The fat fed apoe ko mouse- chris jackson- u of bristol
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This study examined plaque rupture in the brachiocephalic arteries of 98 fat-fed apolipoprotein E knockout mice over time. Ruptured plaques were significantly larger, more occlusive, had thinner fibrous caps, more previous ruptures, and a greater lipid burden than intact plaques. The earliest ruptures occurred after 7 weeks on a high-fat diet. A pravastatin treatment significantly reduced sudden deaths, suggesting statins may prevent plaque rupture.
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Thermography is a new technique for detecting atherosclerotic plaque vulnerability. A new catheter-based system called the Epiphany Thermography System can precisely measure plaque temperature and has shown higher temperatures in proximal versus distal plaque segments. Studies have found that greater temperature differences between segments correlate with increased risk of future cardiac events, with optimal sensitivity of 86% and specificity of 79%. Preliminary research also indicates statin therapy may lower plaque temperatures and heterogeneity. Further clinical studies are still needed but thermography shows promise as an early detection method for vulnerable plaques.
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This document summarizes an editorial discussing a study that found erythrocyte membranes may play a role in atheromatous core formation. The study observed glycophorin-rich cores in pulmonary artery plaques from patients with chronic thromboembolic pulmonary hypertension. Glycophorins are erythrocyte membrane proteins. This suggests thromboembolic material (erythrocyte membranes) contributed to core formation. However, extrapolating these findings to coronary atherosclerosis is challenging given differences in disease etiology and timing of intraplaque hemorrhage. While erythrocyte membranes contain lipid-rich and scavenger receptor-binding constituents associated with atherosclerosis, more evidence is needed to support their direct contribution to
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The more stenotic a coronary segment is at baseline, the more likely it is to progress to occlusion or myocardial infarction. Less obstructive plaques, which far outnumber severely obstructive plaques, are responsible for most occlusions and infarctions because they are more likely to progress. Myocardial infarction often results from plaques that were only mildly or moderately obstructive months or years prior.
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This document describes LightLab OCT technology which uses optical coherence tomography to provide high-resolution real-time imaging of plaque in arteries. It can characterize plaque through morphological imaging as well as spectroscopic, polarization, Doppler, and elastography imaging. These advanced imaging modes give information on plaque structure, composition, and characteristics to help clinicians select and guide appropriate therapies.
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The document describes results from experiments examining iron uptake and macrophage presence in the periaortic and pericoronary fat of mice, rabbits, and humans with atherosclerosis. Mice and rabbits genetically modified to be prone to atherosclerosis showed greater iron uptake and more macrophages in the periaortic fat compared to controls. In humans, macrophages were found not just in atherosclerotic plaques but also in the surrounding pericoronary fat tissue.
114 evaluation of atherosclerotic plaque
1. The study measured temperature, pH, and lactate levels in atherosclerotic plaques from human and animal subjects.
2. They found significant heterogeneity and variation in pH within and between plaques. Lipid-rich areas had higher temperatures and lower pH compared to calcified areas.
3. Inverse correlations were observed between temperature and pH in human carotid plaques and rabbit aortas, but not in human umbilical arteries.
4. The results suggest that inflammation increases plaque temperature and decreases pH through increased metabolic activity of macrophages and anaerobic glycolysis producing lactate. Low pH may promote plaque vulnerability through activation of matrix-degrading enzymes.
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Thermography is a new technique for detecting atherosclerotic plaque vulnerability. A new catheter-based system called the Epiphany Thermography System can precisely measure plaque temperature and has shown higher temperatures in proximal versus distal plaque segments. Studies have found that greater temperature differences between segments correlate with increased risk of future cardiac events, with optimal sensitivity of 86% and specificity of 79%. Preliminary research also indicates statin therapy may lower plaque temperatures and heterogeneity. Further clinical studies are still needed but thermography shows promise as an early detection method for vulnerable plaques.
