Aeha immune mechanisms in atherosclerosis
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This document summarizes the role of the immune system in atherosclerosis. It finds that: 1) Adaptive immunity plays a major role in atherosclerosis as mice lacking T and B cells develop dramatically less atherosclerosis despite similar cholesterol levels. 2) T cells in lesions recognize oxidized LDL and other antigens, activating macrophages and promoting inflammation. 3) NKT cells increase atherosclerosis by recognizing glycolipid antigens, while regulatory T cells and B cells decrease disease by producing anti-inflammatory cytokines like IL-10 and TGF-β. 4) Protective immunization approaches have shown promise in animal models by stimulating antibody production against oxidized LDL and other antigens to decrease plaque formation.
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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.
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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 by attracting immune cells into the arterial wall.
2. HSPs released from dying cells in advanced atherosclerotic plaques can stimulate the innate immune response and promote inflammation, attracting more immune cells and linking to complications like plaque rupture.
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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 and thrombosis.
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2. One study immunized rabbits with the BCG vaccine, which contains HSP-65, and found higher levels of atherosclerotic plaques in immunized rabbits compared to controls. This suggests HSP-65 immunity may enhance atherosclerosis.
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Orthopedic disorders of metabolic bone disease - البروفيسور فريح عوده ابوحسان Prof Freih Abu Hassan البروفيسور فريح ابوحسان
جراحة العظام / علاج العظام في الاردن / افضل دكتور عظام في الاردن / افضل اخصائي عظام في الاردن / استشاري عظام/افضل استشاري عظام في الاردن /جراحة عظام / /عمليات تطويل العظام في الاردن / اطباء العظام في الاردن / دكتور طب عظام في الاردن / الاطباء في الاردن / خلع ورك / عمليات اليزاروف في الاردن /علاج الكسور /خلع الولادة / تركيب المفصل / اوجاع العظام /افضل طبيب عظام اطفال في الاردن / استشاري اطفال عظام في الاردن / /علاج خلع الكتف / علاج التواء الكاحل / التواء الكاحل / علاج الام العظام / علاج هشاشة العظام / ارقام اطباء عظام في الاردن / مشاكل العظام والمفاصل /مستشار جراحة العظام والمفاصل والكسور/ مستشار جراحة عظام الأطفال.
هشاشة العظام ، امراض العظام ، امراض العظام الناتجة عن اضطراب الايضAtherosclerosis
Dr. Steenblock specializes in treating patients with Atherosclerosis and other similar conditions using Stem Cell Treatments. He uses bone marrow stem cells, adipose (fat) stem cells and umbilical cord stem cells. For more information call his office Today! 1-800-300-1063. Websites:
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www.strokedoctor.com
www.stemcelltherapies.org
www.cerebralpalsycure.com
www.davidsteenblock.com
www.davidsteenblock.net
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Orthopedic disorders of metabolic bone disease - البروفيسور فريح عوده ابوحسان
Orthopedic disorders of metabolic bone disease - البروفيسور فريح عوده ابوحسان Prof Freih Abu Hassan البروفيسور فريح ابوحسان
جراحة العظام / علاج العظام في الاردن / افضل دكتور عظام في الاردن / افضل اخصائي عظام في الاردن / استشاري عظام/افضل استشاري عظام في الاردن /جراحة عظام / /عمليات تطويل العظام في الاردن / اطباء العظام في الاردن / دكتور طب عظام في الاردن / الاطباء في الاردن / خلع ورك / عمليات اليزاروف في الاردن /علاج الكسور /خلع الولادة / تركيب المفصل / اوجاع العظام /افضل طبيب عظام اطفال في الاردن / استشاري اطفال عظام في الاردن / /علاج خلع الكتف / علاج التواء الكاحل / التواء الكاحل / علاج الام العظام / علاج هشاشة العظام / ارقام اطباء عظام في الاردن / مشاكل العظام والمفاصل /مستشار جراحة العظام والمفاصل والكسور/ مستشار جراحة عظام الأطفال.
