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.
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.
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.
Fourth universal definition of myocardial infarction (2018)hospital
This document outlines the 2018 universal definition of myocardial infarction and describes its various types. It defines Type 1 MI as detected cardiac troponin rise with symptoms of ischemia. Type 3 MI occurs in patients who experience cardiac death before biomarkers can be obtained. Type 4a MI is elevation of troponin levels more than 5 times the cutoff 48 hours after percutaneous coronary intervention. Type 5 MI involves troponin elevation more than 10 times the cutoff 48 hours after coronary artery bypass grafting. It also describes myocardial infarction with non-obstructive coronary arteries.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
Aortic Dissection with Hemopericardium and Thrombosed Left Common Iliac Arter...Vinod Namana
#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.
Occurrence of a mural thrombus in a diseased descending thoracic aorta (atherosclerotic or aneurysmal) is a well-known and commonly encountered vascular entity. However, thrombus formation in a normal appearing descending thoracic aorta (NADTA) is rarely reported in literature so far. We present an
unusual case report with a brief literature review of an aortic mural thrombus (AMT) in descending thoracic aorta in a young male. He presented at our center in the emergency department with acute onset abdominal pain and underwent a contrast enhanced CT scan that confirmed mural thrombus in
NADTA.
The main hemodynamic interactions that may impact on the diagnosis of multiple and mixed Multiple and Mixed Valvular Heart Diseases:HOW TO USE IMAGINGThe interplay of multiple valve pathology.The clinical challenge of concomitant aortic and mitral valve stenosis
.
.
Contemporary Perspectives on the Diagnosis and Management of Hypertrophic Car...asclepiuspdfs
Hypertrophic cardiomyopathy (HCM) is a cardiovascular disorder with genetic predisposition. The number of treatment modalities has grown in the contemporary era, with use of pharmacotherapy, device therapy, and surgical intervention, though with the relative paucity of data derived from randomized trials. Its clinical course and prognosis are relatively good. The ongoing quest is to establish the optimal treatment strategy in patients with HCM. This is of direct relevance in reducing the mortality burden associated with sudden cardiac death primarily secondary to dysrhythmias. This review summarizes the clinical features, course, and management of HCM. In particular, we highlight advances in cardiac magnetic resonance imaging assessment of HCM and how risk stratification criteria for suitability of implantable cardioverter defibrillators differ between continents.
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.
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.
Fourth universal definition of myocardial infarction (2018)hospital
This document outlines the 2018 universal definition of myocardial infarction and describes its various types. It defines Type 1 MI as detected cardiac troponin rise with symptoms of ischemia. Type 3 MI occurs in patients who experience cardiac death before biomarkers can be obtained. Type 4a MI is elevation of troponin levels more than 5 times the cutoff 48 hours after percutaneous coronary intervention. Type 5 MI involves troponin elevation more than 10 times the cutoff 48 hours after coronary artery bypass grafting. It also describes myocardial infarction with non-obstructive coronary arteries.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
Aortic Dissection with Hemopericardium and Thrombosed Left Common Iliac Arter...Vinod Namana
#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.
Occurrence of a mural thrombus in a diseased descending thoracic aorta (atherosclerotic or aneurysmal) is a well-known and commonly encountered vascular entity. However, thrombus formation in a normal appearing descending thoracic aorta (NADTA) is rarely reported in literature so far. We present an
unusual case report with a brief literature review of an aortic mural thrombus (AMT) in descending thoracic aorta in a young male. He presented at our center in the emergency department with acute onset abdominal pain and underwent a contrast enhanced CT scan that confirmed mural thrombus in
NADTA.
The main hemodynamic interactions that may impact on the diagnosis of multiple and mixed Multiple and Mixed Valvular Heart Diseases:HOW TO USE IMAGINGThe interplay of multiple valve pathology.The clinical challenge of concomitant aortic and mitral valve stenosis
.
.
Contemporary Perspectives on the Diagnosis and Management of Hypertrophic Car...asclepiuspdfs
Hypertrophic cardiomyopathy (HCM) is a cardiovascular disorder with genetic predisposition. The number of treatment modalities has grown in the contemporary era, with use of pharmacotherapy, device therapy, and surgical intervention, though with the relative paucity of data derived from randomized trials. Its clinical course and prognosis are relatively good. The ongoing quest is to establish the optimal treatment strategy in patients with HCM. This is of direct relevance in reducing the mortality burden associated with sudden cardiac death primarily secondary to dysrhythmias. This review summarizes the clinical features, course, and management of HCM. In particular, we highlight advances in cardiac magnetic resonance imaging assessment of HCM and how risk stratification criteria for suitability of implantable cardioverter defibrillators differ between continents.
Universal Definition of Myocardial Infarct Han Naung Tun
1) The document summarizes the 4th Universal Definition of Myocardial Infarction from 2018, outlining 5 types of MI (myocardial infarction).
2) It describes the criteria for each type of MI, including Type 1 due to plaque rupture, Type 2 due to oxygen supply/demand imbalance, and Type 3 where the patient dies before biomarkers can be obtained.
3) It also discusses MI associated with procedures like PCI (Type 4) and CABG (Type 5), and conditions like MINOCA where the coronary arteries are non-obstructive.
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.
Acute aortic syndrome (AAS) refers to emergency aortic conditions including aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. The common feature is disruption of the aortic media layer allowing blood to enter and separate layers. Aortic dissection occurs when a tear in the intima allows blood to flow between layers. Medical management focuses on controlling blood pressure to limit propagation. Type A dissections involving the ascending aorta require emergency surgery while type B dissections of the descending aorta typically receive medical management. Long term follow up is needed to monitor for complications like aneurysm formation.
