Cardiomyopathies are diseases of the heart muscle that can cause cardiac dysfunction. The main types include dilated cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. Dilated cardiomyopathy is characterized by ventricular dilation and impaired contraction, with the majority of cases being idiopathic. Etiologies of dilated cardiomyopathy include infectious, inflammatory, toxic, metabolic, inherited, and peripartum causes. Treatment aims to reduce preload and afterload through medications like diuretics, vasodilators, and ACE inhibitors. Prognosis depends on the underlying etiology.
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left ventricle not caused by ischemic or valvular heart disease. The document discusses the epidemiology, etiology, pathology, genetics, clinical features, diagnosis, and management of idiopathic dilated cardiomyopathy. Key points include:
- The annual incidence is 5-8 per 100,000 people with increased risk in males, blacks, and those with hypertension or chronic beta-agonist use.
- Causes include genetic mutations, viral infections, autoimmune diseases, and drugs. Pathology shows dilatation, myocyte hypertrophy and death, and extracellular matrix remodeling.
- Diagnosis involves ECG
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
CHF.ppt it is internal medicine part 2016 AmboMekdiDan
Congestive Heart Failure is a complex clinical syndrome that results from any structural or functional disorder impairing the ventricle's ability to fill or eject blood. It is characterized by symptoms like dyspnea and fatigue. There are many causes including coronary artery disease, hypertension, and cardiomyopathies. The pathophysiology involves a cascade where the initial cardiac injury leads to neurohormonal activation and remodeling, progressively worsening cardiac function and symptoms. Evaluation includes assessing functional capacity, volume status, labs, and prognosis to guide management and monitor for complications.
Effect of Post-MI Exercise Training on Cardiac Remodeling presentationCastural Thompson
This document summarizes the effects of post-myocardial infarction (MI) exercise training on cardiac remodeling and function. It finds that regular exercise of moderate-high intensity, performed 3 times per week for 4-12 weeks, can:
1) Reduce left ventricular hypertrophy and dilation caused by cardiac remodeling after a MI.
2) Increase baroreflex sensitivity which predicts improved prognosis by decreasing cardiovascular mortality up to 26%.
3) Alter gene and protein expression in ways that improve contractility and calcium sensitivity, helping normalize the heart's electrical activity and reducing the risk of fatal arrhythmias.
Dilated cardiomyopathy is characterized by an enlarged and poorly contracting left ventricle. The main causes include inflammatory, toxic, metabolic, inherited, idiopathic and miscellaneous factors. On evaluation, patients typically present with decreased cardiac output, tachycardia and signs of congestion. Tests include echocardiogram, which shows increased left ventricular size and reduced ejection fraction, and ECG, which may show conduction delays. Treatment focuses on managing symptoms with diuretics and blocking neurohormonal activation to prevent worsening, while devices like ICDs are used in eligible patients.
Heart as a pump, heart failure & its treatmentChirantan MD
The document discusses normal cardiac physiology and heart failure. It describes how cardiac function depends on preload, afterload, heart rate, and ionotropic state. It then discusses the pathophysiology of systolic heart failure, including activation of neurohormonal systems and changes at the molecular level in contractile proteins and calcium homeostasis. Compensatory mechanisms in heart failure and the progression to decompensated heart failure are also summarized.
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left ventricle not caused by ischemic or valvular heart disease. The document discusses the epidemiology, etiology, pathology, genetics, clinical features, diagnosis, and management of idiopathic dilated cardiomyopathy. Key points include:
- The annual incidence is 5-8 per 100,000 people with increased risk in males, blacks, and those with hypertension or chronic beta-agonist use.
- Causes include genetic mutations, viral infections, autoimmune diseases, and drugs. Pathology shows dilatation, myocyte hypertrophy and death, and extracellular matrix remodeling.
- Diagnosis involves ECG
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
CHF.ppt it is internal medicine part 2016 AmboMekdiDan
Congestive Heart Failure is a complex clinical syndrome that results from any structural or functional disorder impairing the ventricle's ability to fill or eject blood. It is characterized by symptoms like dyspnea and fatigue. There are many causes including coronary artery disease, hypertension, and cardiomyopathies. The pathophysiology involves a cascade where the initial cardiac injury leads to neurohormonal activation and remodeling, progressively worsening cardiac function and symptoms. Evaluation includes assessing functional capacity, volume status, labs, and prognosis to guide management and monitor for complications.
Effect of Post-MI Exercise Training on Cardiac Remodeling presentationCastural Thompson
This document summarizes the effects of post-myocardial infarction (MI) exercise training on cardiac remodeling and function. It finds that regular exercise of moderate-high intensity, performed 3 times per week for 4-12 weeks, can:
1) Reduce left ventricular hypertrophy and dilation caused by cardiac remodeling after a MI.
2) Increase baroreflex sensitivity which predicts improved prognosis by decreasing cardiovascular mortality up to 26%.
3) Alter gene and protein expression in ways that improve contractility and calcium sensitivity, helping normalize the heart's electrical activity and reducing the risk of fatal arrhythmias.
Dilated cardiomyopathy is characterized by an enlarged and poorly contracting left ventricle. The main causes include inflammatory, toxic, metabolic, inherited, idiopathic and miscellaneous factors. On evaluation, patients typically present with decreased cardiac output, tachycardia and signs of congestion. Tests include echocardiogram, which shows increased left ventricular size and reduced ejection fraction, and ECG, which may show conduction delays. Treatment focuses on managing symptoms with diuretics and blocking neurohormonal activation to prevent worsening, while devices like ICDs are used in eligible patients.
Heart as a pump, heart failure & its treatmentChirantan MD
The document discusses normal cardiac physiology and heart failure. It describes how cardiac function depends on preload, afterload, heart rate, and ionotropic state. It then discusses the pathophysiology of systolic heart failure, including activation of neurohormonal systems and changes at the molecular level in contractile proteins and calcium homeostasis. Compensatory mechanisms in heart failure and the progression to decompensated heart failure are also summarized.
