#aortic dissection #tamponade #hemopericardium #pericardial effusion #leg ischemia #type a dissection #shock #cardiogenic shock.
An aortic dissection is an uncommon serious condition, which usually presents with chest pain or upper back pain. Symptoms of aortic dissection may mimic those of other diseases, often leading to delay in diagnosis. We report an unusual case of aortic dissection with hemopericardium and thrombosed left common iliac artery presenting as acute limb ischemia. Maintaining a high index of clinical suspicion for aortic pathology could possibly lead to identification and timely management of a greater number of patients who have atypical presentations. This would be especially true for patients who have catastrophic presentations with unexplained symptoms.
Left Ventricular Apical Ballooning, Catecholamine Toxicity, and Cardiomyopathyasclepiuspdfs
Case reports and clinical experiences have implicated catecholamine. Excess likely contributes to the pathophysiologic process as a cause of cardiac dysfunction, impaired hemodynamic function, and poor outcomes. Cardiac dysfunction has also been described in many other diseases; there is likely a common underlying pathophysiology. In this review, we will examine the pathophysiology of cardiac dysfunction after catecholamine surge and discuss the evidence surrounding cardiac dysfunction.
ST-segment Depression: All are Not Created Equal!asclepiuspdfs
ST depression on an electrocardiography can be from various causes including ischemia, acute coronary syndrome, electrolyte imbalance, posterior myocardial infarction, pulmonary embolism and others. Making the right diagnosis and therefore the right treatment is of paramount importance. This article goes into depth explaining why all ST-segment depressions are not created equal.
This document provides an overview of hypertrophic cardiomyopathy (HCM). It defines HCM as an increased left ventricular wall thickness of 15 mm or more that is not due to abnormal loading conditions. HCM is caused by mutations in sarcomere genes. Symptoms can include left ventricular outflow tract obstruction and complications such as heart failure, atrial fibrillation, and sudden cardiac death. The document discusses the diagnosis of HCM using echocardiography, cardiac MRI and other imaging tools. It also reviews treatments such as medications, surgical myectomy to relieve outflow tract obstruction, alcohol septal ablation, implantable cardioverter-defibrillators and heart transplantation.
CVD in cancer survivors.Screening of cancer survivors.Chest Radiotherapy .JACC Scientific Expert Panel
( J Am Coll Cardiol 2019;74:905–27 )manifestations of chest and mediastinal radiotherapy .
The Progression of Hypertensive Heart Disease.From hypertension to heart failuremagdy elmasry
Staging of Hypertensive Heart Disease.Precipitants and clinical sequelae related to LVH and myocardial fibrosis.Imaging in hypertensive heart disease .Differential diagnosis of LVH.Concentric LVH .Eccentric LVH . Concentric remodeling .linking hypertension and atrial fibrillation
Role of echocardiography in acute myocardial infractionRakesh Kumar Messi
Echocardiography is useful in the diagnosis and management of acute myocardial infarction (AMI) for several reasons:
1. It can detect regional wall motion abnormalities (RWMAs) that occur prior to ECG changes during a coronary occlusion, aiding early diagnosis.
2. It is recommended to evaluate ventricular function, detect mechanical complications like thrombus, and stratify risk in patients with confirmed AMI.
3. RWMAs seen on echocardiography localize the area of infarction and correspond to the coronary artery territory. Complications like ventricular septal defects and mitral regurgitation can also be identified.
This document discusses surgical management for hypertrophic obstructive cardiomyopathy (HOCM). It begins by defining HOCM and describing its genetic causes. It then discusses how HOCM can be anatomically classified and the morphology of septal hypertrophy and the mitral valve apparatus. The natural course of the disease and various treatment approaches are outlined, including supportive management, medical management, septal myectomy surgery, and alcohol septal ablation. Septal myectomy is described as the gold standard technique, aiming to relieve left ventricular outflow tract obstruction and mitigate mitral regurgitation. Outcomes of septal myectomy are generally good, but risks include heart block and residual gradients.
Inherited aortopathy can cause complications like aortic dissection and repeated surgeries. This document discusses inherited aortopathies associated with congenital heart defects. Primary aortic dilatation is mainly associated with coarctation of the aorta, bicuspid aortic valve, and conotruncal abnormalities. Secondary dilatation can occur after congenital heart surgery when non-aortic tissue is used. The most serious complication is aortic dissection. Guidelines exist for investigating and treating this life-threatening event, with consideration of underlying hereditary disorders.
Left Ventricular Apical Ballooning, Catecholamine Toxicity, and Cardiomyopathyasclepiuspdfs
Case reports and clinical experiences have implicated catecholamine. Excess likely contributes to the pathophysiologic process as a cause of cardiac dysfunction, impaired hemodynamic function, and poor outcomes. Cardiac dysfunction has also been described in many other diseases; there is likely a common underlying pathophysiology. In this review, we will examine the pathophysiology of cardiac dysfunction after catecholamine surge and discuss the evidence surrounding cardiac dysfunction.
ST-segment Depression: All are Not Created Equal!asclepiuspdfs
ST depression on an electrocardiography can be from various causes including ischemia, acute coronary syndrome, electrolyte imbalance, posterior myocardial infarction, pulmonary embolism and others. Making the right diagnosis and therefore the right treatment is of paramount importance. This article goes into depth explaining why all ST-segment depressions are not created equal.
This document provides an overview of hypertrophic cardiomyopathy (HCM). It defines HCM as an increased left ventricular wall thickness of 15 mm or more that is not due to abnormal loading conditions. HCM is caused by mutations in sarcomere genes. Symptoms can include left ventricular outflow tract obstruction and complications such as heart failure, atrial fibrillation, and sudden cardiac death. The document discusses the diagnosis of HCM using echocardiography, cardiac MRI and other imaging tools. It also reviews treatments such as medications, surgical myectomy to relieve outflow tract obstruction, alcohol septal ablation, implantable cardioverter-defibrillators and heart transplantation.
CVD in cancer survivors.Screening of cancer survivors.Chest Radiotherapy .JACC Scientific Expert Panel
( J Am Coll Cardiol 2019;74:905–27 )manifestations of chest and mediastinal radiotherapy .
The Progression of Hypertensive Heart Disease.From hypertension to heart failuremagdy elmasry
Staging of Hypertensive Heart Disease.Precipitants and clinical sequelae related to LVH and myocardial fibrosis.Imaging in hypertensive heart disease .Differential diagnosis of LVH.Concentric LVH .Eccentric LVH . Concentric remodeling .linking hypertension and atrial fibrillation
Role of echocardiography in acute myocardial infractionRakesh Kumar Messi
Echocardiography is useful in the diagnosis and management of acute myocardial infarction (AMI) for several reasons:
1. It can detect regional wall motion abnormalities (RWMAs) that occur prior to ECG changes during a coronary occlusion, aiding early diagnosis.
2. It is recommended to evaluate ventricular function, detect mechanical complications like thrombus, and stratify risk in patients with confirmed AMI.
3. RWMAs seen on echocardiography localize the area of infarction and correspond to the coronary artery territory. Complications like ventricular septal defects and mitral regurgitation can also be identified.
This document discusses surgical management for hypertrophic obstructive cardiomyopathy (HOCM). It begins by defining HOCM and describing its genetic causes. It then discusses how HOCM can be anatomically classified and the morphology of septal hypertrophy and the mitral valve apparatus. The natural course of the disease and various treatment approaches are outlined, including supportive management, medical management, septal myectomy surgery, and alcohol septal ablation. Septal myectomy is described as the gold standard technique, aiming to relieve left ventricular outflow tract obstruction and mitigate mitral regurgitation. Outcomes of septal myectomy are generally good, but risks include heart block and residual gradients.
Inherited aortopathy can cause complications like aortic dissection and repeated surgeries. This document discusses inherited aortopathies associated with congenital heart defects. Primary aortic dilatation is mainly associated with coarctation of the aorta, bicuspid aortic valve, and conotruncal abnormalities. Secondary dilatation can occur after congenital heart surgery when non-aortic tissue is used. The most serious complication is aortic dissection. Guidelines exist for investigating and treating this life-threatening event, with consideration of underlying hereditary disorders.
