Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. The document discusses the pathophysiology and various treatment approaches for congestive heart failure. Pharmacological treatments discussed include ACE inhibitors, beta-blockers, diuretics, and aldosterone antagonists. Newer potential treatments discussed are coenzyme Q10 and BET protein inhibitors. Non-pharmacological treatments discussed are stem cell therapy, gene therapy, cardiac devices like pacemakers, defibrillators and resynchronization therapy, as well as continuous positive airway pressure. The document concludes that while heart failure was once seen as incurable, new gene and stem cell therapies now offer promise for reversing syst
This document discusses different types of shock and their pathophysiology. It begins with learning objectives about shock states and types of shock including cardiogenic, hypovolemic, septic, neurogenic, anaphylactic, and obstructive shock. It then covers the stages of shock and discusses specific types in more detail, focusing on their causes, pathophysiology, clinical manifestations, diagnosis, and management. The types of shock discussed in depth include hypovolemic, cardiogenic, distributive (septic, neurogenic, anaphylactic), and obstructive shock.
Coagulant & AntiCoagulant Haemostasis (arrest of blood loss) and blood coagulation involve complex interaction between the injury vessel wall, platelets and coagulation factors
Heart failure results from reduced cardiac output and elevated sympathetic discharge, leading to vasoconstriction and sodium and water retention. Drugs used to treat heart failure include diuretics, ACE inhibitors, beta blockers, aldosterone receptor antagonists, and vasodilators. Diuretics are first-line to reduce preload and relieve edema. ACE inhibitors and ARBs reduce afterload while beta blockers attenuate sympathetic activation. Aldosterone receptor antagonists prevent remodeling and reduce mortality.
This document discusses drugs that act on blood components to prevent clotting. It covers anticoagulants like heparin and warfarin that prevent clot formation, fibrinolytics like streptokinase that break down existing clots, and antiplatelets like aspirin and clopidogrel that inhibit platelet aggregation. The stages of coagulation and fibrinolysis are described. Specific drugs are explained including their mechanisms of action, clinical uses, and potential side effects.
This document provides an overview of blood drugs and the coagulation process. It discusses how platelets, coagulation factors, and fibrinogen work together to form blood clots during injury to stop bleeding. It then summarizes different types of drugs that can interfere with coagulation, including platelet inhibitors like aspirin and anticoagulants like heparin. The goal of these drugs is to prevent excessive clotting in certain clinical situations like heart attacks. However, interfering with the body's natural clotting process also increases the risk of bleeding.
This document discusses different types of shock including hypovolemic, cardiogenic, distributive, and neurogenic shock. It provides details on the causes, pathophysiology, clinical signs, and treatment of each type. The main vasopressor agents used to treat shock are also described, including norepinephrine, epinephrine, dopamine, and vasopressin. Septic shock is discussed as a type of distributive shock resulting from an infection and systemic inflammatory response.
Congestive heart failure occurs when the heart cannot pump enough blood to meet the body's needs. Symptoms result from blood backing up in the heart and lungs. The main drugs used to treat CHF are ACE inhibitors, ARBs, diuretics, beta-blockers, digoxin, and vasodilators. Digoxin works by inhibiting the sodium-potassium pump, raising intracellular calcium levels, increasing calcium release from the sarcoplasmic reticulum, and enhancing the actin-myosin interaction to strengthen contraction and cardiac output.
This document discusses different types of shock and their pathophysiology. It begins with learning objectives about shock states and types of shock including cardiogenic, hypovolemic, septic, neurogenic, anaphylactic, and obstructive shock. It then covers the stages of shock and discusses specific types in more detail, focusing on their causes, pathophysiology, clinical manifestations, diagnosis, and management. The types of shock discussed in depth include hypovolemic, cardiogenic, distributive (septic, neurogenic, anaphylactic), and obstructive shock.
Coagulant & AntiCoagulant Haemostasis (arrest of blood loss) and blood coagulation involve complex interaction between the injury vessel wall, platelets and coagulation factors
Heart failure results from reduced cardiac output and elevated sympathetic discharge, leading to vasoconstriction and sodium and water retention. Drugs used to treat heart failure include diuretics, ACE inhibitors, beta blockers, aldosterone receptor antagonists, and vasodilators. Diuretics are first-line to reduce preload and relieve edema. ACE inhibitors and ARBs reduce afterload while beta blockers attenuate sympathetic activation. Aldosterone receptor antagonists prevent remodeling and reduce mortality.
This document discusses drugs that act on blood components to prevent clotting. It covers anticoagulants like heparin and warfarin that prevent clot formation, fibrinolytics like streptokinase that break down existing clots, and antiplatelets like aspirin and clopidogrel that inhibit platelet aggregation. The stages of coagulation and fibrinolysis are described. Specific drugs are explained including their mechanisms of action, clinical uses, and potential side effects.
This document provides an overview of blood drugs and the coagulation process. It discusses how platelets, coagulation factors, and fibrinogen work together to form blood clots during injury to stop bleeding. It then summarizes different types of drugs that can interfere with coagulation, including platelet inhibitors like aspirin and anticoagulants like heparin. The goal of these drugs is to prevent excessive clotting in certain clinical situations like heart attacks. However, interfering with the body's natural clotting process also increases the risk of bleeding.
This document discusses different types of shock including hypovolemic, cardiogenic, distributive, and neurogenic shock. It provides details on the causes, pathophysiology, clinical signs, and treatment of each type. The main vasopressor agents used to treat shock are also described, including norepinephrine, epinephrine, dopamine, and vasopressin. Septic shock is discussed as a type of distributive shock resulting from an infection and systemic inflammatory response.
Congestive heart failure occurs when the heart cannot pump enough blood to meet the body's needs. Symptoms result from blood backing up in the heart and lungs. The main drugs used to treat CHF are ACE inhibitors, ARBs, diuretics, beta-blockers, digoxin, and vasodilators. Digoxin works by inhibiting the sodium-potassium pump, raising intracellular calcium levels, increasing calcium release from the sarcoplasmic reticulum, and enhancing the actin-myosin interaction to strengthen contraction and cardiac output.
