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Atherosclerotic plaque contains iron positive cells such as subendothelial macrophages. Macrophages accumulate in the layers of arteries and contribute to the formation of atherosclerotic plaque. The presence of iron positive macrophages is a characteristic of atherosclerotic plaque building up in arteries.
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204 prevalence of inflammatory cells in non ruptured atherosclerotic plaques
204 prevalence of inflammatory cells in non ruptured atherosclerotic plaquesSociety for Heart Attack Prevention and Eradication
This document summarizes a post-mortem study examining the prevalence of inflammatory cells in non-ruptured atherosclerotic plaques. The study found that moderate or heavy staining for macrophages was present in 45% of femoral artery cross-sections and 84% of femoral arteries had at least one cross-section with moderate/heavy inflammation. There was no observed relationship between the degree of inflammation in the left and right coronary arteries within individuals, indicating the level of local inflammation is locally determined with low predictive value for other arteries.3rd vulnerable plaque rumberger 3 16-02 3
1) Clinical data confirms that coronary calcium detected by electron beam computed tomography (EBT) is found in 96% of patients presenting with or developing acute coronary syndromes, and that these patients have significantly greater coronary artery calcium scores at baseline compared to asymptomatic matched individuals.
2) Histologic studies show that coronary artery calcium occurs in all types of plaques, including stable (43%), rupture-prone (54%), and erosion-prone (77%) plaques.
3) Therefore, coronary artery calcium detected by imaging is a marker of atherosclerotic plaque burden but not necessarily a marker of stable or unstable plaque, as there is considerable overlap in calcium presence between different plaque types.
Aha 2 mr lipid
This document summarizes atherosclerosis and atherothrombosis through multiple figures and references. It describes:
I) The stages of atherosclerosis from early asymptomatic lesions to advanced lesions that can cause angina or acute coronary syndrome.
II) Biological processes involved in atherosclerosis progression and complications like thrombosis, including inflammation, apoptosis, tissue factor expression, and neovascularization.
III) Effects of lipid lowering and PPAR-γ agonists on reducing atherosclerotic plaques, inflammation, and apoptosis in animal and human studies using techniques like MRI and immunohistochemistry.
035 respiratory infection of apo e ko mice
1) Acute respiratory infection caused by influenza virus led to excessive plaque inflammation in the aortas of ApoE knockout mice.
2) One third of infected mice showed inflammatory infiltrates associated with platelet clusters and fibrin near the plaques.
3) The study aimed to investigate if acute respiratory infection can increase plaque inflammation and macrophage infiltration, and to examine related cytokine and receptor expression over the longer term.
248 carotid atherosclerotic lesion models
This document describes models of human carotid arteries that can be used for quality control in clinical trials evaluating atherosclerotic lesions with MRI endpoints. The models are made from cadaveric human carotid arteries and have attributes that closely resemble real carotid arteries, including different stages of atherosclerotic lesions. The models are housed in holders that are compatible with MRI and allow indexing of reference sites. Documentation is provided on the models' composition and standardized MRI acquisition parameters to enable reproducible imaging as an internal standard over long periods.
208 peter libby
Dr. Peter Libby earned his medical degree from the University of California, San Diego and completed his training in internal medicine and cardiology at Brigham and Women's Hospital. He is currently the Mallinckrodt Professor of Medicine at Harvard Medical School and Chief of the Cardiovascular Division at Brigham and Women's Hospital. Dr. Libby's research focuses on the role of inflammation in vascular diseases like atherosclerosis. He has published extensively on cardiovascular medicine and atherosclerosis in journals like Circulation and The New England Journal of Medicine.
044 mice mri
This study aimed to image atherosclerotic plaques in the aortas of Apo E deficient mice using MRI. To visualize the aorta, contrast agent was injected into mice both while inside and outside of the MRI scanner. Respiratory gating was used to reduce motion artifacts from breathing by intubating mice and providing ventilation. Initial scans showed the aorta but more optimization is needed, such as decreasing the dose of iron contrast agent used and adding ECG gating to address motion from the heart. Future plans include further refining the MRI protocol and beginning a similar study in rabbits.