Approach to patient with Dilated CardiomyopathyNizam Uddin
This document provides an overview of dilated cardiomyopathy (DCM), including its definition, classification, etiologies, pathophysiology, clinical presentation, diagnosis and management. Key points include:
1) DCM is characterized by dilation and impaired contraction of the ventricles. Causes include genetic factors, viral myocarditis, toxins and idiopathic cases.
2) Diagnosis involves assessing history, symptoms of heart failure, echocardiogram showing reduced systolic function, and ruling out other potential causes.
3) Presentation varies from asymptomatic to heart failure symptoms. Management focuses on treating heart failure and its causes. Prognosis depends on the severity and reversibility of the underlying
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left or both ventricles not solely caused by abnormal loading conditions or ischemic heart disease. It has an annual incidence of 5-8 per 100,000 people and is more common in males, blacks, and those with hypertension or chronic beta-agonist use. Causes include genetic mutations, viral or autoimmune myocarditis, toxins, and metabolic abnormalities. On pathology, it shows cardiac dilatation and loss of myocytes leading to decreased wall thickness and increased fibrosis. Treatment involves managing heart failure symptoms and its underlying causes. Prognosis depends on factors like functional classification, ejection fraction, and biomarkers, with some patients experiencing improvement or stabilization
This document discusses anesthetic concerns for trauma victims requiring operative intervention who are too sick to anesthetize. It covers cardiac trauma such as blunt myocardial injury, traumatic aortic injury, and cardiac tamponade. It also discusses pulmonary trauma such as pulmonary contusions, flail chest, fat embolism syndrome, and acute lung injury. The case study presented is of an obese man in shock following a motor vehicle crash requiring emergency surgery. The priorities are stabilizing the patient's hemodynamics and oxygenation through fluid resuscitation and ventilation before inducing anesthesia to improve outcomes.
Reverse Takotsubo Cardiomyopathy Following General AnaesthesiaPremier Publishers
Reverse takotsubo cardiomyopathy(r-TTC) is a rare condition in which regional wall motion abnormalities affect the basal segments of left ventricle in absence of significant coronary artery disease. The Diagnosis is established by characteristic echocardiographic findings, clinical manifestations, and laboratory features. In this report we demonstrate a case of general anaesthesia induced cardiomyopathy in 21 years old female.
Takotsubo syndrome diagnostic criteria.
position papers :Mayo clnic ,HFA and InterTAK Diagnostic Criteria.Takotsubo Syndrome and COVID-19.Noninvasive Multimodality Imaging
in the Diagnosis and Management
of Patients with Takotsubo Syndrome
Dilated cardiomyopathy (DCM) can have several underlying mechanisms and etiologies including genetic factors, viral infections, autoimmunity, and toxins. The document discusses the prevalence, clinical presentations, genetic causes, role of inflammation and autoimmunity, and viral persistence in DCM. It also summarizes diagnostic and management approaches for DCM and reviews specific genetic mutations involved like those involving lamin A/C that are associated with the worst survival outcomes.
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by abnormal thickening of the heart muscle. It was first described in 1900 and occurs in 0.02-0.2% of the population. HCM is caused by mutations in genes coding for sarcomere proteins and is usually inherited in an autosomal dominant pattern. Treatment focuses on reducing risks of complications like heart failure and sudden cardiac death through medications, implantable cardioverter-defibrillators, or invasive procedures like septal reduction therapy.
Aortic stenosis is the abnormal narrowing of the aortic valve opening. It can be caused by congenital heart defects, calcification of the valve, or rheumatic fever. Symptoms include chest pain, fainting, fatigue, and heart failure. Diagnosis involves echocardiogram, ECG, chest x-ray and cardiac catheterization. Treatment depends on severity and includes medications, balloon valvuloplasty, transcatheter aortic valve replacement, surgical aortic valve replacement, and lifestyle changes like quitting smoking.
This document discusses thromboprophylaxis in ICU patients. It provides information on:
- The risk of venous thromboembolism (VTE) in hospitalized patients and the potential for prophylaxis to reduce this risk
- Common prophylactic options like enoxaparin, fondaparinux, and unfractionated heparin
- Tools to assess patient risk like the PADUA and IMPROVE scores
- Factors to consider when selecting a prophylactic method, including duration of prophylaxis
The document aims to review best practices for preventing VTE in high-risk hospitalized populations through appropriate thromboprophylaxis.
A genetic study identified a mutation in the Lamin A/C gene associated with dilated cardiomyopathy (DCM) and variable skeletal muscle involvement in a family. 14 members were examined, and 5 had DCM. One member had pure DCM, while others showed mild skeletal muscle weakness. Sequencing of the Lamin A/C gene in one affected member found a mutation, suggesting this gene can cause DCM and related skeletal muscle dystrophy.
Mr. Mohammed Ghouse, a 64-year-old male with hypertension, presented with chest pain and was admitted to the hospital. Tests showed extensive heart ischemia. He underwent coronary angiography which revealed triple vessel disease and atherosclerosis. His condition was stabilized with medications and an IABP device, but he later developed ventricular tachycardia and died despite resuscitative efforts. The cause of death was determined to be an acute myocardial infarction due to reduced blood flow from the blocked coronary arteries.
This document presents the fourth universal definition of myocardial infarction. Key changes include differentiating myocardial infarction from myocardial injury, highlighting peri-procedural myocardial injury after procedures as distinct from infarction, and considering electrical remodeling in assessing repolarization abnormalities. The definition aims to standardize the diagnosis of infarction for improved patient management and research.
1) A study of 900 older adults found that myocardial fibrosis detected by cardiac magnetic resonance (CMR) imaging was common, with myocardial infarction detected in 211 patients, major non-ischemic fibrosis in 54 patients, and minor non-ischemic fibrosis in 238 patients.
2) Patients with major non-ischemic fibrosis detected by CMR had a poorer prognosis than those without late gadolinium enhancement.
3) A study comparing outcomes of unrecognized myocardial infarction detected by CMR versus recognized myocardial infarction found that all-cause mortality was lower in those with unrecognized infarction for at least 5 years.
This document summarizes a presentation on pulmonary embolism given in 2014. It discusses various treatment options for pulmonary embolism including heparin alone, thrombolytics, surgical embolectomy, and catheter directed therapy. It notes that guidelines support thrombolysis for massive PE but are vague on submassive PE. One study showed thrombolysis for submassive PE led to a decrease in mortality but increase in major bleeding. The presentation emphasizes treating high risk PE aggressively with a multidisciplinary team approach and considering thrombolysis or advanced procedures to reduce long term morbidity. It describes the creation of a PE advanced care team at the hospital.
This document discusses venous thrombosis and pulmonary embolism. It covers risk factors, pathophysiology, diagnostic evaluation, and treatment options. The main points are:
1. Venous thrombosis and pulmonary embolism are concerns in postoperative and ICU patients. Thrombi often form silently in leg veins and can break off and travel to the lungs.
2. Diagnostic evaluations include D-dimer, ventilation-perfusion scans, echocardiograms, angiograms. Imaging shows defects from clots blocking blood flow.
3. Treatment involves anticoagulation initially with heparin or low molecular weight heparin. Warfarin is used long-term. Thrombolytics or inferior v
This document discusses cardiovascular pathology and includes the following:
1. It provides an overview and outline of topics to be covered related to heart and vascular diseases including atherosclerosis, myocardial infarction, aneurysms, and others.
2. It discusses the six principal mechanisms of heart disease including failure of the pump, obstruction to flow, regurgitant flow, shunted flow, disorders of conduction, and rupture of the heart or vessels.
3. It provides learning objectives for the presentation that cover topics like atherosclerosis, hypertension, aneurysms, congestive heart failure, and more.
Fourth Universal Definition Of Myocardial Infarction (2018)magdy elmasry
The document discusses the definition and diagnosis of heart attacks. It notes that there has been confusion over how to diagnose heart attacks, but that new 2018 guidelines aim to provide clarity. The guidelines define myocardial infarction based on elevated troponin levels, as well as symptoms and other diagnostic criteria. They distinguish between types of heart attacks based on their underlying causes, such as plaque rupture or an imbalance of oxygen supply and demand. The guidelines emphasize integrating clinical findings, electrocardiograms, imaging, and lab results over time to arrive at an accurate diagnosis.