This document discusses drugs that affect blood coagulation. It begins by describing the normal process of blood coagulation and the intrinsic and extrinsic pathways. It then defines thromboembolic and hemorrhagic disorders. It discusses the actions of anticoagulants, antiplatelets, and thrombolytic drugs. Specific drug classes are then covered in more detail, including indications, mechanisms of action, pharmacokinetics, cautions and interactions. Nursing considerations are provided for various drug categories. The document contains questions to test the reader's understanding.
Shock is defined as a state of cellular hypoxia due to reduced oxygen delivery or utilization. It can be classified as initial/primary shock which is transient and benign, or true/secondary shock which involves a circulatory imbalance at the cellular level. Hinshaw and Cox classify shock into four categories: hypovolemic, cardiogenic, extracardiac obstructive, and distributive. All forms of shock involve reduced circulating blood volume, reduced oxygen supply to tissues leading to anoxia, and release of inflammatory mediators from cellular injury. Compensatory responses aim to maintain circulation and maximize cardiac function to redistribute perfusion to vital organs. Diagnosis involves monitoring physiology, while management focuses on treating the underlying cause, organ
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
The document discusses various agents used to treat coagulation disorders and bleeding risks. It outlines the blood coagulation mechanism and lists common risk factors for blood clots. It then describes different classes of drugs that work at different points in the coagulation cascade, including anticoagulants like heparin and warfarin that prevent clotting, fibrinolytics that break up existing clots, and antiplatelets that reduce platelet aggregation. It also discusses drugs used for bleeding disorders and important drug interactions.
Drugs acting on blood and blood forming organsUrmila Aswar
This document discusses drugs that act on blood and blood forming organs. It covers topics like hemostasis, coagulation factors, coagulation pathways, anticoagulants like heparin and warfarin, fibrinolytics, and antiplatelet drugs. Key points include that hemostasis is the process by which bleeding stops, coagulation involves intrinsic and extrinsic pathways, and anticoagulants prevent clotting through various mechanisms like inhibiting thrombin formation. Common anticoagulants discussed are heparin, low molecular weight heparins, warfarin, and fibrinolytics like streptokinase that lyse clots. Antiplatelet drugs like aspirin are also covered.
This document discusses coagulants and anticoagulants. It describes how coagulants promote coagulation and control bleeding, including systemic coagulants like vitamin K, tranexamic acid, and fibrinogen. Local coagulants called styptics are also discussed. Anticoagulants prevent coagulation and control conditions involving excessive clotting. Common anticoagulants described are heparin, low molecular weight heparin, warfarin and newer oral anticoagulants. Warfarin is a vitamin K antagonist that inhibits vitamin K-dependent clotting factors. Its mechanism of action and factors affecting dosing are summarized.
Individualized Webcam facilitated and e-Classroom USMLE Step 1 Tutorials with Dr. Cray. Starting at $50.00/hr., depending on pre-assessment. 1 BMS Unit is 4 hr. General Principles and some Organ System require multiple units to complete in preparation for the USMLE Step 1 A HIGH YIELD FOCUS IN Biochemistry / Cell Biology, Microbiology / Immunology and the 4 P’s-Phiso, Pathophys, Path and Pharm. Webcam Facilitated USMLE Step 2 Clinical Knowledge and Clinical Skills diadactic tutorials /1 Unit is 4 hours, individualized one-on-one and group sessions, Including all Internal Medicine sub-sub-specitialities. For questions or more information.. drcray@imhotepvirtualmedsch.com
Approach to a child with bleeding for UGsCSN Vittal
This document discusses hemostasis and bleeding disorders. It covers platelet disorders, coagulation factor deficiencies, and vascular disorders that can cause bleeding. Evaluation of bleeding disorders includes obtaining a medical history, physical examination, and laboratory tests like platelet count, bleeding time, prothrombin time, and factor assays. Specific disorders discussed include hemophilia A, hemophilia B, and von Willebrand disease. Treatment involves replacing the deficient clotting factor through blood component transfusion or recombinant factor replacement.
Vitamin K acts as a cofactor in the liver's synthesis of coagulation proteins, and a daily intake of 50-100 micrograms is usually sufficient. Coagulants like plasma fractions containing coagulation factors VIII and IX are used to treat deficiencies that cause bleeding disorders. Anticoagulants prevent thrombus formation and embolism by reducing fibrin formation; they include heparin and low molecular weight heparins, warfarin and related oral anticoagulants, and newer direct factor Xa and thrombin inhibitors. Monitoring of anticoagulant levels is important when they are used to treat conditions involving deep vein thrombosis, pulmonary embolism, myocardial infarction and others.
This document discusses drugs used for treating shock. It describes different types of shock including hypovolemic, septic, cardiogenic, and anaphylactic shock. It then discusses three categories of drugs used to treat shock: vasoconstrictors like epinephrine and norepinephrine which increase blood pressure, cardio tonic drugs like digoxin, dobutamine, and dopamine which increase heart function, and fluid replacement agents like blood, colloids, and crystalloids which replace lost fluids. Epinephrine causes vasoconstriction, increases heart rate and output, and dilates airways. Norepinephrine also causes vasoconstriction. Digoxin increases heart contraction force while
This document provides an overview of a lecture on drugs used to treat cardiovascular disorders. It discusses the function of the cardiovascular system and heart regulation, then outlines therapeutic strategies and drug classes for treating common conditions like hypertension, angina, heart failure, and arrhythmias. The goals are to reduce workload on the heart, improve blood flow, and restore normal heart rhythms.
This document provides an overview of shock, including its definition, types, etiology, pathogenesis, stages, and pathophysiological changes. It discusses the classification of shock into types such as hypovolemic, septic, traumatic, neurogenic, and distributive shock. For septic shock specifically, it covers the etiology as severe infection, pathophysiology involving the immune response and release of toxins, and key features including hypotension, tissue hypoperfusion, and high mortality rates. Treatment focuses on fluid resuscitation and source control for hypovolemic and septic shock.
Trauma-induced coagulopathy and hemorrhagic shock are leading causes of death in trauma patients. The document discusses the etiology and mechanisms of acute traumatic coagulopathy (ATC), which can occur independently of acidosis, hypothermia, or hemodilution. ATC appears to be mediated by dysregulation of the protein C system and thrombin diversion from coagulation to protein C activation under conditions of hypoperfusion. This leads to a hyperfibrinolytic state and impaired clot formation. Understanding ATC may help address one of the most preventable causes of death in trauma patients.
