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This document discusses the use of coronary CT angiography (CTA) to detect and characterize coronary atherosclerosis beyond just detecting coronary stenoses. CTA can identify calcified plaques, non-calcified plaques, and mixed plaques. It can detect atheromas and characterize plaque density. CTA can also identify intracoronary thrombi and myocardial infarction scars. The document outlines the CTA scanning parameters and techniques used to minimize motion artifacts and optimize image quality for plaque detection and characterization.
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060 coronary atherosclerosis with multislice ct
This document discusses the use of coronary CT angiography (CTA) to detect and characterize coronary atherosclerosis beyond just detecting coronary stenoses. CTA can identify calcified plaques, non-calcified plaques, fibrocalcified plaques, thrombus, and acute myocardial infarction scars. It can also detect atheromas and allow for plaque characterization and follow-up under therapy. CTA provides advantages over conventional angiography for coronary plaque detection, characterization, and imaging of acute coronary events.
Acc v porg becker
This document discusses the use of coronary CT angiography (CTA) to detect and characterize coronary atherosclerosis beyond just detecting coronary stenoses. CTA can identify calcified plaques, non-calcified plaques, fibrocalcified plaques, thrombus, and acute myocardial infarction scars. It can also detect atheromas and allow for plaque characterization by density. CTA provides advantages over conventional angiography for atherosclerosis detection, characterization of plaque composition, and identification of acute coronary events or intracoronary thrombus formation. Limitations include artifacts from cardiac motion, breathing, blooming effect and small vessel visualization which can be addressed by technological improvements such as faster rotation times, ECG gating, and thinner slices
Acute coronary syndrome
This document discusses acute coronary syndrome (ACS), including unstable angina and myocardial infarction (MI). It defines the conditions and describes the pathophysiology. For diagnosis of MI, there must be a rise in cardiac biomarkers along with symptoms. Investigations include ECG, biomarkers like troponin, and echocardiography. Management of NSTEMI involves bed rest, oxygen, anti-ischemic and anti-thrombotic drugs. For STEMI, reperfusion therapy like primary PCI or fibrinolytic therapy is used within 2 hours of diagnosis. Complications can include arrhythmias, further ischemia, and embolism.
Abdominal Aortic Aneurysms
This document discusses a case of a 52-year-old male presenting for elective repair of a large abdominal aortic aneurysm (AAA). It provides background on AAAs including risk factors, pathophysiology, epidemiology, presentation, natural history, and treatment options including surveillance and surgical repair. Treatment focuses on risk factor modification, antibiotics, analgesia, DVT prophylaxis, and management of postoperative complications. The patient underwent successful AAA repair with bifemoral bypass and subsequently recovered from postoperative pneumonia and arrhythmia.
Abdominal Aortic Aneurysm
This document discusses abdominal aortic aneurysms. Key points include:
- Abdominal aortic aneurysms are defined as a dilation of the aorta to over 1.5 times its normal diameter. Risk factors include age over 50 for men and 70 for women, family history, and smoking.
- Aneurysms rupture when the wall tension exceeds the strength of the aneurysm wall, which depends on size, shape, blood pressure, and the material properties of the wall.
- Treatment options include open surgical repair or endovascular stent graft placement. Complications can include cardiac, pulmonary, and renal issues. Late complications include anastomotic failures or new aneurysm formation. Five-year survival after
Anesthesia for Lower limb revascularization
This document discusses anaesthesia considerations for lower limb revascularization procedures. It begins with an introduction to peripheral artery disease and classifications. Causes, common sites, and presentations of acute and chronic limb ischemia are described. Preoperative assessment includes cardiovascular and pulmonary evaluation. Risk stratification guidelines are provided. Optimal perioperative management focuses on hemodynamic stability, temperature control, hydration and pain management. Both regional and general anesthesia techniques are reviewed. Postoperative monitoring and analgesia are also discussed.
Deep Vein Pathophysiology: Reflux & Obstruction
By: Peter J. Pappas, M.D.
Visit VeinGlobal at http://www.veinglobal.com/ for more presentations and videos on this topic, or for more information on venous disease news, education and research.
Acute Coronary Syndrome
Acute Coronary Syndrome (ACS) refers to conditions caused by reduced blood flow to the heart due to blockages in the coronary arteries, including unstable angina, NSTEMI, and STEMI. It requires immediate medical treatment as it can lead to myocardial ischemia and infarction. Diagnostics include ECG, blood tests, chest x-ray, and echocardiogram to determine the type and extent of occlusion. Initial management focuses on reperfusion therapy such as primary PCI or fibrinolytic therapy. Long-term management involves medications like ACE inhibitors, beta blockers, aspirin, statins to prevent future cardiac events and complications like arrhythmias, heart failure, and death.
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060 coronary atherosclerosis with multislice ct
This document discusses the use of coronary CT angiography (CTA) to detect and characterize coronary atherosclerosis beyond just detecting coronary stenoses. CTA can identify calcified plaques, non-calcified plaques, fibrocalcified plaques, thrombus, and acute myocardial infarction scars. It can also detect atheromas and allow for plaque characterization and follow-up under therapy. CTA provides advantages over conventional angiography for coronary plaque detection, characterization, and imaging of acute coronary events.
Acc v porg becker
This document discusses the use of coronary CT angiography (CTA) to detect and characterize coronary atherosclerosis beyond just detecting coronary stenoses. CTA can identify calcified plaques, non-calcified plaques, fibrocalcified plaques, thrombus, and acute myocardial infarction scars. It can also detect atheromas and allow for plaque characterization by density. CTA provides advantages over conventional angiography for atherosclerosis detection, characterization of plaque composition, and identification of acute coronary events or intracoronary thrombus formation. Limitations include artifacts from cardiac motion, breathing, blooming effect and small vessel visualization which can be addressed by technological improvements such as faster rotation times, ECG gating, and thinner slices
Acute coronary syndrome
This document discusses acute coronary syndrome (ACS), including unstable angina and myocardial infarction (MI). It defines the conditions and describes the pathophysiology. For diagnosis of MI, there must be a rise in cardiac biomarkers along with symptoms. Investigations include ECG, biomarkers like troponin, and echocardiography. Management of NSTEMI involves bed rest, oxygen, anti-ischemic and anti-thrombotic drugs. For STEMI, reperfusion therapy like primary PCI or fibrinolytic therapy is used within 2 hours of diagnosis. Complications can include arrhythmias, further ischemia, and embolism.
Abdominal Aortic Aneurysms
This document discusses a case of a 52-year-old male presenting for elective repair of a large abdominal aortic aneurysm (AAA). It provides background on AAAs including risk factors, pathophysiology, epidemiology, presentation, natural history, and treatment options including surveillance and surgical repair. Treatment focuses on risk factor modification, antibiotics, analgesia, DVT prophylaxis, and management of postoperative complications. The patient underwent successful AAA repair with bifemoral bypass and subsequently recovered from postoperative pneumonia and arrhythmia.
Abdominal Aortic Aneurysm
This document discusses abdominal aortic aneurysms. Key points include:
- Abdominal aortic aneurysms are defined as a dilation of the aorta to over 1.5 times its normal diameter. Risk factors include age over 50 for men and 70 for women, family history, and smoking.