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This document summarizes an editorial discussing a study that found erythrocyte membranes may play a role in atheromatous core formation. The study observed glycophorin-rich cores in pulmonary artery plaques from patients with chronic thromboembolic pulmonary hypertension. Glycophorins are erythrocyte membrane proteins. This suggests thromboembolic material (erythrocyte membranes) contributed to core formation. However, extrapolating these findings to coronary atherosclerosis is challenging given differences in disease etiology and timing of intraplaque hemorrhage. While erythrocyte membranes contain lipid-rich and scavenger receptor-binding constituents associated with atherosclerosis, more evidence is needed to support their direct contribution to
256 spatial encoding part 2
1. MRI uses spatial encoding gradients and radiofrequency pulses to selectively excite slices of tissue and encode spatial information in the MRI signal. 2. Frequency encoding gradients encode left-right spatial information, while phase encoding gradients are applied in the orthogonal direction to fully spatially encode each image slice. 3. Fourier transformation is used to reconstruct images from the spatially encoded MRI data.
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The document summarizes two MRI scans of a rabbit aorta. The first scan used a superficial coil but lacked penetration, so a volume coil was used for the second scan. The second scan obtained 27 slices with improved parameters. Fat suppression imaging was also performed but requires further optimization to improve results and identify artifacts.
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This document describes LightLab OCT technology which uses optical coherence tomography to provide high-resolution real-time imaging of plaque in arteries. It can characterize plaque through morphological imaging as well as spectroscopic, polarization, Doppler, and elastography imaging. These advanced imaging modes give information on plaque structure, composition, and characteristics to help clinicians select and guide appropriate therapies.
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The document describes results from experiments examining iron uptake and macrophage presence in the periaortic and pericoronary fat of mice, rabbits, and humans with atherosclerosis. Mice and rabbits genetically modified to be prone to atherosclerosis showed greater iron uptake and more macrophages in the periaortic fat compared to controls. In humans, macrophages were found not just in atherosclerotic plaques but also in the surrounding pericoronary fat tissue.
114 evaluation of atherosclerotic plaque
1. The study measured temperature, pH, and lactate levels in atherosclerotic plaques from human and animal subjects.
2. They found significant heterogeneity and variation in pH within and between plaques. Lipid-rich areas had higher temperatures and lower pH compared to calcified areas.
3. Inverse correlations were observed between temperature and pH in human carotid plaques and rabbit aortas, but not in human umbilical arteries.
4. The results suggest that inflammation increases plaque temperature and decreases pH through increased metabolic activity of macrophages and anaerobic glycolysis producing lactate. Low pH may promote plaque vulnerability through activation of matrix-degrading enzymes.
Vogel endothelial function cv es
This document discusses endothelial dysfunction as a marker for cardiovascular events. It summarizes that impaired endothelium-dependent dilation in the coronary and brachial arteries provides prognostic information about future cardiovascular events, with worse endothelial dysfunction correlating to higher event rates. Various clinical tests are presented that measure endothelial function in these arteries. The document also suggests endothelial dysfunction may serve as an index for gauging therapeutic responses, as certain treatments are shown to improve endothelial function and reduce cardiovascular event rates.
Vp watch editorial - v2 n2- 2002
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 characteristics of atherosclerotic lesions developed in each model.
II. It focuses on newer models, including a rabbit model that allows induced plaque rupture and a double knockout LDL/apoE mice model that spontaneously develops extensive coronary lesions and myocardial infarctions at a young age, more closely mimicking human coronary heart disease.
III. However, it notes that while these models improve study of clinical atherosclerosis complications, it remains unclear how closely their plaque pathophysiology and coagulation systems
Spio cytokinejan28-2
This study aimed to compare the presence of iron particles in macrophage-rich atherosclerotic plaques in apo E-deficient mice under normal conditions versus after administration of cytokines TNF-alpha and IL-1beta. Eight female mice were divided into two groups, with five receiving an injection of TNF-alpha and IL-1beta and three receiving a saline injection as a control. All mice then received an injection of iron particles. After seven days, the mice were euthanized and their aortas examined for iron staining and plaque formation.
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1) The document discusses interleukin-18 (IL-18), an inflammatory cytokine that plays a role in atherosclerosis and plaque instability. Studies have shown IL-18 is overexpressed in atherosclerotic plaques and higher levels predict future cardiovascular events.
2) One study found serum IL-18 levels were significantly higher in coronary artery disease patients who suffered fatal cardiovascular events compared to those who did not. High IL-18 levels were an independent predictor of death even after adjusting for other risk factors.