This document discusses various drugs that affect blood fluidity and the hemostatic system. It describes anticoagulants like heparin and warfarin that prevent blood clotting through different mechanisms. It also covers antiplatelet drugs like aspirin and clopidogrel that inhibit platelet aggregation. Thrombolytics like tissue plasminogen activator and streptokinase are discussed as agents that lyse blood clots. The causes and treatments of anemia are summarized, including iron deficiency and megaloblastic anemias related to vitamin B12 and folate deficiencies.
This document discusses hemostasis and mechanisms of coagulation, fibrinolysis, platelet function, and their regulation. It describes the roles of coagulation factors, fibrinolysis, endothelium, platelets, calcium, and vitamins in hemostasis. Direct and indirect acting agents that promote coagulation or inhibit fibrinolysis are discussed. Uses and side effects of heparin, warfarin, aspirin, streptokinase, and aprotinin are summarized.
This document discusses hemostatic agents used to treat thrombi (blood clots). It describes three main types of drugs: platelet aggregation inhibitors like aspirin that decrease new clot formation; anticoagulants like heparin and warfarin that interrupt the clotting cascade; and fibrinolytics like streptokinase that directly break up existing clots. Aspirin is used to treat possible heart attacks, while heparin and warfarin are used long-term in high-risk patients. Fibrinolytics must be given quickly, so paramedics can administer them pre-hospital. The document provides examples and mechanisms of action for several specific drugs in each category.
Pathogenesis and Medicolegal aspect of shock Soreingam Ragui
shock is one of the main cause of death very common encountered in day to day practice,in this presentation we look at how it happen,what are the causes and how we diagnose it in brief and its forensic importance
Slideshare biological actions of endothelium aj Anu Priya
The endothelium forms an interface between circulating blood and the vessel wall. It plays several important biological roles beyond just acting as a covering for blood vessels. Endothelial cells regulate vascular tone through the secretion of vasoactive substances like nitric oxide and endothelin. They also regulate coagulation, inflammation, cell growth, angiogenesis, and other processes. Dysfunction or damage of the endothelium is involved in the development of cardiovascular and other diseases.
shock is a Life threatening clinical syndrome of cardio-vascular collapse characterized by Hypotension and Hypoperfusion. If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.
The document provides an overview of congestive heart failure including its anatomy, physiology, definition, classification, pathophysiology, clinical manifestations, diagnostic evaluations, and management. It discusses the etiology and precipitating causes of heart failure. The management involves pharmacological treatments including diuretics, ACE inhibitors, beta blockers and other vasodilators. Nursing management focuses on monitoring fluid status, administering medications, assessing symptoms and providing patient education.
Drugs used in Congestive heart failure shoaib241087
This document provides an overview of drugs used to treat congestive heart failure (CHF). It begins with definitions and classifications of CHF, then describes diagnostic methods. The main treatment strategies and drugs are discussed, including inotropic drugs like digoxin, dobutamine, and dopamine. Renin-angiotensin system inhibitors like ACE inhibitors are also covered. The document provides details on mechanisms of action, pharmacokinetics, uses, interactions, and side effects of common CHF drugs.
This document discusses drugs that affect blood coagulation. It begins by describing the normal process of blood coagulation and the intrinsic and extrinsic pathways. It then defines thromboembolic and hemorrhagic disorders. It discusses the actions of anticoagulants, antiplatelets, and thrombolytic drugs. Specific drug classes are then covered in more detail, including indications, mechanisms of action, pharmacokinetics, cautions and interactions. Nursing considerations are provided for various drug categories. The document contains questions to test the reader's understanding.
Shock is defined as a state of cellular hypoxia due to reduced oxygen delivery or utilization. It can be classified as initial/primary shock which is transient and benign, or true/secondary shock which involves a circulatory imbalance at the cellular level. Hinshaw and Cox classify shock into four categories: hypovolemic, cardiogenic, extracardiac obstructive, and distributive. All forms of shock involve reduced circulating blood volume, reduced oxygen supply to tissues leading to anoxia, and release of inflammatory mediators from cellular injury. Compensatory responses aim to maintain circulation and maximize cardiac function to redistribute perfusion to vital organs. Diagnosis involves monitoring physiology, while management focuses on treating the underlying cause, organ
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
The document discusses various agents used to treat coagulation disorders and bleeding risks. It outlines the blood coagulation mechanism and lists common risk factors for blood clots. It then describes different classes of drugs that work at different points in the coagulation cascade, including anticoagulants like heparin and warfarin that prevent clotting, fibrinolytics that break up existing clots, and antiplatelets that reduce platelet aggregation. It also discusses drugs used for bleeding disorders and important drug interactions.
Drugs acting on blood and blood forming organsUrmila Aswar
This document discusses drugs that act on blood and blood forming organs. It covers topics like hemostasis, coagulation factors, coagulation pathways, anticoagulants like heparin and warfarin, fibrinolytics, and antiplatelet drugs. Key points include that hemostasis is the process by which bleeding stops, coagulation involves intrinsic and extrinsic pathways, and anticoagulants prevent clotting through various mechanisms like inhibiting thrombin formation. Common anticoagulants discussed are heparin, low molecular weight heparins, warfarin, and fibrinolytics like streptokinase that lyse clots. Antiplatelet drugs like aspirin are also covered.
This document discusses coagulants and anticoagulants. It describes how coagulants promote coagulation and control bleeding, including systemic coagulants like vitamin K, tranexamic acid, and fibrinogen. Local coagulants called styptics are also discussed. Anticoagulants prevent coagulation and control conditions involving excessive clotting. Common anticoagulants described are heparin, low molecular weight heparin, warfarin and newer oral anticoagulants. Warfarin is a vitamin K antagonist that inhibits vitamin K-dependent clotting factors. Its mechanism of action and factors affecting dosing are summarized.
