Study Material
Myocardial infarction (MI), commonly known as a heart attack. MI is a blockage of blood flow to the heart muscle. Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease.
Myocardial infarction, also known as a heart attack, is caused by reduced blood flow to the heart muscle due to blockage of the coronary arteries, usually by atherosclerosis or a blood clot. It causes irreversible damage to heart tissue. Risk factors include age, sex, family history, smoking, hypertension, obesity, diabetes, and high cholesterol. Symptoms include chest pain and tightness, pain in the arms or back, and shortness of breath. Diagnosis involves electrocardiograms, blood tests of cardiac biomarkers, and echocardiograms. Treatment focuses on restoring blood flow, preventing clots, and managing complications like arrhythmias or heart failure.
This document defines myocardial infarction and describes its types, causes, symptoms, complications, diagnostic tests, and treatment options. Myocardial infarction is the death of heart muscle caused by a blockage in one of the coronary arteries that reduces blood flow. It can be anterior, posterior, or other regions. Risk factors include smoking, hypertension, age, and diabetes. Symptoms include chest pain and shortness of breath. Complications include heart failure, arrhythmias, and cardiac rupture. Diagnosis involves electrocardiograms, blood tests of cardiac enzymes, and imaging tests. Treatment includes medications like aspirin, beta-blockers, and statins as well as surgical procedures like coronary artery bypass grafting and angioplasty
ISCHEMIA HEART DISEASE AND MYOCARDIAL INFARETIONfikri asyura
This document discusses ischemic heart disease and myocardial infarction. It covers the pathophysiology of coronary ischemia, including how myocardial oxygen demand and supply are determined. When demand exceeds supply, ischemia occurs. The document details the physiology of coronary blood flow, autoregulation, and flow reserve. It then covers the clinical syndromes of stable angina, unstable angina, and acute myocardial infarction. Key concepts include the progression of atherosclerotic plaque, the vulnerable plaque that can rupture in acute coronary syndromes, and the treatment approaches for stable and unstable ischemia.
This document provides information about myocardial infarction (MI) or heart attack. It defines MI as death of heart muscle cells due to lack of oxygen, usually caused by a blockage in the coronary arteries. It lists risk factors for MI such as smoking, diabetes, hypertension, and family history. It describes the signs and symptoms of MI, diagnostic tests including ECG and cardiac enzymes, types of MI, and treatments including thrombolytics, angioplasty, medications, and lifestyle changes to prevent future heart attacks. The nursing management of MI focuses on reducing pain, improving perfusion, preventing complications, health education, and calling for help if symptoms worsen.
Myocardial infarction, also known as a heart attack, results from a critical imbalance between oxygen supply and demand in the heart muscle. The primary cause is coronary artery occlusion due to atherosclerosis, vasospasm, or embolism. Symptoms may include chest pain, dyspnea, sweating, and anxiety. Diagnosis is made based on elevated cardiac enzyme levels and ECG changes. Initial treatment focuses on pain relief, oxygen, fluids, and aspirin while long-term prevention includes medications like beta-blockers, ACE inhibitors, antiplatelets, and statins to reduce risk of future heart attacks and heart failure.
This document provides an overview of cardiac failure/congestive heart failure. It begins with an introduction and objectives. It then reviews heart anatomy and physiology, including the structure of the heart, conducting system, heart sounds, and ECG. It defines cardiac failure and discusses epidemiology, causes, pathophysiology, clinical manifestations, classifications, diagnostic process, medical management, and complications. Nursing management is also addressed using the nursing process approach.
The document provides guidelines for the diagnosis and management of chronic stable angina, defining it as chest discomfort caused by myocardial ischemia that is typically triggered by exertion or stress. It discusses the pathophysiology, risk factors, diagnostic testing options including ECG, stress testing, and imaging, and recommendations for invasive coronary angiography. The guidelines are intended to help clinicians properly evaluate and treat patients experiencing chronic stable angina.