3) By blocking IL-18 or its receptor in animal models, atherosclerotic plaque development and instability was reduced, suggesting IL-18 promotes plaque inflammation and vulnerability, in part by stimulating interferon-gamma production
The prev of inf cells in nonrupt a. plaque pasterkamp- part 2
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This document discusses various definitions of arterial remodeling used in post-mortem and intravascular ultrasound research. It notes that the different definitions lead to large variations in reported prevalence numbers for expansive, intermediate, and constrictive remodeling. The definitions are analyzed and some are noted to only be suitable for certain study types. It concludes that careful consideration of the remodeling definition used is needed when reporting prevalences, as without a gold standard or serial studies, the reference sites may not be free of atherosclerotic disease and could be remodeled as well.Symposium jang
This document summarizes research on using optical coherence tomography (OCT) to characterize coronary plaques. OCT uses near-infrared light to generate high-resolution cross-sectional images of tissue microstructure. Researchers studied 357 arterial segments ex vivo using OCT and validated plaque types (fibrous, calcific, lipid-rich) against histology with high accuracy. A pilot clinical study of 10 patients found OCT feasible and safe for in vivo coronary imaging before and after percutaneous coronary intervention, identifying a variety of plaque types and stent appositions. While blood obstruction and motion artifacts posed challenges, the results support further evaluation of OCT as a potential "optical biopsy" tool.
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This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It suggests that targeting specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, cells, or small molecule drugs could help shift the immune response away from pathogenic Th1 immunity toward protective Th2 immunity. Certain cytokines like IL-10 and TGFβ may be protective, while IFNγ and TNFα aggravate disease. Immunization experiments with oxidized LDL and heat shock protein 65 have shown promise in reducing lesions in animal models. Statins and pentoxifyllin may also help by inhibiting Th1 responses. However, general immunosuppression poses side effects, so focused immune modulation is a more viable strategy
Spio mri studies by dr naghavi
1) The document discusses a study using magnetic resonance imaging (MRI) to detect active atherosclerotic plaque in mice after injection of superparamagnetic iron oxide (SPIO) nanoparticles.
2) The study found that SPIO nanoparticles were taken up by macrophages within atherosclerotic plaques, darkening the plaques on post-injection MRI scans.
3) Histological analysis confirmed iron particle presence within plaques that correlated with macrophage density, supporting MRI's ability to detect plaque inflammation.
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Thermography is a new catheterization technique using a 3.3F over-the-wire catheter with a basket of 5 temperature sensors and a central blood thermo couple. The study assessed temperature recordings, catheter steerability, and coronary angiograms in 12 patients undergoing thermography of suspected coronary lesions. Temperature increases of up to 0.36°C were detected in focal areas, or "hot spots", in 4 of the 11 patients, which could indicate plaque rupture sites. Thermography was successfully performed in 92% of cases and showed good steerability.
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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.
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
Triggers of cardiovascular events can include physical and emotional stress. Stress from events like earthquakes, blizzards, intense sporting games, and overexertion from activities like snow shoveling have been shown to increase the risk of acute cardiovascular outcomes like myocardial infarction. While modern therapies have improved cardiovascular health, research continues to show temporary increases in cardiovascular mortality associated with highly emotional sporting events even in recent years. Managing risk factors, reducing stress, and utilizing preventative therapies may help reduce the impact of triggers on cardiovascular health.
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.
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This document discusses machine learning applications in cardiac imaging presented by Piotr Slomka. It describes how machine learning can improve image analysis, diagnosis, and risk prediction. Machine learning combines multiple data points like imaging and clinical data to predict outcomes. Deep learning can perform tasks like image segmentation. Machine learning provides quantitative scores that predict disease, need for intervention, or patient outcomes to help clinicians. The goal is to integrate machine learning into clinical decision making.
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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.
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.
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.
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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 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.
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This document discusses endothelial dysfunction as a marker for cardiovascular events. It summarizes that impaired endothelium-dependent dilation in the coronary and brachial arteries provides prognostic information about future cardiovascular events, with worse endothelial dysfunction correlating to higher event rates. Various clinical tests are presented that measure endothelial function in these arteries. The document also suggests endothelial dysfunction may serve as an index for gauging therapeutic responses, as certain treatments are shown to improve endothelial function and reduce cardiovascular event rates.
Vp watch editorial - v2 n2- 2002
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 characteristics of atherosclerotic lesions developed in each model.