- Aneurysms rupture when the wall tension exceeds the strength of the aneurysm wall, which depends on size, shape, blood pressure, and the material properties of the wall.
- Treatment options include open surgical repair or endovascular stent graft placement. Complications can include cardiac, pulmonary, and renal issues. Late complications include anastomotic failures or new aneurysm formation. Five-year survival after
Anesthesia for Lower limb revascularization
This document discusses anaesthesia considerations for lower limb revascularization procedures. It begins with an introduction to peripheral artery disease and classifications. Causes, common sites, and presentations of acute and chronic limb ischemia are described. Preoperative assessment includes cardiovascular and pulmonary evaluation. Risk stratification guidelines are provided. Optimal perioperative management focuses on hemodynamic stability, temperature control, hydration and pain management. Both regional and general anesthesia techniques are reviewed. Postoperative monitoring and analgesia are also discussed.
Deep Vein Pathophysiology: Reflux & Obstruction
By: Peter J. Pappas, M.D.
Visit VeinGlobal at http://www.veinglobal.com/ for more presentations and videos on this topic, or for more information on venous disease news, education and research.
Acute Coronary Syndrome
Acute Coronary Syndrome (ACS) refers to conditions caused by reduced blood flow to the heart due to blockages in the coronary arteries, including unstable angina, NSTEMI, and STEMI. It requires immediate medical treatment as it can lead to myocardial ischemia and infarction. Diagnostics include ECG, blood tests, chest x-ray, and echocardiogram to determine the type and extent of occlusion. Initial management focuses on reperfusion therapy such as primary PCI or fibrinolytic therapy. Long-term management involves medications like ACE inhibitors, beta blockers, aspirin, statins to prevent future cardiac events and complications like arrhythmias, heart failure, and death.
Acute limb ischaemia
Acute limb ischemia occurs when there is a sudden interruption of blood flow to a limb, threatening the viability of the limb. It can be caused by emboli originating from the heart or blood vessels, or from thrombosis of arteries due to conditions like atherosclerosis. Clinical evaluation focuses on the 5 Ps - pain, pallor, pulselessness, paresthesia, and paralysis. Investigations include Doppler ultrasound, angiography, and measurement of ankle-brachial indices. Treatment involves immediate care, thrombolysis, or surgical revascularization depending on the severity. Complications can include reperfusion injury, compartment syndrome, bleeding, and potential limb amputation.
Acute limb ischemia
A 44-year-old man presented with acute onset left leg pain, numbness, and weakness. On examination, his left lower limb was pale, cold, pulseless with reduced sensation. Imaging showed a thrombus in his aorta and left iliac and femoral arteries. He was diagnosed with acute limb ischemia and underwent aortic endarterectomy, femoral embolectomy and patch angioplasty, and fasciotomy to restore blood flow and prevent compartment syndrome. Post-operatively, he required monitoring for reperfusion injuries and long-term anticoagulation to prevent recurrence.
Acute aortic emergencies
A summary presentation on acute aortic emergencies including aortic dissection and aneurysmal disease.
Carotid artery disease
I am a Neurosurgeon with advanced training in Interventional vascular Neurosurgery(FINR) from Zurich, Switzerland, and FMINS-Fellowship in minimally invasive and Endoscopic Neurosurgery from Germany.
I am presently working in Columbia asia hospitals, Bangalore.
My areas of interest are Vascular Neurosurgery, Stroke specialist, interventional neuroradiology, Endoscopic and minimally invasive Neurosurgery, Endoscopic spine surgery.
Acute limb ischemia
1. Acute limb ischemia is a medical emergency that occurs when there is a sudden decrease in blood flow to a limb, threatening the viability of the limb. It requires urgent evaluation and management within 2 weeks of symptom onset.
2. The main treatment options are endovascular therapies like catheter-directed thrombolysis or mechanical thrombectomy, or surgical interventions like thrombectomy or bypass surgery. The goal is to rapidly restore arterial blood flow while minimizing risks to the patient.
3. Factors like the severity of ischemia, time since symptom onset, and patient characteristics help determine which treatment - thrombolysis, surgical thrombectomy, or in some cases immediate amputation - is most appropriate to salvage the limb.
Chronic lower limb ischemia
This document defines peripheral artery disease and describes its causes and presentation. PAD is caused by a reduction of blood flow in the arteries due to stenosis or occlusion. Major causes include atherosclerosis, Buerger's disease, vasospastic disorders like Raynaud's, and vasculitis. Clinical features include trophic skin changes, absent pulses, and symptoms ranging from intermittent claudication to critical limb ischemia. Diagnosis involves imaging like Doppler and angiography. Treatment options include conservative management, endovascular procedures like angioplasty, and open surgeries like bypass grafts and amputation.
Acute limb ischemia
A 64-year-old man presented with sudden onset of pain and loss of sensation in his right leg. Examination found absent pulses, decreased sensation, and an inability to move his toes, indicating acute limb ischemia. The document discusses the etiology, pathophysiology, clinical evaluation, investigations including Doppler ultrasound and angiography, and treatment approaches for acute limb ischemia including thrombolytics, surgery, and amputation. The goal of therapy is to restore blood flow, preserve the limb if possible, and prevent recurrence through anticoagulation.
Acute ischemic limb
Acute limb ischemia is a sudden decrease in limb perfusion that threatens limb viability. It is usually caused by thrombosis of atherosclerotic vessels or embolism from cardiac sources or aneurysms. Clinical manifestations include pain, pallor, coldness, and pulselessness. Imaging can help determine the severity and guide treatment, which may include thrombolysis, embolectomy, bypass surgery, or amputation depending on the classification and etiology. Complications include reperfusion injury and compartment syndrome.
peripherial arterial disease
1) PAD is associated with increased risk of myocardial infarction and ischemic stroke due to shared risk factors of atherosclerosis.
2) Clinical features of PAD range from asymptomatic to intermittent claudication to critical limb ischemia manifested by rest pain, ulcers or gangrene.
3) Diagnosis involves assessment of symptoms and risk factors as well as tests such as ankle-brachial index, duplex ultrasound and angiography. Treatment depends on severity and may include lifestyle modification, medication, angioplasty or bypass surgery.
Chronic lower limb ischemia
1. The document discusses peripheral arterial occlusive disease (PAOD), also known as peripheral artery disease (PAD), which refers to obstruction of arteries outside the heart and brain.
2. Risk factors for PAOD include smoking, diabetes, hypertension, hyperlipidemia, older age, male sex, family history of vascular disease, and certain ethnicities.
3. Symptoms range from intermittent claudication to critical limb ischemia with rest pain and tissue loss. Physical exam findings and tests like the ankle-brachial pressure index can help in diagnosis.
4. Management options discussed include conservative treatment for mild cases as well as endovascular and surgical revascularization procedures for more severe cases.
Chronic limb ischaemia
Lecture on chronic limb ischaemia for medical students. Encompasses basic sciences, classifications and principles of management.
