Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
This document provides an overview of sinus of Valsalva aneurysm (SOVA). Key points include:
- SOVA is a thin-walled bulge that originates from the aortic sinuses, most commonly the right sinus. It can rupture into the right heart chambers.
- Presentation depends on rupture status - ruptured SOVA causes a continuous murmur while unruptured can cause arrhythmias or embolism. Imaging helps confirm diagnosis.
- Surgery is the standard treatment, involving a median sternotomy, cardiopulmonary bypass, and patch closure of the defect from inside the aorta and heart chambers. Device closure is also possible. Outcomes are generally good but
A 45 years old lady presented with generalized weakness and palpitations. She is a diagnosed case of chronic renal failure with Diabetes mellitus and Hypertension. Her serum K+ level is 6.8 meq/L. She had the following ECG.
Case; A 54 years old gentleman complained of chest discomfort on exertion for the last 5 months. He is smoker for 10 years, diabetic for 5 years and hypertensive for 3 years. He had the following ECG.
Case: A 25 years old gentleman presented with chest pain and fever .He was normotensive, non-smoker and non-diabetic. His pulse 128b/min and BP-130/80 mm Hg. Troponin I was normal.
Case: A 58 years old gentleman complained of severe central chest pain with excessive sweating 5 days back. He is smoker for 7 years, diabetic for 5 years and hypertensive for 4 years. His BP-90/70 mm Hg. He had the following ECG.
This document discusses inotropic therapy for heart failure. It begins by outlining the stages of heart failure from pre-clinical to end-stage disease. It then discusses the goals and strategies for treatment at each stage, including drugs routinely used like diuretics, ACE inhibitors, and beta-blockers. The document focuses on positive inotropic drugs, describing commonly used agents like digoxin, dopamine, and dobutamine. It provides details on their mechanisms of action, appropriate uses, and risks. Overall, the document provides a comprehensive overview of inotropic therapy and pharmacological management of heart failure.
- Pulmonary artery hypertension (PAH) is defined as a mean pulmonary artery pressure of ≥25 mmHg at rest. It is characterized by pre-capillary pulmonary hypertension with a pulmonary wedge pressure <15 mmHg and a pulmonary vascular resistance >3 Wood units.
- The pathophysiology involves sustained vasoconstriction, vascular remodeling, in situ thrombosis, and increased arterial stiffness. Genetic factors like BMPR2 mutations also contribute to PAH development.
- Clinical features range from mild breathlessness to signs of right heart failure. Diagnostic tests include echocardiography, CT scans, V/Q scans, right heart catheterization and lab tests.
- Treatment involves oxygen therapy, diure
This document discusses ductus arteriosus dependent congenital heart diseases. It begins by defining ductus dependent circulation as abnormalities where ductus arteriosus patency is required to maintain systemic perfusion. It then describes the anatomy and physiology of the ductus arteriosus, noting its role in diverting blood from the pulmonary to systemic circulation in fetal life. The document outlines conditions of ductus dependent pulmonary and systemic blood flow. It discusses goals of management as minimizing hypoxemia and balancing pulmonary and systemic circulations. Maintaining ductal patency with prostaglandins is emphasized as critical for stabilization in ductus dependent lesions.
1) Pulmonary hypertension (PH) is defined as elevated pulmonary artery pressure, while pulmonary arterial hypertension (PAH) is a subtype caused by constriction and remodeling of small pulmonary arteries.
2) PAH is a progressive disease that involves proliferation of cells in the pulmonary arteries leading to increased pulmonary vascular resistance and right heart failure if left untreated.
3) The document reviews classification of PH, diagnostic testing and evaluation algorithms, goals of treatment, and approved therapies for PAH.
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
This document provides an overview of sinus of Valsalva aneurysm (SOVA). Key points include:
- SOVA is a thin-walled bulge that originates from the aortic sinuses, most commonly the right sinus. It can rupture into the right heart chambers.
- Presentation depends on rupture status - ruptured SOVA causes a continuous murmur while unruptured can cause arrhythmias or embolism. Imaging helps confirm diagnosis.
- Surgery is the standard treatment, involving a median sternotomy, cardiopulmonary bypass, and patch closure of the defect from inside the aorta and heart chambers. Device closure is also possible. Outcomes are generally good but
A 45 years old lady presented with generalized weakness and palpitations. She is a diagnosed case of chronic renal failure with Diabetes mellitus and Hypertension. Her serum K+ level is 6.8 meq/L. She had the following ECG.
Case; A 54 years old gentleman complained of chest discomfort on exertion for the last 5 months. He is smoker for 10 years, diabetic for 5 years and hypertensive for 3 years. He had the following ECG.
Case: A 25 years old gentleman presented with chest pain and fever .He was normotensive, non-smoker and non-diabetic. His pulse 128b/min and BP-130/80 mm Hg. Troponin I was normal.
Case: A 58 years old gentleman complained of severe central chest pain with excessive sweating 5 days back. He is smoker for 7 years, diabetic for 5 years and hypertensive for 4 years. His BP-90/70 mm Hg. He had the following ECG.
This document discusses inotropic therapy for heart failure. It begins by outlining the stages of heart failure from pre-clinical to end-stage disease. It then discusses the goals and strategies for treatment at each stage, including drugs routinely used like diuretics, ACE inhibitors, and beta-blockers. The document focuses on positive inotropic drugs, describing commonly used agents like digoxin, dopamine, and dobutamine. It provides details on their mechanisms of action, appropriate uses, and risks. Overall, the document provides a comprehensive overview of inotropic therapy and pharmacological management of heart failure.