Myocardial infarction, also known as a heart attack, is caused by reduced blood flow to the heart muscle due to blockage of the coronary arteries, usually by atherosclerosis or a blood clot. It causes irreversible damage to heart tissue. Risk factors include age, sex, family history, smoking, hypertension, obesity, diabetes, and high cholesterol. Symptoms include chest pain and tightness, pain in the arms or back, and shortness of breath. Diagnosis involves electrocardiograms, blood tests of cardiac biomarkers, and echocardiograms. Treatment focuses on restoring blood flow, preventing clots, and managing complications like arrhythmias or heart failure.
This document defines myocardial infarction and describes its types, causes, symptoms, complications, diagnostic tests, and treatment options. Myocardial infarction is the death of heart muscle caused by a blockage in one of the coronary arteries that reduces blood flow. It can be anterior, posterior, or other regions. Risk factors include smoking, hypertension, age, and diabetes. Symptoms include chest pain and shortness of breath. Complications include heart failure, arrhythmias, and cardiac rupture. Diagnosis involves electrocardiograms, blood tests of cardiac enzymes, and imaging tests. Treatment includes medications like aspirin, beta-blockers, and statins as well as surgical procedures like coronary artery bypass grafting and angioplasty
ISCHEMIA HEART DISEASE AND MYOCARDIAL INFARETIONfikri asyura
This document discusses ischemic heart disease and myocardial infarction. It covers the pathophysiology of coronary ischemia, including how myocardial oxygen demand and supply are determined. When demand exceeds supply, ischemia occurs. The document details the physiology of coronary blood flow, autoregulation, and flow reserve. It then covers the clinical syndromes of stable angina, unstable angina, and acute myocardial infarction. Key concepts include the progression of atherosclerotic plaque, the vulnerable plaque that can rupture in acute coronary syndromes, and the treatment approaches for stable and unstable ischemia.
This document provides information about myocardial infarction (MI) or heart attack. It defines MI as death of heart muscle cells due to lack of oxygen, usually caused by a blockage in the coronary arteries. It lists risk factors for MI such as smoking, diabetes, hypertension, and family history. It describes the signs and symptoms of MI, diagnostic tests including ECG and cardiac enzymes, types of MI, and treatments including thrombolytics, angioplasty, medications, and lifestyle changes to prevent future heart attacks. The nursing management of MI focuses on reducing pain, improving perfusion, preventing complications, health education, and calling for help if symptoms worsen.
Myocardial infarction, also known as a heart attack, results from a critical imbalance between oxygen supply and demand in the heart muscle. The primary cause is coronary artery occlusion due to atherosclerosis, vasospasm, or embolism. Symptoms may include chest pain, dyspnea, sweating, and anxiety. Diagnosis is made based on elevated cardiac enzyme levels and ECG changes. Initial treatment focuses on pain relief, oxygen, fluids, and aspirin while long-term prevention includes medications like beta-blockers, ACE inhibitors, antiplatelets, and statins to reduce risk of future heart attacks and heart failure.
This document provides an overview of cardiac failure/congestive heart failure. It begins with an introduction and objectives. It then reviews heart anatomy and physiology, including the structure of the heart, conducting system, heart sounds, and ECG. It defines cardiac failure and discusses epidemiology, causes, pathophysiology, clinical manifestations, classifications, diagnostic process, medical management, and complications. Nursing management is also addressed using the nursing process approach.
The document provides guidelines for the diagnosis and management of chronic stable angina, defining it as chest discomfort caused by myocardial ischemia that is typically triggered by exertion or stress. It discusses the pathophysiology, risk factors, diagnostic testing options including ECG, stress testing, and imaging, and recommendations for invasive coronary angiography. The guidelines are intended to help clinicians properly evaluate and treat patients experiencing chronic stable angina.
1. Ischaemic heart disease is caused by an imbalance between myocardial oxygen supply and demand, usually due to atherosclerosis limiting blood flow in the coronary arteries.
2. The main types of ischaemic heart disease are stable angina, unstable angina, myocardial infarction (STEMI and NSTEMI), and sudden cardiac death. Clinical presentation and ECG/biomarker findings are used to distinguish these conditions.