هشاشة العظام ، امراض العظام ، امراض العظام الناتجة عن اضطراب الايضAtherosclerosis
Dr. Steenblock specializes in treating patients with Atherosclerosis and other similar conditions using Stem Cell Treatments. He uses bone marrow stem cells, adipose (fat) stem cells and umbilical cord stem cells. For more information call his office Today! 1-800-300-1063. Websites:
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Role of free radical in the development of atherosclerosis
The document discusses the role of free radicals in the development of atherosclerosis. It provides details on:
- What free radicals are and their sources in the body
- How free radicals can damage LDL cholesterol and lead to atherosclerosis
- The process of atherosclerosis where macrophages take up oxidized LDL and become foam cells that accumulate in artery walls
- The role of antioxidants like superoxide dismutase in neutralizing free radicals and preventing oxidative damage
Atherosclerosis 3
The document discusses the morphology and complications of atherosclerosis. It begins by describing the earliest lesion, the fatty streak, and later atherosclerotic plaques which form in arteries. Plaques are composed of cells, extracellular matrix, lipids, and can rupture or erode. This can lead to complications like myocardial infarction, stroke, and peripheral vascular disease. Diagnosis involves tests like CT scans and treatment includes lifestyle changes and medications like statins to reduce cholesterol and risk of clotting.
Atherosclerosis
Atherosclerosis is a disease affecting large arteries characterized by plaque buildup in the vessel wall containing lipids, inflammatory cells, and smooth muscle cells. It is caused by multiple risk factors like hyperlipidemia, smoking, hypertension, and diabetes. Symptoms vary depending on location and severity of blockages, and may include leg pain with walking, non-healing wounds, or gangrene. Treatment involves lifestyle changes, medications, and procedures like angioplasty or bypass surgery to improve blood flow.
Atherosclerosis
Atherosclerosis is a disease where plaque builds up in the arteries, making them harder and narrower. It is caused by inflammation over time from risk factors like age, family history, obesity, lack of exercise, smoking, high blood pressure, and high cholesterol. Doctors use tests like angiograms to see blockages. Treatment focuses on managing contributing conditions with drugs or procedures like angioplasty and bypass surgery to reopen arteries. Prevention emphasizes lifestyle changes like a healthy diet, exercise, quitting smoking, and stress reduction.
Aterosclerosis diapositivas
La aterosclerosis es la principal causa de muerte e incapacidad en el mundo desarrollado. Se caracteriza por la acumulación de lípidos y el endurecimiento de las arterias. Tiene múltiples factores de riesgo como la hipercolesterolemia, el tabaquismo y la diabetes, y puede causar complicaciones como infartos e isquemias cerebrales. El tratamiento se enfoca en controlar los factores de riesgo a través de cambios en el estilo de vida y medicamentos para prevenir eventos cardiovasculares.
Arteriosclerosis
1. La arteriosclerosis es una enfermedad progresiva de las arterias que se caracteriza por placas sobre elevadas.
2. Existen factores de riesgo modificables como la hipertensión, diabetes y tabaquismo que aceleran el desarrollo de la arteriosclerosis.
3. Los análisis de sangre como el colesterol y los triglicéridos son biomarcadores útiles para evaluar el riesgo cardiovascular asociado a la arteriosclerosis.
Aterosclerosis
La aterosclerosis es una alteración patológica de las arterias caracterizada por el depósito anormal de lípidos y tejido fibroso en la pared arterial, que desorganiza la arquitectura y reduce el flujo sanguíneo. Es causada principalmente por factores de riesgo como la hipertensión, la diabetes, el tabaquismo, la dislipidemia, la obesidad y el sedentarismo. La aterosclerosis sigue siendo la principal causa de muerte prematura en las sociedades desarrolladas.
Aterosclerosis
El documento describe la enfermedad de la aterosclerosis, incluyendo sus causas, progresión y manifestaciones clínicas. La aterosclerosis es una enfermedad de las arterias caracterizada por la formación de placas que reducen la luz vascular. Estas placas están compuestas de lípidos, células y tejido conectivo. Puede provocar déficits de riego sanguíneo y dar lugar a síntomas como angina de pecho o infarto agudo de miocardio. El documento discute diversas teorías sobre la etiolog
Atherosclerosis
Atherosclerosis is characterized by the buildup of fatty plaques, cholesterol, and cellular waste within the inner lining of arteries. Over time, this buildup narrows the arteries and restricts blood flow. The major risk factors for atherosclerosis include increasing age, male gender, family history, smoking, high blood pressure, diabetes, and high cholesterol. The disease process begins with endothelial injury to blood vessels, which allows cholesterol and immune cells like macrophages to accumulate in the artery wall and form fatty streaks. These can progress to raised atherosclerotic plaques made of cells, connective tissue, and lipids that further restrict blood flow. Advanced plaques can rupture or erode, potentially causing heart attacks or strokes if cl
Aterosclerosis
La aterosclerosis es una enfermedad caracterizada por el depósito de sustancias lipídicas en las paredes de las arterias que las endurece y estrecha. Esto se debe a una respuesta inflamatoria crónica iniciada por daño al endotelio vascular que causa acumulación de lípidos y formación de placas ateromatosas. La aterosclerosis puede causar diversos síndromes clínicos como enfermedad cardíaca, accidentes cerebrovasculares y enfermedad vascular periférica debido al estrechamiento de las
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Orthopedic disorders of metabolic bone disease - البروفيسور فريح عوده ابوحسان
Orthopedic disorders of metabolic bone disease - البروفيسور فريح عوده ابوحسان
Role of free radical in the development of atherosclerosis
Role of free radical in the development of atherosclerosis
Similar to Aeha immune mechanisms in atherosclerosis
075 immune modulation
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. Several approaches show promise in animal models, including immunization with oxidized LDL to induce protective antibodies, administration of the heat shock protein HSP65 to reduce lesions, and use of pentoxifyllin or statins which can inhibit Th1 responses and atherosclerosis. However, challenges remain in translating these strategies to chronic human disease given general immunosuppression carries side effects from increased infection risk.