Thermal Imaging for the Diagnosis of Early Vascular Dysfunctions: A Case Reportasclepiuspdfs
Diseases of blood vessels (referred in this article as vascular dysfunction) cause more morbidity and mortality, than combined impact of any other major non-communicable disease including cancer. We strongly feel that the development of a therapy system based on the management of disease of the vessel than management of the risk factors will yield better results and provide greater opportunity for individualized therapy. Detection of early vascular changes before clinical manifestations of endothelial dysfunction, hardening of the arteries, increased intima-media thickness, is of great importance for early identification of individuals with increased risk of accelerated atherosclerosis.
This document describes a case report of a 70-year-old man found to have a giant left atrial myxoma, which is a rare type of heart tumor. Trans-thoracic echocardiography revealed a large irregular mass occupying the entire left atrium. The patient underwent successful surgical excision of the mass. Pathological examination confirmed it was a left atrial myxoma measuring 7.5 x 4.5 x 2.5 cm. Follow-up echocardiography showed no remaining tumor and normal heart function. While rare in the elderly, left atrial myxomas should be considered as a potential cause of cardiac symptoms even in older patients.
Meadows Syndrome as Manifested by Displaced Ischemia of the Lower Limbsemualkaira
Peripartum cardiomyopathy (PPMC) or Meadows syndrome is recognised as a major cause of pregnancy-related heart failure with
high morbidity and mortality. It is a condition of unknown aetiology that manifests itself as heart failure due to systolic dysfunction
of the left ventricle during the last month of pregnancy and up to 5
months after delivery.
Approach to patient with Dilated CardiomyopathyNizam Uddin
This document provides an overview of dilated cardiomyopathy (DCM), including its definition, classification, etiologies, pathophysiology, clinical presentation, diagnosis and management. Key points include:
1) DCM is characterized by dilation and impaired contraction of the ventricles. Causes include genetic factors, viral myocarditis, toxins and idiopathic cases.
2) Diagnosis involves assessing history, symptoms of heart failure, echocardiogram showing reduced systolic function, and ruling out other potential causes.
3) Presentation varies from asymptomatic to heart failure symptoms. Management focuses on treating heart failure and its causes. Prognosis depends on the severity and reversibility of the underlying
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left or both ventricles not solely caused by abnormal loading conditions or ischemic heart disease. It has an annual incidence of 5-8 per 100,000 people and is more common in males, blacks, and those with hypertension or chronic beta-agonist use. Causes include genetic mutations, viral or autoimmune myocarditis, toxins, and metabolic abnormalities. On pathology, it shows cardiac dilatation and loss of myocytes leading to decreased wall thickness and increased fibrosis. Treatment involves managing heart failure symptoms and its underlying causes. Prognosis depends on factors like functional classification, ejection fraction, and biomarkers, with some patients experiencing improvement or stabilization
This document discusses anesthetic concerns for trauma victims requiring operative intervention who are too sick to anesthetize. It covers cardiac trauma such as blunt myocardial injury, traumatic aortic injury, and cardiac tamponade. It also discusses pulmonary trauma such as pulmonary contusions, flail chest, fat embolism syndrome, and acute lung injury. The case study presented is of an obese man in shock following a motor vehicle crash requiring emergency surgery. The priorities are stabilizing the patient's hemodynamics and oxygenation through fluid resuscitation and ventilation before inducing anesthesia to improve outcomes.
Reverse Takotsubo Cardiomyopathy Following General AnaesthesiaPremier Publishers
Reverse takotsubo cardiomyopathy(r-TTC) is a rare condition in which regional wall motion abnormalities affect the basal segments of left ventricle in absence of significant coronary artery disease. The Diagnosis is established by characteristic echocardiographic findings, clinical manifestations, and laboratory features. In this report we demonstrate a case of general anaesthesia induced cardiomyopathy in 21 years old female.
Takotsubo syndrome diagnostic criteria.
position papers :Mayo clnic ,HFA and InterTAK Diagnostic Criteria.Takotsubo Syndrome and COVID-19.Noninvasive Multimodality Imaging
in the Diagnosis and Management
of Patients with Takotsubo Syndrome
Dilated cardiomyopathy (DCM) can have several underlying mechanisms and etiologies including genetic factors, viral infections, autoimmunity, and toxins. The document discusses the prevalence, clinical presentations, genetic causes, role of inflammation and autoimmunity, and viral persistence in DCM. It also summarizes diagnostic and management approaches for DCM and reviews specific genetic mutations involved like those involving lamin A/C that are associated with the worst survival outcomes.
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by abnormal thickening of the heart muscle. It was first described in 1900 and occurs in 0.02-0.2% of the population. HCM is caused by mutations in genes coding for sarcomere proteins and is usually inherited in an autosomal dominant pattern. Treatment focuses on reducing risks of complications like heart failure and sudden cardiac death through medications, implantable cardioverter-defibrillators, or invasive procedures like septal reduction therapy.
Aortic stenosis is the abnormal narrowing of the aortic valve opening. It can be caused by congenital heart defects, calcification of the valve, or rheumatic fever. Symptoms include chest pain, fainting, fatigue, and heart failure. Diagnosis involves echocardiogram, ECG, chest x-ray and cardiac catheterization. Treatment depends on severity and includes medications, balloon valvuloplasty, transcatheter aortic valve replacement, surgical aortic valve replacement, and lifestyle changes like quitting smoking.
This document discusses thromboprophylaxis in ICU patients. It provides information on:
- The risk of venous thromboembolism (VTE) in hospitalized patients and the potential for prophylaxis to reduce this risk
- Common prophylactic options like enoxaparin, fondaparinux, and unfractionated heparin
- Tools to assess patient risk like the PADUA and IMPROVE scores
- Factors to consider when selecting a prophylactic method, including duration of prophylaxis
The document aims to review best practices for preventing VTE in high-risk hospitalized populations through appropriate thromboprophylaxis.
A genetic study identified a mutation in the Lamin A/C gene associated with dilated cardiomyopathy (DCM) and variable skeletal muscle involvement in a family. 14 members were examined, and 5 had DCM. One member had pure DCM, while others showed mild skeletal muscle weakness. Sequencing of the Lamin A/C gene in one affected member found a mutation, suggesting this gene can cause DCM and related skeletal muscle dystrophy.
Mr. Mohammed Ghouse, a 64-year-old male with hypertension, presented with chest pain and was admitted to the hospital. Tests showed extensive heart ischemia. He underwent coronary angiography which revealed triple vessel disease and atherosclerosis. His condition was stabilized with medications and an IABP device, but he later developed ventricular tachycardia and died despite resuscitative efforts. The cause of death was determined to be an acute myocardial infarction due to reduced blood flow from the blocked coronary arteries.
This document presents the fourth universal definition of myocardial infarction. Key changes include differentiating myocardial infarction from myocardial injury, highlighting peri-procedural myocardial injury after procedures as distinct from infarction, and considering electrical remodeling in assessing repolarization abnormalities. The definition aims to standardize the diagnosis of infarction for improved patient management and research.
1) A study of 900 older adults found that myocardial fibrosis detected by cardiac magnetic resonance (CMR) imaging was common, with myocardial infarction detected in 211 patients, major non-ischemic fibrosis in 54 patients, and minor non-ischemic fibrosis in 238 patients.
2) Patients with major non-ischemic fibrosis detected by CMR had a poorer prognosis than those without late gadolinium enhancement.
3) A study comparing outcomes of unrecognized myocardial infarction detected by CMR versus recognized myocardial infarction found that all-cause mortality was lower in those with unrecognized infarction for at least 5 years.
This document summarizes a presentation on pulmonary embolism given in 2014. It discusses various treatment options for pulmonary embolism including heparin alone, thrombolytics, surgical embolectomy, and catheter directed therapy. It notes that guidelines support thrombolysis for massive PE but are vague on submassive PE. One study showed thrombolysis for submassive PE led to a decrease in mortality but increase in major bleeding. The presentation emphasizes treating high risk PE aggressively with a multidisciplinary team approach and considering thrombolysis or advanced procedures to reduce long term morbidity. It describes the creation of a PE advanced care team at the hospital.