This document provides information on peripheral artery disease (PAD), including:
- PAD is caused by blockages in the arteries supplying the lower extremities, most often due to atherosclerosis. It affects 8-10 million Americans and over 200 million worldwide.
- Risk factors include age over 65, smoking, diabetes, and other cardiovascular conditions. Symptoms range from asymptomatic to critical limb ischemia.
- Diagnosis involves ankle-brachial index testing, imaging like ultrasound and CT angiography, and treadmill exercise testing.
- Treatment focuses on risk factor modification through medications, exercise, smoking cessation, and revascularization for severe cases.
An intramural hematoma (IMH) is a thickening of the aortic wall due to bleeding within the media in the absence of an intimal tear. It is considered a precursor to aortic dissection and is classified as a class 2 aortic dissection. A penetrating atherosclerotic ulcer (PAU) is caused by the erosion of an atherosclerotic plaque through the internal elastic lamina into the media. It is classified as a class 4 aortic dissection. Both IMH and PAU can lead to complications like intramural hematoma expansion, pseudoaneurysm formation, aortic dissection, and rupture. Imaging modalities like CT, MRI, TEE, and IVUS
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
This document discusses mitral valve disease and treatment options such as surgical repair/replacement and the MitraClip procedure. Some key points:
- Mitral regurgitation (MR) is the most common valve problem and increases in prevalence with age. Left untreated, MR can lead to heart failure and death.
- Surgical treatment has traditionally been the only option to reliably reduce MR, but many patients are considered too high-risk for surgery.
- The MitraClip procedure is a minimally invasive treatment that fills this gap for inoperable patients by using a clip to repair the mitral valve and reduce MR without open heart surgery.
- Clinical trials show the MitraClip procedure reduces MR
The article discusses new cardiac parametric mapping techniques for T1 and T2 mapping that provide pixel-based maps of myocardial relaxation times. These techniques can detect diffuse myocardial pathologies missed by conventional imaging by quantifying subtle tissue changes. T1 mapping in particular shows potential for diagnosing diseases involving diffuse fibrosis. Standardization of mapping methods is still needed to ensure consistent quantitative results. The efficient, single breath-hold nature of new mapping sequences improves clinical applicability for detecting early disease changes.
Penetrating atherosclerotic ulcer (PAU) is an ulcerating atherosclerotic lesion that penetrates the aortic wall. CT is often used to evaluate PAU, showing features like a focal outpouching with adjacent hematoma. While some cases progress slowly, PAU carries a risk of complications like rupture. Treatment depends on factors like symptoms, expansion rate, and surgical risk. Careful monitoring is important due to variable prognosis.
HCM – Presentation, Hemodynamics and InterventionAnkur Gupta
This document describes a case of a 50-year-old female presenting with symptoms of breathlessness, angina, and presyncope. Echocardiography revealed asymmetric septal hypertrophy and systolic anterior motion of the mitral valve, consistent with hypertrophic obstructive cardiomyopathy (HOCM). The document then provides detailed background information on HOCM, including definitions, pathophysiology, clinical presentation, diagnostic testing, and treatment options such as beta-blockers, septal ablation, and disqualification from competitive sports in severe cases.
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 .
Radiological evaluation of takayasu arteritis Dr. muhammad Bin Zulfiqar Servi...Dr. Muhammad Bin Zulfiqar
Radiological evaluation of takayasu arteritis Dr. muhammad Bin Zulfiqar Services Institute of Medical Sciences Services Hospital Lahore
In this presentation we will discuss the role of imaging in TA.
The document defines no-reflow as inadequate myocardial perfusion through a coronary circulation segment without mechanical vessel obstruction. No-reflow occurs in 30% of patients after reperfusion for myocardial infarction and is associated with worse outcomes. It results from microvascular obstruction from distal embolization, ischemic injury, and reperfusion injury. Diagnosis involves assessing TIMI flow, myocardial blush grade, and imaging techniques. Prevention focuses on reducing embolization using thrombectomy or filters while treatment involves vasodilators like adenosine, verapamil, and glycoprotein IIb/IIIa inhibitors.
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.
An aortic dissection is a tear within the layers of the aortic wall. It can cause severe chest or back pain and risks damage to organs if blood flow is blocked. Prompt diagnosis through imaging tests and treatment are critical to survival. While type A dissections involving the ascending aorta require emergency surgery, type B dissections of the descending aorta can often be treated through intensive blood pressure control and medication to prevent expansion of the tear. Risk factors include hypertension, genetics, trauma, and certain medical conditions.
No reflow and slow flow phenomenon during pcirahul arora
This document discusses strategies and prevention of slow flow and no-reflow phenomenon during percutaneous coronary intervention (PCI). It defines no-reflow as inadequate myocardial perfusion through a coronary artery without mechanical obstruction. No-reflow occurs in 8-11% of primary PCIs and is associated with worse clinical outcomes. The pathophysiology involves distal embolization, ischemic injury, reperfusion injury, and individual patient susceptibility. Preventing no-reflow requires reducing thrombus burden, ischemia time, reperfusion injury through anti-inflammatory drugs, and addressing risk factors like diabetes.