Acute limb ischaemia
Acute limb ischemia is a vascular emergency defined as a sudden interruption of blood supply to a limb, threatening limb viability. It is commonly caused by arterial embolism or thrombosis. The degree of obstruction, site of occlusion, and presence of collateral circulation determine the pathophysiology. Tissues tolerate ischemia at different rates, with nerves being first affected and skin last. Diagnosis involves imaging studies and blood tests. Treatment depends on whether ischemia is reversible or irreversible, with anticoagulation, endovascular intervention, open surgery, or amputation used depending on the situation. Factors like delay in treatment and underlying conditions impact outcomes.
Acute limb ischemia
A 64-year-old male presented with sudden onset of pain and loss of sensation in his right leg. On examination, he was found to have absent pulses below the knee, decreased sensation, and inability to move his toes. Based on the clinical signs of acute limb ischemia, further investigations including Doppler ultrasound and angiography were recommended to determine the appropriate treatment, which may involve thrombolysis, surgery to restore blood flow, or amputation if the ischemia is irreversible.
Chronic lower limb ischemia
The document discusses peripheral artery disease (PAD), specifically critical limb ischemia (CLI). It defines CLI as a severe form of PAD involving ischemic rest pain, ulcers, or gangrene lasting over 2 weeks due to reduced blood flow. CLI is diagnosed using ankle-brachial pressure index testing or angiography and treated through risk factor modification, pharmacotherapy, and revascularization to relieve pain, heal ulcers, and prevent limb loss. The primary goals of CLI treatment are to improve symptoms, function, and survival.
Acute coronary syndrome
Acute coronary syndrome refers to a range of conditions caused by reduced blood flow in the coronary arteries including unstable angina and myocardial infarction. Angina pectoris is characterized by chest pain or pressure that is triggered by physical exertion or stress and relieved by rest. Medical management of angina aims to decrease oxygen demand on the heart and increase supply by using nitrates, beta blockers, and calcium channel blockers to dilate arteries and slow the heart rate. Antiplatelet drugs like aspirin are also used to prevent clots from worsening the condition.
Aortic abdominal aneurism
An abdominal aortic aneurysm (AAA) is a pathological dilatation of the normal aortic lumen that can be either fusiform or saccular in shape. AAAs affect about 2% of the population and rupture risk increases with diameter. Elective repair has a mortality of 1.5% while emergency repair has a 50% mortality rate. Screening is recommended for men aged 65-75 who smoke and men and women over 50 with a family history. Surgical repair or endovascular repair depends on aneurysm anatomy, with endovascular repair allowing for shorter hospital stays and recovery times. Prompt recognition and treatment of a ruptured AAA is critical to reduce high mortality rates from rupture.
108 cetp expression
CETP overexpression in diabetic and obese db/db mice prevented the formation of diet-induced atherosclerotic plaques in the aorta. CETP overexpression lowered total cholesterol concentrations and reduced cholesterol levels in the pro-atherogenic VLDL and IDL/LDL lipoprotein subfractions. This suggests CETP plays an anti-atherogenic role in the context of diabetic obesity by modifying cholesterol distribution among lipoproteins. The authors conclude CETP may help maintain vascular health in humans with diabetic obesity, and its suppression in this population may contribute to higher atherosclerosis risk.
Acc 2002 microarray mehran for print
This document discusses the use of DNA microarrays in vulnerable plaque research. It provides background on atherosclerosis and identifies DNA microarrays as a tool that can be used to investigate the molecular mechanisms underlying plaque vulnerability. The document outlines the basic steps of a DNA microarray experiment and discusses considerations for experimental design, data analysis, and validation of results. It also summarizes several studies that have used DNA microarrays or related techniques to examine gene expression in atherosclerosis.
8
This document discusses in vivo coronary sinus thermography. It shows graphs of temperature differences over time between the coronary sinus and right atrium in controls and CAD patients, finding a significant difference. It lists ongoing research using thermography to study conditions like tachycardia, arrhythmias, medication effects, heart failure, and organ function. It concludes that new catheters are being developed to increase thermography sensitivity and that coronary sinus temperature may someday provide more patient information than just detecting plaque.
125 ct based characterization
Growing evidence suggests that CT-based characterization of coronary plaques and arteries is possible. 16 slice multi-detector CT can reliably detect coronary obstructions when combined with heart rate control. It can also identify soft, intermediate, and calcified plaques. This technology has great potential as an initial non-invasive technique to identify vulnerable plaque or arteries in at-risk populations. The combination of CT imaging with serum markers may provide a powerful predictive tool for assessing vulnerability.
Acc presentation (1)
This document describes a study that introduces a non-invasive method for imaging macrophage infiltration in inflamed atherosclerotic plaques using superparamagnetic iron oxide (SPIO) nanoparticles and MRI. The researchers injected SPIO into hypercholesterolemic and normal rabbits and found that SPIO profoundly accumulated in areas of macrophage infiltration in the atherosclerotic plaques, as confirmed by histology. SPIO-enhanced MRI was able to identify these inflamed plaques non-invasively. The results suggest SPIO-enhanced MRI can be a novel method for detecting rupture-prone inflamed plaques associated with heart attacks and strokes.
246 recombinant apolipoprotein ai milano
Two studies were summarized that examined the effects of apolipoprotein A-I Milano (Apo A-I Milano) on atherosclerosis. One study found that a single high dose of recombinant Apo A-I Milano reduced macrophage and lipid content in plaques of Apo E deficient mice by 40-50% and 29-36%, respectively, within 48 hours. The other study found that carriers of the Apo A-I Milano mutant had normal arterial thickness, unlike low-HDL subjects, suggesting the mutant may protect against atherosclerosis despite low HDL levels. Further research is needed to understand the mechanism and effects of Apo A-I Milano and its potential for stabilizing human plaques.
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Acute limb ischaemia
Acute limb ischemia occurs when there is a sudden interruption of blood flow to a limb, threatening the viability of the limb. It can be caused by emboli originating from the heart or blood vessels, or from thrombosis of arteries due to conditions like atherosclerosis. Clinical evaluation focuses on the 5 Ps - pain, pallor, pulselessness, paresthesia, and paralysis. Investigations include Doppler ultrasound, angiography, and measurement of ankle-brachial indices. Treatment involves immediate care, thrombolysis, or surgical revascularization depending on the severity. Complications can include reperfusion injury, compartment syndrome, bleeding, and potential limb amputation.
Acute limb ischemia
A 44-year-old man presented with acute onset left leg pain, numbness, and weakness. On examination, his left lower limb was pale, cold, pulseless with reduced sensation. Imaging showed a thrombus in his aorta and left iliac and femoral arteries. He was diagnosed with acute limb ischemia and underwent aortic endarterectomy, femoral embolectomy and patch angioplasty, and fasciotomy to restore blood flow and prevent compartment syndrome. Post-operatively, he required monitoring for reperfusion injuries and long-term anticoagulation to prevent recurrence.
Acute aortic emergencies
A summary presentation on acute aortic emergencies including aortic dissection and aneurysmal disease.
