035 respiratory infection of apo e ko mice
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1) Acute respiratory infection caused by influenza virus led to excessive plaque inflammation in the aortas of ApoE knockout mice. 2) One third of infected mice showed inflammatory infiltrates associated with platelet clusters and fibrin near the plaques. 3) The study aimed to investigate if acute respiratory infection can increase plaque inflammation and macrophage infiltration, and to examine related cytokine and receptor expression over the longer term.
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The definition of pyrexia of unknown origin (PUO) dates back to 1961; it was described as a persistent fever above 38.3°C (100°F) that evades diagnosis for at least 3 weeks, including 1 week of investigation in hospital. PUO and present a systematic clinical approach to the investigation and management of patients, recommending potential second-line investigations when the etiology is unclear
Drnaghavi
1) Influenza infection was found to exert prominent inflammatory and thrombotic effects on atherosclerotic plaques in aged Apo E-deficient mice.
2) About one third of the infected mice showed striking intimal infiltrates in the aorta and most of these mice died or were sacrificed between days 4-10 post infection.
3) Administration of cytokines mimicking influenza infection resulted in greater iron accumulation in macrophage-rich regions of plaques compared to controls, indicating enhanced macrophage homing to plaques.
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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.
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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.
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The document provides guidelines for defining vulnerable plaque and vulnerable patients from the Association for Eradication of Heart Attack. It outlines major and minor histopathological and clinical criteria for vulnerable plaque including active inflammation, thin fibrous cap with large lipid core, endothelial denudation, and stenosis. Potential screening and diagnostic methods are discussed at the plaque, systemic, and blood levels ranging from non-invasive imaging to intravascular techniques. Different types of vulnerable plaque that can cause acute coronary events are also categorized.
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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.
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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.
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.
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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.
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035 respiratory infection of apo e ko mice
- 1. Respiratory Infection of Apo E KO Mice Causes Excessive Plaque Inflammation Implication for triggering effect of flu in human heart attack Adeeba Akhtar MD, Silvio Litovsky, MD, Philip Wyde PhD, Mohammad Madjid MD, Ward Casscells MD, James Willerson MD, Morteza Naghavi MD.
- 2. Background • The role of infection in atherosclerosis has been known for years. • A number of pathogens such as C. pneumonia, HSV, CMV have been reported to be present in the plaque and moreover related to CHD • Other chronic infections such as H. pylori, and dental infection were also found to increase likelihood of chronic coronary heart disease.
- 3. Background • However, acute effect of infection in triggering coronary events has not received as much attention. • A number of retrospective epidemiological studies have shown the relationship between acute upper respiratory infection and myocardial infarction.
- 4. Background • The role of inflammation and inflammatory cytokines in the development of vulnerable plaque and plaque rupture is now well established. • Increased circulating cytokines was shown to accelerate plaque formation in Apo E mice. • Influenza infection can increase thrombogenecity of blood by increasing platelet aggregation. • We have previously shown in a case-control study that flu vaccination is associated with reduced recurrence of MI.
- 5. Background Therefore we have hypothesized : • 1) Acute influenza infection of old Apo E deficient mice may cause acute coronary event and heart attack. • 2) Acute influenza infection can increase plaque inflammation and macrophage infiltration, with or without rupture/erosion.
- 6. Study Design 42 ApoE Mice Controls infected with Influenza virus Hong Kong P9 LD50 9 Direct infection 24 Intranasal inoculation 9 33 6 sacrificed 3died 11sacrificed 13died
- 7. Procedure: • We measured the baseline weight , heart rate, pulse oximetry of all the infected mice and measured these parameters again before sacrificing. • This was a short term (15 days) study and the mice were sacrificed at 3, 5, 10, 15 days. • After sacrifice we took the heart and aorta in formalin and cut 5 sections for each aorta and one mid-transverse ventricular section of the heart.
- 8. Examinations • Weight (substitute for Temp) • Oxygen sat. • Pulse • Lung virus titration. • rtPCR for influenza virus. • CBC and Hb. • Blood smear. • Multiple aorta and heart specimens for pathology examinations, H&E, Movat, CD68, TUNEL, actin, CD3 staining.
- 9. General Findings • - As expected based on LD 50%, old mice were prompted to die mainly due to overwhelming lung infection . But we sacrificed most of them at their maximum load of infection. • Significant weight loss occurred in all infected mice but not in control mice.
- 10. Specific Findings • Hot and ground-breaking !!! …
- 13. Control mice 2(power 40)
- 14. Control mice 3(power 10)
- 16. Infected Mice 1(Intra nasal group)Power 10
- 17. Power 40
- 18. Power100
- 19. Infected mice2( Intranasal group) power10
- 20. Power 40
- 21. Power100
- 23. power10
- 24. Power40
- 25. power100
- 27. Power 40
- 28. Power100
- 29. Infected Mice5 (Intranasal group) power 4
- 30. Power10
- 31. Power40
- 33. Power10
- 34. Power40a
- 35. Power40b
- 36. Power100
- 37. Infected Mice 7( Direct group) Power10
- 38. Power40
- 39. Infected Mice8 (Intranasal Group) Power 10
- 40. power40
- 41. Power100
- 42. Infected Mice 1(Intranasal Group) Power10
- 43. Power40
- 45. Power10
- 46. Power40
- 48. Power 10
- 49. Power 40
- 54. KP-1 staining (Power 40)
- 55. Conclusion: • One third of the infected mice developed this inflammatory infiltrate associated with clusters of platelets and occasionally fibrin overlying the infiltrate. • The infiltrate is polymorphic (macrophages, smooth muscle cells, T-lymphocytes). Next set of stainings will be done on frozen tissue to improve antigenicity. • Upregulation of inflammatory and procoagulant cytokines and receptors will be investigated. • Longer-term studies will investigate the possible
- 58. Adeeba ! Mitra ! Mort ! Khawar ! Tania ! Birendra !Mohammad ! Silvio ! Moein ! Sadaf ! Reza !
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