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
MANAGEMENT OF ANTERIOR WALL MI WITH SHOCK IN A NON PCI CENTER Praveen Nagula
Cardiogenic shock is a major cause of death in AMI patients and requires immediate diagnosis and management. The document outlines the definition, causes, predictive indicators, medical and interventional management of cardiogenic shock. It recommends emergency revascularization with PCI or CABG for suitable patients irrespective of time delay from MI onset. For those unsuitable for revascularization, fibrinolytic therapy is recommended if no contraindications. Intra-aortic balloon pump can be useful for hemodynamically unstable patients while alternative devices may be considered for refractory shock.
Lec 4 management of cardiogenic shock for mohsEhealthMoHS
Cardiogenic shock is a life-threatening condition occurring in 4-15% of acute myocardial infarction cases, with a high mortality rate of 50%. It is defined as impaired organ perfusion due to reduced cardiac output and low blood pressure. Treatment involves general supportive measures, inotropic drugs, revascularization procedures, and mechanical circulatory support devices to increase blood pressure and cardiac output. With early reperfusion therapy and intensive care, mortality from cardiogenic shock complicating acute coronary syndrome can be reduced to around 40%.
Sudden cardiac death (SCD/SCA) is an unexpected death due to cardiac causes that occurs in a short time period (generally within 1 hour of symptom onset) in a person with known/unknown cardiac disease.
Patients at risk for SCD may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints.
In the Framingham Study, preexisting CAD was associated with a 2.8- to 5.3-fold increase in risk of SCD
Both left ventricular dysfunction and NYHA class were powerful risk factors for SCD in patients with either ischemic or nonischemic cardiomyopathy
An LVEF of less than 30 % (due to any etiology) is the single most powerful independent indicator for SCD
This document discusses cardiorenal syndrome (CRS), defined as when acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. It describes 5 types of CRS based on whether cardiac or renal dysfunction occurs acutely or chronically. Type 1 involves acute cardiac failure worsening renal function, while Type 2 involves chronic congestive heart failure causing chronic renal dysfunction. Biomarkers like NGAL can aid early diagnosis of CRS Type 1. Management involves diuretics, inotropes, vasodilators, and blocking the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs.
The document discusses cardiogenic shock, outlining its definition, causes, pathophysiology, diagnosis and management, with a focus on shock complicating myocardial infarction. Cardiogenic shock occurs in 5-8% of patients hospitalized with ST-elevation myocardial infarction and has a high mortality rate of 70-80% despite emerging treatments. The document provides details on the hemodynamic parameters defining cardiogenic shock and reviews the various mechanisms that can lead to left or right ventricular failure and shock.
Heart Failure - What to expect from the Investigations?Praveen Nagula
This document discusses investigations for a 65-year-old male patient presenting with worsening shortness of breath. On physical examination, the patient was sweating profusely and in respiratory distress. Investigations that may be useful include laboratory tests to rule out heart failure like BNP or NT-proBNP levels, echocardiography to assess cardiac structure and function, chest X-ray to check for pulmonary congestion, electrocardiography to check for abnormalities, and biomarkers to assess prognosis and guide therapy. The document outlines the role and findings of these various diagnostic tests in evaluating the patient's condition and determining if heart failure is present and the underlying etiology.
This patient is a 25 year old female admitted to the ICU for respiratory failure and hypotension following a 6 day prodromal illness. She is intubated and receiving vasopressors. The differential diagnosis includes sepsis, severe sepsis, or septic shock from an unknown source. Principles of management include identifying the source, administering appropriate antibiotics, optimizing hemodynamics and organ function, and providing lung protective ventilation for her acute respiratory distress syndrome. Early enteral nutrition is important to support her systemic immune response and prevent further organ dysfunction from a cumulative energy deficit.
This document discusses oxygenation and its effects on the cardiovascular and hematologic systems. It covers topics such as ventilation, respiration, circulation, and case studies involving patient assessments. Key areas of focus include the anatomy and physiology of the heart and blood vessels, diagnostic tests, common cardiovascular conditions like heart disease, heart failure, hypertension, and peripheral vascular disease. Nursing interventions are provided for treating related symptoms and managing patient care.
This document provides an overview of hypertrophic cardiomyopathy (HCM). It begins with definitions of cardiomyopathy and HCM. It then discusses the historical perspective, genetic basis, morphology, pathophysiology, clinical features, diagnosis, and management of HCM. Some key points include:
- HCM is a genetic heart condition characterized by unexplained thickening of the heart muscle. It is the most common cause of sudden cardiac death in young people.
- The genetic basis involves mutations in genes encoding sarcomere proteins. This leads to impaired relaxation and increased calcium sensitivity of the heart muscle.
- Morphologically, HCM involves asymmetric left ventricular hypertrophy and abnormalities of the mitral valve apparatus. Hist
Myocardial infarction occurs when there is prolonged ischemia to the heart muscle due to reduced oxygen supply or increased oxygen demand. It is usually caused by formation of a blood clot within a coronary artery blocking blood flow. Diagnosis is made through symptoms, electrocardiogram changes, and cardiac biomarker levels. Treatment involves oxygen, aspirin, nitrates, beta blockers, fibrinolytics or percutaneous coronary intervention to restore blood flow, as well as long term medications like statins to prevent future heart attacks.
A 65-year-old male with a history of mitral valve replacement in 1975 presents with decreased exercise tolerance over the past two months. He has a history of paroxysmal atrial fibrillation for 10 years. Cardiac catheterization was ordered to assess his coronary arteries and measure the gradient across his mitral valve. Tracings from the catheterization show early rapid filling of the ventricles followed by abrupt stopping of ventricular filling in mid diastole, consistent with constrictive pericarditis.