Carotid artery disease
I am a Neurosurgeon with advanced training in Interventional vascular Neurosurgery(FINR) from Zurich, Switzerland, and FMINS-Fellowship in minimally invasive and Endoscopic Neurosurgery from Germany.
I am presently working in Columbia asia hospitals, Bangalore.
My areas of interest are Vascular Neurosurgery, Stroke specialist, interventional neuroradiology, Endoscopic and minimally invasive Neurosurgery, Endoscopic spine surgery.
Acute limb ischemia
1. Acute limb ischemia is a medical emergency that occurs when there is a sudden decrease in blood flow to a limb, threatening the viability of the limb. It requires urgent evaluation and management within 2 weeks of symptom onset.
2. The main treatment options are endovascular therapies like catheter-directed thrombolysis or mechanical thrombectomy, or surgical interventions like thrombectomy or bypass surgery. The goal is to rapidly restore arterial blood flow while minimizing risks to the patient.
3. Factors like the severity of ischemia, time since symptom onset, and patient characteristics help determine which treatment - thrombolysis, surgical thrombectomy, or in some cases immediate amputation - is most appropriate to salvage the limb.
Chronic lower limb ischemia
This document defines peripheral artery disease and describes its causes and presentation. PAD is caused by a reduction of blood flow in the arteries due to stenosis or occlusion. Major causes include atherosclerosis, Buerger's disease, vasospastic disorders like Raynaud's, and vasculitis. Clinical features include trophic skin changes, absent pulses, and symptoms ranging from intermittent claudication to critical limb ischemia. Diagnosis involves imaging like Doppler and angiography. Treatment options include conservative management, endovascular procedures like angioplasty, and open surgeries like bypass grafts and amputation.
Acute limb ischemia
A 64-year-old man presented with sudden onset of pain and loss of sensation in his right leg. Examination found absent pulses, decreased sensation, and an inability to move his toes, indicating acute limb ischemia. The document discusses the etiology, pathophysiology, clinical evaluation, investigations including Doppler ultrasound and angiography, and treatment approaches for acute limb ischemia including thrombolytics, surgery, and amputation. The goal of therapy is to restore blood flow, preserve the limb if possible, and prevent recurrence through anticoagulation.
Acute ischemic limb
Acute limb ischemia is a sudden decrease in limb perfusion that threatens limb viability. It is usually caused by thrombosis of atherosclerotic vessels or embolism from cardiac sources or aneurysms. Clinical manifestations include pain, pallor, coldness, and pulselessness. Imaging can help determine the severity and guide treatment, which may include thrombolysis, embolectomy, bypass surgery, or amputation depending on the classification and etiology. Complications include reperfusion injury and compartment syndrome.
peripherial arterial disease
1) PAD is associated with increased risk of myocardial infarction and ischemic stroke due to shared risk factors of atherosclerosis.
2) Clinical features of PAD range from asymptomatic to intermittent claudication to critical limb ischemia manifested by rest pain, ulcers or gangrene.
3) Diagnosis involves assessment of symptoms and risk factors as well as tests such as ankle-brachial index, duplex ultrasound and angiography. Treatment depends on severity and may include lifestyle modification, medication, angioplasty or bypass surgery.
Chronic lower limb ischemia
1. The document discusses peripheral arterial occlusive disease (PAOD), also known as peripheral artery disease (PAD), which refers to obstruction of arteries outside the heart and brain.
2. Risk factors for PAOD include smoking, diabetes, hypertension, hyperlipidemia, older age, male sex, family history of vascular disease, and certain ethnicities.
3. Symptoms range from intermittent claudication to critical limb ischemia with rest pain and tissue loss. Physical exam findings and tests like the ankle-brachial pressure index can help in diagnosis.
4. Management options discussed include conservative treatment for mild cases as well as endovascular and surgical revascularization procedures for more severe cases.
Chronic limb ischaemia
Lecture on chronic limb ischaemia for medical students. Encompasses basic sciences, classifications and principles of management.
Acute limb ischaemia
Acute limb ischemia is a vascular emergency defined as a sudden interruption of blood supply to a limb, threatening limb viability. It is commonly caused by arterial embolism or thrombosis. The degree of obstruction, site of occlusion, and presence of collateral circulation determine the pathophysiology. Tissues tolerate ischemia at different rates, with nerves being first affected and skin last. Diagnosis involves imaging studies and blood tests. Treatment depends on whether ischemia is reversible or irreversible, with anticoagulation, endovascular intervention, open surgery, or amputation used depending on the situation. Factors like delay in treatment and underlying conditions impact outcomes.
Acute limb ischemia
A 64-year-old male presented with sudden onset of pain and loss of sensation in his right leg. On examination, he was found to have absent pulses below the knee, decreased sensation, and inability to move his toes. Based on the clinical signs of acute limb ischemia, further investigations including Doppler ultrasound and angiography were recommended to determine the appropriate treatment, which may involve thrombolysis, surgery to restore blood flow, or amputation if the ischemia is irreversible.
Chronic lower limb ischemia
The document discusses peripheral artery disease (PAD), specifically critical limb ischemia (CLI). It defines CLI as a severe form of PAD involving ischemic rest pain, ulcers, or gangrene lasting over 2 weeks due to reduced blood flow. CLI is diagnosed using ankle-brachial pressure index testing or angiography and treated through risk factor modification, pharmacotherapy, and revascularization to relieve pain, heal ulcers, and prevent limb loss. The primary goals of CLI treatment are to improve symptoms, function, and survival.
Acute coronary syndrome
Acute coronary syndrome refers to a range of conditions caused by reduced blood flow in the coronary arteries including unstable angina and myocardial infarction. Angina pectoris is characterized by chest pain or pressure that is triggered by physical exertion or stress and relieved by rest. Medical management of angina aims to decrease oxygen demand on the heart and increase supply by using nitrates, beta blockers, and calcium channel blockers to dilate arteries and slow the heart rate. Antiplatelet drugs like aspirin are also used to prevent clots from worsening the condition.
Aortic abdominal aneurism
An abdominal aortic aneurysm (AAA) is a pathological dilatation of the normal aortic lumen that can be either fusiform or saccular in shape. AAAs affect about 2% of the population and rupture risk increases with diameter. Elective repair has a mortality of 1.5% while emergency repair has a 50% mortality rate. Screening is recommended for men aged 65-75 who smoke and men and women over 50 with a family history. Surgical repair or endovascular repair depends on aneurysm anatomy, with endovascular repair allowing for shorter hospital stays and recovery times. Prompt recognition and treatment of a ruptured AAA is critical to reduce high mortality rates from rupture.
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108 cetp expression
CETP overexpression in diabetic and obese db/db mice prevented the formation of diet-induced atherosclerotic plaques in the aorta. CETP overexpression lowered total cholesterol concentrations and reduced cholesterol levels in the pro-atherogenic VLDL and IDL/LDL lipoprotein subfractions. This suggests CETP plays an anti-atherogenic role in the context of diabetic obesity by modifying cholesterol distribution among lipoproteins. The authors conclude CETP may help maintain vascular health in humans with diabetic obesity, and its suppression in this population may contribute to higher atherosclerosis risk.
