506 what is the link between infection and cardiovascular events
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This document summarizes findings from the Heart Outcomes Prevention Evaluation (HOPE) study regarding the relationship between infections and cardiovascular events. The HOPE study analyzed antibodies to four pathogens (Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, hepatitis A virus) in over 3,000 patients over 4.5 years. While C. pneumoniae and H. pylori antibodies showed no significant association, cytomegalovirus antibodies were mildly correlated with increased cardiovascular risk. Having a higher "total pathogen score" based on levels of antibodies to all four pathogens predicted a higher risk of cardiovascular events compared to having none or just one infection.
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Optical Coherence Tomography (OCT) can characterize plaque morphology as fibrous, lipid-rich, or calcified. Unstable plaques tend to be lipid-rich with diffuse borders compared to stable fibrous plaques. Post-acute myocardial infarction studies using OCT found a high incidence of lipid-rich plaques, plaque disruption, residual thrombus, and stent prolapse, indicating unstable plaque morphology contributes to coronary syndromes.
Dr falk's slides part ii
This document summarizes key points from a task force report on identifying and treating asymptomatic patients vulnerable to heart attack. It introduces a new paradigm focused on outcomes studies, measuring disease activity, and identifying the vulnerable plaque and patient. The report was chaired by Morteza Naghavi and had writing contributions from experts in cardiovascular imaging, risk assessment, and prevention. It aims to advance the field beyond traditional risk factor assessment alone.
Old vulnerable patient slides without movies
The document discusses vulnerable plaques and patients. It describes that ruptured plaques are the most common type of culprit lesion, causing around 70% of heart attacks. While stenotic plaques are only responsible for around 20% of heart attacks, non-stenotic plaques which are more frequent, cause around 50% of heart attacks. Both the morphology and activity of plaques need to be assessed to identify vulnerable plaques and patients.
223 edta chelating therapy
1) Studies have shown chelation therapy using EDTA to remove calcium from atherosclerotic plaques is unlikely to provide benefits and may be harmful. Randomized controlled trials have failed to show improvements in outcomes.
2) A recent study of 53 patients with coronary artery disease found no significant differences in endothelial function between those receiving EDTA chelation therapy and placebo over 6 months.
3) There is no evidence chelation therapy is effective or that removing small amounts of calcium from plaques would impact disease. Calcium strengthens plaques and its deposition is an active process, not simply passive buildup.
Esv2n22
Atherosclerotic cardiovascular disease is the leading cause of mortality worldwide, resulting from vulnerable plaque. Vulnerable plaque often causes acute coronary syndromes and sudden cardiac death. A vulnerable patient has vulnerable plaque and/or vulnerable blood and/or vulnerable myocardium, putting them at high risk for sudden cardiac events. Markers of vulnerable plaque include inflammation and thin plaque caps. Markers of vulnerable blood include increased platelet aggregation and coagulation factors. A study found that C-reactive protein (CRP) levels independently predict risk of sudden cardiac death in healthy men, so CRP may help identify vulnerable patients.
Macrophage induced proteolysis zorina galis- emory u
Macrophage induced proteolysis zorina galis- emory uSociety for Heart Attack Prevention and Eradication
This document summarizes research on matrix metalloproteinases (MMPs) and their role in weakening atherosclerotic plaques. It finds that MMPs are expressed in human atherosclerotic plaques, especially in macrophage foam cells located in the vulnerable shoulders of plaques. Several MMPs have been shown to degrade components of the fibrous cap, including collagen. Reactive oxygen species produced by macrophage foam cells can activate latent MMPs. Treatments that reduce oxidative stress, such as N-acetyl cysteine, decrease MMP expression and activity in experimental atherosclerosis. Overall, the document provides evidence that MMPs expressed by macrophage foam cells may weaken plaques through degradation of the fibrous cap, making plaques moreErbel
An intramural hematoma (IMH) is a thickening of the aortic wall due to bleeding within the wall in the absence of an intimal tear. It is considered a precursor to aortic dissection and is classified as a class 2 aortic dissection. A penetrating atherosclerotic ulcer (PAU) is caused by the erosion of an atherosclerotic plaque through the internal elastic lamina into the media. It is classified as a class 4 aortic dissection. Both IMH and PAU can lead to complications like intramural hematoma formation, pseudoaneurysm, aortic dissection, and rupture. Progression from IMH to overt aortic dissection or rupture indicates a
Asme05 ibis
1) The study investigated the relationship between shear stress and plaque vulnerability in human coronary arteries. Shear stress was calculated using 3D lumen and wall data from angiography and IVUS, combined with computational fluid dynamics. Plaque vulnerability was assessed using IVUS-based palpography data to render radial strain maps.