A 65-year-old male with a history of mitral valve replacement in 1975 presents with decreased exercise tolerance over the past two months. He has a history of paroxysmal atrial fibrillation for 10 years. Cardiac catheterization was ordered to assess his coronary arteries and measure the gradient across his mitral valve. Tracings from the catheterization show early rapid filling of the ventricles followed by abrupt stopping of ventricular filling in mid diastole, consistent with constrictive pericarditis.
This document provides an overview of evaluating and managing chest pain. It discusses the many potential causes of chest pain including cardiac, pulmonary, gastrointestinal and psychiatric conditions. Key points include that up to 30% of cardiac catheterizations for suspected coronary artery disease are negative. The diagnostic workup involves considering the patient's history, symptoms, physical exam, ECG, cardiac biomarkers, imaging and ruling out life-threatening causes like aortic dissection and pulmonary embolism. For suspected acute coronary syndrome, treatment involves antiplatelet agents, anticoagulants, nitroglycerin, beta-blockers, oxygen and considering cardiac catheterization if within 90 minutes of symptoms.
1. Mitral stenosis is most commonly caused by rheumatic fever and results in thickening and calcification of the mitral valve, reducing the valve orifice area and obstructing blood flow from the left atrium to ventricle.
2. The pathophysiology involves elevated left atrial pressure, pulmonary hypertension, and reduced cardiac output. Symptoms range from easy fatigability to pulmonary edema.
3. Physical exam findings include an opening snap, rumbling diastolic murmur, and signs of right heart failure in severe cases. Severity is graded based on orifice area, pulmonary artery pressure, and NYHA functional
This document discusses congestive heart failure in infants and children. It begins with background on the main causes of heart failure in children, which are often congenital heart disease and cardiomyopathy rather than issues like coronary artery disease that commonly cause heart failure in adults. The document then covers topics like the pathophysiology and classifications of heart failure in children, as well as diagnostic workup, management, and treatment approaches. Physical exam findings and classifications like Ross and NYHA scores are also outlined to help evaluate heart failure severity in pediatric patients.
This document discusses heart failure in childhood. It defines heart failure as the heart's inability to deliver adequate cardiac output to meet the body's needs. The most common causes in children are congenital defects like VSD, ASD, or acquired conditions like rheumatic heart disease or myocarditis. Symptoms can include feeding difficulties, respiratory distress, or failure to thrive in infants. Diagnosis involves tests like echocardiogram, chest X-ray, and BNP levels to assess cardiac function and rule out other conditions. Treatment focuses on enhancing contractility, reducing preload and afterload, and improving oxygen delivery through medications, diuretics, and surgery or catheterization for congenital defects.
This document provides guidance on intensive care medicine topics that may be covered in the FRCA exam, with a focus on acute liver failure and cardiogenic shock. It discusses 20 specific ICU questions that may appear in the MCQ section and advises candidates to focus on structure in their answers. Example cases are presented on acute liver failure and a postoperative patient with cardiogenic shock, with discussion points provided for each. Key topics in the management of these conditions like encephalopathy, fluid balance and inotropes are reviewed. Candidates are encouraged to answer just the question asked and not provide irrelevant extra details.
Endothelial dysfunction in indian scenarioheartsense
www,heartsense.in. Endothelial dysfunction is the root pathology in the pathogenesis of hypertension, diabetes and IHD. This technical article is aimed towards health care professionals. For patient information on health and heart disease, visit www.heartsense.in.
EVASION OF APOPTOSIS powerpoint presentationJeenaRaj10
Tumor cells evade apoptosis through two major mechanisms: losing the function of the TP53 gene which regulates apoptosis, allowing cells to survive without regulation, or overexpressing anti-apoptotic BCL2 family members like BCL2 itself, protecting tumor cells from apoptosis and enabling survival and drug resistance. Mutations in genes involved in apoptosis pathways are common in cancers and help tumor cells resist programmed cell death.
This document discusses the limitless replicative potential of cancer cells. Normal cells have a limited ability to divide, typically 60-70 times, before reaching senescence. Cancer cells bypass this limitation through several factors. They evade senescence by accumulating genetic changes that deregulate cell cycle controls. They evade mitotic crisis, which is caused by telomere shortening, by expressing telomerase or using alternative lengthening of telomeres mechanisms. Cancer cells also have the property of self-renewal like stem cells, allowing them to perpetually replenish themselves through asymmetrical cell division producing more cancer stem cells.
Heart as a pump, heart failure & its treatmentChirantan MD
This document discusses cardiac physiology and heart failure. It begins by introducing the authors and location. It then discusses normal cardiac physiology parameters such as preload, afterload, heart rate, and ionotropic state. It explores these parameters in depth including how they are altered in heart failure. The document also examines factors that can lead to heart failure like cardiomyopathy or arrhythmias. In summary, it provides a comprehensive overview of cardiac function and the pathophysiology of heart failure.
MANAGEMENT OF ANTERIOR WALL MI WITH SHOCK IN A NON PCI CENTER Praveen Nagula
Cardiogenic shock is a major cause of death in AMI patients and requires immediate diagnosis and management. The document outlines the definition, causes, predictive indicators, medical and interventional management of cardiogenic shock. It recommends emergency revascularization with PCI or CABG for suitable patients irrespective of time delay from MI onset. For those unsuitable for revascularization, fibrinolytic therapy is recommended if no contraindications. Intra-aortic balloon pump can be useful for hemodynamically unstable patients while alternative devices may be considered for refractory shock.
Lec 4 management of cardiogenic shock for mohsEhealthMoHS
Cardiogenic shock is a life-threatening condition occurring in 4-15% of acute myocardial infarction cases, with a high mortality rate of 50%. It is defined as impaired organ perfusion due to reduced cardiac output and low blood pressure. Treatment involves general supportive measures, inotropic drugs, revascularization procedures, and mechanical circulatory support devices to increase blood pressure and cardiac output. With early reperfusion therapy and intensive care, mortality from cardiogenic shock complicating acute coronary syndrome can be reduced to around 40%.