Acc 2002 microarray mehran for print
This document discusses the use of DNA microarrays in vulnerable plaque research. It provides background on atherosclerosis and identifies DNA microarrays as a tool that can be used to investigate the molecular mechanisms underlying plaque vulnerability. The document outlines the basic steps of a DNA microarray experiment and discusses considerations for experimental design, data analysis, and validation of results. It also summarizes several studies that have used DNA microarrays or related techniques to examine gene expression in atherosclerosis.
8
This document discusses in vivo coronary sinus thermography. It shows graphs of temperature differences over time between the coronary sinus and right atrium in controls and CAD patients, finding a significant difference. It lists ongoing research using thermography to study conditions like tachycardia, arrhythmias, medication effects, heart failure, and organ function. It concludes that new catheters are being developed to increase thermography sensitivity and that coronary sinus temperature may someday provide more patient information than just detecting plaque.
125 ct based characterization
Growing evidence suggests that CT-based characterization of coronary plaques and arteries is possible. 16 slice multi-detector CT can reliably detect coronary obstructions when combined with heart rate control. It can also identify soft, intermediate, and calcified plaques. This technology has great potential as an initial non-invasive technique to identify vulnerable plaque or arteries in at-risk populations. The combination of CT imaging with serum markers may provide a powerful predictive tool for assessing vulnerability.
Acc presentation (1)
This document describes a study that introduces a non-invasive method for imaging macrophage infiltration in inflamed atherosclerotic plaques using superparamagnetic iron oxide (SPIO) nanoparticles and MRI. The researchers injected SPIO into hypercholesterolemic and normal rabbits and found that SPIO profoundly accumulated in areas of macrophage infiltration in the atherosclerotic plaques, as confirmed by histology. SPIO-enhanced MRI was able to identify these inflamed plaques non-invasively. The results suggest SPIO-enhanced MRI can be a novel method for detecting rupture-prone inflamed plaques associated with heart attacks and strokes.
246 recombinant apolipoprotein ai milano
Two studies were summarized that examined the effects of apolipoprotein A-I Milano (Apo A-I Milano) on atherosclerosis. One study found that a single high dose of recombinant Apo A-I Milano reduced macrophage and lipid content in plaques of Apo E deficient mice by 40-50% and 29-36%, respectively, within 48 hours. The other study found that carriers of the Apo A-I Milano mutant had normal arterial thickness, unlike low-HDL subjects, suggesting the mutant may protect against atherosclerosis despite low HDL levels. Further research is needed to understand the mechanism and effects of Apo A-I Milano and its potential for stabilizing human plaques.
094 spectroscopic fiber optic catheter
This document describes research on using near-infrared spectroscopy to measure pH levels in atherosclerotic plaque via a fiber optic catheter. Previous studies showed plaque pH heterogeneity and that inflamed regions have lower pH. The researchers collected human carotid plaques and used a 3Fr fiber optic catheter prototype to obtain optical reflectance spectra of 17 tissue sites, which were then calibrated to pH readings from micro-electrodes. A partial least squares model achieved a determination coefficient of 0.63 and root mean squared deviation of 0.14 pH units. Further work aims to increase sample size under physiological conditions to better identify vulnerable plaque based on pH levels in vivo.
177 link between coronary and carotid
1) The document discusses the link between carotid artery disease and coronary artery disease. Studies have found an association between carotid artery plaques and stenosis and higher risk of cardiovascular events.
2) Measuring intima-media thickness (IMT) of the carotid arteries has been used as a surrogate for coronary artery atherosclerosis, though atherosclerosis is non-uniformly distributed. Individual carotid segments may be associated with different risk factors.
3) A recent study found that multiple risk factors cause different morphological changes in carotid artery segments, with systolic blood pressure contributing most to common carotid IMT and age contributing most to carotid bulb IMT. This suggests individual carotid segments may have different prognostic value.
203 pathologic substrate of coronary plaque erosion
This document summarizes a study examining the matrix composition of different types of coronary culprit plaques, including stable plaques and those with erosion or rupture. The study found that plaque erosion was associated with accumulation of hyaluronan and decorin, as well as expression of CD44 and immature smooth muscle cells. Plaque erosion may be promoted by these matrix components, particularly hyaluronan binding to CD44, which could increase thrombosis and smooth muscle cell proliferation/migration. The differential accumulation of matrix proteins provides insights into the pathogenesis of plaque erosion.
209 trans blood vision™
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.
180 aortic thermography catheter
The document discusses a study conducted by the Department of Cardiology at Athens Medical School in 2001 that used a new aortic thermography catheter to measure temperatures in the aorta and coronary sinus of patients. The study involved 18 patients with documented coronary artery disease and 12 patients with normal coronary arteries, as determined by angiography. The purpose was to investigate if there are temperature differences in blood between the coronary sinus and right atrium in patients with left coronary artery lesions compared to those without.
176 coronary pan artritis
This document discusses inflammation in coronary artery plaques and its relationship to vulnerable plaques. It reports that:
1) Inflammation is common in deeper layers of atherosclerotic plaques and is associated with lipid content but not necessarily plaque rupture.
2) Patients with unstable angina tend to have evidence of widespread coronary inflammation, not just at the culprit lesion, suggesting vulnerable plaques may form throughout the arteries.
3) Given that vulnerable patients often have many inflamed plaques, targeting a single coated stent to one region may not be sufficient as a treatment approach for reducing acute coronary events risk.
3rd vulnerable plaque rumberger 3 16-02 1
Electron beam tomography (EBT) is a scanning method introduced in 1984 that images the heart 10 times faster than helical CT. Over 600 papers have been published on EBT validating its ability to determine and quantify coronary artery calcium. Coronary artery calcification is the hardening of the coronary arteries that has been known for 300 years. Recent research in the past 10 years has found that it is an active process that can occur early in atherosclerotic plaque development and is an intimate part of the fibroproliferative and inflammatory pathophysiology of coronary artery disease. Histological examination shows calcium is present within atherosclerotic plaque.
508 search for genomic and proteomic risk factors and protective factors asso...
1. This study aims to identify genomic and proteomic risk factors and protective factors associated with coronary heart disease by analyzing gene and protein expression profiles in blood cells from patients with and without heart disease.
2. The study will recruit patients aged 18-80 categorized into five groups based on having heart disease and traditional risk factors. Gene expression in monocytes and neutrophils will be analyzed using microarray technology and real-time PCR.
3. Differentially expressed genes will be identified by comparing expression profiles between patient groups to uncover new diagnostic markers and therapeutic targets for coronary heart disease.
040 center for vulnerable plaque research
This document discusses vulnerable plaque detection using superparamagnetic iron oxide (SPIO) nanoparticles and MRI. It describes how SPIOs are taken up by macrophages in atherosclerotic plaques, decreasing the MRI signal and allowing plaque visualization. Studies in mice and rabbits show SPIO uptake correlates with plaque inflammation and macrophage content on histology. MRI of rabbits post-SPIO injection detected more signal decrease in hypercholesterolemic rabbits compared to controls, indicating potential to identify vulnerable plaque.