Individualized Webcam facilitated and e-Classroom USMLE Step 1 Tutorials with Dr. Cray. Starting at $50.00/hr., depending on pre-assessment. 1 BMS Unit is 4 hr. General Principles and some Organ System require multiple units to complete in preparation for the USMLE Step 1 A HIGH YIELD FOCUS IN Biochemistry / Cell Biology, Microbiology / Immunology and the 4 P’s-Phiso, Pathophys, Path and Pharm. Webcam Facilitated USMLE Step 2 Clinical Knowledge and Clinical Skills diadactic tutorials /1 Unit is 4 hours, individualized one-on-one and group sessions, Including all Internal Medicine sub-sub-specitialities. For questions or more information.. drcray@imhotepvirtualmedsch.com
Approach to a child with bleeding for UGsCSN Vittal
This document discusses hemostasis and bleeding disorders. It covers platelet disorders, coagulation factor deficiencies, and vascular disorders that can cause bleeding. Evaluation of bleeding disorders includes obtaining a medical history, physical examination, and laboratory tests like platelet count, bleeding time, prothrombin time, and factor assays. Specific disorders discussed include hemophilia A, hemophilia B, and von Willebrand disease. Treatment involves replacing the deficient clotting factor through blood component transfusion or recombinant factor replacement.
Vitamin K acts as a cofactor in the liver's synthesis of coagulation proteins, and a daily intake of 50-100 micrograms is usually sufficient. Coagulants like plasma fractions containing coagulation factors VIII and IX are used to treat deficiencies that cause bleeding disorders. Anticoagulants prevent thrombus formation and embolism by reducing fibrin formation; they include heparin and low molecular weight heparins, warfarin and related oral anticoagulants, and newer direct factor Xa and thrombin inhibitors. Monitoring of anticoagulant levels is important when they are used to treat conditions involving deep vein thrombosis, pulmonary embolism, myocardial infarction and others.
This document discusses drugs used for treating shock. It describes different types of shock including hypovolemic, septic, cardiogenic, and anaphylactic shock. It then discusses three categories of drugs used to treat shock: vasoconstrictors like epinephrine and norepinephrine which increase blood pressure, cardio tonic drugs like digoxin, dobutamine, and dopamine which increase heart function, and fluid replacement agents like blood, colloids, and crystalloids which replace lost fluids. Epinephrine causes vasoconstriction, increases heart rate and output, and dilates airways. Norepinephrine also causes vasoconstriction. Digoxin increases heart contraction force while
This document provides an overview of a lecture on drugs used to treat cardiovascular disorders. It discusses the function of the cardiovascular system and heart regulation, then outlines therapeutic strategies and drug classes for treating common conditions like hypertension, angina, heart failure, and arrhythmias. The goals are to reduce workload on the heart, improve blood flow, and restore normal heart rhythms.
This document provides an overview of shock, including its definition, types, etiology, pathogenesis, stages, and pathophysiological changes. It discusses the classification of shock into types such as hypovolemic, septic, traumatic, neurogenic, and distributive shock. For septic shock specifically, it covers the etiology as severe infection, pathophysiology involving the immune response and release of toxins, and key features including hypotension, tissue hypoperfusion, and high mortality rates. Treatment focuses on fluid resuscitation and source control for hypovolemic and septic shock.
Trauma-induced coagulopathy and hemorrhagic shock are leading causes of death in trauma patients. The document discusses the etiology and mechanisms of acute traumatic coagulopathy (ATC), which can occur independently of acidosis, hypothermia, or hemodilution. ATC appears to be mediated by dysregulation of the protein C system and thrombin diversion from coagulation to protein C activation under conditions of hypoperfusion. This leads to a hyperfibrinolytic state and impaired clot formation. Understanding ATC may help address one of the most preventable causes of death in trauma patients.
This document discusses various drugs that affect blood fluidity and the hemostatic system. It describes anticoagulants like heparin and warfarin that prevent blood clotting through different mechanisms. It also covers antiplatelet drugs like aspirin and clopidogrel that inhibit platelet aggregation. Thrombolytics like tissue plasminogen activator and streptokinase are discussed as agents that lyse blood clots. The causes and treatments of anemia are summarized, including iron deficiency and megaloblastic anemias related to vitamin B12 and folate deficiencies.
This document discusses hemostasis and mechanisms of coagulation, fibrinolysis, platelet function, and their regulation. It describes the roles of coagulation factors, fibrinolysis, endothelium, platelets, calcium, and vitamins in hemostasis. Direct and indirect acting agents that promote coagulation or inhibit fibrinolysis are discussed. Uses and side effects of heparin, warfarin, aspirin, streptokinase, and aprotinin are summarized.
This document discusses hemostatic agents used to treat thrombi (blood clots). It describes three main types of drugs: platelet aggregation inhibitors like aspirin that decrease new clot formation; anticoagulants like heparin and warfarin that interrupt the clotting cascade; and fibrinolytics like streptokinase that directly break up existing clots. Aspirin is used to treat possible heart attacks, while heparin and warfarin are used long-term in high-risk patients. Fibrinolytics must be given quickly, so paramedics can administer them pre-hospital. The document provides examples and mechanisms of action for several specific drugs in each category.
Pathogenesis and Medicolegal aspect of shock Soreingam Ragui
shock is one of the main cause of death very common encountered in day to day practice,in this presentation we look at how it happen,what are the causes and how we diagnose it in brief and its forensic importance
Slideshare biological actions of endothelium aj Anu Priya
The endothelium forms an interface between circulating blood and the vessel wall. It plays several important biological roles beyond just acting as a covering for blood vessels. Endothelial cells regulate vascular tone through the secretion of vasoactive substances like nitric oxide and endothelin. They also regulate coagulation, inflammation, cell growth, angiogenesis, and other processes. Dysfunction or damage of the endothelium is involved in the development of cardiovascular and other diseases.
shock is a Life threatening clinical syndrome of cardio-vascular collapse characterized by Hypotension and Hypoperfusion. If uncompensated, these mechanisms may lead to impaired cellular metabolism and death.
The document provides an overview of congestive heart failure including its anatomy, physiology, definition, classification, pathophysiology, clinical manifestations, diagnostic evaluations, and management. It discusses the etiology and precipitating causes of heart failure. The management involves pharmacological treatments including diuretics, ACE inhibitors, beta blockers and other vasodilators. Nursing management focuses on monitoring fluid status, administering medications, assessing symptoms and providing patient education.
Drugs used in Congestive heart failure shoaib241087
This document provides an overview of drugs used to treat congestive heart failure (CHF). It begins with definitions and classifications of CHF, then describes diagnostic methods. The main treatment strategies and drugs are discussed, including inotropic drugs like digoxin, dobutamine, and dopamine. Renin-angiotensin system inhibitors like ACE inhibitors are also covered. The document provides details on mechanisms of action, pharmacokinetics, uses, interactions, and side effects of common CHF drugs.