This document discusses venous thrombosis and pulmonary embolism. It covers risk factors, pathophysiology, diagnostic evaluation, and treatment options. The main points are:
1. Venous thrombosis and pulmonary embolism are concerns in postoperative and ICU patients. Thrombi often form silently in leg veins and can break off and travel to the lungs.
2. Diagnostic evaluations include D-dimer, ventilation-perfusion scans, echocardiograms, angiograms. Imaging shows defects from clots blocking blood flow.
3. Treatment involves anticoagulation initially with heparin or low molecular weight heparin. Warfarin is used long-term. Thrombolytics or inferior v
This document discusses cardiovascular pathology and includes the following:
1. It provides an overview and outline of topics to be covered related to heart and vascular diseases including atherosclerosis, myocardial infarction, aneurysms, and others.
2. It discusses the six principal mechanisms of heart disease including failure of the pump, obstruction to flow, regurgitant flow, shunted flow, disorders of conduction, and rupture of the heart or vessels.
3. It provides learning objectives for the presentation that cover topics like atherosclerosis, hypertension, aneurysms, congestive heart failure, and more.
Fourth Universal Definition Of Myocardial Infarction (2018)magdy elmasry
The document discusses the definition and diagnosis of heart attacks. It notes that there has been confusion over how to diagnose heart attacks, but that new 2018 guidelines aim to provide clarity. The guidelines define myocardial infarction based on elevated troponin levels, as well as symptoms and other diagnostic criteria. They distinguish between types of heart attacks based on their underlying causes, such as plaque rupture or an imbalance of oxygen supply and demand. The guidelines emphasize integrating clinical findings, electrocardiograms, imaging, and lab results over time to arrive at an accurate diagnosis.
Thermal Imaging for the Diagnosis of Early Vascular Dysfunctions: A Case Reportasclepiuspdfs
Diseases of blood vessels (referred in this article as vascular dysfunction) cause more morbidity and mortality, than combined impact of any other major non-communicable disease including cancer. We strongly feel that the development of a therapy system based on the management of disease of the vessel than management of the risk factors will yield better results and provide greater opportunity for individualized therapy. Detection of early vascular changes before clinical manifestations of endothelial dysfunction, hardening of the arteries, increased intima-media thickness, is of great importance for early identification of individuals with increased risk of accelerated atherosclerosis.
This document describes a case report of a 70-year-old man found to have a giant left atrial myxoma, which is a rare type of heart tumor. Trans-thoracic echocardiography revealed a large irregular mass occupying the entire left atrium. The patient underwent successful surgical excision of the mass. Pathological examination confirmed it was a left atrial myxoma measuring 7.5 x 4.5 x 2.5 cm. Follow-up echocardiography showed no remaining tumor and normal heart function. While rare in the elderly, left atrial myxomas should be considered as a potential cause of cardiac symptoms even in older patients.
Meadows Syndrome as Manifested by Displaced Ischemia of the Lower Limbsemualkaira
Peripartum cardiomyopathy (PPMC) or Meadows syndrome is recognised as a major cause of pregnancy-related heart failure with
high morbidity and mortality. It is a condition of unknown aetiology that manifests itself as heart failure due to systolic dysfunction
of the left ventricle during the last month of pregnancy and up to 5
months after delivery.
Meadows Syndrome as Manifested by Displaced Ischemia of the Lower Limbsemualkaira
Peripartum cardiomyopathy (PPMC) or Meadows syndrome is recognised as a major cause of pregnancy-related heart failure with
high morbidity and mortality. It is a condition of unknown aetiology that manifests itself as heart failure due to systolic dysfunction
of the left ventricle during the last month of pregnancy and up to 5
months after delivery
Meadows Syndrome as Manifested by Displaced Ischemia of the Lower Limbsemualkaira
Peripartum cardiomyopathy (PPMC) or Meadows syndrome is recognised as a major cause of pregnancy-related heart failure with
high morbidity and mortality. It is a condition of unknown aetiology that manifests itself as heart failure due to systolic dysfunction
of the left ventricle during the last month of pregnancy and up to 5
months after delivery.
Meadows Syndrome as Manifested by Displaced Ischemia of the Lower Limbsemualkaira
Peripartum cardiomyopathy (PPMC) or Meadows syndrome is recognised as a major cause of pregnancy-related heart failure with
high morbidity and mortality. It is a condition of unknown aetiology that manifests itself as heart failure due to systolic dysfunction
of the left ventricle during the last month of pregnancy and up to 5
months after delivery
Meadows Syndrome as Manifested by Displaced Ischemia of the Lower Limbsemualkaira
Peripartum cardiomyopathy (PPMC) or Meadows syndrome is recognised as a major cause of pregnancy-related heart failure with
high morbidity and mortality. It is a condition of unknown aetiology that manifests itself as heart failure due to systolic dysfunction
of the left ventricle during the last month of pregnancy and up to 5
months after delivery
Meadows Syndrome as Manifested by Displaced Ischemia of the Lower Limbsemualkaira
Peripartum cardiomyopathy (PPMC) or Meadows syndrome is recognised as a major cause of pregnancy-related heart failure with
high morbidity and mortality. It is a condition of unknown aetiology that manifests itself as heart failure due to systolic dysfunction
of the left ventricle during the last month of pregnancy and up to 5
months after delivery.
A Mistake that has Hurt No One: Sinus Mistakusasclepiuspdfs
There are times when we, the health care providers make a diagnosis and plan to treat that condition accordingly. In the mean time, because of a second opinion or another specialist consult might change the diagnosis completely and therefore the mode of management could change drastically. Here we present a similar case scenario for work-up of chest pains changing the diagnosis and therefore the mode of treatment. However in this process the patient did not get hurt (“Sinus Mistakus”).
The introduction of more sensitive cardiac troponin assays and lower diagnostic thresholds led to a revision of guidelines classifying myocardial injury by cause. The third universal definition differentiated between myocardial infarction due to plaque rupture (type 1) and due to ischemia from other illnesses (type 2), and classified injury without ischemia as acute or chronic injury. Both injury and type 2 infarction are common, occurring in over a third of hospitalized patients, who have poor short and long-term outcomes.
Blunt traumatic pericardial rupture and cardiac herniation is a rare but often fatal injury from severe chest trauma. The authors present two cases of this condition where early diagnosis was missed. Case 1 involved a motorbike accident with subsequent deterioration and discovery of a large pericardial tear and cardiac herniation requiring emergency surgery. Case 2 from a car collision developed hemorrhage from a longitudinal pericardial tear and left ventricular laceration discovered at thoracotomy. Diagnosis is difficult but important signs include unexplained cardiovascular instability, prominent cardiac shadows, and large pneumopericardium on imaging. Prompt surgical repair of pericardial defects and relocation of the heart is the primary treatment when identified
Analysis Of The Pathophysiological Framework Of Dilated...Kristi Anderson
The document discusses a case study of an elderly patient, Mr. P., who is struggling to manage his congestive heart failure and cardiomyopathy. It briefly defines congestive heart failure and cardiomyopathy. The nurse's treatment plan involves educating the patient to better manage his conditions, monitoring his symptoms and medication adherence, and collaborating with his healthcare team to improve his condition and quality of life.
Cardiomyopathies are a group of diseases that affect the myocardium of the heart. They can be classified into different types including dilated, hypertrophic, restrictive, and arrhythmogenic right ventricular cardiomyopathy. Hypertrophic cardiomyopathy is a familial condition characterized by unexplained thickening of the left ventricular wall and septum without an identifiable cause. It is one of the leading causes of sudden cardiac death.
Obstructive Shock, from Diagnosis to Treatment.pdfJonathanPuente6
The document summarizes the diagnosis and treatment of obstructive shock. It defines obstructive shock as shock caused by extra-cardiac diseases that reduce cardiac output through obstruction. The most common causes are listed as pulmonary embolism, pneumothorax, cardiac tamponade, and aortic dissection. The document recommends a three step approach to diagnosis: 1) clinical examination, 2) ultrasound examination using the RUSH protocol, and 3) radiological imaging if needed. Prognosis depends on the underlying cause and how quickly it is treated, with mortality rates ranging from 0.7% for pneumothorax to over 50% for pulmonary embolism with shock.