Aeha multipeptide and passive
This document summarizes research on developing vaccines and passive immunization for atherosclerosis. Key points:
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- Active immunization of mice with specific apo B-100 peptide sequences reduced atherosclerosis by up to 70% and shifted plaque composition.
- Passive immunization of mice with human antibodies against two peptides also reduced atherosclerosis and macrophage content in plaques.
- Some human IgM levels against oxidized LDL peptides correlate with severity of atherosclerosis and plaque composition.
- The research suggests certain oxidized LDL peptides could be targets for vaccines or passive immunotherapy to treat atherosclerosis
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204 prevalence of inflammatory cells in non ruptured atherosclerotic plaques
204 prevalence of inflammatory cells in non ruptured atherosclerotic plaquesSociety for Heart Attack Prevention and Eradication
This document summarizes a post-mortem study examining the prevalence of inflammatory cells in non-ruptured atherosclerotic plaques. The study found that moderate or heavy staining for macrophages was present in 45% of femoral artery cross-sections and 84% of femoral arteries had at least one cross-section with moderate/heavy inflammation. There was no observed relationship between the degree of inflammation in the left and right coronary arteries within individuals, indicating the level of local inflammation is locally determined with low predictive value for other arteries.3rd vulnerable plaque rumberger 3 16-02 3
1) Clinical data confirms that coronary calcium detected by electron beam computed tomography (EBT) is found in 96% of patients presenting with or developing acute coronary syndromes, and that these patients have significantly greater coronary artery calcium scores at baseline compared to asymptomatic matched individuals.
2) Histologic studies show that coronary artery calcium occurs in all types of plaques, including stable (43%), rupture-prone (54%), and erosion-prone (77%) plaques.
3) Therefore, coronary artery calcium detected by imaging is a marker of atherosclerotic plaque burden but not necessarily a marker of stable or unstable plaque, as there is considerable overlap in calcium presence between different plaque types.
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I) The stages of atherosclerosis from early asymptomatic lesions to advanced lesions that can cause angina or acute coronary syndrome.
II) Biological processes involved in atherosclerosis progression and complications like thrombosis, including inflammation, apoptosis, tissue factor expression, and neovascularization.
III) Effects of lipid lowering and PPAR-γ agonists on reducing atherosclerotic plaques, inflammation, and apoptosis in animal and human studies using techniques like MRI and immunohistochemistry.
035 respiratory infection of apo e ko mice
1) Acute respiratory infection caused by influenza virus led to excessive plaque inflammation in the aortas of ApoE knockout mice.
2) One third of infected mice showed inflammatory infiltrates associated with platelet clusters and fibrin near the plaques.
3) The study aimed to investigate if acute respiratory infection can increase plaque inflammation and macrophage infiltration, and to examine related cytokine and receptor expression over the longer term.
248 carotid atherosclerotic lesion models
This document describes models of human carotid arteries that can be used for quality control in clinical trials evaluating atherosclerotic lesions with MRI endpoints. The models are made from cadaveric human carotid arteries and have attributes that closely resemble real carotid arteries, including different stages of atherosclerotic lesions. The models are housed in holders that are compatible with MRI and allow indexing of reference sites. Documentation is provided on the models' composition and standardized MRI acquisition parameters to enable reproducible imaging as an internal standard over long periods.
208 peter libby
Dr. Peter Libby earned his medical degree from the University of California, San Diego and completed his training in internal medicine and cardiology at Brigham and Women's Hospital. He is currently the Mallinckrodt Professor of Medicine at Harvard Medical School and Chief of the Cardiovascular Division at Brigham and Women's Hospital. Dr. Libby's research focuses on the role of inflammation in vascular diseases like atherosclerosis. He has published extensively on cardiovascular medicine and atherosclerosis in journals like Circulation and The New England Journal of Medicine.
