
Gerard Pasterkamp ◽  
Jean-Paul P.M. de Vries ◽  
Lena Bosch ◽  
Judith J. de Haan ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Intraplaque Hemorrhage ◽  
Histopathological Study ◽  
Carotid Plaques ◽  
Microvascular Leakage

scholarly journals Intravascular Ultrasound of Symptomatic Intracranial Stenosis Demonstrates Atherosclerotic Plaque with Intraplaque Hemorrhage: A Case Report

2009 ◽  
Vol 19 (3) ◽  
pp. 266-270 ◽  
Author(s):  
Philip M. Meyers ◽  
H. Christian Schumacher ◽  
William A. Gray ◽  
Johanna Fifi ◽  
John G. Gaudet ◽  
...  
Keyword(s):  
Case Report ◽  
Intravascular Ultrasound ◽  
Atherosclerotic Plaque ◽  
Intracranial Stenosis ◽  
Intraplaque Hemorrhage

scholarly journals Analysis of MicroRNAs Associated With Carotid Atherosclerotic Plaque Rupture With Thrombosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Peng Nie ◽  
Fan Yang ◽  
Fang Wan ◽  
Shuxuan Jin ◽  
Jun Pu
Keyword(s):  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Vascular Wall ◽  
Intraplaque Hemorrhage ◽  
Control Group ◽  
Left Carotid Artery ◽  
Mirna Microarray ◽  
Post Surgery ◽  
Atherosclerotic Plaque Rupture

Atherosclerosis is a progressive vascular wall inflammatory disease, and the rupture of atherosclerotic vulnerable plaques is the leading cause of morbidity and mortality worldwide. This study intended to explore the potential mechanisms behind plaque rupture and thrombosis in ApoE knockout mice. The spontaneous plaque rupture models were established, and left carotid artery tissues at different time points (1-, 2-, 4-, 6-, 8-, 12-, and 16-week post-surgery) were collected. By the extent of plaque rupture, plaque was defined as (1) control groups, (2) atherosclerotic plaque group, and (3) plaque rupture group. Macrophage (CD68), MMP-8, and MMP-13 activities were measured by immunofluorescence. Cytokines and inflammatory markers were measured by ELISA. The left carotid artery sample tissue was collected to evaluate the miRNAs expression level by miRNA-microarray. Bioinformatic analyses were conducted at three levels: (2) vs. (1), (3) vs. (2), and again in seven time series analysis. The plaque rupture with thrombus and intraplaque hemorrhage results peaked at 8 weeks and decreased thereafter. Similar trends were seen in the number of plaque macrophages and lipids, the expression of matrix metalloproteinase, and the atherosclerotic and plasma cytokine levels. MiRNA-microarray showed that miR-322-5p and miR-206-3p were specifically upregulated in the atherosclerotic plaque group compared with those in the control group. Meanwhile, miR-466h-5p was specifically upregulated in the plaque rupture group compared with the atherosclerotic plaque group. The highest incidence of plaque rupture and thrombosis occurred at 8 weeks post-surgery. miR-322-5p and miR-206-3p may be associated with the formation of atherosclerotic plaques. miR-466h-5p may promote atherosclerotic plaque rupture via apoptosis-related pathways.

scholarly journals Glycophorin C in atherosclerotic plaque is associated with major adverse cardiovascular events after carotid endarterectomy.

2021 ◽  
Author(s):  
Joost M. Mekke ◽  
Tim R. Sakkers ◽  
Maarten C. Verwer ◽  
Noortje van den Dungen ◽  
Yipei Song ◽  
...  
Keyword(s):  
Carotid Endarterectomy ◽  
Atherosclerotic Plaque ◽  
Cardiovascular Events ◽  
Neurological Symptoms ◽  
Intraplaque Hemorrhage ◽  
Major Adverse Cardiovascular Events ◽  
Symptomatic Carotid ◽  
Postoperative Risk ◽  
Male Patients ◽  
Glycophorin C