Sudden cardiac death (SCD/SCA) is an unexpected death due to cardiac causes that occurs in a short time period (generally within 1 hour of symptom onset) in a person with known/unknown cardiac disease.
Patients at risk for SCD may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints.
In the Framingham Study, preexisting CAD was associated with a 2.8- to 5.3-fold increase in risk of SCD
Both left ventricular dysfunction and NYHA class were powerful risk factors for SCD in patients with either ischemic or nonischemic cardiomyopathy
An LVEF of less than 30 % (due to any etiology) is the single most powerful independent indicator for SCD
This document discusses cardiorenal syndrome (CRS), defined as when acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. It describes 5 types of CRS based on whether cardiac or renal dysfunction occurs acutely or chronically. Type 1 involves acute cardiac failure worsening renal function, while Type 2 involves chronic congestive heart failure causing chronic renal dysfunction. Biomarkers like NGAL can aid early diagnosis of CRS Type 1. Management involves diuretics, inotropes, vasodilators, and blocking the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs.
The document discusses cardiogenic shock, outlining its definition, causes, pathophysiology, diagnosis and management, with a focus on shock complicating myocardial infarction. Cardiogenic shock occurs in 5-8% of patients hospitalized with ST-elevation myocardial infarction and has a high mortality rate of 70-80% despite emerging treatments. The document provides details on the hemodynamic parameters defining cardiogenic shock and reviews the various mechanisms that can lead to left or right ventricular failure and shock.
Heart Failure - What to expect from the Investigations?Praveen Nagula
This document discusses investigations for a 65-year-old male patient presenting with worsening shortness of breath. On physical examination, the patient was sweating profusely and in respiratory distress. Investigations that may be useful include laboratory tests to rule out heart failure like BNP or NT-proBNP levels, echocardiography to assess cardiac structure and function, chest X-ray to check for pulmonary congestion, electrocardiography to check for abnormalities, and biomarkers to assess prognosis and guide therapy. The document outlines the role and findings of these various diagnostic tests in evaluating the patient's condition and determining if heart failure is present and the underlying etiology.
This patient is a 25 year old female admitted to the ICU for respiratory failure and hypotension following a 6 day prodromal illness. She is intubated and receiving vasopressors. The differential diagnosis includes sepsis, severe sepsis, or septic shock from an unknown source. Principles of management include identifying the source, administering appropriate antibiotics, optimizing hemodynamics and organ function, and providing lung protective ventilation for her acute respiratory distress syndrome. Early enteral nutrition is important to support her systemic immune response and prevent further organ dysfunction from a cumulative energy deficit.
This document discusses oxygenation and its effects on the cardiovascular and hematologic systems. It covers topics such as ventilation, respiration, circulation, and case studies involving patient assessments. Key areas of focus include the anatomy and physiology of the heart and blood vessels, diagnostic tests, common cardiovascular conditions like heart disease, heart failure, hypertension, and peripheral vascular disease. Nursing interventions are provided for treating related symptoms and managing patient care.
This document provides an overview of hypertrophic cardiomyopathy (HCM). It begins with definitions of cardiomyopathy and HCM. It then discusses the historical perspective, genetic basis, morphology, pathophysiology, clinical features, diagnosis, and management of HCM. Some key points include:
- HCM is a genetic heart condition characterized by unexplained thickening of the heart muscle. It is the most common cause of sudden cardiac death in young people.
- The genetic basis involves mutations in genes encoding sarcomere proteins. This leads to impaired relaxation and increased calcium sensitivity of the heart muscle.
- Morphologically, HCM involves asymmetric left ventricular hypertrophy and abnormalities of the mitral valve apparatus. Hist
Myocardial infarction occurs when there is prolonged ischemia to the heart muscle due to reduced oxygen supply or increased oxygen demand. It is usually caused by formation of a blood clot within a coronary artery blocking blood flow. Diagnosis is made through symptoms, electrocardiogram changes, and cardiac biomarker levels. Treatment involves oxygen, aspirin, nitrates, beta blockers, fibrinolytics or percutaneous coronary intervention to restore blood flow, as well as long term medications like statins to prevent future heart attacks.
A 65-year-old male with a history of mitral valve replacement in 1975 presents with decreased exercise tolerance over the past two months. He has a history of paroxysmal atrial fibrillation for 10 years. Cardiac catheterization was ordered to assess his coronary arteries and measure the gradient across his mitral valve. Tracings from the catheterization show early rapid filling of the ventricles followed by abrupt stopping of ventricular filling in mid diastole, consistent with constrictive pericarditis.
A 65-year-old male with a history of mitral valve replacement in 1975 presents with decreased exercise tolerance over the past two months. He has a history of paroxysmal atrial fibrillation for 10 years. Cardiac catheterization was ordered to assess his coronary arteries and measure the gradient across his mitral valve. Tracings from the catheterization show early rapid filling of the ventricles followed by abrupt stopping of ventricular filling in mid diastole, consistent with constrictive pericarditis.
This document provides an overview of evaluating and managing chest pain. It discusses the many potential causes of chest pain including cardiac, pulmonary, gastrointestinal and psychiatric conditions. Key points include that up to 30% of cardiac catheterizations for suspected coronary artery disease are negative. The diagnostic workup involves considering the patient's history, symptoms, physical exam, ECG, cardiac biomarkers, imaging and ruling out life-threatening causes like aortic dissection and pulmonary embolism. For suspected acute coronary syndrome, treatment involves antiplatelet agents, anticoagulants, nitroglycerin, beta-blockers, oxygen and considering cardiac catheterization if within 90 minutes of symptoms.
1. Mitral stenosis is most commonly caused by rheumatic fever and results in thickening and calcification of the mitral valve, reducing the valve orifice area and obstructing blood flow from the left atrium to ventricle.
2. The pathophysiology involves elevated left atrial pressure, pulmonary hypertension, and reduced cardiac output. Symptoms range from easy fatigability to pulmonary edema.