This document provides an outline on heart failure, covering definitions, etiology, pathophysiology, clinical manifestations, complications, diagnosis, and management. Heart failure is defined as a condition where the heart cannot pump enough blood to meet the body's needs. The most common causes are high blood pressure and structural heart issues. The pathophysiology involves compensatory mechanisms like activation of the sympathetic nervous system and renin-angiotensin-aldosterone system. Clinical manifestations include dyspnea, edema, fatigue, and liver enlargement. Management involves drug therapy like diuretics and ACE inhibitors, as well as lifestyle changes like sodium and fluid restriction.
Heart failure is a complex progressive disorder where the heart is unable to pump sufficient blood to meet the body's metabolic requirements. The main causes include impaired ability of the ventricles to fill and eject blood, abnormal increases in blood volume, and diseases affecting the heart such as coronary artery disease, hypertension, and valvular issues. Treatment strategies aim to increase cardiac output, reduce preload and afterload, and increase contractility through various drug classes including diuretics, ACE inhibitors, beta-blockers, and vasodilators.
This presentation is very important for pharmacy students and medication and the kids are not as good as you can do with a bit of snow here and growing physically and mentally drained from and working wonders awaiting results from work tomorrow morning to make sure you can get the money back to you can tell me what you want me when you can get it for pharmacy students and medication and a HS for pharmacy students and medication for pharmacy students and medication for pharmacy students This presentation is very important for pharmacy students and medication and the kids are not as good as you can do with a bit of snow here and growing physically and mentally drained from and working wonders awaiting results from work tomorrow morning to make sure you can get the money back to you can tell me what you want me when you can get it for pharmacy students and medication and a HS for pharmacy students and medication for pharmacy students and medication for pharmacy students This presentation is very important for pharmacy students and medication and the kids are not as good as you can do with a bit of snow here and growing physically and mentally drained from and working wonders awaiting results from work tomorrow morning to make sure you can get the money back to you can tell me what you want me when you can get it for pharmacy students and medication and a HS for pharmacy students and medication for pharmacy students and medication for pharmacy students This presentation is very important for pharmacy students and medication and the kids are not as good as you can do with a bit of snow here and growing physically and mentally drained from and working wonders awaiting results from work tomorrow morning to make sure you can get the money back to you can tell me what you want me when you can get it for pharmacy students and medication and a HS for pharmacy students and medication for pharmacy students and medication for pharmacy students This presentation is very important for pharmacy students and medication and the kids are not as good as you can do with a bit of snow here and growing physically and mentally drained from and working wonders awaiting results from work tomorrow morning to make sure you can get the money back to you can tell me what you want me when you can get it for pharmacy students and medication and a HS for pharmacy students and medication for pharmacy students and medication for pharmacy students This presentation is very important for pharmacy students and medication and the kids are not as good as you can do with a bit of snow here and growing physically and mentally drained from and working wonders awaiting results from work tomorrow morning to make sure you can get the money back to you can tell me what you want me when you can get it for pharmacy students and medication and a HS for pharmacy students and medication for pharmacy students and medication for pharmacy students This presentation is very important for pharmacy stude
The document discusses the biological basis of cardiac repair after myocardial infarction. It notes that massive cardiomyocyte loss due to infarction overwhelms the heart's limited regenerative capacity, resulting in scar formation. Necrotic cells trigger an intense inflammatory response through danger signals and toll-like receptor signaling that recruits leukocytes. As inflammation subsides, fibroblasts proliferate and deposit collagen, maintaining ventricular integrity. Dysregulated inflammation, impaired resolution, or excessive fibrosis can cause adverse remodeling and heart failure. Modulating the inflammatory and reparative response may prevent post-infarction heart failure.
Cardiotoxicity refers to heart damage caused by certain chemotherapy drugs, heavy metals, and other toxins. Three main mechanisms of cardiotoxicity are discussed: interfering with aerobic metabolism in the heart, altering myocardial conduction, and directly damaging heart muscle cells. Symptoms of cardiotoxicity include fatigue, shortness of breath, and swelling. Diagnosis involves physical exams, imaging tests like echocardiograms and MUGA scans, and blood tests. Prevention strategies center around modifying drug treatment plans, using protective medications like dexrazoxane, and controlling risk factors after treatment through medications like ACE inhibitors and beta-blockers.
Myocardial infarction, also known as a heart attack, results from prolonged lack of oxygen supply to heart muscle, causing cell death. It is usually caused by a blockage of a coronary artery from an atherosclerotic plaque rupture. Symptoms include chest pain and shortness of breath. Diagnosis involves evaluating symptoms, electrocardiogram changes, and cardiac enzyme levels. Treatment focuses on restoring blood flow, reducing workload and complications through medications like antiplatelets, anticoagulants, beta blockers, and ACE inhibitors.
Congestive heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It can be caused by conditions present at birth like hypoplastic left heart syndrome. Symptoms include poor weight gain, fast breathing, and edema. Diagnosis involves chest x-ray, electrocardiogram, echocardiogram, and sometimes cardiac catheterization. Treatment focuses on underlying causes, medications to control symptoms like diuretics and digoxin, and surgery when possible to correct structural heart defects.
Heart failure occurs when the heart is unable to pump enough blood to meet the body's needs. It has a high mortality rate. The most common cause is coronary artery disease. When the heart does not contract well, blood backs up in the lungs and periphery. Chronic activation of compensatory mechanisms like the sympathetic nervous system contributes to cardiac remodeling over time.
Right heart failure causes issues like leg swelling and liver enlargement due to blood backing up. Left heart failure can cause pulmonary edema. Treatment focuses on reducing symptoms, slowing disease progression, and improving survival through drugs that target the renin-angiotensin-aldosterone system, beta-blockers, diuretics, and vasodilators. Dentists
This document provides an overview of the pharmacological management of congestive heart failure. It discusses the pathophysiology of heart failure and compensatory mechanisms. It describes the renin-angiotensin-aldosterone system and its role in heart failure. The document outlines the classification, causes, signs and symptoms, and diagnostic criteria of heart failure. It discusses the goals and types of drugs used to treat heart failure, including vasodilators, diuretics, beta blockers, and angiotensin-modulating agents like ACE inhibitors. The document provides details on commonly used ACE inhibitors and their mechanisms and effects in treating heart failure.