- Pulmonary artery hypertension (PAH) is defined as a mean pulmonary artery pressure of ≥25 mmHg at rest. It is characterized by pre-capillary pulmonary hypertension with a pulmonary wedge pressure <15 mmHg and a pulmonary vascular resistance >3 Wood units.
- The pathophysiology involves sustained vasoconstriction, vascular remodeling, in situ thrombosis, and increased arterial stiffness. Genetic factors like BMPR2 mutations also contribute to PAH development.
- Clinical features range from mild breathlessness to signs of right heart failure. Diagnostic tests include echocardiography, CT scans, V/Q scans, right heart catheterization and lab tests.
- Treatment involves oxygen therapy, diure
This document discusses ductus arteriosus dependent congenital heart diseases. It begins by defining ductus dependent circulation as abnormalities where ductus arteriosus patency is required to maintain systemic perfusion. It then describes the anatomy and physiology of the ductus arteriosus, noting its role in diverting blood from the pulmonary to systemic circulation in fetal life. The document outlines conditions of ductus dependent pulmonary and systemic blood flow. It discusses goals of management as minimizing hypoxemia and balancing pulmonary and systemic circulations. Maintaining ductal patency with prostaglandins is emphasized as critical for stabilization in ductus dependent lesions.
1) Pulmonary hypertension (PH) is defined as elevated pulmonary artery pressure, while pulmonary arterial hypertension (PAH) is a subtype caused by constriction and remodeling of small pulmonary arteries.
2) PAH is a progressive disease that involves proliferation of cells in the pulmonary arteries leading to increased pulmonary vascular resistance and right heart failure if left untreated.
3) The document reviews classification of PH, diagnostic testing and evaluation algorithms, goals of treatment, and approved therapies for PAH.
This document discusses heart failure with preserved ejection fraction (HFpEF), formerly known as diastolic heart failure. It provides background on HFpEF versus systolic heart failure and explores the pathophysiology and management of HFpEF. Key points include:
1) HFpEF is a distinct clinical syndrome from heart failure with reduced ejection fraction (HFrEF), with normal ejection fraction but evidence of diastolic dysfunction.
2) Impaired systolic function can be detected in HFpEF patients using strain imaging, despite preserved global ejection fraction.
3) The pathophysiology of HFpEF is complex and multifactorial, involving microvascular inflammation, cardiomyocyte stiff
The document discusses various clinical trials related to cardiovascular diseases. It summarizes the ACCORD BP study which found that targeting a SBP of <120 mm Hg compared to <140 mm Hg in patients with type 2 diabetes did not reduce cardiovascular events. It also summarizes the HOPE trial which found that ramipril reduced cardiovascular deaths, myocardial infarction, and stroke in high-risk patients without low ejection fraction or heart failure. Finally, it summarizes the EUROPA trial which found that perindopril reduced the primary endpoint of cardiovascular mortality, non-fatal MI, and cardiac arrest in patients with stable coronary artery disease.
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
1) A 55-year-old woman presented with shortness of breath and was found to have right ventricular hypertrophy on ECG. Echocardiogram showed an atrial septal defect with pulmonary hypertension.
2) A 35-year-old woman with shortness of breath for 3 years was found to have mitral stenosis and pulmonary hypertension on echocardiogram.
3) A pregnant 25-year-old woman had severe pulmonary hypertension found on echocardiogram.
A 73-year-old male presented with dizziness for 1 year and chest pain for 2 days. His ECG showed left bundle branch block (LBBB) and first-degree atrioventricular block, consistent with possible trifascicular block. Trifascicular block must be confirmed with bundle of His electrogram. The patient has abnormal conduction through one or more divisions of the intraventricular conduction system distal to the bundle of His, presenting as LBBB and first-degree AV block. This suggests involvement of the left and right bundles as well as the AV node, consistent with trifascicular block.
The document discusses various types of valvular heart disease including stenosis, regurgitation, mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, tricuspid stenosis, tricuspid regurgitation, pulmonary stenosis and pulmonary regurgitation. For each condition, the causes, consequences, clinical presentation, investigations, and management are described. Common investigations like echocardiography and treatments like valve replacement surgery are also summarized.
Raja Lahiri provides an overview of coronary angiography. Key points include:
- Coronary angiography is the current gold standard for visualizing the coronary arteries through X-ray imaging with contrast injection.
- The history of coronary angiography began in the 1920s-1940s with early experiments in cerebral and cardiac catheterization.
- Modern techniques involve accessing arteries typically through the femoral or radial arteries to insert a catheter for contrast injection into the coronary arteries under X-ray imaging.
- Multiple angiographic views are needed to visualize different segments of the left and right coronary arteries. Coronary angiography is used to evaluate coronary artery disease, graft patency, and left ventricular function.
The EMPEROR-Reduced trial studied the effects of empagliflozin in patients with chronic heart failure with reduced ejection fraction. The trial included patients with NYHA class II-IV heart failure and an ejection fraction below 40% who were receiving standard guideline-directed medical therapy. Patients were randomly assigned to receive empagliflozin 10 mg daily or placebo and followed for a median of 16 months. The study found that empagliflozin reduced the risk of the composite primary outcome of cardiovascular death or hospitalization for heart failure compared to placebo.