044 mice mri
This study aimed to image atherosclerotic plaques in the aortas of Apo E deficient mice using MRI. To visualize the aorta, contrast agent was injected into mice both while inside and outside of the MRI scanner. Respiratory gating was used to reduce motion artifacts from breathing by intubating mice and providing ventilation. Initial scans showed the aorta but more optimization is needed, such as decreasing the dose of iron contrast agent used and adding ECG gating to address motion from the heart. Future plans include further refining the MRI protocol and beginning a similar study in rabbits.
Aeha multipeptide and passive
This document summarizes research on developing vaccines and passive immunization for atherosclerosis. Key points:
- Antibodies in human plasma bind to oxidized LDL peptide sequences, indicating an immune response against atherosclerosis antigens.
- Active immunization of mice with specific apo B-100 peptide sequences reduced atherosclerosis by up to 70% and shifted plaque composition.
- Passive immunization of mice with human antibodies against two peptides also reduced atherosclerosis and macrophage content in plaques.
- Some human IgM levels against oxidized LDL peptides correlate with severity of atherosclerosis and plaque composition.
- The research suggests certain oxidized LDL peptides could be targets for vaccines or passive immunotherapy to treat atherosclerosis
Arterial remodeling paul sch
This study used intravascular ultrasound to examine arterial remodeling and plaque characteristics in patients with stable angina versus unstable coronary syndromes. It found that lesions in unstable patients had greater plaque burden despite similar lumen narrowing, and a greater extent of positive arterial remodeling compared to stable patients. Lesions in unstable patients also tended to have more echolucent plaque morphology. The results suggest that bulky, remodeled plaques may be more prone to rupture and cause acute coronary syndromes.
213 oral apo ai mimetic peptide for reduction of atherosclerosis
213 oral apo ai mimetic peptide for reduction of atherosclerosisSociety for Heart Attack Prevention and Eradication
I. The document discusses research on using oral apo A-I mimetic peptides synthesized from D-amino acids to reduce atherosclerosis in mice. These peptides dramatically inhibited atherosclerosis by up to 79% without changing total plasma or HDL cholesterol levels.
II. The peptides are thought to protect against atherosclerosis through reverse cholesterol transport and removing oxidized lipids. Orally administered D-amino acid peptides were shown to be stable in circulation and enhance HDL's ability to prevent LDL oxidation.
III. The research suggests D-amino acid apo A-I mimetic peptides could provide a potential oral treatment for atherosclerosis and other diseases caused by oxidized lipids.Vulnerable patient mar 04
This document discusses triggers for sudden cardiac arrest (SCA) and death (SCD). It notes that over 2/3 of SCD cases are unable to be predicted due to a lack of well-established risk factors. While population risk factors can identify at-risk groups, they cannot predict risk for individuals. The document explores various biological, anatomical, and environmental factors that can precipitate fatal arrhythmias and discusses how the timing of transient initiating events is critical for the development of ventricular tachyarrhythmias. It emphasizes that myocardial electrophysiological processes likely determine the onset or lack of VT/VF/SCD and that immediate access to automated external defibrillators is needed to save lives.
3rd vulnerable plaque rumberger 3 16-02 1
Electron beam tomography (EBT) is a scanning method introduced in 1984 that can rapidly image the heart using a scanning electron beam. EBT has been used in over 600 scientific papers to study cardiac imaging and determine coronary artery calcium. Coronary artery calcification is the hardening of the coronary arteries that has been known for 300 years but is now understood to be an active process that can occur early in atherosclerotic plaque development and is intimately involved in the pathophysiology of coronary artery disease, regulated similarly to bone mineralization and repair. EBT images show calcification appears centrally within atherosclerotic plaques.
218 pharmacologic stabilization of vulnerable plaque
218 pharmacologic stabilization of vulnerable plaqueSociety for Heart Attack Prevention and Eradication
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The document discusses that less obstructive plaques pose a greater risk of coronary occlusion than severely obstructed plaques due to their greater numbers. It also states that the aggregate risk of rupture from many non-significant lesions exceeds that of fewer significant lesions, so a myocardial infarction is more likely to originate from a non-significant lesion. Additionally, it explains that while electron beam tomography (EBT) cannot identify vulnerable plaques directly, it can identify vulnerable patients based on their coronary artery calcium (CAC) scores and percentile ranks, as risk increases with higher scores. EBT is also useful for estimating prognosis and tracking changes in plaque in response to treatment over time.
