200 is coated stent the answer
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This document discusses drug-coated stents for preventing restenosis. It summarizes a study showing that stents coated with the immunosuppressant sirolimus reduced restenosis by 50% by inhibiting cell proliferation. While adding dexamethasone provided no additional benefit. If further trials confirm the results, sirolimus-coated stents may become the standard therapy for coronary revascularization. However, questions remain about whether coating and stenting all vulnerable plaques found is the best long-term treatment approach.
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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 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
In stent retenosis pathophysiology
- Drug-eluting stents significantly reduced restenosis rates compared to bare-metal stents, but in-stent restenosis still occurs in 5-10% of cases.
- Restenosis can be focal or diffuse and is classified based on its severity and treatment approach. Higher grades of restenosis are associated with poorer outcomes.
- Factors contributing to in-stent restenosis include patient and lesion characteristics, stent design and materials, drug effects, inflammation, neoatherosclerosis, low wall shear stress areas, and potential thrombus formation.
- Earlier and more rapid neoatherosclerosis may occur inside drug-eluting stents compared to bare-metal stents,
In stent restenosis
The document discusses in-stent restenosis (ISR), defined as the re-narrowing of a stented coronary artery due to neointimal tissue proliferation. ISR rates range from 3-20% with drug-eluting stents and 16-44% with bare-metal stents, usually occurring 3-20 months after stent placement. Predictors of ISR include patient characteristics like diabetes, lesion characteristics like length, and procedural characteristics like stent undersizing. The main mechanism is neointimal tissue proliferation due to arterial wall damage during stenting. ISR treatment involves revascularization like balloon angioplasty or additional stenting.
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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.
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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.
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- Drug-eluting stents significantly reduced restenosis rates compared to bare-metal stents, but in-stent restenosis still occurs in 5-10% of cases.
- Restenosis can be focal or diffuse and is classified based on its severity and treatment approach. Higher grades of restenosis are associated with poorer outcomes.
- Factors contributing to in-stent restenosis include patient and lesion characteristics, stent design and materials, drug effects, inflammation, neoatherosclerosis, low wall shear stress areas, and potential thrombus formation.
- Earlier and more rapid neoatherosclerosis may occur inside drug-eluting stents compared to bare-metal stents,
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This document discusses in-stent neoatherosclerosis, which refers to the development of new atherosclerotic lesions inside coronary stents. Percutaneous coronary intervention procedures like stenting cause endothelial injury and disrupt blood flow, promoting inflammation and accelerated atherosclerosis. Over time, this can lead to problems like in-stent restenosis and late stent thrombosis. While similar to native coronary atherosclerosis, in-stent neoatherosclerosis develops more rapidly. Factors like stent strut design, polymer coatings, and incomplete re-endothelialization all contribute to this pathological process.
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InStent Resetenosis: An Algorithmic Approach to Diagnosis and Treatment
BMS were developed to mitigate elastic recoil and negative remodeling, but they remain prone to NIH. DES were developed to prevent NIH, and these devices (especially first-generation DES) can be accompanied by delayed reendothelialization, which has been associated with stent thrombosis.
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Plasmacytoma
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Esnrt poster cd20
This case report describes a case of refractory acute cellular rejection in a kidney transplant patient that was successfully treated with the monoclonal antibody rituximab. The patient developed sudden graft dysfunction 2 days post-transplant. Initial biopsy showed significant cellular infiltration but no antibody-mediated rejection. Further staining revealed 90% of infiltrating cells were CD20-positive. Treatment with steroids, plasmapheresis, and immunosuppression intensification failed to improve the graft. A single dose of rituximab led to improvement in graft function and disappearance of CD20-positive cells on follow-up biopsy. This highlights the importance of detailed cellular characterization in refractory rejection and targeting therapy to the specific cell population involved.
Total body irradiation
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A 20-year-old male kidney transplant recipient presented with a fever and dental pain from a mass in his lower mandible. Imaging showed a cystic space occupying lesion involving his wisdom tooth. Surgical excision of the mass and extraction of the impacted teeth was performed. Histopathology revealed the mass was a giant cell reparative granuloma. This lesion is a benign non-neoplastic tumor that can develop from local trauma or vascular injury. It is rarely reported in kidney transplant patients and careful monitoring of parathyroid hormone levels and immunosuppression is important for management.
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1) Bone and joint infections are difficult to treat due to bacterial adhesion and biofilm formation on implants which impairs the host immune response. Clindamycin inhibits bacterial adhesion and penetrates biofilms.
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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.
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.
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Vulnerable plaque refers to dangerous forms of atherosclerotic plaques that can rupture or induce thrombosis, disrupting blood flow. The document discusses the history and research around vulnerable plaque, including pioneers in the field and emerging techniques to detect vulnerable plaque such as intravascular ultrasound, optical coherence tomography, and magnetic resonance imaging. It summarizes that vulnerable plaques are typically characterized by a thin fibrous cap, large lipid core, and presence of macrophages.
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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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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 summarizes presentations from symposia on vulnerable plaque and discusses the relationship between plaque, blood, and patients in atherothrombosis. It notes that multiple factors like diabetes, smoking, and hyperlipidemia can make blood more thrombogenic and moderate the severity of acute events after plaque rupture. Statins, aspirin, and other drugs that target tissue factor or thrombin pathways may be promising antithrombotic agents by inhibiting thrombosis initiation and propagation.