Coronary aneurysms are seen in 0.3-5% of patients undergoing coronary angiography. The most common cause is atherosclerosis. Aneurysms form due to disruption of the vessel wall from weakened media allowing dilation from intraluminal pressure. While often asymptomatic, aneurysms can cause angina, embolization, or rupture. Surgical correction via ligation, bypass, or patch repair is preferred but covered stents may be used for larger aneurysms over 10mm to reduce risk of restenosis.
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
Hypertrophic cardiomyopathy (HCM) is a genetic cardiovascular disease characterized by increased and thickened heart muscle. It is the most common cause of sudden cardiac death in young people. HCM can cause symptoms such as chest pain, heart failure, and palpitations. Treatment involves managing left ventricular outflow tract obstruction through medications, septal reduction procedures, or alcohol septal ablation. Patients at high risk for sudden cardiac death may receive an implantable cardioverter defibrillator for prevention. Risk factors include a family history of sudden death, abnormal blood pressure response to exercise, and extensive thickening of the heart muscle.
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by thickened heart muscle. It has an autosomal dominant pattern of inheritance, with mutations in genes encoding sarcomeric proteins. HCM causes a non-dilated, hypertrophied left ventricle and can lead to heart failure, arrhythmias, and sudden cardiac death. Treatment involves medications like beta-blockers or verapamil to reduce symptoms, and interventions like septal reduction procedures or implantable cardioverter-defibrillators to reduce risk of complications. Regular screening of family members is important for early detection of HCM.
This document summarizes hypertrophic cardiomyopathy (HCM), an autosomal dominant genetic heart condition characterized by unexplained left ventricular hypertrophy. Key points include that it has a prevalence of 1 in 500 adults and is caused by over 200 mutations in genes involved in heart muscle proteins. Symptoms range from none to heart failure, arrhythmias, and sudden cardiac death. Diagnosis is typically made by echocardiogram showing left ventricular hypertrophy. Treatment involves managing symptoms and reducing risk of complications like sudden cardiac death.
Universal Definition of Myocardial Infarct Han Naung Tun
1) The document summarizes the 4th Universal Definition of Myocardial Infarction from 2018, outlining 5 types of MI (myocardial infarction).
2) It describes the criteria for each type of MI, including Type 1 due to plaque rupture, Type 2 due to oxygen supply/demand imbalance, and Type 3 where the patient dies before biomarkers can be obtained.
3) It also discusses MI associated with procedures like PCI (Type 4) and CABG (Type 5), and conditions like MINOCA where the coronary arteries are non-obstructive.
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.
Acute aortic syndrome (AAS) refers to emergency aortic conditions including aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. The common feature is disruption of the aortic media layer allowing blood to enter and separate layers. Aortic dissection occurs when a tear in the intima allows blood to flow between layers. Medical management focuses on controlling blood pressure to limit propagation. Type A dissections involving the ascending aorta require emergency surgery while type B dissections of the descending aorta typically receive medical management. Long term follow up is needed to monitor for complications like aneurysm formation.
This document provides information on peripheral artery disease (PAD), including:
- PAD is caused by blockages in the arteries supplying the lower extremities, most often due to atherosclerosis. It affects 8-10 million Americans and over 200 million worldwide.
- Risk factors include age over 65, smoking, diabetes, and other cardiovascular conditions. Symptoms range from asymptomatic to critical limb ischemia.
- Diagnosis involves ankle-brachial index testing, imaging like ultrasound and CT angiography, and treadmill exercise testing.
- Treatment focuses on risk factor modification through medications, exercise, smoking cessation, and revascularization for severe cases.
An intramural hematoma (IMH) is a thickening of the aortic wall due to bleeding within the media in the absence of an intimal tear. It is considered a precursor to aortic dissection and is classified as a class 2 aortic dissection. A penetrating atherosclerotic ulcer (PAU) is caused by the erosion of an atherosclerotic plaque through the internal elastic lamina into the media. It is classified as a class 4 aortic dissection. Both IMH and PAU can lead to complications like intramural hematoma expansion, pseudoaneurysm formation, aortic dissection, and rupture. Imaging modalities like CT, MRI, TEE, and IVUS
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
This document discusses mitral valve disease and treatment options such as surgical repair/replacement and the MitraClip procedure. Some key points:
- Mitral regurgitation (MR) is the most common valve problem and increases in prevalence with age. Left untreated, MR can lead to heart failure and death.
- Surgical treatment has traditionally been the only option to reliably reduce MR, but many patients are considered too high-risk for surgery.
- The MitraClip procedure is a minimally invasive treatment that fills this gap for inoperable patients by using a clip to repair the mitral valve and reduce MR without open heart surgery.
- Clinical trials show the MitraClip procedure reduces MR
The article discusses new cardiac parametric mapping techniques for T1 and T2 mapping that provide pixel-based maps of myocardial relaxation times. These techniques can detect diffuse myocardial pathologies missed by conventional imaging by quantifying subtle tissue changes. T1 mapping in particular shows potential for diagnosing diseases involving diffuse fibrosis. Standardization of mapping methods is still needed to ensure consistent quantitative results. The efficient, single breath-hold nature of new mapping sequences improves clinical applicability for detecting early disease changes.
Penetrating atherosclerotic ulcer (PAU) is an ulcerating atherosclerotic lesion that penetrates the aortic wall. CT is often used to evaluate PAU, showing features like a focal outpouching with adjacent hematoma. While some cases progress slowly, PAU carries a risk of complications like rupture. Treatment depends on factors like symptoms, expansion rate, and surgical risk. Careful monitoring is important due to variable prognosis.