This document provides an overview of the pharmacological management of congestive heart failure. It discusses the pathophysiology of heart failure and compensatory mechanisms. It describes the renin-angiotensin-aldosterone system and its role in heart failure. The document outlines the classification, causes, signs and symptoms, and diagnostic criteria of heart failure. It discusses the goals and types of drugs used to treat heart failure, including vasodilators, diuretics, beta blockers, and angiotensin-modulating agents like ACE inhibitors. The document provides details on commonly used ACE inhibitors and their mechanisms and effects in treating heart failure.
1. Calcium channel blockers decrease cardiac contractility and workload, relaxing smooth muscle and dilating coronary and peripheral vessels. They are used for angina, dysrhythmias, and hypertension.
2. Positive inotropic medications stimulate myocardial contractility, improving cardiac function and output. They are used short-term for advanced heart failure.
3. Both calcium channel blockers and positive inotropic drugs work by regulating calcium levels in cardiac and smooth muscle cells, with calcium channel blockers inhibiting calcium influx and positive inotropics increasing it.
Cardiogenic shock is a condition of diminished cardiac output that severely impairs cardiac perfusion. In this condition in which the heart suddenly can't pump enough blood to meet the body's needs.
Drugs used for the treatment of myocardial ischemiask-yasmeen
This document provides information on drugs used for the treatment of myocardial ischemia. It discusses the types of myocardial ischemia including stable, unstable, and variant angina. It then describes the heart and coronary arteries and risk factors for myocardial ischemia. The main drug classes used for treatment are discussed in detail, including nitrates, calcium channel blockers, beta blockers, potassium channel activators, antiplatelet drugs, ACE inhibitors, and cholesterol lowering medications. Adverse effects, pharmacokinetics and contraindications are summarized for each drug class. Additional treatments beyond medications are also mentioned.
This document provides information on angina pectoris (chest pain), including its types, causes, symptoms, pathogenesis, and treatment options. It discusses the classification and mechanisms of action of various antianginal drug classes - nitrates, beta-blockers, calcium channel blockers, potassium channel activators, and others. Adverse effects and uses are described for representative drugs in each class. The classifications covered are nitrate compounds, beta-blockers, calcium channel blockers, potassium channel activators, and miscellaneous drugs including antiplatelet and cytoprotective agents.
Congestive cardiac failure irene new slideIrene Vadakkan
Congestive cardiac failure is a condition where the heart is unable to pump enough blood to meet the body's needs. It can result from any cardiac disorder that impairs the ventricle's ability to deliver adequate blood flow. The main types are low-output and high-output cardiac failure. Treatment involves managing symptoms, reducing fluid volume, and correcting underlying causes. Pharmacological therapies aim to relieve symptoms, improve pump function, and include diuretics, ACE inhibitors, beta-blockers, and other vasodilators. Lifestyle modifications like diet, exercise, and smoking cessation also play an important role in congestive cardiac failure management.
Ischemic heart disease (IHD) is caused by an inadequate blood supply to the heart muscle due to narrowed coronary arteries. The most common cause is atherosclerosis which develops over many years and is worsened by risk factors like smoking, high cholesterol, and hypertension. Symptoms include chest pain and shortness of breath during physical exertion. Diagnosis involves tests like electrocardiograms, stress tests, and cardiac catheterization. Treatment aims to improve symptoms, prevent heart attacks, and includes risk factor modification, medications like nitrates, beta blockers, and calcium channel blockers, and revascularization procedures like angioplasty and bypass surgery.
This document discusses the classification and mechanisms of action of various classes of antihypertensive drugs used to treat hypertension. It describes beta blockers, diuretics, ACE inhibitors, angiotensin II receptor blockers, and calcium channel blockers. For each class, it provides details on their mechanisms of action in lowering blood pressure, medical uses for treating conditions like heart failure and hypertension, and potential side effects. The document aims to explain the pharmacology of antihypertensive drugs and help understand their different classifications and mechanisms of action.
The file gives the information of Cardiac Failure. Etiology of cardiac failure, types, stages of cardiac failure. It also covers the multisystem effects of cardiac failure, classification of drugs acting on cardiac failure.
Similar to Congestive heart failure a path from conventional to aadvance therapy (20)
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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
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2. CONGESTIVE HEART FAILURE:
A PATH FROM
CONVENTIONAL TO ADVANCE THERAPY
PRESENTED BY
MOMIN ALTAMASH
M PHARM 1 ST YEAR
(PHARMACOLOGY)
ROLL NO. 22
GUIDED BY
http://www.freewebs.com
MR VINOD GUPTA
2
3. Table of Contents :
1.
INTRODUCTION
2.
PATHOPHYSIOLOGY
3.
PHARMACOLOGICAL TREATMENT OF CONGESTIVE HEART FAILURE
4.
NEWER DRUGS UNDER RESEARCH
5.
ADVANCES IN THE TREATMENT
6.
NON PHARMACOLOGICAL TREATMENT
7.
CONCLUSION
8.
REFRENCES
3
4. 1 ) Introduction :
CONGESTIVE HEART FAILURE
Factors that may produce congestive heart failure
Obstruction
Inflammation
Malnutrition
Insufficiency
Oxygen lack
Anaemia
Raised pressure
Toxins
Hyperthyroidism
4
6. 2) Pathophysiology of Congestive Heart Failure :
• Congestive heart failure is the pathophysiologic state in which –
• the heart is unable to pump blood at a rate commensurate with the requirements
of metabolizing tissues, or can do so only from an elevated filling pressure
(Braunwald and Bristow, 2000).
• Heart failure is a complex of symptoms –
• That is fatigue, shortness of breath, and congestion that are related to the
inadequate perfusion of tissue during exertion and often to the retention of fluid.
Its primary cause is an impairment of the heart's ability to fill or empty the left
ventricle properly (Cohn, 1996).
6
8. Preload is a passive stretching force exerted on the
ventricular muscle at the end of diastole. Preload is caused
by the volume of blood in the ventricle at the end of
diastole.