Left-Right ShuntNatural history & Principles of Managementdrranjithmp
This document discusses ventricular septal defects (VSD), the most common congenital heart defect. Key points include:
- VSDs occur in 8 per 1000 live births. The most common type is a perimembranous VSD.
- Clinical presentation depends on the size of the defect and degree of left-to-right shunting. Small defects may close spontaneously.
- Complications can include heart failure, pulmonary vascular disease, infective endocarditis, and aortic valve prolapse/regurgitation.
- Treatment may involve surgery to close the defect, with timing dependent on factors like age, size, and pulmonary pressures.
This document discusses supraventricular tachycardias (SVT). It defines different types of SVT including paroxysmal SVT, which is common in emergency rooms. Quality of life is often poor for those with paroxysmal SVT. The document discusses mechanisms of SVT including reentry circuits, enhanced automaticity, and triggered activity. It provides details on differentiating AV nodal reentrant tachycardia from AV reentrant tachycardia using electrocardiogram findings. Treatment options discussed include carotid sinus massage, adenosine, and catheter ablation.
Takotsubo cardiomyopathy (TC), also known as "broken heart syndrome", is an acute cardiac syndrome that presents similarly to acute coronary syndrome (ACS) but is caused by transient left ventricular dysfunction rather than coronary artery blockages. It often occurs in post-menopausal women in response to severe emotional or physical stress and is characterized by abnormal ventriculograms showing apical ballooning of the left ventricle. While difficult to distinguish from ACS initially, differentiating the two is important to avoid unnecessary thrombolysis in TC patients. The pathophysiology of TC involves excess catecholamine release and microvascular dysfunction resulting in reversible myocardial stunning.
Pulmonary hypertension is elevated pressures in the pulmonary vascular bed defined as a mean pulmonary artery pressure of ≥20 mmHg. The document discusses the pathophysiology, categorization, risk stratification, diagnosis and treatment of pulmonary hypertension. Risk stratification considers a mPAP ≥25 mmHg, PVR >3 Woods Units and PAWP ≤15 mmHg to determine who warrants treatment. Treatment includes vasodilator therapy targeting the prostacyclin, endothelin, and nitric oxide pathways.
Prosthetic heart valves have evolved significantly over the past 70 years from early caged ball designs to modern bileaflet valves. Present day valves include mechanical options like the St. Jude bileaflet valve as well as bioprosthetic options derived from animal tissues like the Medtronic Mosaic porcine valve. Complications remain an issue, though designs aim to improve hemodynamics and reduce thrombosis. Future advances may allow reduced anticoagulation needs.
Tavi,Transcatheter Aortic Valve Replacement, TAVI,TAVR,Dr.Hasan Mahmud
Transcatheter aortic valve implantation (TAVI) has been developed as an alternative to surgical aortic valve replacement for high-risk patients. TAVI involves threading a collapsible valve through blood vessels and implanting it to replace the diseased valve. Over 30,000 high-risk patients with severe aortic stenosis have undergone TAVI, based on evidence from studies showing it is safer than surgery for this group. TAVI indications may expand as longer-term data on outcomes becomes available and the procedure requires a multidisciplinary team approach and dedicated training.
Antiplatelets in stroke recent scenarioNeurologyKota
- Aspirin is recommended within 24-48 hours for acute ischemic stroke (AIS) and after 24 hours if IV thrombolysis is administered.
- For minor strokes, dual antiplatelet therapy with aspirin and clopidogrel for 21 days begun within 24 hours is recommended, followed by clopidogrel alone for 90 days.
- The efficacy of IV antiplatelet drugs like tirofiban and eptifibatide for AIS is not well established and requires further research.
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
Heart failure - pathogenesis and current managementSubhasish Deb
1. Heart failure is defined as the inability of the heart to pump enough blood to meet the body's needs. It can occur when the heart muscle is damaged or weakened.
2. The document discusses the pathogenesis, stages, evaluation, and management of heart failure. Compensatory mechanisms initially help the heart function but eventually cause harm through remodeling if the underlying issue is not addressed.
3. Treatment involves controlling risk factors, using medications like ACE inhibitors and beta blockers, and devices like ICDs and CRT for more advanced cases. Ongoing monitoring is important as the condition can progress despite treatment.
This document discusses heart failure with preserved ejection fraction (HFpEF), formerly known as diastolic heart failure. It provides background on HFpEF versus systolic heart failure and explores the pathophysiology and management of HFpEF. Key points include:
1) HFpEF is a distinct clinical syndrome from heart failure with reduced ejection fraction (HFrEF), with normal ejection fraction but evidence of diastolic dysfunction.
2) Impaired systolic function can be detected in HFpEF patients using strain imaging, despite preserved global ejection fraction.
3) The pathophysiology of HFpEF is complex and multifactorial, involving microvascular inflammation, cardiomyocyte stiff
The document discusses various clinical trials related to cardiovascular diseases. It summarizes the ACCORD BP study which found that targeting a SBP of <120 mm Hg compared to <140 mm Hg in patients with type 2 diabetes did not reduce cardiovascular events. It also summarizes the HOPE trial which found that ramipril reduced cardiovascular deaths, myocardial infarction, and stroke in high-risk patients without low ejection fraction or heart failure. Finally, it summarizes the EUROPA trial which found that perindopril reduced the primary endpoint of cardiovascular mortality, non-fatal MI, and cardiac arrest in patients with stable coronary artery disease.
