3rd vulnerable plaque rumberger 3 16-02 1
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Electron beam tomography (EBT) is a scanning method introduced in 1984 that images the heart 10 times faster than helical CT. Over 600 papers have been published on EBT validating its ability to determine and quantify coronary artery calcium. Coronary artery calcification is the hardening of the coronary arteries that has been known for 300 years. Recent research in the past 10 years has found that it is an active process that can occur early in atherosclerotic plaque development and is an intimate part of the fibroproliferative and inflammatory pathophysiology of coronary artery disease. Histological examination shows calcium is present within atherosclerotic plaque.
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![Electron Beam TomographyElectron Beam Tomography
[EBT][EBT]
Is a unique and established tomographic scanning methodIs a unique and established tomographic scanning method
[1[1stst
introduced in 1984] using a scanning electron beamintroduced in 1984] using a scanning electron beam
rather than a rotating X-ray source [e.g. helical CT]rather than a rotating X-ray source [e.g. helical CT]
Rapidly images the patient’s heart [50 or 100 msec/image,Rapidly images the patient’s heart [50 or 100 msec/image,
Approximately 10 times faster than helical CT]Approximately 10 times faster than helical CT]
Imaging done synchronized at a phase of the cardiacImaging done synchronized at a phase of the cardiac
cycle corresponding to the least ballistic coronary motioncycle corresponding to the least ballistic coronary motion](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
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This document discusses two MRI contrast agents - MS-325 and EP-1873. MS-325 is an albumin-binding agent that enhances the vessel wall in patients with atherosclerosis by binding to extravasated albumin, allowing visualization of plaque. It also prolongs the enhancement of the vessel wall and lumen, enabling high-resolution measurement of plaque burden. EP-1873 is a fibrin-targeted agent that makes thrombotic consequences of plaque rupture directly visible on standard MR scans, with potential applications in assessing thromboembolic risk and monitoring clot resolution after treatment.
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This document discusses non-invasive imaging techniques for coronary artery plaque and vulnerable patients. It notes that while lipid-rich plaque makes up about 20% of total plaque volume, it is often not detectable without invasive techniques. Computed tomography (CT) and electron beam tomography (EBT) are discussed as non-invasive options for imaging plaque characteristics and identifying vulnerable patients. The document considers various scanning parameters, display options, and need for high scan speeds when using these techniques. It concludes that non-invasive coronary imaging can provide benefits like identifying high-risk patients, guiding appropriate interventions, and avoiding unnecessary invasive procedures.Monocyte recruitment into atherosclerotic plaques
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2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture or thrombosis.
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- Over 400 genes are involved in regulating atherosclerotic plaque formation and other processes like inflammation and metabolism. However, the roles of most genes are still unknown.
- Several studies have found associations between certain gene polymorphisms like connexin 37, ACE, NPY, and IL-6, and increased carotid intima-media thickness and plaque formation.
- The presence of carotid plaque shows heritability and a common genetic basis with other cardiovascular
070 visualization of atherosclerotic vulnerable plaque
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093 multi slice fast ct
1) EBT and MSCT can visualize coronary arteries with sufficient resolution due to their temporal and spatial capabilities.
2) Clinical studies have shown coronary calcium detection via EBT can successfully identify asymptomatic individuals at increased risk of coronary events.
3) The prognostic value of non-calcified plaques detected by EBT and MSCT after contrast injection is still unclear. Future studies will help define the role of coronary calcium detection in risk stratification.
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Nicotine enhances the adaptive immune response by upregulating expression of nicotinic acetylcholine receptors on dendritic cells, increasing their production of inflammatory cytokines and ability to activate T cells. It also promotes the recruitment of dendritic cells to atherosclerotic plaques, potentially contributing to plaque destabilization. The findings suggest nicotine has proinflammatory effects that may link smoking to cardiovascular disease by exacerbating atherosclerosis.
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1. Autoimmune reactions against heat shock proteins (HSPs), particularly HSP60, may play an important role in the early development of atherosclerosis.
2. HSPs released from necrotic cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more inflammatory cells. This may link HSPs to complications like plaque rupture or thrombosis.
3. Both humoral and cellular immune reactions against HSP60 work together with classical cardiovascular risk factors to promote atherosclerosis and its complications.
3rd vp 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 examining plaques before and after percutaneous coronary intervention, identifying various plaque types and procedural complications like dissections. While promising, OCT imaging in patients requires overcoming challenges like blood flow obstruction and motion artifacts.
Aeha muller 2
This document discusses various methods for identifying vulnerable plaques, including non-invasive imaging techniques like CT and MRI, as well as invasive techniques like intravascular ultrasound (IVUS) and optical coherence tomography (OCT). It summarizes several studies that examined autopsy specimens to determine the prevalence of thin-capped fibroatheromas and disrupted plaques. The document also describes the goals of using advanced IVUS spectral analysis to characterize plaque composition in vivo and a potential natural history study to determine if detecting vulnerable plaque can predict future cardiovascular events.
241 genetic influence on carotid atherosclerosis
This document discusses the genetic influences and mechanisms involved in the development of carotid atherosclerosis and carotid artery plaque. Some key points:
- Atherosclerosis has both environmental and strong genetic components. Studies in twins show genetics plays a major role.
- Over 400 genes are involved in regulating atherosclerotic plaque formation and other processes like inflammation and metabolism. However, the roles of most genes are still unknown.
- Several studies have found associations between certain gene polymorphisms like connexin 37, ACE, NPY, and IL-6, and increased carotid intima-media thickness and plaque formation.