Afterload is the force resisting the contraction of the
cardiac muscle fibers. Afterload can also be considered
as the blood pressure exerted on the Atrial Valve during
diastole
John Burton,
MD- Albany
Medical CenterAlbany, New
York
Contractility refers to the ability of cardiac muscle fibers to
shorten when stimulated (strength
8
10. • Compensatory mechanisms may restore CO to near-normal.
• But, if excessive the compensatory mechanisms can worsen heart failure because . . .
• Vasoconstriction: ↑’s the resistance against which heart has to pump (i.e., ↑’s
afterload), and may therefore ↓ CO
• Na and water retention: ↑’s fluid volume, which ↑’s preload. If too much “stretch” ↓
strength of contraction and ↓’s CO
• Excessive tachycardia → ↓’d diastolic filling time → ↓’d ventricular filling → ↓’d SV
and CO
10
11. 3) PHARMACOLOGICAL TREATMENT
CONGESTIVE OF HEART FAILURE :
Drug Classes
Used To Treat
CHF :
Cardiac
Glycosides
β blockers
(ACE Inhibitors)
and AT1 Receptor
Antagonists
Diuretics
Vasodilators
Aldosterone
Antagonists
11
12. 3.1] The Cardiac Glycosides (Cardenolides):
•
Drug Members :
i.
Digitoxin (Crystodigin)
ii. Digoxin (Lanoxin)
iii. Deslanoside (Cedilanid-D)
•
Mechanisms of Action :
http://cvpharmacology.com
12
13. • The net effect of the glycosides on the heart is as follows :
a. heart rate is slowed
b. contraction is greater due to increased filling volumes
c. ejection fraction is improved
d. increased ejection velocity
• Adverse Side Effects Of The Glycosides :
Fatigue, delirium, anorexia, headaches, hallucinations.
13
14. 3.2] Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors) and
AT1 Receptor Antagonists:
•
Drug Members:
• Captopril (Capoten)
• Enalapril (Vasotec)
• Lisinopril (Prinivil)
Mechanism:
•
AT1 receptor antagonists should
at present be viewed as the preferred
alternative when ACE inhibitors cannot be tolerated
http://www.uspharmacist.com
•
Adverse Side Effects : GI distress, dizziness, skin rashes, hypotension
14
15. 3.3) BETA-BLOCKERS:
http://www.cardiachealth.org
Beta-blockers may work by slowing the heart rate, which allows the left
ventricle (the main pumping chamber of the heart) to fill more completely.
some of these medicines may also help open or widen blood vessels in the
body. this makes them especially useful in some people with certain forms of
heart failure who may also have high blood pressure
15
19. 4) NEWER DRUGS UNDER RESEARCH
•
4.1) Coenzyme Q10 :
•
occurs naturally in the body and is essential to survival.
• Acts as an electron carrier in the mitochondria,
http://www.netrition.com
• CoQ10 levels are decreased in the heart muscle of patients with heart failure,
• Double blind controlled trials have shown that CoQ10 improves symptoms,
functional capacity and quality of life in patients with heart failure with no side
effects
• "Other heart failure medications block rather than enhance cellular processes and
may have side effects.
• Supplementation with CoQ10, which is a natural and safe
19
20. • It corrects a deficiency in the body and blocks the vicious metabolic cycle
in chronic heart failure called the energy starved heart.“
•
sources-Q10 is present in food, including red meat, plants and fish, but
levels are insufficient to impact on heart failure.
• CoQ10 is also sold over the counter as a food supplement.
•
Coenzyme Q10 decreases all cause mortality by half.
•
It is the first drug to improve heart failure mortality in over a decade and
can be added to standard treatment .
http://www.vitacost.com
20
21. •4.2) Bromodomain and extraterminal domain (BET) protein inhibitors :
Current therapies are not adequately effective at improving health and preventing
deaths.
Bromodomain and extraterminal domain (BET) proteins activates genes that
contribute to heart failure.
Heart failure may be triggered by the activation of a large set of genes that cause
the walls of the heart to thicken and develop scar tissue, impairing the organ's
ability to pump blood normally.
21
22. BET proteins can have a huge impact on gene activity because they belong to a
class of molecules called epigenetic readers, which recognize special marks on
DNAprotein complexes and attract gene-activating proteins to those spots.
BET inhibitor called JQ1 shows promise in treating heart failure. JQ1 protect
against heart-wall thickening, the formation of scar tissue, and pump failure
22
24. 5.1) Stem cell therapy.
• Stem cells - These are undifferentiated cells that can differentiate into
specialized cell types. stem cells come from 3 main sources:
i.
Embryonic stem cells,
ii. Adult tissue (adult stem cells).
iii. Endometrial stem cells.
24
25. CLASSIFICATION
1
Adult stem cells
2
Embryionic stem cells
3
Endometrial stem cells
Exist throughout the body after
embryonic development. found in tissues
such as the brain, bone marrow, blood,
blood vessels, skeletal muscles, skin, and
the liver.
Derived from a four- or five-day-old human
embryo that is in the blastocyst phase of
development. in IVF (in vitro fertilization)
clinics there are extra embryos. only one is
implanted into a woman from several eggs
fertilized in a test tube.
It involves extraction of a small amount of
menstrual blood from young healthy donors
that is called as endometrial stem cells.
25
27. • Possible mechanisms of recovery include:
• Generation of heart muscle cells,
• Stimulation of growth of new blood vessels to repopulate damaged heart
tissue,
• Secretion of growth factors,
• Assistance via some other mechanism,
27
28. • PROCEDURE OF STEM CELL THERAPY
1.
COLLECTION
2. PROCESSING AND
CRYOPRESRVATION
3. INFUSION
4. ENGRAFMENT
AND RECOVERY
28
29. 5.2) GENE THERAPY :
• Gene therapy is the use of DNA as a pharmaceutical agent to
treat disease. Gene therapy is a technique that uses genes to treat
or prevent disease.
• Researchers are testing several approaches to gene therapy,
including:
• Replacing a mutated gene that causes disease with a healthy
copy of the gene.
• Inactivating, or “knocking out,” a mutated gene that is
functioning improperly.
• Introducing a new gene into the body to help fight a disease .
29
31. • SARCOENDOPLASMIC RETICULUM (SER):
• Sarcoplasmic reticulum activated by Ca2+ leads to contraction.
• In heart failure, decrease expression of Ca2+ causes impairment of SER.