The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
1) A 55-year-old woman presented with shortness of breath and was found to have right ventricular hypertrophy on ECG. Echocardiogram showed an atrial septal defect with pulmonary hypertension.
2) A 35-year-old woman with shortness of breath for 3 years was found to have mitral stenosis and pulmonary hypertension on echocardiogram.
3) A pregnant 25-year-old woman had severe pulmonary hypertension found on echocardiogram.
A 73-year-old male presented with dizziness for 1 year and chest pain for 2 days. His ECG showed left bundle branch block (LBBB) and first-degree atrioventricular block, consistent with possible trifascicular block. Trifascicular block must be confirmed with bundle of His electrogram. The patient has abnormal conduction through one or more divisions of the intraventricular conduction system distal to the bundle of His, presenting as LBBB and first-degree AV block. This suggests involvement of the left and right bundles as well as the AV node, consistent with trifascicular block.
The document discusses various types of valvular heart disease including stenosis, regurgitation, mitral stenosis, mitral regurgitation, aortic stenosis, aortic regurgitation, tricuspid stenosis, tricuspid regurgitation, pulmonary stenosis and pulmonary regurgitation. For each condition, the causes, consequences, clinical presentation, investigations, and management are described. Common investigations like echocardiography and treatments like valve replacement surgery are also summarized.
Raja Lahiri provides an overview of coronary angiography. Key points include:
- Coronary angiography is the current gold standard for visualizing the coronary arteries through X-ray imaging with contrast injection.
- The history of coronary angiography began in the 1920s-1940s with early experiments in cerebral and cardiac catheterization.
- Modern techniques involve accessing arteries typically through the femoral or radial arteries to insert a catheter for contrast injection into the coronary arteries under X-ray imaging.
- Multiple angiographic views are needed to visualize different segments of the left and right coronary arteries. Coronary angiography is used to evaluate coronary artery disease, graft patency, and left ventricular function.
The EMPEROR-Reduced trial studied the effects of empagliflozin in patients with chronic heart failure with reduced ejection fraction. The trial included patients with NYHA class II-IV heart failure and an ejection fraction below 40% who were receiving standard guideline-directed medical therapy. Patients were randomly assigned to receive empagliflozin 10 mg daily or placebo and followed for a median of 16 months. The study found that empagliflozin reduced the risk of the composite primary outcome of cardiovascular death or hospitalization for heart failure compared to placebo.
Left-Right ShuntNatural history & Principles of Managementdrranjithmp
This document discusses ventricular septal defects (VSD), the most common congenital heart defect. Key points include:
- VSDs occur in 8 per 1000 live births. The most common type is a perimembranous VSD.
- Clinical presentation depends on the size of the defect and degree of left-to-right shunting. Small defects may close spontaneously.
- Complications can include heart failure, pulmonary vascular disease, infective endocarditis, and aortic valve prolapse/regurgitation.
- Treatment may involve surgery to close the defect, with timing dependent on factors like age, size, and pulmonary pressures.
This document discusses supraventricular tachycardias (SVT). It defines different types of SVT including paroxysmal SVT, which is common in emergency rooms. Quality of life is often poor for those with paroxysmal SVT. The document discusses mechanisms of SVT including reentry circuits, enhanced automaticity, and triggered activity. It provides details on differentiating AV nodal reentrant tachycardia from AV reentrant tachycardia using electrocardiogram findings. Treatment options discussed include carotid sinus massage, adenosine, and catheter ablation.
Takotsubo cardiomyopathy (TC), also known as "broken heart syndrome", is an acute cardiac syndrome that presents similarly to acute coronary syndrome (ACS) but is caused by transient left ventricular dysfunction rather than coronary artery blockages. It often occurs in post-menopausal women in response to severe emotional or physical stress and is characterized by abnormal ventriculograms showing apical ballooning of the left ventricle. While difficult to distinguish from ACS initially, differentiating the two is important to avoid unnecessary thrombolysis in TC patients. The pathophysiology of TC involves excess catecholamine release and microvascular dysfunction resulting in reversible myocardial stunning.
Pulmonary hypertension is elevated pressures in the pulmonary vascular bed defined as a mean pulmonary artery pressure of ≥20 mmHg. The document discusses the pathophysiology, categorization, risk stratification, diagnosis and treatment of pulmonary hypertension. Risk stratification considers a mPAP ≥25 mmHg, PVR >3 Woods Units and PAWP ≤15 mmHg to determine who warrants treatment. Treatment includes vasodilator therapy targeting the prostacyclin, endothelin, and nitric oxide pathways.
Prosthetic heart valves have evolved significantly over the past 70 years from early caged ball designs to modern bileaflet valves. Present day valves include mechanical options like the St. Jude bileaflet valve as well as bioprosthetic options derived from animal tissues like the Medtronic Mosaic porcine valve. Complications remain an issue, though designs aim to improve hemodynamics and reduce thrombosis. Future advances may allow reduced anticoagulation needs.
Tavi,Transcatheter Aortic Valve Replacement, TAVI,TAVR,Dr.Hasan Mahmud
Transcatheter aortic valve implantation (TAVI) has been developed as an alternative to surgical aortic valve replacement for high-risk patients. TAVI involves threading a collapsible valve through blood vessels and implanting it to replace the diseased valve. Over 30,000 high-risk patients with severe aortic stenosis have undergone TAVI, based on evidence from studies showing it is safer than surgery for this group. TAVI indications may expand as longer-term data on outcomes becomes available and the procedure requires a multidisciplinary team approach and dedicated training.