511 first steps towards understanding
This study investigated genetic differences in vascular remodeling and shear stress regulation in response to altered blood flow in four inbred rat strains. The results showed significant differences among strains in their ability to maintain normal endothelial shear stress levels through outward arterial remodeling when flow was increased or decreased. Specifically, the GH strain was better able to regulate shear stress through remodeling compared to the SHR-SP strain. These genetic differences in vascular responses to changes in blood flow have important implications for understanding the variable manifestations of atherosclerosis and susceptibility to cardiovascular disease in individuals and populations. Future studies are needed to investigate whether similar genetic differences exist in humans and their role in clinical outcomes.
220 statin therapy and coronary calcification
This study investigated whether statin therapy can slow or reverse coronary calcification in hyperlipidemic patients. 72 patients underwent electron beam tomography scans at years 1 and 2: the first year with no lipid treatment, the second year taking cerivastatin. Cerivastatin significantly reduced LDL cholesterol and slowed the progression of coronary calcification, demonstrating an 8.8% increase in calcium volume score from years 1 to 2 compared to a 25% increase with no treatment. While reversal was not shown for the whole group, patients achieving an LDL <100 mg/dl had a slightly negative calcium change. This provides further evidence that statins can slow atherosclerotic progression.
044 mice mri
This study aimed to image atherosclerotic plaques in the aortas of Apo E deficient mice using MRI. To visualize the aorta, contrast agent was injected into mice both while inside and outside of the MRI scanner. Respiratory gating was used to reduce motion artifacts from breathing by intubating mice and providing ventilation. Initial scans showed the aorta but further refinement is needed, including decreasing the dose of iron contrast agent to improve image resolution without excessive signal loss. Future plans include ECG gating to reduce cardiac motion and starting similar studies in rabbits.
225 animal models of heart attack part 2
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.
098 red wine and heart disease
1) The study found that red wines from France increased expression of the endothelial nitric oxide synthase (eNOS) gene and protein in human endothelial cells, whereas red wines from Germany did not.
2) French red wines were also found to increase activity of the eNOS promoter and stability of eNOS mRNA, resulting in increased production of bioactive nitric oxide (NO) from the endothelial cells.
3) The increase in eNOS expression, activity, and NO production brought about by French red wines may contribute to the cardiovascular benefits associated with moderate red wine consumption.
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This document discusses the use of coronary CT angiography (CTA) to detect and characterize coronary atherosclerosis beyond just detecting coronary stenoses. CTA can identify calcified plaques, non-calcified plaques, mixed plaques, atheromas, thrombi, and myocardial infarction scars. CTA provides information on plaque composition and distribution that can help understand coronary artery disease and be used to follow patients under therapy. The limitations of CTA include artifacts from cardiac motion, breathing, blooming effect, and poor contrast opacification of small vessels. Advances in multislice CT technology are helping to address some of these limitations.
060 coronary atherosclerosis with multislice ct
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SPECT/CT shows promise for atherosclerosis imaging by combining anatomical CT imaging of plaque volume with molecular SPECT imaging of plaque activity. SPECT could potentially image multiple molecular processes simultaneously, such as apoptosis, oxidized LDL, or inflammation. Recent advances in SPECT technology include improved resolution, sensitivity, and the ability to perform dynamic cardiac SPECT to quantify blood flow and endothelial function. Pairing molecular SPECT imaging with anatomical CT may allow characterization of plaque vulnerability beyond quantification of volume. However, further developments are still needed including new tracers, multimodality technology, and software.
Berman shape 05 fin
SPECT/CT shows promise for atherosclerosis imaging by combining anatomical CT imaging of plaque volume with molecular SPECT imaging of plaque activity. SPECT could potentially image multiple molecular processes simultaneously, such as apoptosis, oxidized LDL, or inflammation. Recent advances in SPECT technology include improved resolution, sensitivity, and the ability to perform dynamic cardiac SPECT to quantify blood flow and endothelial function. Combined structural and molecular imaging may allow more accurate risk assessment and monitoring of treatment response than anatomical methods alone. However, further developments are still needed, including new tracers approved for human use.
Acute Upper GI bleed.pptx
1) Acute gastrointestinal bleeding can originate from the upper GI tract and has many potential causes, including peptic ulcers, esophageal and gastric varices, erosive mucosal disease, and tumors.
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The document discusses intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). ICH can be caused by hypertension, trauma, vascular malformations, or coagulopathies. Common symptoms include focal neurological deficits, severe headache, and decreased consciousness. Diagnosis involves CT scan or MRI to detect bleeding, and management focuses on controlling blood pressure, reducing ICP, and preventing vasospasm in SAH. SAH is often caused by aneurysm rupture and presents with sudden, explosive headache. Diagnosis involves CT, lumbar puncture, or angiography. Treatment focuses on monitoring for rebleeding, vasospasm, and surgically clipping aneurysms. Prognosis depends
072 ct angiography
This document discusses the promises and limitations of fast CT angiography for coronary artery imaging. It summarizes that CT techniques have improved over time, with multislice spiral CT now able to acquire images with high spatial resolution and good contrast in less than 500 ms. However, temporal resolution remains a challenge, especially at higher heart rates. CT coronary angiography has high negative predictive value for ruling out significant stenoses when image quality is sufficient, but it cannot replace cardiac catheterization and has limitations for patients with arrhythmias or unevaluable arteries. The detection of coronary plaque is also discussed as a potential role for CT, but accuracy and reproducibility require further study.
072 ct angiography
This document discusses the promises and limitations of fast CT angiography for coronary artery imaging. It summarizes that CT techniques have improved over time, with multislice spiral CT now able to acquire images with high spatial resolution and good contrast in less than 500 ms. However, temporal resolution remains a challenge, especially at higher heart rates. CT coronary angiography has high negative predictive value for ruling out significant stenoses when image quality is sufficient, but it cannot replace cardiac catheterization and has limitations for patients with arrhythmias or unevaluable arteries. The detection of coronary plaque is also discussed as a potential role for CT, but accuracy and reproducibility require further study.
Achenbach
This document discusses the promises and limitations of fast CT angiography for coronary artery imaging. It summarizes the development of electron beam tomography and multislice spiral CT techniques which have improved temporal resolution to 50-100ms, allowing feasible coronary imaging. However, limitations remain such as slice thickness and radiation dose. Studies show high negative predictive value (~95%) for ruling out significant stenoses when image quality is sufficient. While CT may replace cardiac catheterization for "ruling out" disease, it is not recommended for screening or evaluating patients with clear symptoms. CT also shows potential for detecting plaques and evaluating bypass grafts and stents but accuracy of plaque quantification requires further study.
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CCS + Revas.pptx
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CTCA - CT Coronary Angiography Plaque Characterization
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Cardiac ct
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Lecture vienna september 16 2005
This document summarizes the use of noninvasive MDCT imaging of the coronary arteries. It discusses the challenges of imaging small, rapidly moving coronary vessels. MDCT allows for successful coronary imaging with temporal resolution of 330-400ms, spatial resolution of 0.4-0.75mm, coverage of the heart in a single breath hold of 8-14 seconds. Sensitivity for detecting coronary stenosis is 80-86% for 4-16 slice MDCT and specificity is 90-97%. Potential clinical applications include decreasing invasive angiograms, improving risk assessment, detecting anomalies, and evaluating bypass grafts. Larger clinical trials are still needed to determine the impact on patient management.