HCM – Presentation, Hemodynamics and InterventionAnkur Gupta
This document describes a case of a 50-year-old female presenting with symptoms of breathlessness, angina, and presyncope. Echocardiography revealed asymmetric septal hypertrophy and systolic anterior motion of the mitral valve, consistent with hypertrophic obstructive cardiomyopathy (HOCM). The document then provides detailed background information on HOCM, including definitions, pathophysiology, clinical presentation, diagnostic testing, and treatment options such as beta-blockers, septal ablation, and disqualification from competitive sports in severe cases.
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 .
Radiological evaluation of takayasu arteritis Dr. muhammad Bin Zulfiqar Servi...Dr. Muhammad Bin Zulfiqar
Radiological evaluation of takayasu arteritis Dr. muhammad Bin Zulfiqar Services Institute of Medical Sciences Services Hospital Lahore
In this presentation we will discuss the role of imaging in TA.
The document defines no-reflow as inadequate myocardial perfusion through a coronary circulation segment without mechanical vessel obstruction. No-reflow occurs in 30% of patients after reperfusion for myocardial infarction and is associated with worse outcomes. It results from microvascular obstruction from distal embolization, ischemic injury, and reperfusion injury. Diagnosis involves assessing TIMI flow, myocardial blush grade, and imaging techniques. Prevention focuses on reducing embolization using thrombectomy or filters while treatment involves vasodilators like adenosine, verapamil, and glycoprotein IIb/IIIa inhibitors.
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.
An aortic dissection is a tear within the layers of the aortic wall. It can cause severe chest or back pain and risks damage to organs if blood flow is blocked. Prompt diagnosis through imaging tests and treatment are critical to survival. While type A dissections involving the ascending aorta require emergency surgery, type B dissections of the descending aorta can often be treated through intensive blood pressure control and medication to prevent expansion of the tear. Risk factors include hypertension, genetics, trauma, and certain medical conditions.
No reflow and slow flow phenomenon during pcirahul arora
This document discusses strategies and prevention of slow flow and no-reflow phenomenon during percutaneous coronary intervention (PCI). It defines no-reflow as inadequate myocardial perfusion through a coronary artery without mechanical obstruction. No-reflow occurs in 8-11% of primary PCIs and is associated with worse clinical outcomes. The pathophysiology involves distal embolization, ischemic injury, reperfusion injury, and individual patient susceptibility. Preventing no-reflow requires reducing thrombus burden, ischemia time, reperfusion injury through anti-inflammatory drugs, and addressing risk factors like diabetes.
Coronary aneurysms are seen in 0.3-5% of patients undergoing coronary angiography. The most common cause is atherosclerosis. Aneurysms form due to disruption of the vessel wall from weakened media allowing dilation from intraluminal pressure. While often asymptomatic, aneurysms can cause angina, embolization, or rupture. Surgical correction via ligation, bypass, or patch repair is preferred but covered stents may be used for larger aneurysms over 10mm to reduce risk of restenosis.
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
Hypertrophic cardiomyopathy (HCM) is a genetic cardiovascular disease characterized by increased and thickened heart muscle. It is the most common cause of sudden cardiac death in young people. HCM can cause symptoms such as chest pain, heart failure, and palpitations. Treatment involves managing left ventricular outflow tract obstruction through medications, septal reduction procedures, or alcohol septal ablation. Patients at high risk for sudden cardiac death may receive an implantable cardioverter defibrillator for prevention. Risk factors include a family history of sudden death, abnormal blood pressure response to exercise, and extensive thickening of the heart muscle.
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by thickened heart muscle. It has an autosomal dominant pattern of inheritance, with mutations in genes encoding sarcomeric proteins. HCM causes a non-dilated, hypertrophied left ventricle and can lead to heart failure, arrhythmias, and sudden cardiac death. Treatment involves medications like beta-blockers or verapamil to reduce symptoms, and interventions like septal reduction procedures or implantable cardioverter-defibrillators to reduce risk of complications. Regular screening of family members is important for early detection of HCM.
This document summarizes hypertrophic cardiomyopathy (HCM), an autosomal dominant genetic heart condition characterized by unexplained left ventricular hypertrophy. Key points include that it has a prevalence of 1 in 500 adults and is caused by over 200 mutations in genes involved in heart muscle proteins. Symptoms range from none to heart failure, arrhythmias, and sudden cardiac death. Diagnosis is typically made by echocardiogram showing left ventricular hypertrophy. Treatment involves managing symptoms and reducing risk of complications like sudden cardiac death.
Hypertrophic cardiomyopathy (HCM) is defined by a thickened left ventricular wall without an identifiable cause. It can range from asymptomatic to causing heart failure, arrhythmias, or sudden cardiac death. Treatment depends on whether the left ventricular outflow tract (LVOT) is obstructed. For symptomatic patients with LVOT obstruction despite maximum medical therapy, septal reduction procedures like alcohol septal ablation or surgical myectomy are recommended. Alcohol septal ablation involves injecting alcohol into a septal perforator artery to ablate tissue and reduce the gradient. Surgical myectomy directly resects septal muscle. Both procedures significantly reduce gradients and improve symptoms but surgical myectomy provides better gradient and symptom reduction with a lower risk of
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.