This document discusses venous thromboembolism (VTE) and the risks for marathon athletes. It notes that marathon athletes have several thrombogenic risk factors due to intensive training over long periods. These include dehydration, injury/inflammation, and immobilization during travel. The document outlines Virchow's triad of factors contributing to VTE risk and notes marathon athletes are at risk in all three areas. It provides tables with information on preventing VTE, signs and symptoms, considerations for medical practitioners, and return-to-training advice. The overall message is that marathon athletes have heightened VTE risk that requires awareness and preventive measures.
This document provides an overview of carotid artery stenosis. It discusses the anatomy of the carotid arteries and how stenosis can increase the risk of stroke by reducing blood flow to the brain. Symptoms of stenosis range from transient ischemic attacks to full strokes, depending on the location and severity of the blockage. Imaging plays a key role in detecting and evaluating carotid artery stenosis. Treatment may involve medications, lifestyle changes, or carotid endarterectomy surgery to remove plaque buildup.
Acute myocardial infarction critical care cardiologyGiovanna Trujillo
This document discusses the evaluation and diagnosis of acute chest pain in the intensive care unit setting. It describes that chest pain requires immediate evaluation to diagnose potentially life-threatening causes like acute myocardial infarction. While AMI is a major concern, there are many cardiac and non-cardiac causes of chest pain that require testing and diagnostic evaluation. Common causes discussed in detail include pericarditis, pulmonary embolism, musculoskeletal pain, and acute myocarditis.
Anaesthetic Management of a Patient with Ischaemic Heart DiseaseZareer Tafadar
This document discusses the anaesthetic management of patients with ischemic heart disease undergoing non-cardiac surgery. It begins by defining ischemic heart disease and outlining its various manifestations including stable angina, unstable angina, and myocardial infarction. It then discusses preoperative evaluation and risk stratification of these patients, including medical history, physical exam, ECG, stress testing, and coronary angiography. Intraoperative management focuses on minimizing myocardial ischemia through beta-blockers, tight blood pressure control, and avoidance of tachycardia or hypotension.
We present the case of a 49-year-old male who was referred from Emergency department with worsening
breathlessness, chest tightness for last 24 hours. He had a background history of Asthma and Hypertension. Initial ECG revealed symmetric T wave inversions in anterior leads and found to have raised
troponin levels. Patient was diagnosed and treated as NSTEMI. While waiting for his coronary angiogram
he underwent echocardiogram whose findings were consistent with right sided impairment. Differential
diagnosis of Pulmonary Embolism has been made and CT Pulmonary Angiogram done that confirmed
diagnosis of Pulmonary Embolism. Early advice from the Respiratory team was sought and patient was
treated with rivaroxaban. After a hospital stay, he made a remarkable recovery.
This document discusses a case of blunt traumatic pericardial rupture and cardiac herniation in a 21-year old male following a motorbike accident. Key findings from imaging included a 10cm tear in the right pericardium, pneumopericardium, and herniation of the heart into the right hemithorax. The patient underwent thoracotomy for repair of the pericardial tear. Diagnosis of blunt traumatic pericardial rupture can be difficult due to subtle clinical signs and associated injuries from polytrauma. Imaging modalities like CT are useful for diagnosis. Surgical closure is usually required for moderate to large tears to prevent further herniation and hemodynamic compromise.
Broken Heart Syndrome: A Stress Responseasclepiuspdfs
This case report describes a 76-year-old female who presented with symptoms of chest pain and dyspnea after experiencing recent physical stress from pneumonia. She underwent pre-operative testing in preparation for hiatal hernia repair surgery. During induction of anesthesia, she went into ventricular fibrillation but self-converted to sinus rhythm. She was diagnosed with Takotsubo cardiomyopathy after cardiac catheterization found no significant coronary artery blockages. Takotsubo cardiomyopathy, also known as broken heart syndrome, is a type of reversible left ventricular dysfunction that can mimic acute coronary syndrome. It is often preceded by physical or emotional stress and predominantly affects postmenopausal women.
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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
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
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TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
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2. 339 American Journal of Medical Case Reports
Figure 2. Computed Tomography of chest showing aortic dissection
involving aortic root
Figure 3. Computed Tomography of chest showing hemopericardium
and descending aortic dissection
Figure 4. Computed Tomography of chest showing thrombosis of left
common iliac artery
Initial work up that included electrocardiogram, chest
radiography and basic labs were completely normal.
Vascular surgery was consulted to rule out acute limb
ischemia. In next couple of hour’s patient’s BP dropped to
78/50 with HR ranging from 114-130 beats per minute.
Patient did not respond to fluid bolus and was started on a
norepinephrine drip. Repeat labs showed drop in
hemoglobin from 13.2 to 12.1 g/dl, increase in blood urea
nitrogen/creatinine 16/1.0 to 19/2.2 mg/dl, lactic acid > 12
mmol/L and negative troponins. After stabilizing the
patient, CT chest, abdomen, pelvis and lower extremity
was done which revealed large hemopericardium [Figure 1]
with aortic dissection originating at the aortic root,
extending into the distal thoracic aorta [Figure 2, Figure 3]
with thrombosed left common iliac artery [Figure 4].
Patient was evaluated by vascular and cardio-thoracic
surgery and was transferred to other facility for emergent
surgery. Patient underwent replacement of ascending aorta,
hemi-arch and resuspension and repair of aortic valve with
a 32 mm Hemashield double Velour Dacron graft. Total
circulatory arrest time was 42 minutes and received
antergrade cerebral perfusion for 41 min. Patient also
underwent femoral-femoral bypass surgery. After the
surgery, patient’s limb got better and was transferred to
rehabilitation center. Patient continues to follow at
cardiovascular and vascular surgery clinics and was doing
well for the last 18 months.
3. Discussion
3.1. Introduction
AD is an uncommon serious condition, which usually
presents with chest pain and upper back pain but can have
many atypical presentations such as stroke, myocardial
infarction, syncope, mesenteric and limb ischemia
[1,2,3,4]. Many patients die even before they present to
the ED or prior to the diagnosis [5]. Our patient presented
with low back pain and acute lower limb ischemia and
found to have type A aortic dissection with
hemopericardium in addition to occlusive thrombus;
incidentally diagnosed on complete vascular imaging,
which was done to investigate the cause of hemodynamic
instability. Aortic dissection can present with impaired or
absent blood flow in peripheral vessels (carotid, brachial,
femoral) [1]. This pulse deficit most commonly results
from intimal flap or compression by a hematoma [5].
Literature review showed, very few cases have been
reported with concomitant AD and acute distal arterial
thromboembolic occlusion of a vessel [6,7,8,9].
Olsson C. et al. reported an incidence of 9.1 cases per
100,000 in women increasing to 16.3 per 100,000 in men
based on study from national heath care registry data and
out of hospital death autopsies [10,11] and Howard et al.
reported incidence of 6 cases per 100,000 population in
Oxford Vascular study [12]. AD is more frequently seen
in men compared to females in a ratio of 1.5: 1 and men
developed at younger age compared to females (79.3
verses 67.1 years) per Oxford vascular study [12]. Marfan
syndrome patients develop AD at very young age (less
then 40 years) [5]. Diagnosis is often missed in up to 38%
of cases on initial evaluation and first established in 28%
of cases during autopsy [1,13].