3. Treatment involves lifestyle modifications and medications like nitrates, beta-blockers, and calcium channel blockers to reduce oxygen demand and increase supply. Revascularization procedures like PCI or CABG may also be used in certain patients.
1. Ischemic heart disease (IHD), also known as coronary artery disease, is caused by an imbalance between the heart's oxygen supply and demand, and is commonly seen in middle-aged men and post-menopausal women.
2. The major cause is coronary atherosclerosis, which causes plaque buildup in the coronary arteries and can lead to conditions like angina, acute myocardial infarction (MI), and sudden cardiac death.
3. Acute MI occurs when a coronary artery becomes blocked, causing localized heart muscle cell death from lack of oxygen. It is a medical emergency characterized by chest pain and changes in electrocardiogram (ECG) and cardiac enzyme levels.
1. A myocardial infarction occurs when blood flow to the heart is blocked, damaging heart muscle.
2. It is caused most often by atherosclerosis and plaque buildup that obstruct coronary arteries.
3. Symptoms include chest pain and other signs of reduced blood supply to the heart. Diagnosis is based on symptoms, electrocardiogram changes, and blood tests showing cardiac enzyme levels.
Myocardial infarction occurs when blood flow to the heart is obstructed, causing death of heart muscle tissue. It is usually caused by atherosclerosis leading to coronary artery occlusion. Risk factors include conditions like diabetes, smoking, high cholesterol, and family history. Symptoms include chest pain and potential complications are arrhythmias, heart failure, or cardiac rupture. Diagnosis involves cardiac enzyme and troponin levels, electrocardiogram, and other imaging tests. Treatment focuses on restoring blood flow, reducing risk factors, managing pain and symptoms, and monitoring for complications.
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
This document discusses ischemic heart disease and coronary artery disease. Coronary artery disease is caused by atherosclerosis which develops due to risk factors like smoking, high blood pressure, high cholesterol, and diabetes. Clinical presentations include stable angina, unstable angina, non-ST elevation myocardial infarction, and ST elevation myocardial infarction. Treatment involves lifestyle modifications, medications like antiplatelets, anticoagulants, and statins, as well as procedures like percutaneous coronary intervention and coronary artery bypass grafting.
Myocarditis is an inflammatory disease of the heart muscle that is usually caused by viral infections. It can lead to dilated cardiomyopathy and heart failure. Viruses are the most common cause, with adenovirus now more prevalent than coxsackievirus. Myocarditis presents with symptoms of heart failure, chest pain, or arrhythmias. Diagnosis involves EKG, cardiac biomarkers, echocardiogram, cardiac MRI, and endomyocardial biopsy. Treatment focuses on managing arrhythmias and heart failure with medications, while immunosuppression may benefit some forms of myocarditis but not others.
Congestive cardiac failure is defined as a chronic condition where the heart is unable to pump enough blood to meet the body's needs. It can be classified as systolic, diastolic, acute or chronic. Common causes include arrhythmias, myocardial infarction, hypertension, and obesity. Symptoms include fatigue, shortness of breath, and edema while signs include tachycardia and edema. Diagnosis involves tests such as ECG, echocardiogram, and blood tests. Management consists of medications like ACE inhibitors, diuretics, beta-blockers and lifestyle modifications like diet, exercise and smoking cessation.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
This document defines acute myocardial infarction (AMI or heart attack) and discusses its causes, risk factors, signs and symptoms, diagnostic testing, treatment options, and long-term management. An AMI occurs when blood flow to the heart is reduced, damaging heart muscle. The main causes are blockages in the coronary arteries, often due to blood clots forming on top of plaques. Risk factors include age, family history, smoking, diabetes, high blood pressure, high cholesterol, obesity, and physical inactivity. Treatment focuses on restoring blood flow through medications, angioplasty, or bypass surgery, along with long-term lifestyle changes and medications to prevent future issues.