2) Results showed that low shear stress downstream of plaques related to low strain, indicating less vulnerable plaques. High shear stress predicted locations of high strain spots, confirming the hypothesis that high shear stress relates to plaque vulnerability.
3) Follow-up data is still needed to confirm this relationship between high shear stress and plaque vulnerability. The study provides insight into how hemodynamics relate to plaque
505 definitions of arterial remodeling in post mortem and intravascular ultra...
505 definitions of arterial remodeling in post mortem and intravascular ultra...Society for Heart Attack Prevention and Eradication
This document discusses various definitions of arterial remodeling used in post-mortem and intravascular ultrasound research. It notes that the different definitions lead to large variations in reported prevalence numbers for expansive, intermediate, and constrictive remodeling. The definitions are analyzed and some are noted to only be suitable for certain study types. It concludes that careful consideration of the remodeling definition used is needed when reporting prevalences, as without a gold standard or serial studies, the reference sites may not be free of atherosclerotic disease and could themselves be remodeled.Out of hospital 2
The document discusses out of hospital sudden cardiac death (SCD) and whether rates are declining or escalating. Key points include:
1. Over 400,000 SCDs occur annually out of hospital or upon arrival to the emergency room.
2. Pre-hospital delay times in the U.S. have not declined in recent decades and impede treatment of SCD, which remains a major public health challenge.
3. Improving early recognition of heart attack symptoms and rapid intervention through public health initiatives could help reduce SCD rates and save more lives.
Pandemic of cvd atlanta
This document provides guidelines from the Association for Eradication of Heart Attack on defining vulnerable plaques and vulnerable patients. It outlines major and minor histopathological and clinical criteria for defining vulnerable plaque, including active inflammation, thin fibrous cap, endothelial dysfunction, and intraplaque hemorrhage. Potential diagnostic methods are discussed for plaque-level and systemic-level screening and diagnosis of vulnerability, such as MRI, ultrasound, spectroscopy and blood biomarkers. Different types of vulnerable plaques that can cause acute coronary events are also categorized.
Ebt rumberger- ohio state u- part 4
The document discusses that less obstructive plaques pose a greater risk of coronary occlusion than severely obstructed plaques due to their greater numbers. It also states that the aggregate risk of rupture from many non-significant lesions exceeds that of fewer significant lesions, so a myocardial infarction is more likely to originate from a non-significant lesion. Additionally, it explains that while electron beam tomography (EBT) cannot identify vulnerable plaques directly, it can identify vulnerable patients based on their coronary artery calcium (CAC) scores and percentile ranks, as risk increases with higher scores. EBT is also useful for estimating prognosis and tracking changes in plaque in response to treatment over time.
Dr maseri aeha_neworleans_mar2004
1) The document discusses different types of patients presenting with acute coronary syndromes (ACS) and whether their clinical characteristics and triggers of ACS can help identify specific causes.
2) It identifies two types of ACS - Type 1 involves infarction out of the blue with complete stability before and after, while Type 2 involves unstable angina progressing to infarction and recurrent ACS.
3) Elevated C-reactive protein (CRP) levels are found in most unstable angina, myocardial infarctions preceded by unstable angina, and predict recurrent instability, suggesting its role in inflammation underlying ACS.
Esv2n15
I. The document summarizes several studies that investigated the role of the immune system, particularly B cells, in atherosclerosis using mouse models.
II. One study found that RAG-1 deficient mice, which lack functional B and T cells, exhibited increased neointimal formation following arterial injury compared to wild type mice. Transferring B cells from wild type mice to RAG-1 deficient mice reduced neointimal formation.