Teplizumab
Présentation réalisée dans le cadre de l\’option "Méthodes Modernes de Découverte et de Développement de Médicaments"
233 cd40
CD40 and its ligand CD40L play an important role in atherosclerosis by promoting inflammation. Statins can limit the expression of CD40 and CD40L, thereby reducing inflammation. Oxidized LDL increases the expression of CD40 and CD40L on endothelial cells, smooth muscle cells, and macrophages, further promoting atherosclerosis. CD40L also contributes to thrombosis and restenosis. While CD40 does not seem to affect early plaque formation, its deficiency is associated with more stable plaques at advanced stages of atherosclerosis.
Esv2n48
CD40 and its ligand CD40L play an important role in atherosclerosis by promoting inflammation. Statins can limit the expression of CD40 and CD40L, thereby reducing inflammation. Oxidized LDL increases the expression of CD40 and CD40L on endothelial cells, smooth muscle cells, and macrophages, further promoting atherosclerosis. CD40L also contributes to thrombosis and restenosis. While CD40 does not seem to affect early plaque formation, its deficiency is associated with more stable plaques at advanced stages of atherosclerosis.
233 cd40
CD40 and its ligand CD40L play an important role in atherosclerosis by promoting inflammation. Statins can limit the expression of CD40 and CD40L, thereby reducing inflammation. Oxidized LDL increases the expression of CD40 and CD40L on endothelial cells, smooth muscle cells, and macrophages, further promoting atherosclerosis. CD40L also contributes to thrombosis and restenosis. While CD40 does not seem to affect early plaque formation, its deficiency is associated with more stable plaques at advanced stages of atherosclerosis.
Cellular Adhesion in Inflammation
This document summarizes cellular adhesion molecules that are involved in the inflammatory process. It discusses selectins, integrins, and their roles and ligands in leukocyte trafficking and extravasation from blood vessels into tissues during inflammation. Selectins such as L-selectin, E-selectin, and P-selectin mediate initial tethering and rolling of leukocytes on endothelial cells, while integrins such as LFA-1 and VLA-4 are involved in tight adhesion and transmigration. Diseases associated with deficiencies in these adhesion molecules and attempts to target them therapeutically in human allergic inflammation and diseases like asthma are also summarized.
178 vaccination against atherosclerosis
There is promising research into developing vaccines against atherosclerosis. Studies have found that vaccination against oxidized LDL and certain ApoB-100 peptides can reduce the development of atherosclerosis in animal models by up to 60%. A recent study immunized ApoE null mice with ApoB-100 peptide sequences and found a 60% reduction in atherosclerotic plaque in the aorta. Further research is still needed but vaccination shows potential as a way to prevent atherosclerosis and vulnerable plaques in humans. International collaboration could help advance this area towards developing heart attack prevention through immune modulation.
178 vaccination against atherosclerosis
Vaccination against atherosclerosis shows promise as an exciting new therapy. Studies in animal models have found that vaccination against oxidized LDL or specific ApoB-100 peptides can significantly reduce atherosclerosis. This study investigated immunization with novel ApoB-100 peptide sequences in ApoE null mice. It found a 60% reduction in atherosclerotic plaque in the aorta of immunized mice, along with increased collagen content in plaques. While more research is still needed, these results suggest that targeted vaccination against antigens involved in atherosclerosis, such as specific oxidized LDL peptides, could potentially be developed into a novel strategy for preventing heart attacks.