4th vulnerable plaque symposium
This study found that temperature heterogeneity in atherosclerotic plaques in rabbits is associated with macrophage accumulation and metalloproteinase (MMP) activity. Thermography detected hot and cold areas that correlated with higher macrophage levels and MMP-2 and MMP-9 activity. More macrophages and MMPs were present in hot areas compared to cold areas of plaques. However, blood flow obscured temperature differences, so flow was stopped to measure temperatures accurately. The results suggest temperature changes detect active macrophages and their effects on plaque vulnerability.
255 in vivo coronary sinus thermography
This document discusses in vivo coronary sinus thermography. It shows graphs of temperature differences over time between the coronary sinus and right atrium in controls and CAD patients, finding a significant difference. It lists ongoing research using thermography to study tachycardia, arrhythmias, medication effects, heart failure, and organ function. It concludes that new catheters are being developed to increase thermography sensitivity, it is being used in other parts of the cardiovascular system, and coronary sinus temperature may provide future information about patients, not just plaque.
037 association for eradication of heart attack
This document discusses vulnerable plaque and the history of research on plaque vulnerability. It provides definitions of vulnerable plaque and different types of vulnerable plaque such as rupture-prone plaques. The document outlines pioneers in plaque research and emerging techniques for detecting vulnerable plaque both invasively, such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT), and non-invasively using magnetic resonance imaging (MRI). It summarizes the natural history of vulnerable plaques and their role in acute coronary events.
Aha periadventitial fat
1. The study found that periadventitial fat tissue in atherosclerotic mouse models takes up more SPIO nanoparticles, a MRI contrast agent, than normal mice, and contains more macrophage-like cells.
2. Preliminary studies in rabbits and humans also showed greater SPIO uptake and more CD68+ cells in periadventitial fat of diseased vessels compared to healthy vessels.
3. The cells in periadventitial fat share properties with stromal vascular fraction cells and may introduce inflammation near plaques, affecting plaque vulnerability, though more study is needed to understand their significance in disease progression.
Vulnerable plaque overview
Vulnerable plaque refers to dangerous forms of atherosclerotic plaques that can rupture or induce thrombosis, disrupting blood flow. The document discusses the history and research around vulnerable plaque, including pioneers in the field and emerging techniques to detect vulnerable plaque such as intravascular ultrasound, optical coherence tomography, and magnetic resonance imaging. It summarizes that vulnerable plaques are typically characterized by a thin fibrous cap, large lipid core, and presence of macrophages.
AHA SHAPE Symposium 2017 Dr. Naghavi Presentation
AHA SHAPE Symposium 2017 Dr. Naghavi PresentationSociety for Heart Attack Prevention and Eradication
This document discusses developing an artificial intelligence system to predict short-term cardiovascular disease (CVD) events. The goal is to eradicate unexpected heart attacks by predicting risk similar to hurricane forecasts. Existing studies are cited that show over 50% of heart attacks are first symptoms of underlying disease. The document outlines previous work by SHAPE to define vulnerable patients and release guidelines. It proposes using machine learning on existing cohort data to develop algorithms predicting heart attacks within 12 months, and validate the system. The hope is this can trigger preventative actions and add over 10 years to life expectancy. Funding is needed to implement the proposed "Machine Learning Vulnerable Patient Project".AHA SHAPE Symposium 2017 Dr. Kloner Presentation
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AHA SHAPE Symposium 2017 Dr. Greenland Presentation
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A machine learning model outperformed the ACC/AHA Pooled Cohort Equations Risk Calculator in detecting high-risk asymptomatic individuals and recommending statin treatment for cardiovascular disease prevention in the Multi-Ethnic Study of Atherosclerosis. The machine learning model used support vector machines and data augmentation to derive a CVD risk predictor from nine variables in the MESA study population. It demonstrated higher sensitivity, specificity, and AUC compared to the ACC/AHA risk calculator, recommending statin treatment for fewer individuals while missing fewer cardiovascular events.