II. It focuses on newer models, including a rabbit model that allows induced plaque rupture and a double knockout LDL/apoE mice model that spontaneously develops extensive coronary lesions and myocardial infarctions at a young age, more closely mimicking human coronary heart disease.
III. However, it notes that while these models improve study of clinical atherosclerosis complications, it remains unclear how closely their plaque pathophysiology and coagulation systems
Spio cytokinejan28-2
This study aimed to compare the presence of iron particles in macrophage-rich atherosclerotic plaques in apo E-deficient mice under normal conditions versus after administration of cytokines TNF-alpha and IL-1beta. Eight female mice were divided into two groups, with five receiving an injection of TNF-alpha and IL-1beta and three receiving a saline injection as a control. All mice then received an injection of iron particles. After seven days, the mice were euthanized and their aortas examined for iron staining and plaque formation.
258 dr renu virmani
Dr. Renu Virmani is the Chairperson of the Department of Cardiovascular Pathology at the Armed Forces Institute of Pathology in Washington, DC. She received her medical degrees in India and has held positions at multiple universities in the United States. Dr. Virmani has established an independent research program focused on cardiovascular pathology, publishing over 300 papers. Her work has helped establish an international reputation for evaluating devices and the pathology of sudden coronary death.
227 which serum should be used
1) The document discusses interleukin-18 (IL-18), an inflammatory cytokine that plays a role in atherosclerosis and plaque instability. Studies have shown IL-18 is overexpressed in atherosclerotic plaques and higher levels predict future cardiovascular events.
2) One study found serum IL-18 levels were significantly higher in coronary artery disease patients who suffered fatal cardiovascular events compared to those who did not. High IL-18 levels were an independent predictor of death even after adjusting for other risk factors.
3) By blocking IL-18 or its receptor in animal models, atherosclerotic plaque development and instability was reduced, suggesting IL-18 promotes plaque inflammation and vulnerability, in part by stimulating interferon-gamma production
The prev of inf cells in nonrupt a. plaque pasterkamp- part 2
The prev of inf cells in nonrupt a. plaque pasterkamp- part 2Society for Heart Attack Prevention and Eradication
This document discusses various definitions of arterial remodeling used in post-mortem and intravascular ultrasound research. It notes that the different definitions lead to large variations in reported prevalence numbers for expansive, intermediate, and constrictive remodeling. The definitions are analyzed and some are noted to only be suitable for certain study types. It concludes that careful consideration of the remodeling definition used is needed when reporting prevalences, as without a gold standard or serial studies, the reference sites may not be free of atherosclerotic disease and could be remodeled as well.Symposium jang
This document summarizes research on using optical coherence tomography (OCT) to characterize coronary plaques. OCT uses near-infrared light to generate high-resolution cross-sectional images of tissue microstructure. Researchers studied 357 arterial segments ex vivo using OCT and validated plaque types (fibrous, calcific, lipid-rich) against histology with high accuracy. A pilot clinical study of 10 patients found OCT feasible and safe for in vivo coronary imaging before and after percutaneous coronary intervention, identifying a variety of plaque types and stent appositions. While blood obstruction and motion artifacts posed challenges, the results support further evaluation of OCT as a potential "optical biopsy" tool.
Towards immune modulation vp
This document discusses potential immune-based therapies for modulating atherosclerosis and vulnerable plaque. It suggests that targeting specific antigens, co-stimulatory molecules, cytokines, vaccines, recombinant proteins, antibodies, cells, or small molecule drugs could help shift the immune response away from pathogenic Th1 immunity toward protective Th2 immunity. Certain cytokines like IL-10 and TGFβ may be protective, while IFNγ and TNFα aggravate disease. Immunization experiments with oxidized LDL and heat shock protein 65 have shown promise in reducing lesions in animal models. Statins and pentoxifyllin may also help by inhibiting Th1 responses. However, general immunosuppression poses side effects, so focused immune modulation is a more viable strategy
Spio mri studies by dr naghavi
1) The document discusses a study using magnetic resonance imaging (MRI) to detect active atherosclerotic plaque in mice after injection of superparamagnetic iron oxide (SPIO) nanoparticles.