This document provides information on alcohol septal ablation (ASA) as a treatment for hypertrophic cardiomyopathy (HCM) with left ventricular outflow tract obstruction. It defines HCM and outlines when ASA is considered, including when medical treatments are no longer effective for symptomatic patients. The procedure involves injecting ethanol into the septal branch of the coronary artery, causing scarring and reducing the ventricular septal thickness. Risks include heart block, but success is defined as a 50% reduction in outflow tract gradient. Factors like the ethanol dose and number of branches treated impact the risk of heart block.
AORTIC DISSECTION and management of aortic dissectiondrhanifmohdali
Aortic emergencies are life-threatening conditions involving the aorta that require timely diagnosis and management. Aortic dissection, a tear in the aortic wall that causes blood to flow abnormally within the wall, is a common aortic emergency. It is usually caused by high blood pressure damaging the aortic wall. Symptoms include a sudden, severe chest pain and pulse abnormalities. Diagnosis involves imaging tests like CT, MRI, or angiography. Treatment aims to lower blood pressure and heart contractility to prevent dissection progression, often using beta blockers. Surgery is usually recommended for type A dissections involving the ascending aorta, while type B dissections of the descending aorta may be treated medically or
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 acute aortic syndrome, including a case presentation of a 55-year-old female with chest pain. Key details include:
1. The patient presented with sudden onset chest pain and was found to have hypertension on examination.
2. Initial workup including ECG, labs and chest x-ray were non-diagnostic but showed a widened mediastinum.
3. Echocardiogram and CT angiogram revealed an aortic dissection involving the aortic arch and descending thoracic aorta.
4. She was referred urgently for cardiovascular surgery to treat this life-threatening condition within 24 hours of presentation.
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY (HOCM)Kurian Joseph
Hypertrophic cardiomyopathy (HCM) is a genetic heart condition characterized by excessive thickening of the heart muscle. It was initially described in the 1950s and causes significant morbidity and mortality due to heart failure, arrhythmias, and sudden cardiac death. The pathophysiology involves left ventricular outflow tract obstruction, diastolic dysfunction, myocardial ischemia, and mitral regurgitation. Treatment involves medications, septal reduction procedures like myectomy or alcohol ablation, and implantable cardioverter-defibrillators in high-risk patients. Prognosis depends on symptom severity and risk factors for sudden cardiac death.
Hypertrophic cardiomyopathy new guidlines ACC 2020DrKamalMehta
This document discusses guidelines for the diagnosis and treatment of hypertrophic cardiomyopathy (HCM). Some key points:
- HCM is a common genetic heart disease characterized by thickened heart muscle. Its prevalence varies from 1:200 to 1:500 in the US.
- Diagnosis involves identifying unexplained thickening of the heart on imaging such as echocardiogram. Genetic testing can identify pathogenic variants in genes linked to HCM in 70% of cases.
- Complications of HCM include sudden cardiac death, heart failure, stroke from atrial fibrillation, and chest pain from issues like left ventricular outflow tract obstruction.
- Evaluation and management focuses on risk stratification
This document discusses the echocardiographic evaluation of hypertrophic obstructive cardiomyopathy (HCM). Key points include:
- Echocardiography is used to diagnose HCM based on unexplained left ventricular hypertrophy and rule out other causes. Asymmetric septal hypertrophy is a characteristic pattern.
- Doppler echocardiography is used to detect left ventricular outflow tract obstruction at rest and with provocative maneuvers like Valsalva.
- Features like systolic anterior motion of the mitral valve indicate dynamic obstruction and need to be monitored with maneuvers.
- Differential diagnosis includes secondary causes of left ventricular hypertrophy from things like hypertension which present differently on echocard
This document discusses dilated cardiomyopathy (DCM), the most common type of cardiomyopathy. It provides details on:
1) The causes, symptoms, signs, diagnostic tests and goals of treatment for DCM. The mainstay of therapy includes vasodilators, digoxin and diuretics.
2) The morphological and microscopic features of DCM which involve enlargement and spherical dilation of the heart chambers.
3) Disease progression can lead to marked left ventricular dilatation and circulatory failure if left untreated. Management aims to relieve symptoms and slow progression.
This document discusses the classification and management of ventricular arrhythmias. It is divided into sections on classification by clinical presentation, electrocardiography, disease entity. Management of VT in structurally abnormal hearts is discussed, including those related to coronary artery disease, dilated cardiomyopathy, bundle branch reentrant tachycardia, arrhythmogenic right ventricular dysplasia, and other conditions. Clinical presentation, mechanisms, diagnostic testing, and treatment options are summarized for each condition.
The document discusses various types of cardiomyopathies including dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy (HCM), and restrictive cardiomyopathy (RCM). It provides details on the definition, causes, symptoms, diagnostic criteria and treatment options for each type. DCM is the most common cardiomyopathy, usually caused by idiopathic or viral factors, leading to ventricular dilation and dysfunction. HCM is a genetic disease causing left ventricular hypertrophy that can lead to obstruction of blood flow. RCM involves restrictive filling of the ventricles with normal wall thickness.