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acute coronary syndrome (MI)
Acute coronary syndrome (ACS) encompasses unstable angina and myocardial infarction (MI). It is characterized by new or worsening chest pain and is caused by dynamic obstruction of the coronary arteries, often due to thrombus formation. Diagnosis involves detecting elevated cardiac biomarkers and ECG changes. Treatment includes analgesics, antithrombotic drugs like aspirin and clopidogrel, anticoagulants, anti-anginal medications, and reperfusion therapies like percutaneous coronary intervention (PCI) or thrombolysis within 2 hours of symptoms for STEMI. Goals of management are to relieve symptoms, prevent complications like arrhythmias, and reduce mortality risk through revascularization. Long term secondary prevention focuses on lifestyle modifications
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Coronary artery disease : CAD, atherosclerotic heart disease
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This document provides background on Jacques Barth, an expert in cardiovascular imaging and risk assessment. It discusses the evolution of ultrasound technology for measuring intima-media thickness (IMT) from 1986 to 2005. IMT is an early marker of atherosclerosis and cardiovascular risk. The document also addresses issues around vulnerable plaques, reporting IMT measurements, and assessing cardiovascular risk in children and adolescents.
Braunwald
This document outlines an approach to identifying and managing coronary risk. It recommends that prevention must be the primary goal through intensive global risk factor reduction for all patients with clinically apparent heart disease. It also recommends identifying asymptomatic high-risk individuals through testing like the Framingham Risk Score so they can receive prevention. It proposes a risk stratification approach from low to very high risk based on annual risk levels and corresponding testing and treatments, with very high risk patients receiving the most intensive treatments like invasive detection of unstable plaques and procedures like CABG or multiple drug-eluting stents.
Acc vp-org 3-02 stone
This document describes a study that uses intravascular ultrasound (IVUS), biplane coronary angiography, and blood flow measurements to characterize endothelial shear stress (ESS) in coronary arteries. It found that over 6 months, areas of low ESS demonstrated plaque progression, areas of normal ESS remained stable, and areas of high ESS developed outward remodeling. The technology allows in vivo determination of intracoronary flow velocity and ESS, which has not previously been possible. This provides a method to predict progression of atherosclerosis and vascular remodeling. A pilot study applied this technique in 8 patients at baseline and 6 months to analyze changes in native coronary artery disease and in-stent restenosis while taking candesartan vs fel
101205 shape aha 2005 f
Zahi A. Fayad is an Associate Professor who studies molecular imaging of atherosclerosis using MRI. His research focuses on developing targeted contrast agents to noninvasively detect unstable plaque. Some agents under investigation include annexin A5 labeled with a radioisotope to detect apoptosis, FDG-PET to assess plaque activity, and fibrin-targeted and MMP-targeting Gd-based contrasts. Additional work involves lipid-based particulate agents using reconstituted HDL or iron oxide nanoparticles. The goal is to improve MRI detection sensitivity and specificity for high-risk plaque characterization.
Acc 2005-1, v pl-vp
This document discusses approaches to cardiovascular disease (CVD) and the need for new approaches. It summarizes that the emphasis is shifting from high risk plaques to high risk symptomatic patients, and from high risk asymptomatic to intermediate and low risk patients. It discusses diagnostic tools like magnetic resonance imaging to identify high risk asymptomatic patients and computed tomography to identify intermediate risk patients using coronary artery calcium scoring and CRP biomarkers. It also discusses prevention and treatment strategies like a polypill for acute coronary syndrome patients and those with chronic atherothrombosis.
Acc presentation macrophage (1)
This document proposes a non-invasive method using SPIO (super paramagnetic iron oxide) nanoparticles to image macrophage infiltration and inflammation in vulnerable atherosclerotic plaques. Rabbits and mice were injected with SPIO, which accumulated in inflamed plaque areas correlated with macrophage density. SPIO-enhanced MRI then successfully identified these inflamed plaques non-invasively in vivo. This technique could provide a way to detect rupture-prone plaques and better understand plaque vulnerability.
Ac cculprit
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.
Acc presentation lipid coated(2)
This document discusses a novel tracer for MRI imaging of macrophage infiltration in atherosclerotic plaque. It summarizes research into lipid-coated superparamagnetic iron oxide nanoparticles (SPIOs) that are phagocytosed by macrophages. The researchers tested various SPIO coatings and sizes to maximize macrophage uptake while minimizing oxidative stress. Lipid-coated SPIOs combined with certain aminoglycans showed the highest uptake and lowest induction of reactive oxygen species. The goal is to develop an MRI contrast agent that can noninvasively image vulnerable, inflamed plaques by detecting macrophage presence.
Acc booth inventory
The document provides details about AEHA's booth at the ACC/AEHA Exhibition from March 30 to April 1, 2003. It lists the booth equipment and inventory, proposed activities like an Ecode on Friday morning and a VP Symposium. Giveaways include Magellan GPS devices in a raffle and Dove chocolates. It also discusses the need for an immediate membership sign-up page on the AEHA website and a vision for the future of AEHA.
Acc 04 vuln pt
This document discusses approaches to identifying and managing coronary risk. It states that the primary goal should be preventing acute cardiac events through intensive risk factor reduction for all patients with clinically apparent heart disease. Additionally, it notes that one third of sudden cardiac deaths and heart attacks occur in previously asymptomatic individuals with undiagnosed risk factors or pre-clinical disease. The document proposes identifying high-risk asymptomatic individuals through testing to provide prevention. It presents a risk stratification approach using testing like CRP, cholesterol, glucose and imaging to guide different levels of risk factor reduction and management.
Acc 2002 mehran for print
This document discusses the use of DNA microarrays in studying vulnerable atherosclerotic plaques. It provides background on atherosclerosis and plaque rupture. DNA microarrays allow high-throughput analysis of gene and protein expression, which can provide insights into molecular mechanisms underlying plaque vulnerability. One study used microarrays to analyze gene expression differences between ruptured and stable plaques, identifying perilipin as upregulated in ruptured plaques. However, microarray analysis of atherosclerosis is still in its early stages with many technical challenges to address.
Acc2002 thermography
Vulnerable plaques are prone to rupture and cause heart attacks. This document proposes criteria for defining vulnerable plaques based on histopathology and clinical factors. It also explores using infrared thermography to identify vulnerable plaques by detecting heat from macrophage inflammation. Studies in animal models and humans found temperature heterogeneity in atherosclerotic arteries that correlated with plaque vulnerability features. Further research aims to develop non-invasive thermography techniques to accurately detect vulnerable plaques and help predict heart attack risk.