III. Overall, the studies suggest that B cells may play a protective role against atherosclerosis by reducing plaque formation and progression. The mechanism may involve antibodies that target oxidation-specific epitopes, but this requires further investigation.
Litovsky1
The document discusses several factors that are considered predictors of plaque vulnerability, including luminal narrowing, plaque volume and composition, fibrous cap thickness, and plaque inflammation. It reviews studies that show myocardial infarction can develop from previously non-severe lesions and that lipid content, cap thickness, inflammation, and stress factors like circumferential stress are correlated with plaque stability and vulnerability. In conclusion, the size and composition of the lipid core, thickness and composition of the fibrous cap, and inflammation are well-established predictors of plaque rupture.
Percutaneous coronary intervention by hossein
This document discusses animal models for studying vulnerable plaque and atherosclerosis. It describes how the chicken, pig, mouse, and rabbit models each have advantages and limitations for replicating human disease. The mouse has been genetically modified to better model plaque development. No current animal model fully captures plaque rupture seen in humans. The rabbit model with an embedded inflatable balloon shows promise for experimentally inducing plaque rupture.
Contrast enhanced mri of vulnerable plaque black or white
Contrast enhanced mri of vulnerable plaque black or whiteSociety for Heart Attack Prevention and Eradication
1. Gadolinium-based contrast agents accumulate in inflamed regions of arterial walls, highlighting areas of increased endothelial permeability, tissue water, and neovascularization associated with inflammation.
2. Studies have shown gadolinium contrast-enhanced MRI can identify arterial inflammation earlier than increases in wall thickness and is associated with elevated serum markers of inflammation.
3. Similarly, superparamagnetic iron oxide (SPIO) nanoparticles have demonstrated potential as a negative contrast agent for MRI detection of atherosclerotic plaques by accumulating in plaque macrophages and creating dark spots in inflamed areas.Ebt and coronary artery calcium
Coronary artery calcium detected by electron beam tomography (EBT) establishes a diagnosis of coronary atherosclerosis, as there are no false positive calcium measurements. The amount of calcium seen on EBT correlates directly with the actual amount of coronary plaque measured by intravascular ultrasound and histopathology. Studies have also shown that a higher coronary artery calcium score on EBT is associated with greater risk of future myocardial infarction, sudden cardiac death, or ischemia over follow-up periods of 3-6 years.
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Macrophage induced proteolysis zorina galis- emory u
Macrophage induced proteolysis zorina galis- emory u
505 definitions of arterial remodeling in post mortem and intravascular ultra...
505 definitions of arterial remodeling in post mortem and intravascular ultra...
Contrast enhanced mri of vulnerable plaque black or white
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Similar to 506 what is the link between infection and cardiovascular events
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Rheumatic heart disease is a major health problem in developing countries caused by heart lesions following rheumatic fever episodes in 30-45% of patients with untreated strep throat infections. Rheumatic fever results from an autoimmune reaction triggered by strep throat that leads to valvular damage in genetically susceptible individuals. Molecular mimicry between proteins in the streptococcus bacteria and human heart proteins is thought to underlie the pathogenesis of rheumatic heart disease.
Cell Salvage in PBM
This document contains summaries of multiple studies that have found associations between red blood cell transfusions and negative health outcomes in critically ill and surgical patients. Specifically:
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A fresh look at cell salvage
This study analyzed 45 observational studies including over 272,000 patients to determine the association between red blood cell transfusion and morbidity and mortality in high-risk hospitalized patients. The analysis found that in 42 of the 45 studies, the risks of red blood cell transfusion outweighed the benefits, with transfusion associated with increased risk of death, infections, multi-organ dysfunction syndrome, and acute respiratory distress syndrome. A meta-analysis found that transfusion was associated with 70% higher odds of death and 80% higher odds of developing an infectious complication. The study suggests current transfusion practices may need reevaluation given the risks appear to outweigh the benefits in most patients.