3. Physical exam findings include an opening snap, rumbling diastolic murmur, and signs of right heart failure in severe cases. Severity is graded based on orifice area, pulmonary artery pressure, and NYHA functional
This document discusses congestive heart failure in infants and children. It begins with background on the main causes of heart failure in children, which are often congenital heart disease and cardiomyopathy rather than issues like coronary artery disease that commonly cause heart failure in adults. The document then covers topics like the pathophysiology and classifications of heart failure in children, as well as diagnostic workup, management, and treatment approaches. Physical exam findings and classifications like Ross and NYHA scores are also outlined to help evaluate heart failure severity in pediatric patients.
This document discusses heart failure in childhood. It defines heart failure as the heart's inability to deliver adequate cardiac output to meet the body's needs. The most common causes in children are congenital defects like VSD, ASD, or acquired conditions like rheumatic heart disease or myocarditis. Symptoms can include feeding difficulties, respiratory distress, or failure to thrive in infants. Diagnosis involves tests like echocardiogram, chest X-ray, and BNP levels to assess cardiac function and rule out other conditions. Treatment focuses on enhancing contractility, reducing preload and afterload, and improving oxygen delivery through medications, diuretics, and surgery or catheterization for congenital defects.
This document provides guidance on intensive care medicine topics that may be covered in the FRCA exam, with a focus on acute liver failure and cardiogenic shock. It discusses 20 specific ICU questions that may appear in the MCQ section and advises candidates to focus on structure in their answers. Example cases are presented on acute liver failure and a postoperative patient with cardiogenic shock, with discussion points provided for each. Key topics in the management of these conditions like encephalopathy, fluid balance and inotropes are reviewed. Candidates are encouraged to answer just the question asked and not provide irrelevant extra details.
Endothelial dysfunction in indian scenarioheartsense
www,heartsense.in. Endothelial dysfunction is the root pathology in the pathogenesis of hypertension, diabetes and IHD. This technical article is aimed towards health care professionals. For patient information on health and heart disease, visit www.heartsense.in.
EVASION OF APOPTOSIS powerpoint presentationJeenaRaj10
Tumor cells evade apoptosis through two major mechanisms: losing the function of the TP53 gene which regulates apoptosis, allowing cells to survive without regulation, or overexpressing anti-apoptotic BCL2 family members like BCL2 itself, protecting tumor cells from apoptosis and enabling survival and drug resistance. Mutations in genes involved in apoptosis pathways are common in cancers and help tumor cells resist programmed cell death.
This document discusses the limitless replicative potential of cancer cells. Normal cells have a limited ability to divide, typically 60-70 times, before reaching senescence. Cancer cells bypass this limitation through several factors. They evade senescence by accumulating genetic changes that deregulate cell cycle controls. They evade mitotic crisis, which is caused by telomere shortening, by expressing telomerase or using alternative lengthening of telomeres mechanisms. Cancer cells also have the property of self-renewal like stem cells, allowing them to perpetually replenish themselves through asymmetrical cell division producing more cancer stem cells.
This document discusses angiogenesis, invasion, and metastasis of tumors. It describes how angiogenesis allows tumors to grow beyond 1-2mm by developing new blood vessels. The metastatic cascade is explained as a two-step process involving invasion of the extracellular matrix and vascular dissemination. Key factors and genetic alterations that influence angiogenesis and the various steps of invasion and metastasis are also outlined.
RED INFARCTS powerpoint presentation basicsJeenaRaj10
1) Red infarcts occur in tissues with dual blood supply, loose connective tissue, or venous outflow issues. They appear as sharply demarcated red or purple areas of necrosis.
2) Microscopically, red infarcts show ischemic coagulative necrosis within 4-12 hours. Acute inflammation infiltrates the area in the following days. Necrotic cells and blood are phagocytosed by macrophages.
3) Red infarcts can occur when blood flow is restored to a previously ischemic area, such as after an arterial blockage is treated. Affected organs include the lung, liver, intestine, and heart.
Factors influencing the development of an infarct.pptxJeenaRaj10
The document discusses factors that influence the development of an infarct. It explains that an infarct is caused by occlusion of the arterial supply or venous drainage of an area, ranging from tissue dysfunction to necrosis. Tissues with more connections like lungs and liver are less vulnerable due to dual blood supply. The rate of occlusion also influences outcomes, as slower occlusions allow for collateral vessel formation. Different tissues are more susceptible to hypoxic injury, with neurons vulnerable within minutes and fibroblasts only after hours of ischemia. Blood oxygen content additionally impacts infarct development.
Presentation1 powerpoint necrosis form of cell deathJeenaRaj10
Necrosis is the death of cells and living tissue. It can be caused by ischemia, physical or chemical agents, or immunological injury. There are several types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Coagulative necrosis involves denaturation of proteins and enzymatic digestion of cells while preserving tissue architecture. Liquefactive necrosis causes tissue to become a liquid mass. Caseous necrosis is seen in tuberculosis and leaves tissue with a cheesy white appearance.
ORBITAL INFLAMMATION powerpoint presentationJeenaRaj10
The document discusses different types of orbital inflammation including preseptal cellulitis, orbital cellulitis, and cavernous sinus thrombosis. Preseptal cellulitis involves structures anterior to the orbital septum and causes swelling and redness of the eyelids but does not affect vision or eye movements. Orbital cellulitis is a purulent inflammation behind the orbital septum that can cause proptosis, restricted eye movements, and vision loss. Cavernous sinus thrombosis is a serious complication where infection and blood clots spread from the face or orbit to the cavernous sinus, which can lead to issues like paralysis of cranial nerves. Broad spectrum antibiotics, monitoring for complications, and surgical drainage may be
Pathology of Pneumonia POWERPOINT PRESENTATIONJeenaRaj10
This document provides information on pneumonia, including:
1. It describes the lung defense mechanisms against infection such as mucociliary clearance, phagocytosis by alveolar macrophages and neutrophils, and serum complement.