2) The study found that SPIO nanoparticles were taken up by macrophages within atherosclerotic plaques, darkening the plaques on post-injection MRI scans.
3) Histological analysis confirmed iron particle presence within plaques that correlated with macrophage density, supporting MRI's ability to detect plaque inflammation.
Thermography iii
Thermography is a new catheterization technique using a 3.3F over-the-wire catheter with a basket of 5 temperature sensors and a central blood thermo couple. The study assessed temperature recordings, catheter steerability, and coronary angiograms in 12 patients undergoing thermography of suspected coronary lesions. Temperature increases of up to 0.36°C were detected in focal areas, or "hot spots", in 4 of the 11 patients, which could indicate plaque rupture sites. Thermography was successfully performed in 92% of cases and showed good steerability.
Vp meeting orlando2003_new template
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 prev of inf cells in nonrupt a. plaque pasterkamp- part 2
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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 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.
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Vuln plaque poster burke
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.
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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
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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.
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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 fat fed apoe ko mouse- chris jackson- u of bristol
- 1. The Fat-Fed Apolipoprotein E Knockout Mouse Chris Jackson Bristol Heart Institute, University of Bristol, UK Emerging Animal Models of Vulnerable Plaque
- 2. Animals • Closed outbred colony of C57:129 homozygous apoE knockout mice • Diet supplemented with 21% lard, 0.15% cholesterol • Age at start of study was 6 to 8 weeks
- 3. Study Design • 98 animals (51 male) were put on study • 34 animals: scheduled termination • Pressure perfusion fixed (10% formalin) at a constant pressure of 100mmHg • 64 animals: sudden death • Not pressure perfusion fixed
- 4. Sudden Deaths 60565248444036322824201612840 0 10 20 30 40 50 60 70 80 90 100 Time (weeks) Survival (%)
- 6. Parameters Measured • Presence or absence of rupture • Plaque cross-sectional area • Media cross-sectional area • Plaque/media area ratio • % Lumenal occlusion • Cap thickness • Number of previous ruptures • Lipid burden
- 7. Incidence of Rupture • 64 sudden deaths • 35 ruptured brachiocephalics • 34 scheduled terminations • 16 ruptured brachiocephalics
- 8. Time Course of Rupture 605550454035302520151050 0 5 10 15 20 25 30 35 Time (Weeks) Cumulative Ruptures
- 9. Plaque Characterisation • Acutely ruptured (“ruptured”) • Visible tear or discontinuity in the cap • Blood-derived components within the lesion • Healed previous rupture (“intact”) • Buried fibrous cap
- 10. Vessel Dimensions Intact Ruptured 0 25000 50000 75000 100000 125000 150000 175000 200000 225000 Media Area Plaque Area Area (sq µm) NS p=0.0015
- 12. Lumenal Occlusion Intact Ruptured 0 10 20 30 40 50 60 Occlusion (%) p<0.0001
- 13. Cap Thickness Intact Ruptured 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 5.5 Cap Thickness (um) p=0.0004
- 14. Previous Healed Ruptures Intact Ruptured 0.0 0.5 1.0 1.5 2.0 2.5 3.0 Buried Caps p<0.0001
- 15. Lipid Burden Intact Ruptured 0 5 10 15 20 25 30 35 40 45 50 55 Lipid Content (%) p=0.0019
- 16. Summary • Ruptured plaques: • Are 56% bigger • Are 52% more occlusive • Have caps that are 57% thinner • Have 151% more previous ruptures • Have a 36% greater lipid burden
- 17. Intervention Study Design • To detect ∆(rupture, intact) with 80% power: • Cap thickness: 17 mice • Lipid content: 22 mice • Lumenal occlusion: 24 mice • Rupture frequency: 33 mice • Plaque area: 53 mice
- 18. Late-Breaking News • Earliest ruptures are seen after 7 weeks of high-fat diet • 75% of males have ruptures after 8 weeks • Pravastatin significantly reduces the incidence of sudden death • PAI-1-/- /apoE-/- double knockouts have significantly more plaque ruptures than apoE-/- single knockouts
- 19. Acknowledgments • Helen Williams, PhD • Jason Johnson, MSc • Kevin Carson, MB ChB • Ray Bush, PhD • Deb Watkins, BSc • British Heart Foundation • Organon Laboratories • Pfizer • AstraZeneca