Antiplatelets in stroke recent scenarioNeurologyKota
- Aspirin is recommended within 24-48 hours for acute ischemic stroke (AIS) and after 24 hours if IV thrombolysis is administered.
- For minor strokes, dual antiplatelet therapy with aspirin and clopidogrel for 21 days begun within 24 hours is recommended, followed by clopidogrel alone for 90 days.
- The efficacy of IV antiplatelet drugs like tirofiban and eptifibatide for AIS is not well established and requires further research.
1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles.
2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension.
3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns.
4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.
Heart failure - pathogenesis and current managementSubhasish Deb
1. Heart failure is defined as the inability of the heart to pump enough blood to meet the body's needs. It can occur when the heart muscle is damaged or weakened.
2. The document discusses the pathogenesis, stages, evaluation, and management of heart failure. Compensatory mechanisms initially help the heart function but eventually cause harm through remodeling if the underlying issue is not addressed.
3. Treatment involves controlling risk factors, using medications like ACE inhibitors and beta blockers, and devices like ICDs and CRT for more advanced cases. Ongoing monitoring is important as the condition can progress despite treatment.
Secondary Prevention after ACS: Focused on Anticoagulant TherapyPERKI Pekanbaru
Dr. Nathania Marliani Kristanti, SpJP, FIHA. 3rd Pekanbaru Cardiology Update, August 25th 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com
Emergency Medical System Network for STEMI ManagementPERKI Pekanbaru
This document discusses the emergency medical system network for managing ST-elevation myocardial infarction (STEMI). It outlines the importance of rapid diagnosis through early electrocardiograms and treatment through reperfusion therapies like primary percutaneous coronary intervention (PCI) or fibrinolysis. The target is first medical contact to reperfusion within 90 minutes for primary PCI or 30 minutes for fibrinolysis. It also discusses long-term secondary prevention therapies.
Strategy to Go for Goal in Dyslipidemia with Acute Coronary Syndrome PatientsPERKI Pekanbaru
Dr. A. Fauzi Yahya, SpJP (K), FIHA, FAsCC. 3rd Pekanbaru Cardiology Update, August 24th 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com
1) The document discusses fibrinolytic therapy for ST-elevation myocardial infarction (STEMI). STEMI is defined as new ST elevation and biomarkers of necrosis.
2) Immediate reperfusion therapy with either primary percutaneous coronary intervention (PCI) or fibrinolysis is recommended for STEMI patients. The goals are to perform primary PCI within 90 minutes of first medical contact or give fibrinolysis within 30 minutes.
3) Several fibrinolytic agents are discussed including alteplase, reteplase, tenecteplase, and streptokinase. Their properties, dosages, and effectiveness are compared. Successful reperfusion is assessed by resolution of symptoms and ECG changes.
Prof. DR. Dr. Rochmad Romdoni, SpJP(K), FINASIM, FIHA, FAsCC. 3rd Pekanbaru Cardiology Update, August 24th 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com
The document provides an overview of heart failure, including its etiology, pathophysiology, diagnosis, and treatment. It discusses the incidence and prevalence of heart failure, common causes, compensatory mechanisms in the body, assessment methods, and current treatment approaches such as medications, device therapies, and lifestyle modifications. The goal is to educate medical practitioners on managing the complex clinical syndrome of heart failure.
Enoxaparin has been shown to be effective across the spectrum of acute coronary syndromes based on multiple randomized controlled trials. For conservative management of unstable angina/NSTEMI, enoxaparin was found to be superior to unfractionated heparin in reducing the primary composite outcome of death and myocardial infarction at 1 year follow-up, with similar rates of major hemorrhage. For high risk ACS patients undergoing an early invasive strategy, enoxaparin was at least as effective as unfractionated heparin with a higher rate of minor bleeding. In STEMI patients, enoxaparin was superior to unfractionated heparin for efficacy when used with fibrinolysis or
Guidelines and beyond new drug therapy for heart failure with reduced ejectio...ahvc0858
This document provides information on new guidelines and therapies for heart failure patients. It begins by outlining the challenges of managing heart failure patients and their high mortality rates. It then discusses the history of heart failure treatments from ACE inhibitors in the 1990s to newer drugs like ARNi's. The document defines the different types of heart failure - HFrEF, HFmrEF, and HFpEF - and their diagnostic criteria. It explains how neprilysin inhibition enhances natriuretic peptides while simultaneously suppressing the RAAS. Finally, it summarizes that the new drug LCZ696 combines neprilysin inhibition with an ARB to reduce mortality and hospitalization in heart failure patients beyond existing neurohormonal therapies
1. Rate control has equivalent efficacy to rhythm control for managing atrial fibrillation and has less drug-related side effects.
2. Drugs like digoxin, beta blockers, and calcium channel blockers can be used for rate control, while antiarrhythmics like amiodarone, dofetilide and sotalol are used for rhythm control.
3. Electrical cardioversion can be used to restore sinus rhythm but has a risk of recurrence, so anticoagulation is recommended afterwards to prevent stroke from clots that may form during the arrhythmia.
1. The document discusses cardiorenal syndrome (CRS), where acute or chronic dysfunction of the heart or kidneys can cause dysfunction in the other organ.