AHA SHAPE Symposium 2017 Dr. Slomka Presentation
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Vu lplaque1 pasterkamp
This document summarizes a post-mortem study examining the prevalence of inflammatory cells in non-ruptured atherosclerotic plaques. The study found that moderate or heavy staining for macrophages was present in 45% of femoral artery cross-sections and 84% of femoral arteries had at least one cross-section with moderate/heavy inflammation. There was no observed relationship between the degree of inflammation in the left and right coronary arteries within individuals, indicating the level of local inflammation is locally determined with little predictive value for other arteries.
Vulnerable plaque vulnerable patient
The document provides guidelines for defining vulnerable plaque and vulnerable patients from the Association for Eradication of Heart Attack. It outlines major and minor histopathological and clinical criteria for vulnerable plaque including active inflammation, thin fibrous cap with large lipid core, endothelial denudation, and stenosis. Potential screening and diagnostic methods are discussed at the plaque, systemic, and blood levels ranging from non-invasive imaging to intravascular techniques. Different types of vulnerable plaque that can cause acute coronary events are also categorized.
Vulnerable patient talk in poland
The document summarizes research on vulnerable plaques and markers of vulnerability. It finds that ruptured plaques are the most common type of culprit lesion, accounting for around 70% of cases. Major criteria for defining vulnerable plaque include outward remodeling, endothelial dysfunction, and a thin fibrous cap with a large lipid core. Both plaque morphology and activity need to be assessed to identify vulnerability.
Vulnerable patient slides without movies
This document contains a summary of a presentation on vulnerable patient syndrome. It includes PowerPoint slides and videos on defining and identifying vulnerable plaques and patients. It thanks sponsors for their support of the educational event. The slides define vulnerable plaques as those likely to rupture in the future, causing heart attacks, and provide criteria for identifying them based on morphology and activity. Biomarkers and conditions that increase plaque and myocardial vulnerability are also summarized. The presentation outlines a pyramid approach for screening, diagnosing, and treating vulnerable patients annually to help reduce heart attacks and their high costs.
Vulnerable (thrombogenic blood
This document summarizes presentations from symposia on vulnerable plaque and discusses the relationship between plaque, blood, and patients in atherothrombosis. It notes that multiple factors like diabetes, smoking, and hyperlipidemia can make blood more thrombogenic and moderate the severity of acute events after plaque rupture. Statins, aspirin, and other drugs that target tissue factor or thrombin pathways may be promising antithrombotic agents by inhibiting thrombosis initiation and propagation.
Vuln shape aha 2005
The document discusses vulnerable plaque and challenges in detecting and treating it. It describes various imaging techniques for detecting vulnerable plaque such as thermography, MRI, CT angiography, and optical coherence tomography. However, it notes that while these can identify high-risk features, it remains unclear what exactly defines vulnerable plaque and whether imaging findings truly correlate with risk. The document also notes that while statins reduce events, the relationship between plaque burden and events is unclear, and better defining and detecting the disease is still needed before new therapies can be developed.
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Arterial remodeling paul sch
This study used intravascular ultrasound to examine arterial remodeling and plaque characteristics in patients with stable angina versus unstable coronary syndromes. It found that lesions in unstable patients had greater plaque burden despite similar lumen narrowing, and a greater extent of positive arterial remodeling compared to stable patients. Lesions in unstable patients also tended to have more echolucent plaque morphology. The results suggest that bulky, remodeled plaques may be more prone to rupture and cause acute coronary syndromes.
213 oral apo ai mimetic peptide for reduction of atherosclerosis
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II. The peptides are thought to protect against atherosclerosis through reverse cholesterol transport and removing oxidized lipids. Orally administered D-amino acid peptides were shown to be stable in circulation and enhance HDL's ability to prevent LDL oxidation.