Introduction Histological assessment studies have identified the presence of intraplaque hemorrhage (IPH) as an indicator of plaque instability and resulting ischemic cerebral sequelae. Although the presence of IPH has been studied extensively in relation to neurological symptoms preceding carotid endarterectomy (CEA) or as a predictor for postoperative risk of major adverse cardiovascular events (MACE), the degree of IPH has not been studied before. Glycophorin, an erythrocyte-specific protein, has been suggested as a marker for the degree of previous hemorrhages in atherosclerotic plaque since erythrocytes are prominently present in IPH. We hypothesized that quantified plaque glycophorin C, as a proxy for the degree of IPH, is associated with destabilizing plaque characteristics, preprocedural symptoms, and increased postoperative risk for MACE. Methods We quantified glycophorin C and six other plaque characteristics with the slideToolkit method. We used human atherosclerotic plaque samples from 1971 consecutive asymptomatic and symptomatic (carotid endarterectomy) patients in the Athero-Express Biobank. Results The total area of glycophorin C in plaque was larger in individuals with a plaque with IPH compared to individuals with plaque without IPH (p<0.001). Quantified glycophorin C was significantly associated with ipsilateral pre-procedural neurological symptoms (OR:1.27, 95%CI:1.06-1.41, p=0.005). In addition, quantified glycophorin C was independently associated with an increased postoperative risk for MACE (HR:1.31, 95%CI:1.01-1.68, p=0.04). Stratified by sex, quantified glycophorin C was associated with an increased postoperative risk for MACE in male patients (HR:1.50, 95%CI:1.13-1.97, p=0.004), but not in female patients (HR:0.70, 95%CI:0.39-1.27, p=0.23). Conclusion Quantified glycophorin C, as a proxy for the degree of IPH, was independently associated with the presence of IPH, symptomatic preprocedural symptoms, and with an increased three-year postoperative risk of MACE. These findings indicate that quantified plaque glycophorin C can be considered as a marker for identifying male patients with a high residual risk for secondary MACE after CEA.

scholarly journals Serum insulin levels are associated with vulnerable plaque components in the carotid artery: the Rotterdam Study

2020 ◽  
Vol 182 (3) ◽  
pp. 343-350
Author(s):  
Blerim Mujaj ◽  
Daniel Bos ◽  
Maryam Kavousi ◽  
Aad van der Lugt ◽  
Jan A Staessen ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Carotid Artery ◽  
Atherosclerotic Plaque ◽  
Carotid Atherosclerosis ◽  
Serum Insulin ◽  
Intraplaque Hemorrhage ◽  
Rotterdam Study ◽  
Lipid Core ◽  
Insulin Levels ◽  
Glucose Levels

Background To investigate the association between fasting serum insulin and glucose levels with atherosclerotic plaque composition in the carotid artery. Impaired insulin and glucose levels are implicated in the etiology of cardiovascular disease; however, their influence on the formation and composition of atherosclerotic plaque remains unclear. Methods In 1740 participants (mean age 72.9 years, 46% women, 14.4% diabetes mellitus) from the population-based Rotterdam Study, we performed carotid MRI to evaluate the presence of calcification, lipid core, and intraplaque hemorrhage in carotid atherosclerosis. All participants also underwent blood sampling to obtain information on serum insulin and glucose levels. Using logistic regression models, we assessed the association of serum insulin and glucose levels (per s.d. and in tertiles) with the different plaque components, while adjusting for sex, age, intima-media thickness, and cardiovascular risk factors. Results Serum insulin levels were associated with the presence of intraplaque hemorrhage (adjusted odds ratio (OR): 1.42 (95% CI: 1.12–1.7)) We found no association with the presence of calcification or lipid core. Sensitivity analyses restricted to individuals without diabetes mellitus yielded similar results. No associations were found between serum glucose levels and any of the plaque components. Conclusions Serum insulin levels are associated with the presence of vulnerable components of carotid plaque, specifically with intraplaque hemorrhage. These findings suggest a complex role for serum insulin in the pathophysiology of carotid atherosclerosis and in plaque vulnerability.

Abstract 1143: Imaging of Vasa Vasorum in Atherosclerotic Plaque with 99m Tc-labeled single chain-VEGF

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Satoru Ohshima ◽  
Shinichiro Fujimoto ◽  
Sotirios Tsimikas ◽  
Frank D Kolodgie ◽  
Renu Virmani ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Ex Vivo ◽  
Imaging Modality ◽  
Atherosclerotic Lesion ◽  
Vasa Vasorum ◽  
Intraplaque Hemorrhage ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Single Chain

Introduction: Adventitial vasa vasorum proliferation and neointimal neovascularization are associated with intraplaque hemorrhage, expansion of necrotic core and hence plaque vulnerability. Increased expression of VEGF and its receptors accompany neoangiogenic process. We used 99m Tc -labeled single chain VEGF (TcV) for developing potentially noninvasive imaging modality in experimentally induced aortic atherosclerotic lesion. Methods : Noninva-sive radionuclide imaging was performed with TcV (6.85 ±0. 27 mCi) in 6 NZW rabbits receiving high cholesterol diet (0.2% cholesterol, 4% fat) for one year and compared with 3 control rabbits receiving normal rabbit chow. Four hours after intravenous administration of TcV, micro SPECT/microCT imaging was performed for in vivo localization of tracer activity. Aortas were then explanted, and gamma counted for determination of % injected dose per gram (%ID/g). The aortas were then submitted for histopathologic characterization. Results : The uptake in thoracic aorta was clearly visualized non-invasively by TcV in vivo imaging in 4 of 5 rabbits in hypercholesterolemic rabbits, but not in the control animals. The %ID/g of each parts of aorta in hypercholesterolemic rabbits (Arch : 0.036 ± 0.020 %, Thoracic : 0.026 ± 0.012 %, Abd : 0.019 ± 0.009 %) was about 2.5-fold higher than that in control group (Arch : 0.014 ± 0.004 %, Thoracic : 0.009 ± 0.003 %, Abd : 0.009 ± 0.003 %) (figure a ). Ex vivo images of each group are shown as figure b . Conclusions : This preliminary study suggests a potentially novel strategy for non-invasive imaging of neoangiogenesis in atherosclerotic plaque and may allow identification of unstable plaques.