2. CRS is classified into 5 types depending on the rapidity of onset and primary organ affected. Various biomarkers can help classify CRS along with clinical evaluation.
3. Management of CRS is challenging and includes diuretics, ACE inhibitors, ARBs, beta-blockers, and renal replacement therapy. However, many treatments require careful use in patients with kidney disease.
This document summarizes guidelines from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII). It provides recommendations on lifestyle modifications, measurement of blood pressure, causes and treatment of hypertension, and evidence from clinical trials on blood pressure control. The key recommendations include lifestyle modifications like weight loss, following the DASH diet, reducing sodium, regular exercise, and moderate alcohol intake to control blood pressure. It also provides guidance on drug therapy based on blood pressure levels and number of medications typically needed to achieve control.
Low dose dopamine increases GFR and RBF. The DAD-HF trial investigated 60 patients randomized to low dose furosemide (continuous infusion 0.5 mg/kg/day) with or without low dose dopamine (2 μg/kg/min). Dopamine preserved renal function compared to furosemide alone in patients with acute decompensated heart failure. There were no significant differences found in a trial comparing high vs low dose furosemide or bolus vs continuous infusion on renal function or symptoms. Novel agents targeting fluid overload, renal function, contractility, and vasomotion may provide new therapeutic options for acute heart failure.
Prof. U. C. SAMAL provides an overview of acute decompensated heart failure and what is new in the field. He discusses similarities and differences between acute myocardial infarction and acute heart failure syndromes. Mortality rates are high for both conditions, though clinical benefits of interventions are greater for acute MI based on published clinical trials. The document then discusses definitions and classifications of acute heart failure syndromes, as well as guidelines for diagnosis and treatment from ESC and ACC/AHA. Biomarkers that can help with diagnosis, prognosis, and guiding therapy are also summarized.
Atrial fibrillation is the most common arrhythmia and increases mortality risk. It is classified as paroxysmal, persistent, or permanent based on duration. The CHA2DS2-VASc score is used to assess stroke risk and determine need for anticoagulation. Treatment focuses on rate control with medications like calcium channel blockers or cardioversion for hemodynamic instability. Anticoagulation is recommended for CHA2DS2-VASc score over 2 to prevent stroke.
HF Essentials-PD- Case based discussion_Cardio.CP.Nephro.pptxsandeepkumarGarg4
Based on the information provided:
1. Kartik has HFrEF with an LVEF of 34% and is on guideline directed medical therapy including ACEi/ARB and beta-blocker.
2. However, he continues to have mild symptoms of fatigue and shortness of breath with elevated NT-proBNP and worsening renal function.
3. Mortality remains high in HFrEF patients despite standard therapies. A new class of drug that provides greater reduction in mortality is needed.
The next appropriate step would be to add sacubitril/valsartan (ARB/neprilysin inhibitor) to his medical regimen to further reduce the risk of mortality based on its proven
Opciones farmacológicas en el manejo de insuficiencia cardiaca - Revisión Can...Juan José Araya Cortés
This review summarizes the pharmacologic options for managing systolic heart failure, focusing on modulating pathways through the renin-angiotensin-aldosterone system. Angiotensin converting enzyme (ACE) inhibitors are recommended for all patients with reduced ejection fraction as clinical trials showed they reduce mortality and attenuate ventricular remodeling. Angiotensin receptor blockers (ARBs) are an alternative for those intolerant of ACE inhibitors. Mineralocorticoid receptor antagonists further block the renin-angiotensin-aldosterone system and clinical trials demonstrated reduced mortality when added to standard therapy.
Atrial fibrillation in advanced heart failure role of rate controldrucsamal
1) Treating atrial fibrillation in patients with advanced heart failure remains a challenge due to the risks of both rate and rhythm control strategies.
2) Rate control is preferred over rhythm control, though strict heart rate targets may not be necessary, and beta blockers provide less clear benefit for rate control in AF patients with heart failure compared to those in sinus rhythm.
3) Antiarrhythmic drugs for rhythm control have been shown to increase risks of death and hospitalization, so non-pharmacological approaches and newer agents are being explored.
The document discusses heart failure, including its definition, stages, causes, symptoms, and treatment guidelines. It provides an overview of epidemiology and costs of heart failure. Guidelines from ACC/AHA classify heart failure into stages A through D based on risk or presence of symptoms. Treatment involves managing risk factors, addressing neurohormonal activation, and following medication protocols tailored to each stage.
1. Cardio-renal syndrome (CRS) describes conditions where acute or chronic dysfunction in one organ induces acute or chronic dysfunction in the other organ.
2. Management of CRS is challenging and involves diuretics, ACE inhibitors, beta blockers, and dialysis. However, treatment outcomes remain poor, with high mortality and rates of rehospitalization.
3. While advances have been made, CRS continues to significantly impact morbidity and mortality. Early multidisciplinary management may help improve outcomes, but effective new therapies are still needed to better treat and prevent this challenging condition.
Acute Decompensated Heart Failure : What is New ?drucsamal
Prof. U. C. SAMAL is an expert in cardiology who has held leadership positions in several cardiological societies. The document discusses the management of acute decompensated heart failure and summarizes recent changes to guidelines. It provides an overview of pharmacological interventions for acute heart failure such as diuretics, vasodilators, and inotropes. Non-invasive ventilation and risk stratification scores are also mentioned. The document emphasizes the importance of both short-term stabilization and long-term management through multi-disciplinary programs to prevent readmissions.