This document discusses ischemic heart disease and angina. It defines ischemic heart disease as a condition where there is inadequate blood supply and oxygen to the heart muscle. Angina is described as chest pain or discomfort caused by an imbalance between the heart's oxygen supply and demand. The document outlines the causes, types, risk factors, diagnosis, and management of angina through lifestyle modifications and medications like aspirin to control symptoms and reduce health risks.
Myocarditis is defined as inflammation of the myocardium that is characterized by inflammatory cell infiltrates and myocyte degeneration or necrosis. It is most often caused by viruses, which can damage the myocardium in three phases: acute viral replication, autoimmune injury, and a chronic dilated cardiomyopathy phase. Symptoms range from being asymptomatic to acute cardiogenic shock and sudden death, and may include fever, respiratory distress, chest discomfort, and signs of heart failure. Diagnosis involves electrocardiogram changes, chest x-ray showing cardiomegaly, echocardiogram demonstrating reduced systolic function, and endomyocardial biopsy identifying inflammation. Treatment is supportive with medications like ACE inhibitors, beta-blockers
Cardiomyopathy is a disease that affects the structure and function of the heart muscle. There are three main types: dilated cardiomyopathy which enlarges the heart ventricles, hypertrophic cardiomyopathy which causes thickening of the heart muscle, and restrictive cardiomyopathy which stiffens the heart muscle. Causes include genetics, infections, hypertension, alcohol use, and other factors. Symptoms vary depending on the type but can include fatigue, shortness of breath, irregular heartbeats, and fluid buildup. Diagnosis involves examinations, tests like echocardiograms, and biopsies. Treatment focuses on managing symptoms with medications, surgery in some cases, and lifestyle changes.
This document provides an overview of congenital and acquired valvular heart diseases. It defines valvular heart disease and describes the four main types of valves in the heart. It then discusses several specific congenital valvular diseases that can occur, including pulmonary atresia, pulmonary stenosis, tricuspid atresia, and bicuspid aortic valve disease. Symptoms, causes, investigations, treatments and complications are outlined for each one. It also discusses acquired valvular diseases such as aortic stenosis and mitral regurgitation.
Heart failure is caused by conditions that weaken the heart muscle such as coronary artery disease and hypertension. The body compensates through mechanisms like the renin-angiotensin system which cause fluid retention, edema, and increased cardiac workload worsening the failure. Treatment goals include reducing preload and afterload through diuretics and vasodilators, improving oxygenation, and increasing contractility. Medications target neurohormonal activation through ACE inhibitors, ARBs, beta-blockers and aldosterone blockade. For severe cases, devices like ICDs, CRT, LVADs and transplantation are used. Lifestyle changes and treating the underlying cause are also important.
1. An aneurysm is an abnormal dilation of a blood vessel that can be congenital or acquired due to weakening of the vessel wall.
2. Aneurysms are classified based on composition, shape, location, and pathogenetic mechanism. The most common type is atherosclerotic aneurysms, which often affect the abdominal aorta.
3. Complications of aneurysms include rupture, which can lead to fatal hemorrhaging, as well as compression of surrounding structures. timely diagnosis and treatment are important to prevent such complications.
Cardiomyopathy refers to diseases of the heart muscle that weaken the heart's ability to pump blood effectively. The three main types are dilated, hypertrophic, and restrictive cardiomyopathy. Dilated cardiomyopathy causes the left ventricle to enlarge and weaken, impairing its ability to pump blood. Causes include viral infections, toxins, genetic factors, and hypertension. Symptoms include fatigue, shortness of breath, and fluid retention. Diagnosis involves echocardiograms, electrocardiograms, and cardiac catheterization. Treatment focuses on managing symptoms through medications, lifestyle changes, and potentially surgery or transplantation.
This document discusses congenital heart disease, specifically atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). It defines each condition, describes their signs and symptoms, risk factors, pathophysiology, diagnosis, and management including both medical and surgical treatment options. The prognosis for each condition with and without treatment is addressed. The document provides a detailed yet concise overview of these three common types of acyanotic heart disease.