- The presence of carotid plaque shows heritability and a common genetic basis with other cardiovascular
070 visualization of atherosclerotic vulnerable plaque
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This document discusses using super paramagnetic iron oxide (SPIO) as a contrast agent for MRI to visualize vulnerable atherosclerotic plaques. SPIO can accumulate in macrophages and be taken up by plaques through fissures or thin caps. MRI after SPIO injection may show active macrophages in inflamed vulnerable plaques through changes in T1 and T2 relaxation times. Preliminary studies show SPIO particles trapped in RES organs of mice and some pulmonary macrophages. Future studies aim to use SPIO and other contrast agents to image carotid plaques in rabbits with dedicated MRI coils.Acc v porg becker
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097 atherosclerotic lesions have regions of low p h
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Macrophages in atherosclerotic lesions release lactic acid, lowering the extracellular pH. This study directly measured the pH of human and rabbit atherosclerotic lesions for the first time, finding lipid-rich areas had pH as low as 7.0. Regions with more macrophages had lower pH, inversely correlated with temperature, suggesting acidity arose from macrophage metabolism rather than hypoxia. These findings have implications for understanding how acidic pH affects processes like LDL oxidation and protease activity in lesions.144 physics of mri
A 71-year-old man with a history of diabetes, coronary artery disease status post myocardial infarction times three, and hypercholesterolemia was found to have an accidental left carotid stenosis and was scheduled for a left carotid endarterectomy. MRI of the carotid arteries was performed using SPIO contrast to better evaluate the extent of disease prior to surgery.
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This document discusses the use of electron beam tomography (EBT) and multi-slice computed tomography (MSCT) to detect and quantify coronary artery calcification as a means to identify asymptomatic individuals at increased risk of coronary events. Several clinical studies have demonstrated the prognostic value of coronary calcium detected by EBT. EBT and MSCT have sufficient resolution to visualize coronary arteries non-invasively. While calcium does not indicate vulnerable plaque, the amount of calcium correlates with overall plaque burden. Future studies will help define the role of calcium detection in clinical risk stratification, though MSCT has not yet been used in outcome studies. The meaning of non-calcified plaque detected by EBT and MSCT also requires further clarification.
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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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The document introduces the All of Us Research Program, which aims to collect health data from one million Americans to advance precision medicine research. It was announced by President Obama in 2015. The program receives funding from the federal government and private partners. It collects various types of health data from participants through surveys, health records, samples, and devices. The data is stored and shared securely while protecting privacy. The goal is to generate new medical discoveries and more personalized healthcare through collaboration between researchers and participants.AHA SHAPE Symposium 2017 Dr. Yen Presentation
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
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.
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 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.
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 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.
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.
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.
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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- 1. EBT Calcium Score:EBT Calcium Score: A Clue to Invulnerable PlaquesA Clue to Invulnerable Plaques In Vulnerable PatientsIn Vulnerable Patients John A. Rumberger, PhD, MD, FACCJohn A. Rumberger, PhD, MD, FACC Clinical Professor of Medicine, Ohio State UniversityClinical Professor of Medicine, Ohio State University Medical Director, OhioHeartMedical Director, OhioHeart Columbus, OhioColumbus, Ohio The 3rd Vulnerable Plaque Symposium 51st Annual ACC, Atlanta GA, 3/16/02
- 2. Electron Beam TomographyElectron Beam Tomography [EBT][EBT] Is a unique and established tomographic scanning methodIs a unique and established tomographic scanning method [1[1stst introduced in 1984] using a scanning electron beamintroduced in 1984] using a scanning electron beam rather than a rotating X-ray source [e.g. helical CT]rather than a rotating X-ray source [e.g. helical CT] Rapidly images the patient’s heart [50 or 100 msec/image,Rapidly images the patient’s heart [50 or 100 msec/image, Approximately 10 times faster than helical CT]Approximately 10 times faster than helical CT] Imaging done synchronized at a phase of the cardiacImaging done synchronized at a phase of the cardiac cycle corresponding to the least ballistic coronary motioncycle corresponding to the least ballistic coronary motion
- 3. Electron Beam TomographyElectron Beam Tomography Over the past 18 years there have > 600 scientificOver the past 18 years there have > 600 scientific papers published regarding EBT validation andpapers published regarding EBT validation and applications for cardiac imagingapplications for cardiac imaging However, theHowever, the applicationapplication receiving the mostreceiving the most ““notice” (and controversy) has been its ability tonotice” (and controversy) has been its ability to determine and quantify Coronary Artery Calciumdetermine and quantify Coronary Artery Calcium
- 4. Coronary Artery CalcificationCoronary Artery Calcification ““Hardening”Hardening” of the coronary arteries has known for 300 years; but over the pastthe past 10 years10 years we havewe have found it is:found it is: An ActiveAn Active ((notnot passive)passive) processprocess CanCan OccurOccur earlyearly in ASO plaque developmentin ASO plaque development AnAn Intimate part ofIntimate part of the fibroproliferative andthe fibroproliferative and inflammatory pathophysiology of CADinflammatory pathophysiology of CAD RegulatedRegulated in a fashion similar to bonein a fashion similar to bone mineralization and repairmineralization and repair
- 5. Coronary Artery CalciumCoronary Artery Calcium and Atherosclerotic Plaqueand Atherosclerotic Plaque Histology X-Ray
- 6. Coronary Artery CalciumCoronary Artery Calcium and Atherosclerotic Plaqueand Atherosclerotic Plaque Histology X-Ray