This document provides an overview of heart failure, with a focus on heart failure with preserved ejection fraction (HFpEF). It discusses the pathophysiology, diagnosis, and management of HFpEF. Key points include:
- HFpEF accounts for about 1/3 to 1/2 of heart failure cases and is associated with abnormal diastolic function.
- Diagnosis involves assessing symptoms, imaging like echocardiography to evaluate diastolic dysfunction, and ruling out other potential causes.
- Treatment focuses on controlling risk factors like hypertension, fluid management, and some evidence that ARBs, ARNI, and statins may provide benefits. Prognosis is similar to heart failure with reduced eject
This document summarizes management of congestive cardiac failure. It discusses current medical therapies including ACE inhibitors, beta blockers, and aldosterone antagonists which have been shown to improve survival. Device therapies like biventricular pacing and implantable cardioverter defibrillators are also used to treat heart failure and reduce mortality and sudden death. Lifestyle modifications and multidisciplinary management in the community can further benefit patients.
1) The document discusses new oral anticoagulants (NOACs) for stroke prevention in patients with atrial fibrillation (AF), comparing them to warfarin.
2) NOACs like apixaban, rivaroxaban, and dabigatran are preferable to warfarin due to their more predictable dosing, fewer drug and food interactions, and lack of required monitoring.
3) Clinical trials found NOACs to have similar or better efficacy in stroke prevention compared to warfarin, with lower risks of intracranial hemorrhage and death.
Heart failure Update as per, 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the
Management of Heart Failure and 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
Similar to Recent Updated Pathogenesis and Management of Heart Failure: (20)
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Recent Updated Pathogenesis and Management of Heart Failure:
1. Recent Updated Pathogenesis and
Management of Heart Failure:
The role of Angiotensin Receptor Blockers?
Dr. dr. ANWAR SANTOSO, SpJP(K), FIHA, FAsCC, FICA.
Dept. of Cardiology – Faculty of Medicine ~ University of Indonesia
National Cardiovascular Centre – Harapan Kita Hospital - INDONESIA
2. VBWG
Diabetes is the No. 1 risk factor
for HF in women with coronary disease
Bibbins-Domingo K Jr et al. Circulation.2004;110:1424-30.
Adjusted hazard ratio
Diabetes
Atrial fibrillation
Myocardial infarction >1 event
Creatinine clearance <40
Current smoking
BMI >35
Left bundle branch block
LV hypertrophy
Systolic BP ≥140
3.1
2.9
2.5
2.3
2.1
1.9
1.9
1.6
1.5
0 0.5 1 1.5 2 2.5 3 3.5
HERS study
3. The Donkey AnalogyThe Donkey AnalogyThe Donkey AnalogyThe Donkey Analogy
Ventricular dysfunction limits a patient's ability to perform the
routine activities of daily living…
4. ↑↑↑↑MAP = (↑↑↑↑SV x ↑↑↑↑HR) x ↑↑↑↑TPR
Sympathetic Nervous System
↑ Contractility Tachycardia Vasoconstriction
Compensatory Mechanisms:Compensatory Mechanisms:Compensatory Mechanisms:Compensatory Mechanisms:
Sympathetic Nervous SystemSympathetic Nervous SystemSympathetic Nervous SystemSympathetic Nervous System
Decreased MAP
5. Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.
↑ CNS sympathetic outflow
Disease progression
↑ Cardiac sympathetic
activity
β1-
receptors
β2-
receptors
α1-
receptors
Vasoconstriction
Sodium retention
Myocardial toxicity
Increased arrhythmias
↑ Sympathetic
activity to kidneys
+ peripheral vasculature
Activation
of RAS
α1- β1-
Sympathetic Activation in Heart FailureSympathetic Activation in Heart FailureSympathetic Activation in Heart FailureSympathetic Activation in Heart Failure
6. Vasoconstriction
Oxidative Stress
Cell Growth Proteinuria
LV remodeling
Vascular remodeling
Angiotensinogen
Angiotensin I
Angiotensin II
AT I receptor
Renin
Angiotensin
Converting
Enzyme
Compensatory Mechanisms:Compensatory Mechanisms:Compensatory Mechanisms:Compensatory Mechanisms:
ReninReninReninRenin----AngiotensinAngiotensinAngiotensinAngiotensin----Aldosterone (RAAS)Aldosterone (RAAS)Aldosterone (RAAS)Aldosterone (RAAS)
10. Proposed Pathogenesis of Heart Failure
Gonzales A, et. al. J Am Coll Cardiol 2011; 58: 1833 - 43
11. Curry CW, et al. Mechanical dyssynchrony in dilated cardiomyopathy with intraventricular conduction
delay as depicted by 3D tagged magnetic resonance imaging. Circulation 2000 Jan 4;101(1):E2.
Compensatory MechanismsCompensatory MechanismsCompensatory MechanismsCompensatory Mechanisms
Ventricular Remodeling
Alterations in the heart’s size, shape, structure, and function brought about
by the chronic hemodynamic stresses experienced by the failing heart.
12. Classification of Heart Failure
ACCF/AHA Stages of HF NYHA Functional Classification
A At high risk for HF but without structural
heart disease or symptoms of HF.
None
B Structural heart disease but without signs
or symptoms of HF.
I No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
C Structural heart disease with prior or
current symptoms of HF.
I No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
II Slight limitation of physical activity.
Comfortable at rest, but ordinary physical
activity results in symptoms of HF.