This document summarizes hypertrophic cardiomyopathy (HCM), beginning with its pathology and pathogenesis. HCM causes thickening of the ventricular walls asymmetrically, most commonly affecting the interventricular septum. The main pathophysiological mechanisms include dynamic left ventricular outflow tract obstruction, mitral regurgitation, diastolic dysfunction, myocardial ischemia, and cardiac arrhythmias. Clinical manifestations range from no symptoms to dyspnea, fatigue, syncope, and sudden cardiac death. Diagnosis is made primarily via echocardiogram. Treatment involves medications, septal reduction procedures, or implantable cardioverter-defibrillators depending on symptoms and risk factors. Prognosis depends on factors like degree of
The document discusses postpericardiotomy syndrome, which is an inflammatory condition that can occur after surgery involving opening of the pericardium. It has three key characteristics:
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1. SURGICAL MANAGEMENT FOR
HYPERTROPHIC OBSTRUCTIVE
CARDIOMYOPATHY
Dr. Hari Kumar Sampath
CTVS Resident , NUH
Moderator: Dr. SorokinVitaly
Sr Consultant Cardiac Surgeon, NUH
2. Definition
♥ Left ventricular hypertrophy in the absence of underlying cause –
Hypertension, Aortic stenosis
♥ LVOTO results from septal hypertrophy combined with systolic anterior
Motion of the mitral valve (SAM) which also produces variable degree of MR
♥ Obstruction - 70% (J Maron et al 2009)
3. Genetics
1 in 500 . Genetically determined 60-80%
familial
De - Novo 20-40%
0.2% of phenotypically expressed disease
>400 mutations in 1 or more of the 15
identified genes that encode components
the cardiac sarcomere complex
Mutation to 3 protein encoding genes
30-70 % in beta Myosin heavy chain (MYH7)
15-25% in Myosin binding protein
(MYBPC3)
15-20% in CardiacTroponinType 2 (TNNP2)
Benefits of genetic analysis
■ Pre clinical diagnosis in patients with
family history of SCD
■ InThose with a malignant mutation
that predisposes them to a severe
phenotype
■ To know the precise genetic defect in
HCM among asymptomatic family
members who carry the mutation and
might be at risk of SCD
Richard P, Charron P, Carrier L, et al. Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of
mutations, and implications for a molecular diagnosis strategy [published correction appears in Circulation. 2004
Jun 29;109(25):3258]. Circulation. 2003;107(17):2227‐2232. doi:10.1161/01.CIR.0000066323.15244.54
5. From a surgical perspective, sub-classified on the basis of the site of maximum
septal hypertrophy, although other wall segments are usually also hypertrophied:
♥ Subaortic HCM—hypertrophy of the basal interventricular septum that creates a
relatively elliptical left ventricular (LV) cavity with a marked nodule.This results in
LVOTO caused by SAM
♥ Midventricular HCM—mid septal hypertrophy that forms a crescent-shaped LV
cavity and may be also associated with SAM and LVOTO
♥ Apical HCM—a predominantly apical distribution of hypertrophy that reduces the
size of the apical region of the LV cavity. Isolated apical HCM is not associated with
LVOTO
7. Morphology of Mitral valve apparatus
■ Mitral anterior leaflet moves anteriorly in systole
■ Posterior mitral leaflet moves and closes against
the free edge of the anterior leaflet and narrows
the LVOT
■ Causes MR with jet directed posterolaterally
■ Whitish endothelial scar is the guide during septal
myectomy
■ 15-25% Papillary muscle anamoly –
Direct insertion of papillary muscle into
anterior leaflet
Papillary muscle fusion to septum
Accessory muscles & Accessory anamolous
Chordae
8. Morphology of Coronary Artery Disease
■ Atherosclerotic coronary artery
disease (CAD) 5-15% in HCM
■ Mayo clinic – 26% of patients
underwent coronary angiogram had
significantCAD
■ 15% had bridging of epicardial
coronary disease – which is more
significant in children with angina
compared to adults (Yetman et al. N
Eng J med 1998)
■ Survival is reduced in presence of
significantCAD
9. Diastolic
dysfunction
• Elevation of LV end diastolic pressure is the principle pathophysiology
• Results in LA enlargement,
• Increase in Pulmonary pressure
• Atrial arrhythmias
• Insufficient myocardial oxygen supply because of the very thick and hypertrophied myocardium;
LVOTO
• Direct effect on increasing end diastolic pressure
• Indirect effect on hemodynamics through association with MR
Mitral
regurgitation
• Intrinsic mitral valve disease may contribute to valvular lesion
• Rupture of chordae leads to CCF
Pathophysiology
10. Clinical presentation
♥ asymptomatic
♥ severely disabling symptoms of fatigue, dyspnea, chest pain, syncope and sudden
cardiac death (SCD)
♥ The overall mortality rate of patients with HCM is less than 1 % per year, most
commonly the result of SCD due to ventricular arrhythmias
♥ It is the most common cause of SCD in young athletes
11. Natural course of the disease
■ symptoms due to LVOTO
■ Asymptomatic with no pressure gradient until 4th -6th decade of life
■ Onset of AF (30%) precipitates symptoms leading to embolism in ( 6%) of the HCM
■ Infective endocarditis 1.4/1000 person per year
■ 1% mortality
12. Diagnosis
ECHO Findings - HCM patients are classified
as having obstruction based on
the measurement of peak systolic
velocity in the left ventricular outflow
tract (LVOT) at rest and in asymptomatic
cases after provocation >30 mm Hg
systolic anterior motion (SAM) of the
anterior leaflet of the mitral valve
resulting in a posteriorly directed jet of
regurgitation
Presence of MR
Differentiate MR jet & true LVOT velocity
mid-systolic closure of the aortic valve
Average LV wall thickness 20-22 mm, but
in 5-10% patients 30-50 mm
LA dilatation, PHT, Diastolic dysfunction
Bos JM,Towbin JA, Ackerman MJ. Diagnostic, prognostic,
and therapeutic implications of genetic testing for
hypertrophic cardiomyopathy. J Am Coll
Cardiol 2009;54:201-211
13. Diagnosis
Cardiac MRI
In case not recognised in 2D ECHO
in anterolateral free wall and apical
hypertrophy
Detects the severity of myocardial
fibrosis which is known risk factor
for ventricular arrhythmias
Invasive Catheterization
■ Rarely indicated
■ Only if symptoms of angina
■ Family history of CAD
■ Abnormal Lipids
■ Older age
14. S
Refractory SymptomsTreatment Failure
Subaortic obstruction Non Obstruction
Severe Symptoms NYHA Class III/IV
Dysopyramide + Beta Blockers Verapamil + Diuretics
Mild to moderate symptoms Class I/II
Beta blockers Verapamil
Septal Myectomy
Alcohol Septal Ablation
HeartTransplantation
15. Supportive management
Avoid
■ dehydration
■ excessive alcohol consumption as volume depletion
exacerbates the pressure gradient
■ Similarly, vasodilating drugs including nitrates to be avoided
■ digoxin, which has positive inotropic effects
16. Medical management
♥ First-line medical therapy : β-adrenergic blocking agents,
- negative inotropic and negative chronotropic effects
- help alleviate obstruction, and
- dosage should be titrated to the maximum tolerated
♥ Second line management : Calcium antagonist Verapamil, which
- improves ventricular relaxation and decreases LV contractility.