2. It classifies pneumonia based on etiology (infective, viral, bacterial, fungal, tuberculosis), morphology (lobar, bronchial, interstitial), duration (acute, chronic), and location (community-acquired, hospital-acquired). Common causative organisms are discussed for each type.
3. The pathogenesis of pneumonia is outlined as entry of microbes, followed by inflammation in the alveoli and surrounding tissues. Complications like abscesses and empy
NECROSIS AND APOPTOSIS POWERPOINT PRESENTATIONJeenaRaj10
This document discusses different types of cell death: necrosis, apoptosis, and necroptosis. Necrosis is unprogrammed cell death due to external factors like toxins or hypoxia. Apoptosis is programmed cell death that helps eliminate unwanted cells through activation of genes and enzymes. Necroptosis shares characteristics of both necrosis and apoptosis - it is caspase-independent cell death triggered by signaling pathways involving the kinases RIPK1 and RIPK3, which phosphorylate MLKL leading to plasma membrane disruption and cell rupture in a programmed manner. Necroptosis plays roles in processes like bone growth, diseases like pancreatitis, and host defense against viruses.
This document discusses various anticoagulants used in hematology. It defines anticoagulants as agents that prevent blood clot formation and lists their uses in preventing disorders caused by abnormal clots. The document describes characteristics anticoagulants must have for hematological examination and lists commonly used anticoagulants like EDTA, oxalates, sodium heparin, sodium citrate, and sodium fluoride/potassium oxalate mixture. Each anticoagulant is classified and their modes of action, concentrations, advantages and disadvantages are detailed.
Necrosis is irreversible injury and death of cells and living tissue. There are several patterns of necrosis that can occur in tissues including coagulative, liquefactive, and caseous necrosis. Coagulative necrosis involves the maintenance of cell outlines but loss of cellular details. The dead tissues remain in the body for a long period. Liquefactive necrosis results from the rapid dissolution of dead cells, often leading to abscess formation. Caseous necrosis converts dead tissue into a granular mass resembling cottage cheese, associated with tuberculosis lesions.
Necrosis is cell death in living tissue that can have various causes and appearances. There are several types of necrosis including coagulative, liquefactive, caseous, fat, and fibrinoid necrosis. Coagulative necrosis involves protein denaturation and enzymatic cell digestion that preserves tissue architecture. Liquefactive necrosis causes tissues to become a liquid mass. Caseous necrosis in tuberculosis infections leads to cheesy white tissue. Fat necrosis in the pancreas and breast appears chalky white.
This document provides an overview of gestational trophoblastic diseases (GTD), including their classification, histopathology, diagnosis, and management. Key points include:
1. GTD are classified by the WHO and include complete and partial hydatidiform moles, as well as benign and malignant trophoblastic lesions. Hydatidiform moles can develop into gestational trophoblastic neoplasia in a minority of cases.
2. Complete hydatidiform moles show diffuse hydropic changes of chorionic villi with abnormal trophoblastic hyperplasia, while partial moles have a mixture of normal and hydropic villi.
3. Malignant trophob
The immune system protects the body from infectious disease. Infectious disease is caused by pathogens like bacteria, viruses, fungi and parasites that invade the body. The immune system uses nonspecific defenses like skin, fever and inflammation that provide a fast response. It also uses specific defenses like white blood cells and antibodies that recognize and attack specific pathogens. B cells produce antibodies that mark pathogens for destruction by macrophages and killer T cells. Memory B cells provide faster immunity upon second exposure to the same pathogen through antibodies.
Tuberculosis is an infection caused by Mycobacterium tuberculosis that mainly affects the lungs. It can spread through droplets in the air from coughing or sneezing. Symptoms include persistent cough, chest pain, coughing up blood, fatigue, and fever. TB is classified as pulmonary or extra-pulmonary depending on the affected area. Diagnosis involves sputum tests, chest x-rays, and the tuberculin skin test. Treatment requires a multi-drug regimen over several months. Preventive measures include BCG vaccination, isolation, and proper ventilation. Drug-resistant forms like MDR-TB and XDR-TB are major challenges. Co-infection with HIV increases the risks of TB infection and
1) Dilated cardiomyopathy is characterized by dilation and impaired contraction of the ventricles, often leading to heart failure. The majority of cases are idiopathic, but it can result from various infectious, toxic, metabolic, inherited and other etiologies.
2) Peripartum cardiomyopathy presents in the last month of pregnancy or within 5 months postpartum, and has an unknown etiology but may involve inflammatory cytokines. It carries a risk of death and recurrence with future pregnancies.
3) Treatment of dilated cardiomyopathy focuses on reducing preload and afterload through medications like diuretics, ACE inhibitors, and beta-blockers to help compensate for impaired contractility and prevent ventricular
This document discusses the process of healing through regeneration and repair. It describes the key stages and phases of wound healing, including inflammation, granulation tissue formation, epithelialization, and scar formation. Factors that can affect healing, both locally such as infection or poor blood supply, and generally such as age, obesity, or malnutrition are also outlined. Complications from improper or delayed healing include infection, cysts, scarring issues, and hernias.
The PATH program aims to help homeless individuals and families in Los Angeles County access stable housing and supportive services to achieve long-term stability. It provides short-term rental assistance and case management to quickly rehouse homeless people and connect them to resources to address challenges like lack of income, untreated mental illness or substance abuse issues. The goal is to transition participants into permanent housing within a few months through this intensive temporary support and help acquiring job skills or public benefits.
Malabsorption results from defects in intraluminal digestion, terminal digestion, transepithelial transport, and lymphatic transport. It is characterized by weight loss, abdominal distention, diarrhea, and steatorrhea. Causes of malabsorption include cystic fibrosis, celiac disease, lactase deficiency, and environmental enteropathy. Microscopic findings depend on the specific condition but may include villous blunting, increased intraepithelial lymphocytes, and lipid vacuoles.