Mathematical modeling
This document provides a summary of mathematical modeling of HIV/AIDS treatment. It discusses the background and history of the HIV epidemic, noting that the number of people living with HIV has increased to 32-38 million globally since 1981. Prevention programs like antiretroviral treatment (ART) have helped reduce prevalence since 1999. The document examines the natural history and transmission of HIV, antiretroviral therapy, socioeconomic risks, and the genetic structure and replication cycle of HIV. It states the problem is determining the optimal timing for ART initiation to increase immunity and decrease mortality and mobility from the disease.
Cardiovascular Disease in HIV-Infected Patients.Predict It and Prevent It.2015
In this downloadable slideset, Priscilla Y. Hsue, MD, and David A. Wohl, MD, discuss data on using traditional and newer markers and modalities to predict and prevent cardiovascular disease in HIV-infected patients.
Format: Microsoft PowerPoint (.ppt)
File size: 3.21 MB
Date posted: 7/16/2015
Сердечно-сосудистые заболевания у ВИЧ-инфицированных пациентов : предсказать ...
Cardiovascular Disease in HIV-Infected Patients.Predict It and Prevent It. 2015
In this downloadable slideset, Priscilla Y. Hsue, MD, and David A. Wohl, MD, discuss data on using traditional and newer markers and modalities to predict and prevent cardiovascular disease in HIV-infected patients.
Format: Microsoft PowerPoint (.ppt)
File size: 3.21 MB
Date posted: 7/16/2015
HCV in CKD
This document discusses treatment of hepatitis C in patients with chronic kidney disease. It begins by establishing the association between HCV infection and CKD, noting that HCV can cause renal impairment and progression of kidney disease through various mechanisms. It then reviews outcomes in this population such as increased prevalence of CKD, faster progression to ESRD, higher mortality rates, and poorer outcomes after renal transplant compared to those without HCV infection. The document next evaluates earlier treatment options with interferon-based regimens, which had low efficacy and significant side effects. It then discusses approval and study of newer direct-acting antiviral regimens, finding improved efficacy and safety particularly with sofosbuvir and glecaprevir/pibrentasvir
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This document reviews literature on anaesthetic considerations for HIV-positive parturients. Several studies found that regional anaesthesia can be safely administered and does not negatively impact immune function or disease progression in asymptomatic HIV-positive women. While some early concerns existed around potential neurological complications, more recent research has found no increased risk. The choice of anaesthesia should be based on standard obstetric factors, with regional anaesthesia being a good option for caesarean delivery when there are no contraindications. Overall, the literature indicates that with proper clinical management including antiretroviral therapy, both general and regional anaesthesia can be used safely in HIV-positive parturients.
Global Burden Of Hypertension In People Living With HIV.docx
Global Burden Of Hypertension In People Living With HIV analyzes the prevalence of hypertension in people living with HIV (PLHIV) across different regions. About 24% of PLHIV have hypertension, totaling nearly 8.9 million affected globally. A meta-analysis found the prevalence of hypertension was significantly higher in PLHIV in North America and lower in sub-Saharan Africa and Asia, with no difference in South America and Europe. The association between HIV and hypertension is determined by biological factors like endothelial dysfunction and inflammation caused by HIV and antiretroviral therapy, which increase blood pressure in PLHIV. However, mortality due to AIDS is still higher in low-income countries like sub-Saharan Africa, so PLHIV
Rheumatic feve 2018
Rheumatic heart disease is a major health problem in many developing countries. It results from autoimmune reactions triggered by untreated streptococcal throat infections, leading to valvular damage. Genetics play a role in susceptibility. The pathogenesis involves molecular mimicry between antigens in group A streptococcus bacteria and human proteins, which can induce cross-reactive antibody responses and result in autoimmune-mediated damage to heart valves and other tissues. Cytokines and specific immune responses are also involved in the progression of rheumatic heart disease.
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The document discusses cardiovascular risk in HIV patients. It finds that HIV patients have approximately double the risk of heart attacks and myocardial infarction compared to HIV-negative people after adjusting for traditional risk factors. Interrupting antiretroviral therapy, as shown in the SMART study, increases the risk of opportunistic disease, death, and non-AIDS events like cardiovascular or renal disease compared to continuous treatment. Protease inhibitors have been associated with a slightly higher risk of heart attacks than non-nucleoside reverse transcriptase inhibitors.