Esv3n12
Vaccination against atherosclerosis shows promise as an exciting new therapy. Studies in animal models have found that vaccination against oxidized LDL or specific ApoB-100 peptides can significantly reduce atherosclerosis. This study investigated immunization with novel ApoB-100 peptide sequences in ApoE null mice. It found a 60% reduction in atherosclerotic plaque in the aorta of immunized mice, along with increased collagen content in plaques. While more research is still needed, these results suggest that targeted vaccination against antigens involved in atherosclerosis, such as specific oxidized LDL peptides, could potentially be developed into a novel strategy for preventing heart attacks and strokes.
109 anatomy of the atherosclerotic plaque
This document contains multiple figures and descriptions related to atherosclerosis and HDL metabolism. It discusses the anatomy of atherosclerotic plaques, how plaque rupture can cause acute coronary syndromes, and how statin drugs may stabilize vulnerable plaques. It also summarizes HDL metabolism, reverse cholesterol transport, the role of CETP, and potential strategies for increasing HDL as a therapeutic target for atherosclerosis.
1031 talk2
The document discusses the role of lipoproteins, particularly LDL and HDL, in inflammation and atherosclerosis. LDL readily enters the artery wall where it can become modified, making it proinflammatory. Modified LDL stimulates expression of MCP-1, which recruits monocytes. Modified LDL also promotes differentiation of monocytes into macrophages. In contrast, HDL is potentially anti-inflammatory. Atherosclerosis is characterized as an inflammatory disease where lipoproteins influence multiple aspects of inflammation.
109 anatomy of the atherosclerotic plaque
The document discusses the role of lipoproteins, particularly LDL and HDL, in inflammation and atherosclerosis. LDL readily enters the artery wall where it can become modified, making it proinflammatory. Modified LDL stimulates expression of MCP-1, which recruits monocytes. Modified LDL also promotes differentiation of monocytes into macrophages. In contrast, HDL is potentially anti-inflammatory. Atherosclerosis is characterized as an inflammatory disease where lipoproteins influence multiple aspects of inflammation.
1031 talk2
This document contains multiple figures and descriptions related to atherosclerosis and HDL metabolism. It discusses the anatomy of atherosclerotic plaques, how plaque rupture can cause acute coronary syndromes, and how statin drugs may stabilize plaques over time by reducing inflammation. It also summarizes HDL metabolism, how genes and proteins involved can be targeted for new therapies, and how increased apo A-I production through gene transfer has been shown to reduce atherosclerosis in animal models.
Cord Blood Natural Killer Cells for Immunotherapy
Cord blood is a potential source of natural killer (NK) cells for cancer immunotherapy. NK cells can be expanded from cord blood units to sufficient clinical scales for treatment. Expanded cord blood NK cells have been shown to be as cytotoxic against tumors as peripheral blood NK cells. They have demonstrated activity against multiple myeloma and chronic lymphocytic leukemia in preclinical studies. A phase I/II clinical trial is exploring the use of ex vivo expanded cord blood NK cells combined with chemotherapy and autologous stem cell transplant for multiple myeloma. Additional strategies are being investigated to enhance the anti-tumor activity of cord blood NK cells, such as using lenalidomide or engineering the cells to improve homing to the bone marrow micro
Mast cell activation syndrome.pdf
The document discusses mast cell activation syndrome (MCAS), including the development and classification of mast cells, clinical manifestations of MCAS, diagnostic criteria for MCAS under various consensus guidelines from 2010 to 2022, and treatments for MCAS. MCAS is diagnosed based on recurrent symptoms affecting multiple organ systems as well as elevated mast cell mediators that respond to treatments targeting mast cell mediators. Diagnostic criteria have evolved over time to rely more on clinical symptoms and treatment response compared to specific mast cell marker thresholds.
Immunosenescence11
The document discusses how the immune system deteriorates with age, known as immunosenescence. Key points include:
- Innate immune cells like neutrophils and monocytes/macrophages show functional declines with aging, including altered receptor expression and signaling.
- The adaptive immune system also deteriorates with age. B cell and humoral immunity show reduced costimulatory molecule expression and defects in signaling. T cell immunity declines in naïve cell numbers, cytotoxic function, and proliferation ability. Memory CD8+ T cells lose co-stimulatory molecules like CD28 with age.