This document defines pericardial effusion and cardiac tamponade, discusses their pathophysiology, etiology, clinical presentation, investigations, and management. Pericardial effusion is an abnormal amount of fluid in the pericardial space, while cardiac tamponade is acute heart failure caused by compression of the heart from a large or rapidly developing effusion. Clinical manifestations depend on the rate of fluid accumulation and include chest pain, lightheadedness, and decreased pulse pressure. Investigations include echocardiography, electrocardiography, and pericardiocentesis. Management involves bed rest, medications, drainage procedures, and surgery in severe cases.
This document discusses the assessment, investigation, and treatment of chronic stable angina. It defines chronic stable angina as chest pain or discomfort that is reproducibly associated with exertion or stress and relieved by rest. The document outlines how to evaluate patients presenting with chest pain through history, physical exam, risk factor assessment, and probability estimation models. It recommends initial tests like ECG, cardiac biomarkers, and stress testing. Treatment focuses on lifestyle changes, medications like aspirin, beta-blockers, calcium channel blockers, and revascularization if needed. Regular patient follow up and education are also emphasized.
Cerebrovascular accident, also known as stroke, is caused by a sudden blockage or rupture of an artery in the brain, cutting off blood flow. There are two main types - ischemic (caused by clot) and hemorrhagic (caused by bleeding). Risk factors include hypertension, smoking, diabetes, heart disease, and family history. Symptoms depend on the affected brain region but may include weakness, numbness, trouble speaking, and loss of coordination. Treatment focuses on restoring blood flow, preventing further damage, and rehabilitation. Control of risk factors can help prevent strokes.
Myocardial infarction occurs when there is prolonged ischemia to the heart muscle due to reduced oxygen supply or increased oxygen demand. It is usually caused by formation of a blood clot within a coronary artery blocking blood flow. Diagnosis is made through symptoms, electrocardiogram changes, and cardiac biomarker levels. Treatment involves oxygen, aspirin, nitrates, beta blockers, fibrinolytics or percutaneous coronary intervention to restore blood flow, as well as long term medications like statins to prevent future heart attacks.
1. Ischaemic heart disease is caused by an imbalance between myocardial oxygen supply and demand, usually due to atherosclerosis limiting blood flow in the coronary arteries.
2. The main types of ischaemic heart disease are stable angina, unstable angina, myocardial infarction (STEMI and NSTEMI), and sudden cardiac death. Clinical presentation and ECG/biomarker findings are used to distinguish these conditions.
3. Treatment involves lifestyle modifications and medications like nitrates, beta-blockers, and calcium channel blockers to reduce oxygen demand and increase supply. Revascularization procedures like PCI or CABG may also be used in certain patients.
1. Ischemic heart disease (IHD), also known as coronary artery disease, is caused by an imbalance between the heart's oxygen supply and demand, and is commonly seen in middle-aged men and post-menopausal women.
2. The major cause is coronary atherosclerosis, which causes plaque buildup in the coronary arteries and can lead to conditions like angina, acute myocardial infarction (MI), and sudden cardiac death.
3. Acute MI occurs when a coronary artery becomes blocked, causing localized heart muscle cell death from lack of oxygen. It is a medical emergency characterized by chest pain and changes in electrocardiogram (ECG) and cardiac enzyme levels.
1. A myocardial infarction occurs when blood flow to the heart is blocked, damaging heart muscle.
2. It is caused most often by atherosclerosis and plaque buildup that obstruct coronary arteries.
3. Symptoms include chest pain and other signs of reduced blood supply to the heart. Diagnosis is based on symptoms, electrocardiogram changes, and blood tests showing cardiac enzyme levels.
Myocardial infarction occurs when blood flow to the heart is obstructed, causing death of heart muscle tissue. It is usually caused by atherosclerosis leading to coronary artery occlusion. Risk factors include conditions like diabetes, smoking, high cholesterol, and family history. Symptoms include chest pain and potential complications are arrhythmias, heart failure, or cardiac rupture. Diagnosis involves cardiac enzyme and troponin levels, electrocardiogram, and other imaging tests. Treatment focuses on restoring blood flow, reducing risk factors, managing pain and symptoms, and monitoring for complications.