RA-ILD Infection Poster ACR 2016 (Final Version)
This study examined the risk of serious infection in patients with rheumatoid arthritis (RA) and interstitial lung disease (ILD). The study identified 181 RA patients with ILD between 1998-2014. It found that these patients faced a high risk of serious infections requiring hospitalization, with an overall rate of 7.4 infections per 100 person-years. The risk was highest for patients with organizing pneumonia ILD (27.1 per 100 person-years) and lower for nonspecific interstitial pneumonia and usual interstitial pneumonia. Use of high-dose prednisone (>10mg per day) was also linked to greater infection risk. Identifying patients at highest risk could help reduce infection-related morbidity.
2015-42-4_6
This document discusses a study investigating hospital-acquired pneumonia (HAP) and the association between HAP and chronic comorbidities. The study included 213 HAP patients and found the most common pathogens were Streptococcus spp. for early-onset pneumonia and Acinetobacter spp. for late-onset pneumonia. Antibiotics like quinolones, cephalosporins and carbapenems were most commonly used but showed high resistance rates. Higher Chronic Disease Scores, older age, cancer, and mechanical ventilation were associated with worse treatment outcomes.
HCV MANAGEMENT IN PATIENT WITH KIDNEY DISEASE..reuploaded
HCV infection is associated with an increased risk of chronic kidney disease and renal impairment. Treatment of HCV in patients with renal disease prior to direct-acting antivirals was not very effective due to significant side effects of interferon-based regimens. The introduction of direct-acting antivirals such as sofosbuvir provided more effective and tolerable treatment options, though patients with severe renal impairment still experienced worse side effects and lower response rates. Effective treatment of HCV in patients with renal disease is important given their risk of faster liver disease progression and greater liver-related morbidity and mortality compared to those with normal renal function.
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Antibiotics bugs- us1 [autosaved]
This document discusses nosocomial (hospital-acquired) infections, specifically one case involving a woman who developed septic shock after being discharged from the hospital. The key points are:
1) The woman was hospitalized for heart failure but developed a fever and signs of septic shock 4 days after discharge.
2) Testing revealed she had a urinary tract infection caused by E. coli, likely acquired from an indwelling urinary catheter placed in the hospital.
3) Nosocomial infections pose a major safety issue, increasing length of stay, costs, and mortality. Gram-negative bacteria are a particular concern due to their ability to rapidly develop antibiotic resistance.
4) Prevention strategies
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A 35-year-old male patient with HIV was admitted with complaints of painful swelling in his right lower limb. Doppler imaging showed deep vein thrombosis in the right leg. The patient had no other risk factors for DVT. He was treated with anticoagulation therapy and his symptoms improved. Deep vein thrombosis is more common in HIV-infected individuals due to factors causing a hypercoagulable state induced by the virus. The report examines the case of DVT in an HIV-positive patient without other risk factors.
Journal of Hepatitis Research
There are significant gender differences in hepatitis B and C virus infections. Men are more likely than women to become chronic carriers of HBV and to develop hepatocellular carcinoma. Women have slower progression of HCV infection to cirrhosis and lower risk of developing HCC. Viral and host factors likely contribute to these disparities, including sex hormones like testosterone and estradiol. Testosterone enhances HBV replication while estradiol reduces HCV production and promotes immune response. Understanding these gender differences can help improve treatment and prevention strategies.
Journal of Hepatitis Research
Journal of Hepatitis Research is a peer-reviewed, open access journal published by Austin Publishers. It provides easy access to high quality Manuscripts in all related aspects of different hepatitis symptoms and treatments caused by viral hepatitis, including hepatitis A, hepatitis B, and hepatitis which are distinct diseases that affect the liver. It focuses upon all the pathophysiology and treatments for the illness caused by Hepatitis.
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More from Society for Heart Attack Prevention and Eradication
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
AHA SHAPE Symposium 2017 Dr. Greenland PresentationSociety for Heart Attack Prevention and Eradication
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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AHA SHAPE Symposium 2017 Dr. Greenland Presentation
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Recently uploaded
The Electrocardiogram - Physiologic Principles
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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506 what is the link between infection and cardiovascular events
- 1. Editorial Slides VP Watch, January 29, 2003, Volume 4, Issue 4 What is the link between infection and cardiovascular events?