♥ Disopyramide is a type I-A antiarrhythmic agent with an anticholinergic effect,
- often used in combination with a β-blocker if this is only partially effective
- In atrial fibrillation, used in combination with an AV node blocker, as AF may be
accompanied by a rapid ventricular response.
19. Surgical management
♥ Goal of any surgical technique is to relieve LVOT obstruction,
♥ avoid the occurrence and/or recurrence of systolic anterior movement (SAM) of the
anterior mitral leaflet (AML) if present—reduce mitral valve (MV)
♥ Depending on the configuration of LVOT obstruction, myectomy with/without MV
replacement has been the “gold standard” in surgical treatment of HOCM.
♥ considering the known disadvantages of artificial valves, MV preserving techniques
will improve postoperative outcomes and decrease major adverse events in the
long term
20. Septal reduction therapy
♥ NewYork Heart Association functional classes III and IV despite maximum tolerated
pharmacotherapy.
♥ Specifically, with a peak outflow gradient of ≤50 mmHg as measured with Doppler
echocardiography either under resting conditions or by physiological provocation
through exercise
♥ Moreover, the required minimum thickness of the interventricular septum required
for surgery is specified at 15 mm
♥ By restoring diastolic activity, septal myectomy is able to provide long term
alleviation of HCM-related symptoms.
21. septal myectomy
- Best in patient with proximal LVOTO and mid ventricular
obstruction
- Not a great option for other variants (apical)
22. ♥ Predictable result with accurate removal of muscle in thickness, length &
width
♥ Can attend to mitral valve issues
♥ Low morbidity & mortality procedure
♥ Other manipulations if needed – CABG, MR
♥ Only high risk for PPM
septal myectomy
23. septal myectomy
♥ GA
♥ Midline sternotomy
♥ Cardiopulmonary by pass
♥ Transthoracic approach
24. Transaortic septal myectomy
♥ The pericardium is opened vertically over the centre of the ascending aorta.
♥ Multiple pericardial sutures are used to suspend the right pericardium to the adjacent
superior sternal edge.
♥ Left pericardial suspension sutures are placed from the aortic annulus level to the
pericardial reflection only as this allows the left ventricular apex to drop into the left chest.
♥ This maneuver elevates the aorta to the sternal level and facilitates visualization during the
procedure
♥ Cardiopulmonary bypass with single two-stage right atrial cannulation and
♥ venting of the left ventricle via the right superior pulmonary vein is established
25. The patient is systemically cooled to 34 degrees centigrade following placement of an aortic
cross clamp,
normothermic cardioplegia solution is used to arrest the heart followed by cooling until the
myocardium reaches 15 degrees centigrade.
A transverse aortotomy is fashioned approximately 0.5 cm above the sinotubular junction
(STJ).
It is important not to cross the STJ with the incision as this may distort the aortic valve with
closure of the aortotomy which can result in aortic insufficiency.
The distal aorta at the incision line is then tacked to the pericardial reflection at the level of the
superior vena cava for exposure
26. ♥ The first myectomy incision is made oriented towards the LV apex beginning 2mm below the right
coronary leaflet hinge point and 2 mm towards the membranous septum.
♥ The depth of the incision is usually 1-1.5 cm and length 3.5-5 cm as guided by the preoperative
echocardiogram.
♥ The incision is made parallel to the LVOT (towards the apex) to a depth of the proposed resection,
with the goal of a residual septal thickness of 0.8 to 1.0 cm.
♥ A tendency is to direct the incision too far to the left of the apex.
♥ To avoid this, the surgeon can make the incision with the left hand.
♥ The length of the incision depends on the extent of the hypertrophy
♥ but is generally 35–50 mm long.
♥ In patients with concomitant mid-ventricular obstruction, the incision should extend to at least the
level of the antero-septal papillary muscle head
27. The second incision is approximately 2.0 mm in depth and 2.0 mm below the right coronary leaflet hinge
and is carried into the sub-commissural area beginning at the base of the first incision.