III. The research suggests D-amino acid apo A-I mimetic peptides could provide a potential oral treatment for atherosclerosis and other diseases caused by oxidized lipids.Vulnerable patient mar 04
This document discusses triggers for sudden cardiac arrest (SCA) and death (SCD). It notes that over 2/3 of SCD cases are unable to be predicted due to a lack of well-established risk factors. While population risk factors can identify at-risk groups, they cannot predict risk for individuals. The document explores various biological, anatomical, and environmental factors that can precipitate fatal arrhythmias and discusses how the timing of transient initiating events is critical for the development of ventricular tachyarrhythmias. It emphasizes that myocardial electrophysiological processes likely determine the onset or lack of VT/VF/SCD and that immediate access to automated external defibrillators is needed to save lives.
3rd vulnerable plaque rumberger 3 16-02 1
Electron beam tomography (EBT) is a scanning method introduced in 1984 that can rapidly image the heart using a scanning electron beam. EBT has been used in over 600 scientific papers to study cardiac imaging and determine coronary artery calcium. Coronary artery calcification is the hardening of the coronary arteries that has been known for 300 years but is now understood to be an active process that can occur early in atherosclerotic plaque development and is intimately involved in the pathophysiology of coronary artery disease, regulated similarly to bone mineralization and repair. EBT images show calcification appears centrally within atherosclerotic plaques.
218 pharmacologic stabilization of vulnerable plaque
218 pharmacologic stabilization of vulnerable plaqueSociety for Heart Attack Prevention and Eradication
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The document discusses that less obstructive plaques pose a greater risk of coronary occlusion than severely obstructed plaques due to their greater numbers. It also states that the aggregate risk of rupture from many non-significant lesions exceeds that of fewer significant lesions, so a myocardial infarction is more likely to originate from a non-significant lesion. Additionally, it explains that while electron beam tomography (EBT) cannot identify vulnerable plaques directly, it can identify vulnerable patients based on their coronary artery calcium (CAC) scores and percentile ranks, as risk increases with higher scores. EBT is also useful for estimating prognosis and tracking changes in plaque in response to treatment over time.
4th vulnerable plaque symposium
This study found that temperature heterogeneity in atherosclerotic plaques in rabbits is associated with macrophage accumulation and metalloproteinase (MMP) activity. Thermography detected hot and cold areas that correlated with higher macrophage levels and MMP-2 and MMP-9 activity. More macrophages and MMPs were present in hot areas compared to cold areas of plaques. However, blood flow obscured temperature differences, so flow was stopped to measure temperatures accurately. The results suggest temperature changes detect active macrophages and their effects on plaque vulnerability.
255 in vivo coronary sinus thermography
This document discusses in vivo coronary sinus thermography. It shows graphs of temperature differences over time between the coronary sinus and right atrium in controls and CAD patients, finding a significant difference. It lists ongoing research using thermography to study tachycardia, arrhythmias, medication effects, heart failure, and organ function. It concludes that new catheters are being developed to increase thermography sensitivity, it is being used in other parts of the cardiovascular system, and coronary sinus temperature may provide future information about patients, not just plaque.
037 association for eradication of heart attack
This document discusses vulnerable plaque and the history of research on plaque vulnerability. It provides definitions of vulnerable plaque and different types of vulnerable plaque such as rupture-prone plaques. The document outlines pioneers in plaque research and emerging techniques for detecting vulnerable plaque both invasively, such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT), and non-invasively using magnetic resonance imaging (MRI). It summarizes the natural history of vulnerable plaques and their role in acute coronary events.
Aha periadventitial fat
1. The study found that periadventitial fat tissue in atherosclerotic mouse models takes up more SPIO nanoparticles, a MRI contrast agent, than normal mice, and contains more macrophage-like cells.
2. Preliminary studies in rabbits and humans also showed greater SPIO uptake and more CD68+ cells in periadventitial fat of diseased vessels compared to healthy vessels.
3. The cells in periadventitial fat share properties with stromal vascular fraction cells and may introduce inflammation near plaques, affecting plaque vulnerability, though more study is needed to understand their significance in disease progression.
Vulnerable plaque overview
Vulnerable plaque refers to dangerous forms of atherosclerotic plaques that can rupture or induce thrombosis, disrupting blood flow. The document discusses the history and research around vulnerable plaque, including pioneers in the field and emerging techniques to detect vulnerable plaque such as intravascular ultrasound, optical coherence tomography, and magnetic resonance imaging. It summarizes that vulnerable plaques are typically characterized by a thin fibrous cap, large lipid core, and presence of macrophages.