Healing is the body's response to injury and involves regeneration and repair. Regeneration involves proliferation of original cells to reconstitute tissue, while repair forms scar tissue. The healing process involves inflammation, granulation tissue formation, epithelialization, and scar maturation. Local factors like infection and poor blood supply as well as general factors like smoking and malnutrition can affect wound healing. Complications include infection, scarring, and hernia formation.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
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
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Hiranandani Hospital in Powai, Mumbai, is a premier healthcare institution that has been serving the community with exceptional medical care since its establishment. As a part of the renowned Hiranandani Group, the hospital is committed to delivering world-class healthcare services across a wide range of specialties, including kidney transplantation. With its state-of-the-art facilities, advanced medical technology, and a team of highly skilled healthcare professionals, Hiranandani Hospital has earned a reputation as a trusted name in the healthcare industry. The hospital's patient-centric approach, coupled with its focus on innovation and excellence, ensures that patients receive the highest standard of care in a compassionate and supportive environment.
- 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
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
2. Cardiomyopathies
Definition: diseases of heart muscle
1980 WHO: unknown causes
– Not clinically relevant
1995 WHO: “diseases of the
myocardium associated with cardiac
dysfunction “
– pathophysiology
– each with multiple etiologies
5. Dilated Cardiomyopathy
•Dilation and impaired contraction of ventricles:
•Reduced systolic function with or without heart failure
•Characterized by myocyte damage
•Multiple etiologies with similar resultant pathophysiology
•Majority of cases are idiopathic
•incidence of idiopathic dilated CM 5-8/100,000
•incidence likely higher due to mild, asymptomatic cases
•3X more prevalent among males and African-Americans
7. Prognosis depends on Etiology
1230 pts. referred for unexplained CM. Felker GM. NEJM 2000;342:1077
8. DCM: Infectious
Acute viral myocarditis
Coxasackie B or echovirus
Self-limited infection in young people
Mechanism?:
– Myocyte cell death and fibrosis
– Immune mediated injury
– BUT:
No change with immunosuppressive drugs
9. DCM: toxic
Alcoholic cardiomyopathy
Chronic use
Reversible with abstinence
Mechanism?:
– Myocyte cell death and fibrosis
– Directly inhibits:
mitochondrial oxidative phosphorylation
Fatty acid oxidation
10. DCM: inherited
Familial cardiomyopathy
30% of ‘idiopathic’
Inheritance patterns
– Autosommal dom/rec, x-linked, mitochondrial
Associated phenotypes:
– Skeletal muscle abn, neurologic, auditory
Mechanism:
– Abnormalities in:
Energy production
Contractile force generation
– Specific genes coding for:
Myosin, actin, dystophin…
29. Influence of EF on Survival in
Patients with Heart Failure
Vasan RS et al. J Am Coll Cardiol. 1999;33:1948-55
30. Class 1: No limitation of physical activity.
Ordinary physical activity w/o fatigue, palpitation, or dyspnea.
Class 2: Slight limitation of physical activity. Comfortable at rest, but
symptoms w/ ordinary physical activity
Class 3: Marked limitation of physical activity. Comfortable at rest, but less
than ordinary activity causes fatigue, palpitation, or dyspnea.
Class 4: Unable to carry out any physical activity without discomfort.
Symptoms include cardiac insufficiency at rest. If any physical
activity is undertaken, discomfort is increased.
J Cardiac Failure 1999;5:357-382
Criteria for NYHA Functional Classification
32. Vasodilator Agents in Heart Failure
Drug Mechanism Action Use
Nitroglycerin
and long-
acting nitrates*
Direct via nitric
oxide
Veno /
arterioloar
Hemodynamic;
anti-ischemic;
long term
Nitroprusside Direct via nitric
oxide
Arteriolar >
venodilation
Hemodynamic
Hydralazine* Direct Arteriolar ?long term*
ACE
inhibitors#
Reduced A-II
Incr. bradykinin
Veno /
arterioloar
Long-term
*Hydralazine and a long-nitrate shown to reduce mortality long-term
# Other actions (aside from vasodilation) likely to be important
34. Electrical and Mechanical
Ventricular Dyssynchrony
Experimentally induced LBBB has effect on:
– expression of regional stress kinases
– calcium-handling proteins.
Expression of p38-MAPK (a stress kinase) is
elevated in the endocardium of the late-
activated region, whereas phospholamban is
decreased.
Sarcoplasmatic reticulum Ca2+-ATPase is
decreased in the region of early activation.
46. What is the difference
between systolic and
diastolic LV dysfunction?
47. Hypertrophic Cardiomyopathy
Left ventricular hypertrophy not due to pressure overload
Hypertrpohy is variable in both severity and location:
-asymmetric septal hypertrophy
-symmetric (non-obstructive)
-apical hypertrophy
Vigorous systolic function, but impaired diastolic function
impaired relaxation of ventricles
elevated diastolic pressures
prevalence as high as 1/500 in general population
mortality in selected populations 4-6% (institutional)
probably more favorable (1%)
48. Etiology
Familial in ~ 55% of cases with autosomal dominant transmission
Mutations in one of 4 genes encoding proteins of cardiac sarcomere
account for majority of familial cases
-MHC
cardiac troponin T
myosin binding protein C
-tropomyosin
Remainder are
spontaneous
mutations.
54. HCM with outflow obstruction
Dynamic LVOT obstruction (may not be present at rest)
SAM (systolic anterior motion of mitral valve)
LVOT Obstruction LVOT gradient
wall stress MVO2 ischemia/angina
LVOT gradient: HR (DFP), preload (LVEDV),
afterload(BP).
LVOT gradient: BP (Afterload), LVEDV(preload)
Symptoms of dyspnea and angina more related to diastolic
dysfunction than to outflow tract obstruction
Syncope: LVOT obstruction (failure to increase CO during exercise
or after vasodilatory stress) or arrhythmia.