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The document discusses vulnerable plaque and challenges in detecting and treating it. It describes various imaging techniques for detecting vulnerable plaque such as thermography, MRI, CT angiography, and optical coherence tomography. However, it notes that while these can identify high-risk features, it remains unclear what exactly defines vulnerable plaque and whether imaging findings truly correlate with risk. The document also notes that while statins reduce events, the relationship between plaque burden and events is unclear, and better defining and detecting the disease is still needed before new therapies can be developed.
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1) The study examined 92 hearts from patients with severe coronary artery disease who died suddenly. The hearts were sectioned and plaque types were classified.
2) The number of "vulnerable" plaques, particularly thin cap atheromas, was highest in hearts of patients who died from acute plaque rupture and lowest in those with incidental disease.
3) Thin cap atheromas and other unstable plaque types were concentrated in the proximal coronary segments, similar to the distribution of plaque ruptures. The study suggests vulnerable plaques contribute to acute coronary syndromes and are non-uniformly distributed within the coronary arteries.
Vp watch editorial_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 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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The document discusses magnetic resonance imaging (MRI) studies of atherosclerosis in human carotid arteries. It summarizes several studies examining features of carotid plaques such as calcified regions, neovasculature and necrotic cores, reproducibility of measurements, appearance of intraplaque hemorrhage, and MRI appearance of thick fibrous caps. The document includes MRI images and photomicrographs comparing MRI findings to histology.
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200 is coated stent the answer
- 1. Editorial Slides - VP Watch, September 5th , 2001, Volume 1, Issue 25 Is coated stent THE answer?
- 2. In-Stent Restenosis = Neointimal Hyperplasia The long-term clinical efficacy of intracoronary stenting is limited by restenosis which, occurs in 15-30 % of patients. In- stent restenosis is due solely to neointimal hyperplasia. Shape and chemical biocompatibility of stent, and the extent of inflammatory response to stenting are among major factors predicting restenosis. Intravascular radiation has shown significant benefit however the cost, repated interventions, radiation safety, short and long term adverse effect all remain unresolved issues. Experimental data suggest that in-situ immunosuppressant and inhibitors of cell cycle progression may be an effective strategy to prevent restenosis.
- 3. Effects of drug-coated stents on arterial repair Suzuki et al., Circulation. 2001;104:1188 Endothelium SM C Fibrin 0 1/2 1 1 1/2 2 2 1/2 3 Repairscore Control Dexametasone Sirolimus SRL+DEX From VP Watch this week: High-power photomicrographs of bare metal (B) and SRL-coated (C) stents
- 4. As highlighted in VP Watch this week, Suzuki, Carter, et al. determined that stents coated with a nonerodable polymer matrix containing 185 µg SRL compared with a bare metal stent reduces restenosis by 50% through inhibiting cellular proliferation. The dose-response effects for this SRL-eluting stent are incompletely characterized but, they indicated a dose- dependent reduction in intimal hyperplasia with 60 µg to 200 µg SRL–coated stents in the rabbit model. Circulation 2001;104:1188 Also Suzuki et al. also showed that stent-based delivery of dexamethasone (DEX) alone is insufficient to inhibit neointimal formation. They did not observed any synergism in combination of dexamethasonwith SRL. Circulation 2001;104:1188
- 5. It was shown years go that intraperitoneal administration of SRL, a potent immunosuppressive agent, resulted in a dose-dependent inhibition of arterial intimal thickening caused by either chronic alloimmune or mechanical injury in a rat model. (Gregory CR, Huie P, Billingham ME, et al., Transplantation. 1993; 55: 1409–1418) Other studies about the effect of Sirolimus on restenosis: Other studies also show that SRL inhibits the proliferation of vascular SMC in human and rat in vitro by blocking the G1 /S transition. (Poon M et al., J Clin Invest. 1996; 98: 2277–2283 and Marx SO et al., Circ Res. 1995; 76: 412– 417) Study of Gallo et al. indicates that systemic SRL therapy significantly reduces the proliferative response after coronary angioplasty in the porcine model. (Circulation. 1999; 99: 2164–2170)
- 6. Latest on Sirulimon restenosis clinical trial: The RAVEL study this week reported “zero” restenosis at 210 days. Congress of European Society of Cardiology Stockholm Sep 1-5th
- 7. Conclusion: Stent-based delivery of Sirolimus via a nonerodable polymer matrix is feasible and effectively reduces restenosis. Adding dexamethasone did not offer additional benefit. If RAVEL holds true for 5 years, the immunosuppressant RAPAMUNE® (Sirolimus) coated stents becomes the standard therapy for coronary revascularization.
- 8. Questions: Feel free to send your response to: Discussion-Group@VulnerablePlaque.org Knowing atherosclerosis as a diffuse disease, do you think that stenting vulnerable plaques with coated stents can be the treatment of choice besides statins? If the coated stent reduces restenosis by 90%, will you stent every vulnerable plaque? What if you find 3, 4, 5 or more vulnerable plaques in one patient?