3D In Vivo IVUS-Based Anisotropic FSI Models With Cyclic Bending for Human Coronary Atherosclerotic Plaque Mechanical Analysis

2009 ◽  
Author(s):  
Dalin Tang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Pamela K. Woodard ◽  
Kristen Billiar ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Computational Models ◽  
Material Model ◽  
3D Models ◽  
Mechanical Analysis ◽  
Intraplaque Hemorrhage ◽  
Plaque Vulnerability ◽  
Cardiovascular Research ◽  
Cyclic Bending

Assessing atherosclerotic plaque vulnerability based on limited in vivo patient data has been a major challenge in cardiovascular research and clinical practice. Considerable advances in medical imaging technology have been made in recent years to identify vulnerable atherosclerotic carotid plaques in vivo with information about plaque components including lipid-rich necrotic pools, calcification, intraplaque hemorrhage, loose matrix, thrombosis, and ulcers, subject to resolution limitations of current technology [1]. Image-based computational models have also been developed which combine mechanical analysis with image technology aiming for more accurate assessment of plaque vulnerability and better diagnostic and treatment decisions [2]. However, 3D models with fluid-structure interactions (FSI), cyclic bending and anisotropic properties based on in vivo IVUS images for human coronary atherosclerotic plaques are lacking in the current literature. In this paper, we introduce 3D FSI models based on in vivo IVUS images to perform mechanical analysis for human coronary plaques. Cyclic bending is included to represent deformation caused by cardiac motion. An anisotropic material model was used for the vessel so that the models would be more realistic for more accurate computational flow and stress/strain predictions.

Abstract 1947: Chymase Inhibition Reduces the Incidence of Intraplaque Hemorrhage and Induces a Stable Atherosclerotic Plaque Phenotype in ApoE Deficient Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ilze Bot ◽  
Marijke M Westra ◽  
Sandra H van Heiningen ◽  
Hans Hilpert ◽  
Inge M Lankhuizen ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Atherosclerotic Plaque ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Intraplaque Hemorrhage ◽  
Plaque Stability ◽  
Plaque Destabilization

Mast cells are abundantly present in perivascular tissue during atherosclerotic plaque progression and were previously demonstrated to contribute significantly to plaque destabilization. In this study, we aimed to investigate to what extent inhibition of chymase, one of the mast cell proteases, could enhance plaque stability. We demonstrated earlier that the specific chymase inhibitor RO501 (1 μM) was able to quench mast cell activation in vitro , as illustrated by a decreased β-hexosaminidase (−41% and −80%, respectively; P<0.05) as well as chymase activity in the releasate of activated MC/9 and peritoneal mast cells (−71% and −65%, respectively; P<0.05). Next, we assessed whether chymase inhibition was also effective in vivo. Atherosclerotic carotid artery lesions were induced in ApoE −/− mice by perivascular collar placement and mast cells were activated by DNP challenge systemically during lesion development. RO501 (50 mg/kg/day) was administered as diet supplement, leading to serum concentrations of ~2 μM. While plaque size after 6 weeks of treatment did not differ, collagen content of the lesions was 2-fold enhanced in mice treated with RO501 compared to controls (1.4 ± 0.5% and 0.7 ± 0.2%, respectively). This was accompanied by a significant decrease in necrotic core size of the plaques (controls: 52 ± 3% versus RO501: 41 ± 4%, P<0.05). To determine the effects of chymase inhibition after acute mast cell activation in advanced plaques, perivascular mast cells were focally activated in the adventitia of advanced lesions in ApoE −/− mice, which were treated with RO501 as described above. At three days after focal mast cell challenge, the incidence of intraplaque hemorrhage (IPH) was inhibited from 23% in control mice to 4.5% in RO501 treated mice, while also the plaque erythrocyte area was reduced by >90% from 1.2 ± 0.6*10 3 to 0.1 ± 0.08*10 3 μm 2 (P<0.05). Also, we observed a reduction in apoptotic cells (RO501: 0.68 ± 0.20% vs. 1.01 ± 0.36% for IPH negative controls and 1.23 ± 0.42% for IPH + plaques). In conclusion, our data suggest that chymase inhibition at least partly prevents the detrimental effects of perivascular mast cells on plaque stability, identifying chymase inhibition as a new therapeutic approach in the prevention of acute coronary syndromes.

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