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
This document discusses ischemic heart disease and coronary artery disease. Coronary artery disease is caused by atherosclerosis which develops due to risk factors like smoking, high blood pressure, high cholesterol, and diabetes. Clinical presentations include stable angina, unstable angina, non-ST elevation myocardial infarction, and ST elevation myocardial infarction. Treatment involves lifestyle modifications, medications like antiplatelets, anticoagulants, and statins, as well as procedures like percutaneous coronary intervention and coronary artery bypass grafting.
Myocarditis is an inflammatory disease of the heart muscle that is usually caused by viral infections. It can lead to dilated cardiomyopathy and heart failure. Viruses are the most common cause, with adenovirus now more prevalent than coxsackievirus. Myocarditis presents with symptoms of heart failure, chest pain, or arrhythmias. Diagnosis involves EKG, cardiac biomarkers, echocardiogram, cardiac MRI, and endomyocardial biopsy. Treatment focuses on managing arrhythmias and heart failure with medications, while immunosuppression may benefit some forms of myocarditis but not others.
Congestive cardiac failure is defined as a chronic condition where the heart is unable to pump enough blood to meet the body's needs. It can be classified as systolic, diastolic, acute or chronic. Common causes include arrhythmias, myocardial infarction, hypertension, and obesity. Symptoms include fatigue, shortness of breath, and edema while signs include tachycardia and edema. Diagnosis involves tests such as ECG, echocardiogram, and blood tests. Management consists of medications like ACE inhibitors, diuretics, beta-blockers and lifestyle modifications like diet, exercise and smoking cessation.
Acute Coronary Syndrome (ACS) refers to a range of conditions caused by reduced blood flow in the coronary arteries. It includes Unstable Angina (UA), Non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). ACS is diagnosed based on electrocardiogram (ECG) findings and cardiac enzyme levels. STEMI shows ST elevations and enzyme elevations, while NSTEMI shows ST depressions/inversions and enzyme elevations without ST elevations. UA shows non-specific ECG changes and normal enzymes. Risk stratification systems like the TIMI score are used for NSTEMI/UA patients to guide management, which may
This document defines acute myocardial infarction (AMI or heart attack) and discusses its causes, risk factors, signs and symptoms, diagnostic testing, treatment options, and long-term management. An AMI occurs when blood flow to the heart is reduced, damaging heart muscle. The main causes are blockages in the coronary arteries, often due to blood clots forming on top of plaques. Risk factors include age, family history, smoking, diabetes, high blood pressure, high cholesterol, obesity, and physical inactivity. Treatment focuses on restoring blood flow through medications, angioplasty, or bypass surgery, along with long-term lifestyle changes and medications to prevent future issues.
This document discusses ischemic heart disease and angina. It defines ischemic heart disease as a condition where there is inadequate blood supply and oxygen to the heart muscle. Angina is described as chest pain or discomfort caused by an imbalance between the heart's oxygen supply and demand. The document outlines the causes, types, risk factors, diagnosis, and management of angina through lifestyle modifications and medications like aspirin to control symptoms and reduce health risks.
Myocarditis is defined as inflammation of the myocardium that is characterized by inflammatory cell infiltrates and myocyte degeneration or necrosis. It is most often caused by viruses, which can damage the myocardium in three phases: acute viral replication, autoimmune injury, and a chronic dilated cardiomyopathy phase. Symptoms range from being asymptomatic to acute cardiogenic shock and sudden death, and may include fever, respiratory distress, chest discomfort, and signs of heart failure. Diagnosis involves electrocardiogram changes, chest x-ray showing cardiomegaly, echocardiogram demonstrating reduced systolic function, and endomyocardial biopsy identifying inflammation. Treatment is supportive with medications like ACE inhibitors, beta-blockers
Cardiomyopathy is a disease that affects the structure and function of the heart muscle. There are three main types: dilated cardiomyopathy which enlarges the heart ventricles, hypertrophic cardiomyopathy which causes thickening of the heart muscle, and restrictive cardiomyopathy which stiffens the heart muscle. Causes include genetics, infections, hypertension, alcohol use, and other factors. Symptoms vary depending on the type but can include fatigue, shortness of breath, irregular heartbeats, and fluid buildup. Diagnosis involves examinations, tests like echocardiograms, and biopsies. Treatment focuses on managing symptoms with medications, surgery in some cases, and lifestyle changes.