• widely used viruses for gene delivery to heart are recombinant AAVs (adeno
associated virus).They are relatively sective for cardiac myocites
• There is high diastolic and low systolic Ca2+ levels when SER is impaired.
Studies has shown that by increasing SER Ca2+ expression by viral transduction
of SER Ca2+ transgene, heart failure can be treated .
31
32. • OTHER TARGETS
a) PHOSPHOLAMBAN:
•
It is a protein that regulates the calcium pump in cardiac muscle.
•
This protein is a potent inhibitor of sarcoplasmic reticulum ca 2+ ATPase in
unphosphorylated state, but inhibition is relieved upon phosphorylation.
•
Inhibitory phospholamban, antisense and psuedophosphorylated state mutant is
used in heart failure by viral delivery.
32
33. b) ADENYLYL
CYCLASE 6
protein kinase a
phosphorylates
phospholamban
and SERCA2A
activity is
enhanced.
FIG: ROLE OF ADENYLYL CYCLASE (AC6) IN HEART
CONTRACTION
http:/www.sciencedirect.com
Symptoms of
heart failure is
alleviated by viral
delivery of AC6
transgene as result
of SERCA2a
function.
33
34. c) PROTEIN PHOSPHATASE 1
•
It is involved in the regulation of a variety of cellular processes,.
• Increased PP1 activity has been observed in the end stage of heart
failure
• SR ca2+ upake is suppressed by the (ppi) because it
dephosphorylates the phospholamban.
•
Pp1 is reduced using (sh)RNA and has showed improved cardiac
function and reduced interstitial fibrosis in mouse model of heart
failure.
34
35. d) SMALL UBIQUITINE LIKE MODIFIER (SUMO 1 ) :
• SUMO 1 is a key component in cardiac function .
• The interaction between SUMO 1 and SERCA2A is crucial for
regulating calcium levels inside cardiac myocytes.
• Reduction in SUMO 1 protein reduces SERCa2+, and thus
efficient calcium handling in patients with failing hearts .
• Introduction of SUMO 1 through gene therapy is associated with
improved activity of SERCA2A, which resulted in improved
cardiac function through an augmentation of cardiac contractility.
35
37. • GENE DELIVERY METHODS ;
A) Transvascular
intracoronary antegrade and retrograde delivery :
B) Direct intramyocardial delivery :
http://www.sciencedirect.com
37
38. 6) Device therapy :
• Damage to the heart muscle can cause changes in the
electrical system of the heart.
• There are three different types of devices that can be
used in the treatment of heart failure to correct an
abnormal heartbeat.
38
39. I. Pacemakers :
• The traditional pacemaker has two parts: lead wires
and a pulse generator, which houses a battery and a
tiny computer.
• The lead wires sense the heart's electrical activity, and
when the computer determines that the heart rhythm is
off, it responds by sending electrical impulses to the
heart muscle to correct its rate.
• Pacemakers are usually used to treat heart rhythms that
are too slow. But they can also be used to treat fast
rhythms or to increase the heart rate in response to
changes in the patient's activity level
39
41. 3) Internal cardioverter defibrillator (ICD):
ICD senses electrical activity and sends a shock to the heart if it
detects a dangerous heart rhythm implantable cardiac
defibrillators reduce the risk of death from sudden cardiac arrest
by 23 percent in patients with heart failure
41
42. • Continuous positive airway pressure(CPAP):
• To improve the prognosis of CHF, additional novel approaches to its
therapy are required. One promising approach is the use of
continuous positive airway pressure (CPAP ).
• When applied via a nasal mask, CPAP provides a noninvasive
mechanical assist to the failing heart by increasing intrathoracic
pressure and augmenting stroke volume and cardiac output,CPAP
improves the mechanical efficiency of the failing heart possibly
through reverse ventricular remodeling.
42
43. 7)
Conclusion
Heart failure is a major health issue with a high rate of
morbidity and mortality
Thus, there is a substantial need for new strategies to
prevent the progression of heart failure.
Until now, heart
failure was seen as an incurable disease.
However, gene
therapy approach have offered the promise of an effective
therapy for reversing systolic heart failure
Great advances in understanding the pathobiology
of HF and their application to further improvements of patient care are withun reach
43
44. Time will tell whether a single target
approach is sufficient to restore heart function and prevent
deterioration or whether multiple gene targets are needed
along with stem cell therapy to eventually replace the
injured myocardium.
Using a viral-delivery gene therapy
approach to treat heart failure by enhancing contractility is
not yet a reality, but substantial progress in that direction
has been made in the last few years.
Great advances in understanding the pathobiology
of HF and their application to further improvements of patient care are
within reach
44
45. •
Refrences
•
1. Beltrami, A.P., Urbanek, K., Kajstura, J., Yan, S.M., Finato, N., Bussani, R., Nadal-Ginard, B., Silvestri, F.,
Leri, A.,
Beltrami, C.A., and Anversa, P. (2001). Evidence that human cardiac myocytes divide after myocardial infarction.
N. Engl. J. Med. 344, 1750–1757.
•
2 . Itskovitz-Eldor, J., Schuldiner, M., Karsenti, D., Eden, A., Yanuka, O., Amit, M., Soreq, H., and Benvenisty, N.
(2000).
Differentiation of human embryonic stem cells into embryoid bodies comprising the three embryonic germ layers.
Mol. Med.
6, 88–95.
•
3. Jackson, K.A., Majka, S.M., Wang, H., Pocius, J., Hartley, C.J., Majesky, M.W., Entman, M.L., Michael, L.H.,
Hirschi, K.K.,
and Goodell, M.A. (2001). Regeneration of ischemic cardiac muscle and vascular endothelium by adult stem cells.
J. Clin.
Invest. 107, 1–8.
•
4. Kehat, I., Kenyagin-Karsenti, D., Druckmann, M., Segev, H., Amit, M., Gepstein, A., Livne, E., Binah, O.,
Itskovitz-Eldor,
J., and Gepstein, L. (2001). Human embryonic stem cells can differentiate into myocytes portraying
cardiomyocytic
structural and functional properties. J. Clin. Invest. (in press)
•
5. Kessler, P.D. and Byrne, B.J. (1999). Myoblast cell grafting into heart muscle: cellular biology and potential
applications.
Annu. Rev. Physiol. 61, 219–242.
45