- These immune changes contribute to the chronic low-grade inflammation, or "inflamm-aging", seen in older individuals
Autoinflammatory diseases
This document discusses autoinflammatory diseases, which are characterized by dysregulation of the innate immune system leading to recurrent, unprovoked inflammation without high autoantibodies or T cells. Common autoinflammatory diseases are caused by mutations that activate the inflammasomes or interferon pathways. Autoinflammatory diseases typically begin in childhood and can cause fever, rash, and organ inflammation. The pathophysiology involves cytosolic pattern recognition receptors such as NLRs, RLRs, and DNA sensors that activate the inflammasomes or interferon response when mutated.
Pasterkamp
This document discusses how balloon dilatation during percutaneous coronary intervention decreases the responsiveness and expression of Toll-like receptors 2 and 4 on immune cells. It found that coronary balloon dilatation reduced the production of TNF-alpha in response to TLR2 and TLR4 ligands, as well as decreasing the expression of TLR2 and TLR4 on granulocytes and monocytes. These anti-inflammatory effects were also seen to a lesser extent in patients who did not undergo balloon dilatation. The document concludes that understanding mechanisms of innate immune system tolerance could provide new targets for modulating inflammation.
Inflammatory Mediators Corrigan
This document summarizes various inflammatory mediators including cytokines, chemokines, lipid mediators, and neuropeptides. It describes the sources and functions of different cytokines such as IL-1, TNF-α, IFN-γ, and chemokines such as IL-8 and RANTES. It also discusses the roles of lipid mediators like leukotrienes and prostaglandins in inflammation.
Dr. Santos Manes - Simposio Internacional 'Terapias oncológicas avanzadas'
Los días 15 y 16 de octubre de 2014, la Fundación Ramón Areces y la Real Academia Nacional de Farmacia, en colaboración con la Fundación de la Innovación Bankinter, reunieron en Madrid a algunos de los mayores expertos mundiales en nuevas terapias contra el cáncer. El Simposio Internacional, coordinado por la profesora y académica María José Alonso, analizó el momento actual de la lucha contra esta enfermedad. También fue un punto de encuentro para científicos de los más innovadores institutos de investigación en oncología, quienes debatieron sobre tres grandes temas: la Medicina Personalizada contra el cáncer, los nanomedicamentos en la terapia del cáncer y las terapias basadas en la inmunomodulación.
Similar to Aeha immune mechanisms in atherosclerosis (20)
Dr. Santos Manes - Simposio Internacional 'Terapias oncológicas avanzadas'
Dr. Santos Manes - Simposio Internacional 'Terapias oncológicas avanzadas'
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AHA SHAPE Symposium 2017 Dr. Naghavi Presentation
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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
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.
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.
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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4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
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Aeha immune mechanisms in atherosclerosis
- 1. Vaccine for atherosclerosis – a review on the role of immunity in atherosclerosis Jan Nilsson, Lund University Göran K Hansson, Karolinska Institutet, Sweden
- 2. Atherosclerosis – an inflammatory response to lipid retention LDL entry LDL retentionLDL retention & modification& modification Adhesion molecules Chemokines Proinflammatory lipids activate EC and Mø LDL uptakeLDL uptake and presentationand presentation T cell activation ProinflammatoryProinflammatory cytokinescytokines Inflammation Destruction & remodeling Lesion growth & activation Foam cell formation G K Hansson & J Nilsson In: Crawford & DiMarco, Cardiology
- 3. Innate immunity in plaque inflammation Inflammatory cytokines Proteases Procoagulant Pro-apoptotic TLR LPS, HSP60, oxLDL(?) TLR Natural antibodies G K Hansson
- 4. Atherosclerosis in the absence of adaptive immunity? (G K Hansson & J Nilsson, in: Crawford & DiMarco, Cardiology)
- 5. Lack of adaptive immunity leads to dramatic reduction in atherosclerosis – without affecting cholesterol levels * ApoE- SCID ApoE- T and B cells No Yes Aortic lesion size Zhou, Nicoletti, Elhage & Hansson Circ 102:2919 2000 Similar - but not as striking - effects in immunodeficient RAG1 x apoE KO Dansky, PNAS 97 Daugherty, JCI 97
- 6. Atherosclerosis in the absence of adaptive immunity? (G K Hansson & J Nilsson, in: Crawford & DiMarco, Cardiology)
- 7. Splenectomy leads to accelerated atherosclerosis in apoE -/- mice 0 20 40 60 80 100 120 140 160 Sham Splenectomy *Lesionsizex103 µm Sx at 6 weeks, analysis at 18 weeks age Caligiuri et al, JCI 109:745, 2002
- 8. B cells of atherosclerotic mice carry atheroprotective immunity 0 50 100 150 200 250 Sham Sx Sx Sx Transfer - - T B * * ‡ ‡ Lesionsize Caligiuri et al, JCI 109:745, 2002
- 9. Do T cells recognize antigens in atherosclerosis?