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213 oral apo ai mimetic peptide for reduction of atherosclerosis
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This document discusses developing an artificial intelligence system to predict short-term cardiovascular disease (CVD) events. The goal is to eradicate unexpected heart attacks by predicting risk similar to hurricane forecasts. Existing studies are cited that show over 50% of heart attacks are first symptoms of underlying disease. The document outlines previous work by SHAPE to define vulnerable patients and release guidelines. It proposes using machine learning on existing cohort data to develop algorithms predicting heart attacks within 12 months, and validate the system. The hope is this can trigger preventative actions and add over 10 years to life expectancy. Funding is needed to implement the proposed "Machine Learning Vulnerable Patient Project".AHA SHAPE Symposium 2017 Dr. Kloner Presentation
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Vu lplaque1 pasterkamp
This document summarizes a post-mortem study examining the prevalence of inflammatory cells in non-ruptured atherosclerotic plaques. The study found that moderate or heavy staining for macrophages was present in 45% of femoral artery cross-sections and 84% of femoral arteries had at least one cross-section with moderate/heavy inflammation. There was no observed relationship between the degree of inflammation in the left and right coronary arteries within individuals, indicating the level of local inflammation is locally determined with little predictive value for other arteries.
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The document provides guidelines for defining vulnerable plaque and vulnerable patients from the Association for Eradication of Heart Attack. It outlines major and minor histopathological and clinical criteria for vulnerable plaque including active inflammation, thin fibrous cap with large lipid core, endothelial denudation, and stenosis. Potential screening and diagnostic methods are discussed at the plaque, systemic, and blood levels ranging from non-invasive imaging to intravascular techniques. Different types of vulnerable plaque that can cause acute coronary events are also categorized.
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The document summarizes research on vulnerable plaques and markers of vulnerability. It finds that ruptured plaques are the most common type of culprit lesion, accounting for around 70% of cases. Major criteria for defining vulnerable plaque include outward remodeling, endothelial dysfunction, and a thin fibrous cap with a large lipid core. Both plaque morphology and activity need to be assessed to identify vulnerability.
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This document summarizes presentations from symposia on vulnerable plaque and discusses the relationship between plaque, blood, and patients in atherothrombosis. It notes that multiple factors like diabetes, smoking, and hyperlipidemia can make blood more thrombogenic and moderate the severity of acute events after plaque rupture. Statins, aspirin, and other drugs that target tissue factor or thrombin pathways may be promising antithrombotic agents by inhibiting thrombosis initiation and propagation.
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The document discusses vulnerable plaque and challenges in detecting and treating it. It describes various imaging techniques for detecting vulnerable plaque such as thermography, MRI, CT angiography, and optical coherence tomography. However, it notes that while these can identify high-risk features, it remains unclear what exactly defines vulnerable plaque and whether imaging findings truly correlate with risk. The document also notes that while statins reduce events, the relationship between plaque burden and events is unclear, and better defining and detecting the disease is still needed before new therapies can be developed.
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1) The study examined 92 hearts from patients with severe coronary artery disease who died suddenly. The hearts were sectioned and plaque types were classified.
2) The number of "vulnerable" plaques, particularly thin cap atheromas, was highest in hearts of patients who died from acute plaque rupture and lowest in those with incidental disease.
3) Thin cap atheromas and other unstable plaque types were concentrated in the proximal coronary segments, similar to the distribution of plaque ruptures. The study suggests vulnerable plaques contribute to acute coronary syndromes and are non-uniformly distributed within the coronary arteries.
Vp watch editorial_slide 25short-
1) Drug-coated stents, particularly those coated with sirolimus, have shown promise in reducing restenosis compared to bare metal stents. Sirolimus inhibits cell proliferation and has been shown in studies to reduce intimal hyperplasia and restenosis in animal models by 50% or more.