3. American Journal of Medical Case Reports 340
3.2. Etiology and Pathogenesis
AD is a longitudinal tear initiated in intima progressing
to disruption of the medial layer thus creating true and
false lumen, which could extend the tear in either
directions of aorta resulting in rupture of aorta,
hemopericardium, massive blood loss, end organ ischemic
damage as in our case and death [5,6,11]. AD is described
as acute if symptom onset is less than 2 weeks and chronic
if more than 2 weeks [5,11]. AD type based on anatomy is
classified by two classification systems. Stanford system
classifies dissections that involve the ascending aorta as
type A and all other dissections as type B regardless of the
site of primary intimal tear. [2,4,5,11] Where as the
DeBakey classifies as type I involving the ascending aorta
and the aortic arch, type II involving the ascending aorta
only and type III involving the descending aorta only [2,5,
11]. Chronic systemic hypertension is the most common
predisposing risk factor implicated in AD. It is prevalent
in 62 to 78% patients with AD [1,5,11,12,13] and
increases the aortic wall stress initiating the tear in intima
[5,11]. Hypertension leads to structural (atherosclerosis,
myo-intimal thickening) and functional (increased
stiffness, loss of endothelial function) changes in the
arterial system and eventually leading to structural
changes of left ventricle (hypertrophy). This interplay
between ventricle and arterial system is called as
ventricular-vascular coupling [14]. Initially it is an
adaptive phenomenon and over time with chronic
hypertension, aging and other factors lead to heightened
arterial stiffness, change in pressure wave amplifications,
velocity and its timing, leading to ventricular-vascular
mismatch which acts as a main underlying
pathophysiology for cardiovascular diseases such as
myocardial ischemia, heart failure, aneurysms and
dissections [14]. Understanding ventricular-vascular
coupling helps in determining pathophysiology of
cardiovascular manifestations [14]. Other etiologies that
would increase the wall stress are physical trauma,
deceleration injury in motor vehicle accidents and falls
[15,16] pheochromocytoma and cocaine use from
catechocholamine surge [17], and coarctation of aorta.
Smoking also increases the risk of dissection by affecting
Transforming growth factor TGF-B that promotes smooth
muscle growth and function in the media [11]. Our patient
had chronic systemic hypertension, chronic smoker and
also experienced motor vehicle accident which would be
predisposing factors for AD. Other predisposing factor
contributing to AD is medial degeneration seen in
conditions such as Marfans syndrome, Noonan syndrome,
Ehlers-Danlos syndrome, Turner syndrome, inflammatory
diseases of aorta and bicuspid aortic valve [7,18,19].
Hagan et al. reported 4.3% in IRAD study [13] Litchford
et al. [20] and Archer AG et al. [21] reported 5% had
direct iatrogenic AD from previous cardiac surgery during
arterial cannulation or during catheter based diagnostic or
therapeutic interventions. Most of the iatrogenic
dissections result in type B dissections.
3.3. Management
Having high index of clinical suspicion is the foremost
important step in diagnosing devastating disease.
Computed tomography (CT) is most common, readily
available and widely used modality for quick diagnosis of
AD. It has high sensitivity (83-94%) and specificity (87-
100%) in diagnosing AD [22]. The presence of an intimal
flap is characteristic of AD as shown in Figure 2 and
Figure 3. Helical or spiral CT is shown to be superior
compared to conventional CT in detecting AD. Trans-
esophageal echocardiogram is highly sensitive (97-99%)
and specific (97-100%) in diagnosing AD, identifying the
entry site of dissection, presence or absence of thrombus,
involvement of coronaries and arch vessels, aortic valve
involvement and hemodynamics across the aortic valve
and pericardial effusion [23,24,25]. Magnetic resonance
imaging also has very high sensitivity and specificity in
range of 95-100%, provides all the information
comparable to TEE and helpful in patients with previous
aortic disease, surgical repair and in construction of three
dimensional images [26,27]. Chest radiography,
electrocardiogram and trans-thoracic echocardiogram are
less specific in diagnosing AD. Chest radiography lacks
specificity but helps in predicting the disease. Widened
mediastinum is seen in 50% of cases with AD. Presence of
non-specific changes on electrocardiogram in a patient
with chest pain, diagnosis points towards AD over
myocardial infarction. Aortography is an invasive, time
consuming procedure and rarely used in recent days.
Type A dissections require urgent surgical intervention
where as Type B dissections are managed medically with
blood pressure control and pain management [2,4,5].
Understanding ventricular-vascular coupling helps in
determining pathophysiology of cardiovascular
manifestations and its management modulation [14].
Unoperated type A dissections have estimated mortality
rate of 1% per hour to 2% per hour during first 48 hours
[28]. AD resulting in rupture has a 90% mortality rate [6].
Fann et al. reported overall operative mortality rate for
acute AD is 24% ± 8%, acute type A AD it is 26% ± 3%,
acute type B dissection 39% ± 8% [29] and 50 to 70% for
renal ischemic patients [30]. Per IRAD study in-hospital
mortality rate for type A dissection patients treated
surgically was 27 % compared to medical management
(high operative risk and elderly patient population) was
58% and for type B dissection patients managed medically
was 10.7 % and 31.4% in surgical group.
Surgery is the standard of care and it is indicated in all
type A dissections, unless serious comorbidities preclude
surgical intervention [31]. The aim of surgery is to excise
and replace the aortic segment with dissection but not to
replace entire dissected aorta and to maintain aortic valve
integrity. Best-known surgical procedures for type A
dissections are the Bentall, David (valve sparing), Yacoub,
Ross, aortic homograft and Elephant technique
[5,11,19,32]. Glue aortoplasty is usually combined with
AD surgical procedure. Our patient underwent valve
sparing aortic root replacement surgery (David procedure).
There is no role for endovascular stents in type A
dissections [33].
Type B dissections are managed medically unless
complicated. Medical management is shown to be superior
to management with either surgical or endovascular stent
approach in uncomplicated type B dissections. The
cornerstone of medical management is tight Blood
pressure and heart rate control with B-blockers and
vasodilators such as Angiotensin-converting-enzyme
inhibitors (ACEI) aiming to reduce the force of left
ventricular contractions, to decrease steepness of the rise
4. 341 American Journal of Medical Case Reports
of the aortic pulse wave (ie, dp/dt) and pain management
[5]. Surgical or endovascular intervention is indicated in
complicated type B dissections, which comprise of type B
dissection with persistent or recurrent pain despite
adequate antihypertensive therapy with at least two
parenteral agents at moderate to high dose, aortic diameter
≥ 5.5 cm, diameter increase > 4mm, acute expansion of
the false lumen, periaortic or mediastinal hematoma
(contained rupture) and in visceral, renal or limb
malperfusion syndrome [34]. Surgical interventions
include replacement of aorta or bypass surgery. Our
patient underwent femoral-femoral bypass surgery, which
resulted in complete recovery of left leg ischemia. Hybrid
procedure includes combination vascular surgical
procedure and endovascular stents. IRAD study showed,
patients who underwent thoracic endovascular aortic
replacement (TEVAR) for type B dissections had lower 5-
year mortality compared to patients treated medically
[11,35]. Based on IRAD study data, the food and drug
administration (FDA), Society for Vascular surgery (SAS),
American Association for Thoracic surgery, Society of
Thoracic Surgeons and the Society for Interventional
Radiology recommended TEVAR for complicated type B
dissections [11,36].
AD managed medically or surgically needs long-term
care and follow up as they have potential to develop aortic
aneurysm and propagate dissection. Long-term management
consists of aggressive blood pressure control, smoking
cessation and clinical and imaging assessment of the aorta
for early detection and correction of the potential
complications [5,37]. Tight blood pressure control may
reduce incidence of re-dissection in about one third of
patients [38]. IRAD database showed B-blockers are
associated with improved survival in type A dissections
[39].
Our patient presented with concomitant Stanford type A
AD and left common iliac arterial thrombosis. It presents a
therapeutic dilemma as the management of arterial
thrombosis usually involves inhibition of the coagulation
cascade. There were no clear guidelines for management
of AD with malperfusion or arterial thrombosis and use of
anticoagulants, but the general consensus was to treat
aortic dissection first as it would correct malperfusion in
most patients [40]. Thoracic aortic surgery is associated
with hemorrhage due to numerous interrelated causes such
extensive surgical exploration, arterial and venous
bleeding, consumptive coagulopathy, antithrombotic use,
platelet dysfunction, coronary bypass and hypothermia
[40]. The Society of Thoracic Surgeons (STS) and The
Society of Cardiovascular anesthesiologists (SCA) have
defined clinical practical guidelines for use of blood
products during perioperative period. However there was
no clear time frame defined to start anticoagulation or
venous thromboembolic prophylaxis post-operatively [41].