III Marked limitation of physical activity.
Comfortable at rest, but less than ordinary
activity causes symptoms of HF.
IV Unable to carry on any physical activity
without symptoms of HF, or symptoms of
HF at rest.
D Refractory HF requiring specialized
interventions.
17. Diuretics, ACE Inhibitors and ARB’sDiuretics, ACE Inhibitors and ARB’sDiuretics, ACE Inhibitors and ARB’sDiuretics, ACE Inhibitors and ARB’s
Reduce the number of sacks on the wagon
19. Pharmacological Treatment for
Stage C HFrEF (cont.)
Diuretics are recommended in patients with HFrEF who
have evidence of fluid retention, unless contraindicated, to
improve symptoms.
ACE inhibitors are recommended in patients with HFrEF
and current or prior symptoms, unless contraindicated, to
reduce morbidity and mortality.
ARBs are recommended in patients with HFrEF with
current or prior symptoms who are ACE inhibitor-
intolerant, unless contraindicated, to reduce morbidity
and mortality.
I IIa IIb III
I IIa IIb III
I IIa IIb III
20. Drugs Commonly Used for HFrEF
(Stage C HF)
Drug Initial Daily Dose(s) Maximum Doses(s)
Mean Doses Achieved in
Clinical Trials
ACE Inhibitors
Captopril 6.25 mg 3 times 50 mg 3 times 122.7 mg/d (421)
Enalapril 2.5 mg twice 10 to 20 mg twice 16.6 mg/d (412)
Fosinopril 5 to 10 mg once 40 mg once ---------
Lisinopril 2.5 to 5 mg once 20 to 40 mg once 32.5 to 35.0 mg/d (444)
Perindopril 2 mg once 8 to 16 mg once ---------
Quinapril 5 mg twice 20 mg twice ---------
Ramipril 1.25 to 2.5 mg once 10 mg once ---------
Trandolapril 1 mg once 4 mg once ---------
ARBs
Candesartan 4 to 8 mg once 32 mg once 24 mg/d (419)
Losartan 25 to 50 mg once 50 to 150 mg once 129 mg/d (420)
Valsartan 20 to 40 mg twice 160 mg twice 254 mg/d (109)
Aldosterone Antagonists
Spironolactone 12.5 to 25 mg once 25 mg once or twice 26 mg/d (424)
Eplerenone 25 mg once 50 mg once 42.6 mg/d (445)
21. Pharmacological Treatment for
Stage C HFrEF (cont.)
ARBs are reasonable to reduce morbidity and mortality as
alternatives to ACE inhibitors as first-line therapy for
patients with HFrEF, especially for patients already taking
ARBs for other indications, unless contraindicated.
Addition of an ARB may be considered in persistently
symptomatic patients with HFrEF who are already being
treated with an ACE inhibitor and a beta blocker in
whom an aldosterone antagonist is not indicated or
tolerated.
I IIa IIb III
I IIa IIb III
22. Pharmacological Treatment for
Stage C HFrEF (cont.)
Routine combined use of an ACE inhibitor, ARB, and
aldosterone antagonist is potentially harmful for
patients with HFrEF.
Use of 1 of the 3 beta blockers proven to reduce mortality
(i.e., bisoprolol, carvedilol, and sustained-release
metoprolol succinate) is recommended for all patients with
current or prior symptoms of HFrEF, unless
contraindicated, to reduce morbidity and mortality.
I IIa IIb III
I IIa IIb III
Harm
30. VBWG
ACC/AHA stages of systolic HF
and treatment options
Jessup M, Brozena S. N Engl J Med. 2003;348:2007-18.*In appropriate patients
31. M’c Murray JJV, et. al. Eur Heart J 2012; doi: 10. 1093/eurhj/ehs.104
Pharmacological treatments in (NYHA class II – IV)
symptomatic systolic Heart Failure
32. M’c Murray JJV, et. al. Eur Heart J 2012; doi: 10. 1093/eurhj/ehs.104
Treatments that may cause harm in
symptomatic Heart Failure
33. • EvidenceEvidenceEvidenceEvidence----based guidelinebased guidelinebased guidelinebased guideline directed diagnosis, evaluation and
therapy should be the mainstay for all patients with HF.
• Effective implementation of guideline-directed best quality
care reduces mortality, improves QOL and preserves healthreduces mortality, improves QOL and preserves healthreduces mortality, improves QOL and preserves healthreduces mortality, improves QOL and preserves health
care resourcescare resourcescare resourcescare resources.
• Ongoing research is needed to answer the remaining
questions including: prevention, nonpharmacological therapy
of HF including dietary adjustments, treatment of HFdietary adjustments, treatment of HFdietary adjustments, treatment of HFdietary adjustments, treatment of HFppppEF,EF,EF,EF,
management of hospitalized HF, effective reduction in HFmanagement of hospitalized HF, effective reduction in HFmanagement of hospitalized HF, effective reduction in HFmanagement of hospitalized HF, effective reduction in HF
readmissions, more precise use of devicereadmissions, more precise use of devicereadmissions, more precise use of devicereadmissions, more precise use of device----based therapy,based therapy,based therapy,based therapy,
smaller MCS platforms and cellsmaller MCS platforms and cellsmaller MCS platforms and cellsmaller MCS platforms and cell----based regenerative therapybased regenerative therapybased regenerative therapybased regenerative therapy.
Conclusions