2) A study by Suzuki et al. found that a sirolimus-coated stent reduced restenosis by 50% through inhibiting cellular proliferation in a dose-dependent manner compared to a bare metal stent. Adding dexamethasone to the coating did not provide additional benefit.
3) If results of the RAVEL clinical trial showing "zero" restenosis out to 5 years
Vp watch editorial_slide25
This document discusses drug-coated stents for preventing restenosis. It summarizes a study showing that stents coated with sirolimus via a polymer matrix reduced restenosis by 50% by inhibiting cell proliferation. Adding dexamethasone provided no additional benefit. Other studies also showed sirolimus inhibits smooth muscle cell proliferation. If results of the RAVEL trial showing "zero" restenosis at 210 days hold true long-term, sirolimus-coated stents may become the standard therapy for coronary revascularization. Questions are raised about whether coating vulnerable plaques could be a primary treatment and if multiple vulnerable plaques would all be stented.
Vp watch editorial_slide25short-
1) Drug-coated stents, particularly those coated with sirolimus, have shown promise in reducing restenosis compared to bare metal stents. Sirolimus inhibits cell proliferation and has been shown in studies to reduce intimal hyperplasia and restenosis in animal models by 50% or more.
2) A study by Suzuki et al. found that a sirolimus-coated stent reduced restenosis by 50% through inhibiting cellular proliferation in a dose-dependent manner compared to a bare metal stent. Adding dexamethasone to the coating did not provide additional benefit.
3) If results of the RAVEL clinical trial showing "zero" restenosis out to 5 years
Vp watch2002
I. This document discusses various animal models that have been used to study atherosclerosis and plaque rupture, including quail, pigeons, chickens, dogs, monkeys, pigs, rats, rabbits, and mice. It provides details on the types of lesions developed and similarities to human disease for each model.
II. The double knockout LDL/apoE mice are highlighted as offering improvements in studying clinical complications of atherosclerosis like human heart disease. However, it is unclear how closely they model vulnerable plaques.
III. Questions are raised about how closely the coagulation systems of these animal models resemble humans and whether any model fully captures repeated plaque ruptures and the role of aging in natural history as seen in humans.
Vp symposium31602
Trans-Blood Vision is a patented infrared technique that uses short-wave infrared wavelengths to see directly through blood. It has the potential to find vulnerable plaque lesions without first entering them, determine their size and surface characteristics in high resolution, and look at their material constituents both on and below the surface. While it cannot provide direct visual guidance for therapy or penetrate as deeply as ultrasound, combining it with augmentative technologies could allow for real-time multi-mode detection, analysis, and therapy guidance of vulnerable plaque lesions. The document concludes that Trans-Blood Vision warrants significant investigation, possibly in combination with other emerging technologies.
Vpschoenhagen
This study used intravascular ultrasound to examine arterial remodeling and plaque characteristics in 131 patients with either stable angina or recent unstable symptoms. Patients with unstable presentations had greater plaque burden at the culprit lesion despite similar luminal narrowing, and a greater extent of positive arterial remodeling compared to those with stable angina. The culprit lesions in unstable patients also showed a higher rate of echolucent plaque morphology. This suggests that bulky, remodeled plaques may be more vulnerable to rupture, leading to acute coronary syndromes. Further prospective study is needed to better understand the relationship between clinical presentation and plaque features.
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The document discusses ways to improve prediction of coronary events beyond the traditional Framingham Risk Score (FRS). It finds that adding C-reactive protein (CRP) measurement to the FRS results in a better model that significantly improves risk prediction, especially for those at intermediate risk. Measuring coronary artery calcium via scanning also seems to enhance prediction over the FRS alone. However, these findings require replication in other patient populations before firmly concluding CRP and calcium scoring can modify physician interpretation of patient risk based on the FRS.
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The document discusses magnetic resonance imaging (MRI) studies of atherosclerosis in human carotid arteries. It summarizes several studies examining features of carotid plaques such as calcified regions, neovasculature and necrotic cores, reproducibility of measurements, appearance of intraplaque hemorrhage, and MRI appearance of thick fibrous caps. The document includes MRI images and photomicrographs comparing MRI findings to histology.
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