Study by Kincaid et al. showed that patients receiving low
molecular weight heparin (LMWH) within 12 hours of
cardiac surgery have significantly greater blood loss and
increased blood transfusion compared with patients
receiving intravenous heparin or a dose of LMWH more
than 12 hours before operation [42]. Medalion et al.
showed that the risk of postoperative bleeding or
transfusion requirement is less if enoxaparin administered
more than 8 hours before coronary artery bypass surgery
[43]. For patients undergoing cardiac surgery, it is
recommended to use mechanical prophylaxis with intermittent
pneumatic compressions (IPC) in uncomplicated post
operative course, low dose unfractionated heparin (LDUH)
or LMWH in addition to IPC in patients whose hospital
course is complicated by one or more non hemorrhagic
surgical complications and in patients with moderate risk
for venous thromboembolism (VTE) and not high risk for
perioperative bleeding, LDUH or LMWH or mechanical
prophylaxis with IPC over no prophylaxis [44].
Unfractionated Heparin is widely used in perioperative
period especially in cardiac surgery [40] due its shorter
half life, less bleeding risk and availability of strong
reversal agent, but its use is limited by concerns of heparin
rebound, heparin resistance, protamine reaction, heparin-
induced thrombocytopenia, heparin- induced platelet
dysfunction and less anti-thrombotic activity compared to
LMWH. Literature review showed wide spread usage of a
second generation LMWH - Bemiparin, in Europe in
perioperative period including high-risk surgical
procedure [45]. Its usage is getting wider given its better
pharmacological profile – anti-factor Xa:anti-factor IIa
(8:1), increase in release of tissue factor pathway inhibitor
from endothelial cells under both static and shear stress
conditions, more favorable efficacy: safety ratio and
shown to be superior to fondaparinex, and unfractionated
heparin in suppressing angiogenesis and vasculogenesis
[45]. Bemiparin may have a potential for use in cardiac
surgeries with malperfusion like our case in perioperative
period but needs further studies evaluating its use. Our
patient was severely coagulopathic after he was rewarmed
and weaned of cardiopulmonary bypass necessitating
multiple rounds of clotting factors. He was placed on
venodyne boots in perioperative period and started on
subcutaneous heparin on first post-operative day.
4. Conclusion
Maintaining a high index of clinical suspicion for aortic
pathology could possibly lead to identification and timely
management of a greater number of patients who have
atypical presentations [1,2,4,5,13]. This would be
especially true for patients who have catastrophic
presentations with unexplained symptoms.
Acknowledgement, Conflicts of Interests
and Grant information
None.
References
[1] P. C. Spittell, J. A. Spittell, Jr., J. W. Joyce, A. J. Tajik, W. D.
Edwards, H. V. Schaff, et al., “Clinical features and differential
diagnosis of aortic dissection: experience with 236 cases (1980
through 1990),” Mayo Clin Proc, vol. 68, pp. 642-51, Jul 1993.
[2] C. A. Nienaber and K. A. Eagle, “Aortic dissection: new frontiers
in diagnosis and management: Part I: from etiology to diagnostic
strategies,” Circulation, vol. 108, pp. 628-35, Aug 5 2003.
[3] Y. von Kodolitsch, A. G. Schwartz, and C. A. Nienaber, “Clinical
prediction of acute aortic dissection,” Arch Intern Med, vol. 160,
pp. 2977-82, Oct 23 2000.
[4] I. A. De Leon Ayala and Y. F. Chen, “Acute aortic dissection: an
update,” Kaohsiung J Med Sci, vol. 28, pp. 299-305, Jun 2012.
5. American Journal of Medical Case Reports 342
[5] I. A. Khan and C. K. Nair, “Clinical, diagnostic, and management
perspectives of aortic dissection,” Chest, vol. 122, pp. 311-28, Jul
2002.
[6] S. M. Huang, F. Du, C. Y. Wang, M. J. Bair, and K. T. Wang,
“Aortic dissection presenting as isolated lower extremity pain in a
young man,” Am J Emerg Med, vol. 28, pp. 1061 e1-3, Nov 2010.
[7] D. Barbic and W. Grad, “Aortic dissection presenting as left leg
numbness and paralysis,” Am J Emerg Med, vol. 28, pp. 1063 e7-8,
Nov 2010.
[8] G. Avegliano, A. Evangelista, C. Elorz, T. Gonzalez-Alujas, H.
Garcia del Castillo, and J. Soler-Soler, “Acute peripheral arterial
ischemia and suspected aortic dissection: usefulness of
transesophageal echocardiography in differential diagnosis with
aortic thrombosis,” Am J Cardiol, vol. 90, pp. 674-7, Sep 15 2002.
[9] N. Raby, J. Giles, and H. Walters, “Aortic dissection presenting as
acute leg ischaemia,” Clinical Radiology, vol. 42, pp. 116-117,
August 1990 1990.
[10] C. Olsson, S. Thelin, E. Stahle, A. Ekbom, and F. Granath,
“Thoracic aortic aneurysm and dissection: increasing prevalence
and improved outcomes reported in a nationwide population-based
study of more than 14,000 cases from 1987 to 2002,” Circulation,
vol. 114, pp. 2611-8, Dec 12 2006.
[11] J. Z. Goldfinger, J. L. Halperin, M. L. Marin, A. S. Stewart, K. A.
Eagle, and V. Fuster, “Thoracic aortic aneurysm and dissection,” J
Am Coll Cardiol, vol. 64, pp. 1725-39, Oct 21 2014.
[12] D. P. Howard, A. Banerjee, J. F. Fairhead, J. Perkins, L. E. Silver,
P. M. Rothwell, et al., “Population-based study of incidence and
outcome of acute aortic dissection and premorbid risk factor
control: 10-year results from the Oxford Vascular Study,”
Circulation, vol. 127, pp. 2031-7, May 21 2013.
[13] P. G. Hagan, C. A. Nienaber, E. M. Isselbacher, D. Bruckman, D.
J. Karavite, P. L. Russman, et al., “The International Registry of
Acute Aortic Dissection (IRAD): new insights into an old
disease,” JAMA, vol. 283, pp. 897-903, Feb 16 2000.
[14] P. S. Saba, M. Cameli, G. Casalnuovo, M. M. Ciccone, A. Ganau,
M. Maiello, et al., “Ventricular-vascular coupling in hypertension:
methodological considerations and clinical implications,” J
Cardiovasc Med (Hagerstown), vol. 15, pp. 773-87, Nov 2014.
[15] J. A. Elefteriades, I. Hatzaras, M. A. Tranquilli, A. J. Elefteriades,
R. Stout, R. K. Shaw, et al., “Weight lifting and rupture of silent
aortic aneurysms,” JAMA, vol. 290, p. 2803, Dec 3 2003.
[16] I. Hatzaras, M. Tranquilli, M. Coady, P. M. Barrett, J. Bible, and J.
A. Elefteriades, “Weight lifting and aortic dissection: more
evidence for a connection,” Cardiology, vol. 107, pp. 103-6, 2007.
[17] R. A. Lange and L. D. Hillis, “Cardiovascular complications of
cocaine use,” N Engl J Med, vol. 345, pp. 351-8, Aug 2 2001.
[18] M. J. Eisenberg, S. A. Rice, A. Paraschos, G. R. Caputo, and N. B.
Schiller, “The clinical spectrum of patients with aneurysms of the
ascending aorta,” Am Heart J, vol. 125, pp. 1380-5, May 1993.
[19] J. AUER, R. Berent, and B. Eber, “Aortic dissection: incidence,
natural history and impact of surgery,” Journal of Clinical and
Basic Cardiology vol. 3, pp. 151-154, 2000 2003.
[20] B. Litchford, J. E. Okies, S. Sugimura, and A. Starr, “Acute aortic
dissection from cross-clamp injury,” J Thorac Cardiovasc Surg,
vol. 72, pp. 709-13, Nov 1976.
[21] A. G. Archer, P. L. Choyke, R. K. Zeman, C. E. Green, and M.
Zuckerman, “Aortic dissection following coronary artery bypass
surgery: diagnosis by CT,” Cardiovasc Intervent Radiol, vol. 9, pp.