- 2. A possible role for infections in atherosclerosis has been intensely investigated since the landmark demonstration of herpes virus-induced atherosclerosis in chickens by Fabricant in 19781 .
- 3. Human atherosclerotic disease has been associated with previous exposure to several microorganisms including Chlamydia pneumoniae, Porphyromonas gingivalis, CMV, HSV-1, HSV-2, hepatitis A virus, influenza virus, enterovirus, etc. Prospective studies are, however, limited.
- 4. A relatively recent approach suggests that the total pathologic burden is a stronger predictor of cardiovascular events than any particular infection2,3,4 . Large randomized trials of antibiotic for secondary prevention of cardiovascular disease have been performed or are ongoing5,6 but even failure of those treatments should not be construed as evidence that the infectious theories are incorrect.
- 5. As highlighted in VP Watch of this week, Smieja et al7 , for the Heart Outcomes Prevention Evaluation (HOPE) study, analyzed sera from 3168 patients for antibodies to Chlamydia pneumonia, H. Pylori, CMV and hepatitis A and followed the patients over 4.5 years of follow-up.
- 6. (Figure 1)
- 7. Figure 1 depicts a Kaplan- Meier plot for cumulative cardiovascular events by titer levels of C. pneumoniae IgG (A) and IgA(B). No statistical significance was found.
- 8. (Figure 2)
- 9. Figure 2 depicts a Kaplan- Meier plot for cumulative cardiovascular events by presence or absence of antibody to H. pylori, CMV, and HAV. Serology for CMV shows a mild predictive correlation with cardiovascular events with a hazard ratio (HR) of 1.24.
- 10. (Figure 3)
- 11. Figure 3 depicts a Kaplan-Meier plot for cumulative cardiovascular events by total pathogen score (C pneumoniae IgG 512 or IgA 64; H pylori >40 AU; CMV >0.4 mIU/mL; and HAV >20 IU/mL). HR compares total pathogen score of 4 versus 0 or 1 combined. A score of 4 had an adjusted HR of 1.41 versus 0 or 1.
- 12. Exposure to CMV but not C. pneumoniae, H. pylori or HAV was associated with a slight excess risk of subsequent cardiovascular events (myocardial infarction, stroke, cardiovascular death) Conclusion
- 13. Total pathogen score based on these 4 infections predicted an increase hazard of cardiovascular events compared to the presence of none or only one of these infections. Con’t
- 14. ReferencesReferences 1. Fabricant CG, Fabricant J, Litrenta MM, et al. Virus- induced atherosclerosis. J Exp Med. 1978; 148: 335–340. 2. Zhu J, Nieto FJ, Horne BD, et al. Prospective study of pathogen burden and risk of myocardial infarction or death. Circulation. 2001; 103: 45–51. 3. Zhu J, Quyyumi AA, Norman JE, et al. Effects of total pathogen burden on coronary artery disease risk and C- reactive protein levels. Am J Cardiol. 2000; 85: 140–146 4. Rupprecht HJ, Blankenberg S, Bickel C, et al. Impact of viral and bacterial infectious burden on long-term prognosis in patients with coronary artery disease. Circulation. 2001; 104: 25–31.
- 15. References 5. Dunne MW. Rationale, and design of a secondary prevention trial of antibiotic use in patients after myocardial infarction: the WIZARD (Weekly Intervention with Zithromax [Azithromycin] for Atherosclerosis and Its Related Disorders) Trial. J Infect Dis. 2000; 181 (suppl 3): S572–S578. 6. Jackson LA. Description and status of the Azithromycin and Coronary Events Study (ACES). J Infect Dis. 2000; 181 (suppl 3): S579–S581. 7. Smieja M, Gnarpe J, Lonn E, Gnarpe H, Olsson G, Yi Q, Dzavik V, McQueen M, Yusuf S. Heart Outcomes Prevention Evaluation (HOPE) Study Investigators. Circulation 2003;107:251-7