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The document presents findings on the A20 gene, which encodes a zinc finger protein that inhibits NF-kB activity and TNF-induced apoptosis. The study found that C57 and FVB mouse strains have a coding difference in A20 that generates a phosphorylation site in C57 mice. C57-A20 was less effective at shutting down TNF-induced NF-kB activity and C57 cells were less susceptible to TNF-induced apoptosis compared to FVB cells. This suggests less active A20 in C57 mice leads to increased inflammation and reduced apoptosis, while more active A20 in FVB mice decreases inflammation and increases apoptosis, contributing to differences in atherosclerosis susceptibility between the strains.
#1 killer of human beings in the 21st century
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.
A20 is an atherosclerosis
The document presents findings on the A20 gene, which encodes a zinc finger protein that inhibits NF-kB activity and TNF-induced apoptosis. The study found that C57 and FVB mouse strains have a coding difference in A20 that generates a putative phosphorylation site in C57 mice. Experiments showed the C57 version of A20 is less effective at shutting down NF-kB activity and C57 cells are less susceptible to TNF-induced apoptosis. This suggests the A20 variation could contribute to differences in atherosclerosis susceptibility between C57 and FVB strains by affecting inflammation and apoptosis.
103100
This progress report discusses ongoing near-infrared (NIR) spectroscopy studies. It notes that a new probe design is being developed to improve signal detection in the NIR range. Characterization of a new light source and additional tissue phantom studies are needed. The report identifies ongoing difficulties with depth penetration studies and experimental setup issues. Priorities include analyzing existing data to inform probe redesign, characterizing the new light source, conducting depth penetration and tissue phantom studies, and addressing experimental setup challenges.
259 crp as a risk factor
This document discusses the use of C-reactive protein (CRP) and low-density lipoprotein (LDL) cholesterol levels to predict cardiovascular risk. It summarizes a study that found CRP to be a stronger predictor of future cardiovascular events than LDL. The study measured CRP and LDL levels in 27,939 healthy women and followed them for 8 years, finding that most cardiovascular events occurred in women with normal or low LDL (<160 mg/dl) but elevated CRP. The document concludes that combining CRP and LDL measurements provides better risk assessment than either marker alone.
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This document contains fluorescence intensity measurements from a fluorescence-based assay using different concentrations of FITC-labeled superparamagnetic iron oxide nanoparticles (FITC SPIO). The measurements are organized in a table with concentrations of FITC SPIO along the left and average fluorescence units per well and standard deviations for different samples labeled with letters in the cells.
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.
510 does lxr links lipid metabolism to inflammation, or ppar
The document discusses the roles of Liver X receptors (LXRs) and peroxisome proliferator-activated receptors (PPARs) in regulating matrix metalloproteinase-9 (MMP-9) expression in macrophages and their implications in atherosclerosis. It reports that LXR and PPAR activation inhibits MMP-9 expression, reducing foam cell accumulation and atherosclerosis progression in mice studies. While PPARγ ligands suppress MMP-9 even in PPARγ deficient cells, the mechanisms of this effect and whether LXR ligands similarly regulate MMP-9 in LXR deficient cells requires further investigation. The LXR agonist GW3965 may have potential for stabilizing vulnerable atherosclerotic plaques by downregulating
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Acc v porg
- 1. Coronary Atherosclerosis with Multislice CT: What is beyond coronary atherosclerosis Konstantin Nikolaou Tobias Jakobs Bernd Wintersperger Radiology Alexander Becker Andreas Knez Alexander Leber Cardiology Michael Muders Pathology Christoph R Becker
- 3. CTA Inclusion Criteria • Asymptomatic patients • CV risk factors • Positive calcium scan • Symptomatic patients • No CAD history • Atypical chest pain • Inconsistent stress test < 100 mg CaHA
- 4. Patient Preparation 82 bpm • β-blocker • R/o Contra indications • Informed consent • Metoprolol • 50 - 100 mg orally • 30 - 90 min prior • HR 50 - 60 bpm 65 bpm
- 5. Coronary CTA Parameters • Testbolus 20 ml @ 4 ml/sTestbolus 20 ml @ 4 ml/s • 120 ml (300 mg iodine) @ 3120 ml (300 mg iodine) @ 3 ml/sml/s + NaCl 60 ml+ NaCl 60 ml @ 3 ml/s@ 3 ml/s • 500 ms gantry rotation500 ms gantry rotation • 120 kV, 300 mA120 kV, 300 mA • 4 x 1 mm collimation4 x 1 mm collimation • 3 mm/s table feed3 mm/s table feed • 40 s breath hold40 s breath hold
- 6. ECG Tube Current Modulation Pitch <0,4 250 ms 250 ms250 ms 100% 20% mAs
- 8. Left Coronary Artery (RAO) Coronary Angiography MDCT & VRT
- 9. LAO 60Coronary Angiography MDCT & VRT Right Coronary Artery (LAO)
- 10. Detection of Coronary Stenoses MDCT Coronary Angiography
- 11. Coronary Stenoses CTA & Angiography Author Journal PPV NPV n.a. n Niemann Lancet 2001 81% 97% 30% 35 Achenbach Circulation 2001 59% 98% 32% 64 Mean/sum 70% 98% 31% 99
- 12. CTA Limitations • Artifacts • Cardiac motion • Breathing • Blooming • Poor opacification • Small vessel
- 13. Solutions < Rot. time & β−blocker • Cardiac motion artifacts < Scan times • Breathing artifacts • CM utilization < Slice thickness • Small vessels • Blooming artifact
- 14. 16 Detector Row CT Angiography • 200 ms • 9 Lp/cm • 0.8 mm • 20 s breath hold • 60 ml CM
- 15. Coronary Plaque Imaging MDCT Coronary Angiography
- 16. Non Calcified Plaque Density
- 17. Coronary Atherosclerosis Calcified Nodule Wall changes Occlusion ThrombusFibrocalcified Plaque Stenoses Intimal Thickening Atheroma Healing Hemorrhage Rupture/Erosion
- 18. Atheroma • 38 YOM • Non specific complain • Risk Factors – Cholesterin – Smoker • No calcium 50 HU 50 HU
- 19. Calcified Nodule • 62 YOM • Suspicion of CAD • 12 mg CaHA
- 21. Thrombus • 42 YOM • Epigastric chest pain • Risk Factors – Hypertension – Smoker • No calcium 20 HU
- 22. Thrombus
- 23. Acute Posterior Wall Infarction
- 25. CT Plaque Density Lipid Fibrose50 ± 12 HU 89 ± 31 HU p = 0.018 Lipid Fibrosis
- 26. CTA vs IVUS Schröder Heart 2001;85:576
- 27. Carotid Atherosclerosis Estes 1998 J Cardiovasc Surg 39:527
- 28. Plaque Distribution Leber 2001 Circulation Non- calcified 13% Mixed 33% Calcified 54% Myocardial Infarction n = 12 122 Plaque Stable Angina n = 12 135 Plaque Non- calcified 6% Mixed 14% Calcified 80%
- 29. Summary • Detection of stenoses – Calcium – Small vessels • Characterization of plaques • Identify atheromas • Follow up under therapy • Acute coronary event • Intracoronary thrombus • Myocardial infarction
- 30. www.CT2002.org
Editor's Notes
- Significant stenosis = stenosis for intervention Indication for bypass surgery