The third incision begins in the subcommissural area running parallel and 2.0 mm below the left coronary
cusp hinge ending 4–5 mm from the mitral annulus
28. UsingArgentine forceps, the ‘LVOT flap’ is grasped and distracted inferiorly.
Now a second 2.0 mm deep incision is made at the superior border of incisions 2 and 3.
In the region of the sub-commissural area the two original incisions are rounded with subsequent
incisions.
The process is repeated eventually forming a flap in the LVOT resection is terminated by placing
downward traction on the specimen and incising across the base.
29. The lateral aspect of the resection at the mitral annulus is completed with scissors, again with care
to avoid trauma to the mitral sub-valvular apparatus
30. With the retractor placed in the resection site, the distal base of the resection can be
extended 1–2 cm laterally under the membranous septum with the resection narrowed as it
is carried towards the annulus.
By producing a traction point, the distal most portion of the resection can also be elongated
if necessary
31. Surgery for HOCM
Mitral valve replacement for HOCM
■ Popularized by Cooley as a quick and uncomplicated fix
■ Does solve the problem of the LVOTO
■ Technical concepts:
Has to be a low profile mechanical valve. Biological valve with struts or high profile
mechanical valves(currently unavailable)Can independently produce LVOTO
All leaflet tissue and chordal apparatus along with, occasionally, the heads of the papillary
muscles have to be resected to open up the LVOT and mid cavity completely.
Issues:
Creates a lifelong dependency on anti-coagulation in a relatively young person
Current role:
Residual LVOTO after previous surgery with inadequate muscle available for repeat resection
32. Resection-Plication-Release operation
■ Abnormal positioning and size of the mitral valve contributes to the dynamic LVOTO
independent of the PSH only
■ Transaortic approach and standard septal myectomy
■ The anterior mitral leaflet is foreshortened by applying 2-4 vertical sutures in the mid body
of the leaflet where it is usually devoid of chords
■ The abnormal attachments of the papillary muscles are release to allow the chordal
apparatus of the MV to fall away from the LVOT
■ Excellent operation for a dynamic LVOTO from complex pathophysiology
33. Correcting a bad result from a septal myectomy
Evaluate the operation andTEE
IS there any scope for more muscle resection?
Are there independent MV issues or mild cavity issues?
Back on bypass
Muscle- Extended resection
Modified Konno procedure for augmenting the LVOT
Mitral valve
Plication
Release of papillary muscle
MV Replacement
Role foe the Alfieri edge to edge suture
Limited –Bailout only cause the whole assembly to move into the LVOT
34. Evaluating a septal myectomy
Gradients
Can be done byTEE or direct needle measuremnts
Reduction in the resting gradient and most importantly the post ectopic potentiation must be
abolished
Role of administration of chronotropes foe evaluation
Mitral valve
SAM to be abolished completely
Trace to mild MR
Why is it adequate?
Inadequate muscle resection
independent mitral valve pathology
35. Pitfalls in a septal myectomy
The trough is not long enough-residual gradient
Damage to aortic valve
Injury during retraction of the leaflet
Trough too close to the base of the RCC destabilzing it.
Damage to mitral valve
Injury to leaflet or chordal apparatus during muscle resection
Ventricular septal defect
Too much muscle resected. Cavalier in evaluation and resection
Heart block
36. Outcomes
Early
■ 1% mortality in experienced centre
■ Complete heart block<1-2%
■ Iatrogenic ventricular septal
perforation
Late
■ >90% shown improvement from
more 2 classes
■ Relief of gradient decrease the atrial
size
■ Decreases AF
37. Survival
■ 98, 96, 83% in 1,5 & 10 years post operatively ( omen et al study)
■ Extent of LVH important determinant of survival
successful myetectomy results in regression LVH
In patients with ICD , myectomy group had less discharges compared to non operative
patients ( Mc Cleod and associates)
38. Alcohol Septal Ablation – Pros & Cons
■ less invasive technique
■ more suitable for elderly or high-risk patients than surgical myectomy because there
may be reduced procedural all-cause mortality rate.
■ However, there is an increased risk of heart block
■ permanent pacemaker requirement, and
■ slightly higher post-procedural resting LVOT gradients
40. Which of the following is not true
regarding morphology of HCM?
■ A.The phenotype closely correlates with genotype
■ B. Upto 20 % of patients will have anamolies of papillary muscles
■ C. Coronary flow is reduced
■ D. CAD is present in 5-15 % of the patients
■ E. LAD muscular bridging is found in 15%
41. Which of the following histopathologic and
genetic findings are true in patients with
HCM?
■ A.The myocardial fibres are hypertrophied and arranged in parallel sheets
■ B.There is organised whirling of fibres
■ C. Most cases are not familial
■ D. It is genetically diverse disease
■ E.All family members should undergo genetic testing
42. HCM results in?
■ A. Systolic dysfunction
■ B. LVOTO
■ C. Functional mitral stenosis
■ D.Asymmetrical left ventricular free wall thickening
■ E. Central mitral insufficiency due to SAM
43. Surgical repair of HCM may include all of
the following except:
■ A. Septal myectomy
■ B. Incision of the ventricular wall below the commissure between the left and right
coronary cusps
■ C. Mitral valve replacement
■ D. Unroofing of the LAD
■ E. Extension of the ventricular incision towards the apex
44. Results after surgery for HCM include?
■ A. Operative mortality of 5%
■ B. Heart block & pacemaker incidence around 5%
■ C. Relief of symptoms in over 90% of the patients
■ D. Long term survival below the general population
■ E. Higher incidence of new right bundle branch block compared to Alcohol septal
ablation