142-5, 1986.
[22] J. E. Cigarroa, E. M. Isselbacher, R. W. DeSanctis, and K. A.
Eagle, “Diagnostic imaging in the evaluation of suspected aortic
dissection. Old standards and new directions,” N Engl J Med, vol.
328, pp. 35-43, Jan 7 1993.
[23] R. Erbel, R. Engberding, W. Daniel, J. Roelandt, C. Visser, and H.
Rennollet, “Echocardiography in diagnosis of aortic dissection,”
Lancet, vol. 1, pp. 457-61, Mar 4 1989.
[24] A. Keren, C. B. Kim, B. S. Hu, I. Eyngorina, M. E. Billingham, R.
S. Mitchell, et al., “Accuracy of biplane and multiplane
transesophageal echocardiography in diagnosis of typical acute
aortic dissection and intramural hematoma,” J Am Coll Cardiol,
vol. 28, pp. 627-36, Sep 1996.
[25] R. S. Ballal, N. C. Nanda, R. Gatewood, B. D'Arcy, T. E.
Samdarshi, W. L. Holman, et al., “Usefulness of transesophageal
echocardiography in assessment of aortic dissection,” Circulation,
vol. 84, pp. 1903-14, Nov 1991.
[26] C. A. Nienaber, Y. von Kodolitsch, V. Nicolas, V. Siglow, A.
Piepho, C. Brockhoff, et al., “The diagnosis of thoracic aortic
dissection by noninvasive imaging procedures,” N Engl J Med, vol.
328, pp. 1-9, Jan 7 1993.
[27] A. L. Pucillo, A. G. Schechter, R. A. Moggio, R. H. Kay, M. S.
Tenner, and M. V. Herman, “Postoperative evaluation of
ascending aortic prosthetic conduits by magnetic resonance
imaging,” Chest, vol. 97, pp. 106-10, Jan 1990.
[28] H. Eggebrecht, D. Baumgart, U. Herold, J. Piotrowski, J.
Barkhausen, R. Wiesemes, et al., “Interventional management of
aortic dissection,” Herz, vol. 27, pp. 539-47, Sep 2002.
[29] J. I. Fann, J. A. Smith, D. C. Miller, R. S. Mitchell, K. A. Moore,
G. Grunkemeier, et al., “Surgical management of aortic dissection
during a 30-year period,” Circulation, vol. 92, pp. II113-21, Nov 1
1995.
[30] J. Laas, M. Heinemann, H. J. Schaefers, W. Daniel, and H. G.
Borst, “Management of thoracoabdominal malperfusion in aortic
dissection,” Circulation, vol. 84, pp. III20-4, Nov 1991.
[31] H. G. Borst and J. Laas, “Surgical treatment of thoracic aortic
aneurysms,” Adv Card Surg, vol. 4, pp. 47-87, 1993.
[32] H. Takayama, C. R. Smith, M. E. Bowdish, and A. S. Stewart,
“Open distal anastomosis in aortic root replacement using axillary
cannulation and moderate hypothermia,” J Thorac Cardiovasc
Surg, vol. 137, pp. 1450-3, Jun 2009.
[33] R. Rolph, J. M. Duffy, B. Modarai, R. E. Clough, P. Taylor, and
M. Waltham, “Stent graft types for endovascular repair of thoracic
aortic aneurysms,” Cochrane Database Syst Rev, vol. 3, p.
CD008448, 2013.
[34] R. Fattori, P. Cao, P. De Rango, M. Czerny, A. Evangelista, C.
Nienaber, et al., “Interdisciplinary expert consensus document on
management of type B aortic dissection,” J Am Coll Cardiol, vol.
61, pp. 1661-78, Apr 23 2013.
[35] R. Fattori, D. Montgomery, L. Lovato, S. Kische, M. Di Eusanio,
H. Ince, et al., “Survival after endovascular therapy in patients
with type B aortic dissection: a report from the International
Registry of Acute Aortic Dissection (IRAD),” JACC Cardiovasc
Interv, vol. 6, pp. 876-82, Aug 2013.
[36] R. A. White, D. C. Miller, F. J. Criado, M. D. Dake, E. B.
Diethrich, R. K. Greenberg, et al., “Report on the results of
thoracic endovascular aortic repair for acute, complicated, type B
aortic dissection at 30 days and 1 year from a multidisciplinary
subcommittee of the Society for Vascular Surgery Outcomes
Committee,” J Vasc Surg, vol. 53, pp. 1082-90, Apr 2011.
[37] S. Pansini, P. V. Gagliardotto, E. Pompei, F. Parisi, G. Bardi, E.
Castenetto, et al., “Early and late risk factors in surgical treatment
of acute type A aortic dissection,” Ann Thorac Surg, vol. 66, pp.
779-84, Sep 1998.
[38] M. E. DeBakey, C. H. McCollum, E. S. Crawford, G. C. Morris,
Jr., J. Howell, G. P. Noon, et al., “Dissection and dissecting
aneurysms of the aorta: twenty-year follow-up of five hundred
twenty-seven patients treated surgically,” Surgery, vol. 92, pp.
1118-34, Dec 1982.
[39] T. Suzuki, E. M. Isselbacher, C. A. Nienaber, R. E. Pyeritz, K. A.
Eagle, T. T. Tsai, et al., “Type-selective benefits of medications in
treatment of acute aortic dissection (from the International
Registry of Acute Aortic Dissection [IRAD]),” Am J Cardiol, vol.
109, pp. 122-7, Jan 1 2012.
[40] L. F. Hiratzka, G. L. Bakris, J. A. Beckman, R. M. Bersin, V. F.
Carr, D. E. Casey, Jr., et al., “2010
ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM
guidelines for the diagnosis and management of patients with
Thoracic Aortic Disease: a report of the American College of
Cardiology Foundation/American Heart Association Task Force
on Practice Guidelines, American Association for Thoracic
Surgery, American College of Radiology, American Stroke
Association, Society of Cardiovascular Anesthesiologists, Society
for Cardiovascular Angiography and Interventions, Society of
Interventional Radiology, Society of Thoracic Surgeons, and
Society for Vascular Medicine,” Circulation, vol. 121, pp. e266-
369, Apr 6 2010.
[41] The Society of Thoracic Surgeons Blood Conservation Guideline
Task, V. A. Ferraris, S. P. Ferraris, S. P. Saha, E. A. Hessel, 2nd,
C. K. Haan, et al., “Perioperative blood transfusion and blood
conservation in cardiac surgery: the Society of Thoracic Surgeons
and The Society of Cardiovascular Anesthesiologists clinical
practice guideline,” Ann Thorac Surg, vol. 83, pp. S27-86, May
2007.
[42] E. H. Kincaid, M. L. Monroe, D. L. Saliba, N. D. Kon, W. G.
Byerly, and M. G. Reichert, “Effects of preoperative enoxaparin
versus unfractionated heparin on bleeding indices in patients
6. 343 American Journal of Medical Case Reports
undergoing coronary artery bypass grafting,” Ann Thorac Surg,
vol. 76, pp. 124-8; discussion 128, Jul 2003.
[43] B. Medalion, G. Frenkel, P. Patachenko, E. Hauptman, L. Sasson,
and A. Schachner, “Preoperative use of enoxaparin is not a risk
factor for postoperative bleeding after coronary artery bypass
surgery,” J Thorac Cardiovasc Surg, vol. 126, pp. 1875-9, Dec
2003.
[44] G. H. Guyatt, E. A. Akl, M. Crowther, D. D. Gutterman, H. J.
Schuunemann, T. American College of Chest Physicians
Antithrombotic, et al., “Executive summary: Antithrombotic
Therapy and Prevention of Thrombosis, 9th ed: American College
of Chest Physicians Evidence-Based Clinical Practice Guidelines,”
Chest, vol. 141, pp. 7S-47S, Feb 2012.
[45] M. M. Ciccone, F. Cortese, F. Corbo, N. E. Corrales, A. K. Al-
Momen, A. Silva, et al., “Bemiparin, an effective and safe low
molecular weight heparin: a review,” Vascul Pharmacol, vol. 62,
pp. 32-7, Jul 2014.