- 10. 0 1 2 3 4 5 oxLDL - - + + + + MC + - - + + + MAb - - - - anti-DR Ctrl ab T cells of human plaques recognize oxLDL as antigen Stemme et al PNAS 1995
- 11. G Cooper, The Cell CD4+ T cells recognize oligopeptide epitopes What about the lipids?
- 12. NKT cells are specialised T cells that recognize glycolipid antigens NKT NKT cells use TCRαβ to recognize glycolipids CD1 binds glycolipid antigens presentation to NKT cells NKT APC G K Hansson
- 13. A role for NKT cells in atherosclerosis? Experimental strategies: • Cross apoE0 with CD1d0 • Activate NKT cells in apoE0 with ”artificial” lipid antigen, α−Galactosyl Ceramide E Tupin et al, J Exp Med 2004; 199:417-422
- 14. E Tupin et al, J Exp Med 2004; 199:417-422 NKT cells increase atherosclerosis αGalCer activates NKT and increases atheroscl No effect of αGalCer in CD1d-/- apoE-/- Reduced atherosclerosis in CD1d-/- apoE-/- mice Lesions at 15 wk
- 15. TGF-β inhibits T cell activation - role in atherosclerosis? - TNFα IL-4 IL-10 IFNγ Non-functional receptors TGFβ APC T cell No effect of dampening signal! Mouse carrying a dominant-negative TGFβR in T cells (Gorelik & Flavell 2000) Cross w/ apoE-/- mouse
- 16. Dramatically increased atherosclerosis in mice lacking TGF-β regulation of T cells Dominant-negative TGFβR under CD4 promoter x apoE-/- Robertson et al, J Clin Invest 2003; 112:1342-50
- 17. Adhesion Chemotaxis Recruitment of immune cells to forming atherosclerotic lesions G K Hansson
- 18. APC CD4+T NKT Antigens activate T cells in lesions oxLDL, HSP60, others? Activation & Th1 differentiation IL-12 IL-18, IL-15 G K Hansson
- 19. Activation of macrophages, endothelial and smooth muscle cells IFN-γ IFN-γ TNF-α CD40L/R Th1 MΦ EC SMC Adhesion Permeability Prothrombotic state Proteases ↓ proliferation ↓ collagen ↓ actin IL-6 Inflammatory mediators G K Hansson
- 20. Regulation of immune activity IL-10 TGF-β TGF-β Treg Th2 Th1 MΦ SMC EC Antigen-specific Treg activation
- 21. Atheroprotective immune mechanisms • Regulatory T cells – Produce antiinflammatory/immunosuppressive cytokines – TGF-β • Robertson JCI 03; Mallat Blood 03; – IL-10 • Mallat Circ Res 99; Pinderski ATVB 99; Caligiuri Mol Med 02 • B cells – Spleen B cells; B1 cells – Stimulated by IL-5 – Possibly due to production of ”natural” antibodies • Caligiuri JCI 02; Binder Nat Med 02, JCI 04
- 22. Can we use protective immunity to protect against atherosclerosis?
- 23. Protective immunization Model: Mutant rabbits, mice Antigen: OxLDL, MDA-LDL, HSP60, beta 2- glycoprotein Administration: Th2 adjuvant sc or mucosal Significant protection after 3 months! Palinski PNAS 95; Ameli ATVB 96; George Athero 99; Zhou ATVB 00 Harats JACC 02; Maron Circ 02
- 24. Vaccination against atherosclerosis? • Antigen-specific protective immunity • Mediated by B cells and regulatory T cells (?) • Protective immunization works in models – MDA-LDL; Phosphorylcholine; HSP65/60 • Many remaining questions and challenges: – Precise epitopes, pure antigens – Administration routes, adjuvants
- 25. Inflammation Repair Innate immunity Adaptive Th1 immunity IFN-γ IL-18 TNF-α IL-1 Antiinflammatory immunity Humoral immunity IL-10 TGF-β Anti-oxLDL MΦ activation Endothelial activation Radicals Proteinases Prothrombotic state Antiinflammation Fibrosis SMC proliferation Plaque stability Antibody clearance Immune regulation of plaque activity G K Hansson
- 26. Nilsson, Hansson, Shah, ATVB, in press