55. Physical Exam
Bisferiens pulse (“spike and dome”)
S4 gallop
Crescendo/Descrescendo systolic ejection murmur
HOCM vs. Valvular AS Intensity of murmur
HOCM AS
Valsalva (preload, afterload)
Squatting ( preload, afterload)
Standing (preload, afterload)
Holosystolic apical blowing murmur of mitral regurgitation
58. Atrial Fibrillation
Acute A. Fib is poorly tolerated -Acute Pulmonary Edema and Shock
Chronic a fib - Fatigue, dyspnea and angina
Rapid HR - decreased time for diastolic filling and LV relaxation
Loss of atrial “Kick” – decreased LV filling
- decreased SV and increased outflow tract obstruction
Rate slowing with -blockers and Ca2+ channel blockers
Digitalis is relatively contra-indicated- positive inotrope
DC Cardioversion
No p wave P wave present
59. Treatment
For symptomatic benefit
-blockers
mvO2
gradient (exercise)
arrythmias
Calcium Channel blockers
Anti-arrhythmics
afib
amiodorone
Disopyramide
AICD for sudden death
antibiotic prophylaxis for endocarditis
No therapy has been shown to improve mortality
60. HCM: Surgical Treatment
For severe symptoms with large outflow gradient (>50mmHg)
Does not prevent Sudden Cardiac Death
Myomyectomy
removal of small portion of upper IV septum
+/- mitral valve replacement
5 year symptomatic benefit in ~ 70% of patients
Dual Camber (DDD pacemaker) pacing
decreases LVOT gradient (by~25%)
randomized trials have shown little longterm benefit
possible favorable morphologic changes
ETOH septal ablation
AICD to prevent sudden death
61. Hypertrophic CM
Most common cause of death in young people.
The magnitude of left ventricular hypertrophy is
directly correlated to the risk of SCD.
Young pts with extreme hypertrophy and few or no
symptoms are at substantial long-term risk of SCD.
.
Spirito P. N Engl J Med. 1997;336:775-785.
Maron BJ. N Engl J Med. 2000;342:365-373.
62. Wall Thickness and
Sudden Death in HCM
Spirito P. N Engl J Med. 2000;342:1778-
1785.
0
2
4
6
8
10
12
14
16
18
20
< 15 16-19 20-24 25-29 > 30
Maximum Left-Ventricular-Wall Thickness (mm)
Incidence
of
Sudden
Death
(per
1,000
person/yr)
0
2.6
7.4
11.0
18.2
63. Prognosis
Sudden Death 2-4%/year in adults
4-6% in children/adolescents
AICD for: survivors of SCD with Vfib
episodes of Sustained VT
pts with family hx of SCD in young family members
High risk mutation (TnT, Arg403Gln)
Predictors of adverse prognosis:
early age of diagnosis
familial form with SCD in 1st degree relative
history of syncope
ischemia
presence of ventricular arrhythmias on Holter (EPS)
EPS
Amiodorone (low dose)
Prophylactic AICD?
64. HCM vs Athletes Heart
Endurance training:
– Physiologic increase in LV mass
Wall thickness and cavity size
Early HCM vs Athlete’s heart
– DEFINITION: Symmetric, <13mm
– 947 elite athletes: 16 thickness=13-16mm
15 rowers, EDD=55-63 c/w 728 athletes/22 other
NEJM1991;324:295
– 286 cyclists: 25 thickness 13-15
50% increased EDD w/ 12% reduced LVEF
JACC 2004;44:144.
66. Restrictive Cardiomyopathy
Characterized by:
• impaired ventricular filling due to an abnormally stiff (rigid) ventricle
•normal systolic function (early on in disease)
•intraventricular pressure rises precipitously with small increases in volume
Pressure
Volume
Causes : infiltration of myocardium by abnormal substance
fibrosis or scarring of endocardium
normal
restriction
68. Amyloidosis
Primary Amyloidosis
immunoglobulin light chains -- multiple myeloma
Secondary Amyloidosis
deposition of protein other than immunoglobulin
senile
familial
chronic inflammatory process
restriction caused by replacement of normal myocardial contractile
elements by infiltrative interstitial deposits
72. Endomyocardial Fibrosis
Endemic in parts of Africa, India, South and Central America, Asia
15-25% of cardiac deaths in equatorial Africa
hypereosinophilic syndrome (Loffler’s endocarditis)
Thickening of basal inferior wall
endocardial deposition of thrombus
apical obliteration
mitral regurgitation
80-90% die within 1-2 years
73. Pathophysiology of Restriction
Elevated systemic and pulmonary venous pressures
right and left sided congestion
reduced ventricular cavity size with SV and CO
74. Clinical Findings
Right > Left heart failure
Dyspnea
Orthopnea/PND
Peripheral edema
Ascites/Hepatomegaly
Fatigue/ exercise tolerance
Clinically mimics constrictive Pericarditis
75. Diagnostic Studies
2D-Echo/Doppler-
mitral in-flow velocity
rapid early diastolic filling
Catheterization –
diastolic pressure equilibration
restrictive vs constrictive
hemodynamics
Endomyocardial biopsy-
definite Dx of restrictive pathology
76. Cardiac Catheterization
Prominent y descent “dip and plateau”
rapid atrial emptying rapid ventricular filling
then abrupt cessation of blood flow due to non-compliant myocardium
78. Treatment
Treat underlying cause
r/o constriction which is treatable (restriction poor prognosis)
amyloid (melphalan/prednisone/colchicine)
Endomyocardial Fibrosis (steroids, cytotoxic drugs, MVR)
Hemochromatosis (chelation, phlebotomy)
Sarcoidosis (steroids)
Diuretics
For congestive symptoms, but LV/RV filling CO
Digoxin (avoid in amyloidosis)
Antiarrhythmics for afib
amiodorone
Pacemaker for conduction system disease
Anticoagulation for thrombus (esp in atrial appendages)