This document provides an overview of congenital and acquired valvular heart diseases. It defines valvular heart disease and describes the four main types of valves in the heart. It then discusses several specific congenital valvular diseases that can occur, including pulmonary atresia, pulmonary stenosis, tricuspid atresia, and bicuspid aortic valve disease. Symptoms, causes, investigations, treatments and complications are outlined for each one. It also discusses acquired valvular diseases such as aortic stenosis and mitral regurgitation.
Heart failure is caused by conditions that weaken the heart muscle such as coronary artery disease and hypertension. The body compensates through mechanisms like the renin-angiotensin system which cause fluid retention, edema, and increased cardiac workload worsening the failure. Treatment goals include reducing preload and afterload through diuretics and vasodilators, improving oxygenation, and increasing contractility. Medications target neurohormonal activation through ACE inhibitors, ARBs, beta-blockers and aldosterone blockade. For severe cases, devices like ICDs, CRT, LVADs and transplantation are used. Lifestyle changes and treating the underlying cause are also important.
1. An aneurysm is an abnormal dilation of a blood vessel that can be congenital or acquired due to weakening of the vessel wall.
2. Aneurysms are classified based on composition, shape, location, and pathogenetic mechanism. The most common type is atherosclerotic aneurysms, which often affect the abdominal aorta.
3. Complications of aneurysms include rupture, which can lead to fatal hemorrhaging, as well as compression of surrounding structures. timely diagnosis and treatment are important to prevent such complications.
Cardiomyopathy refers to diseases of the heart muscle that weaken the heart's ability to pump blood effectively. The three main types are dilated, hypertrophic, and restrictive cardiomyopathy. Dilated cardiomyopathy causes the left ventricle to enlarge and weaken, impairing its ability to pump blood. Causes include viral infections, toxins, genetic factors, and hypertension. Symptoms include fatigue, shortness of breath, and fluid retention. Diagnosis involves echocardiograms, electrocardiograms, and cardiac catheterization. Treatment focuses on managing symptoms through medications, lifestyle changes, and potentially surgery or transplantation.
This document discusses congenital heart disease, specifically atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA). It defines each condition, describes their signs and symptoms, risk factors, pathophysiology, diagnosis, and management including both medical and surgical treatment options. The prognosis for each condition with and without treatment is addressed. The document provides a detailed yet concise overview of these three common types of acyanotic heart disease.
This document defines pericardial effusion and cardiac tamponade, discusses their pathophysiology, etiology, clinical presentation, investigations, and management. Pericardial effusion is an abnormal amount of fluid in the pericardial space, while cardiac tamponade is acute heart failure caused by compression of the heart from a large or rapidly developing effusion. Clinical manifestations depend on the rate of fluid accumulation and include chest pain, lightheadedness, and decreased pulse pressure. Investigations include echocardiography, electrocardiography, and pericardiocentesis. Management involves bed rest, medications, drainage procedures, and surgery in severe cases.
This document discusses the assessment, investigation, and treatment of chronic stable angina. It defines chronic stable angina as chest pain or discomfort that is reproducibly associated with exertion or stress and relieved by rest. The document outlines how to evaluate patients presenting with chest pain through history, physical exam, risk factor assessment, and probability estimation models. It recommends initial tests like ECG, cardiac biomarkers, and stress testing. Treatment focuses on lifestyle changes, medications like aspirin, beta-blockers, calcium channel blockers, and revascularization if needed. Regular patient follow up and education are also emphasized.
Cerebrovascular accident, also known as stroke, is caused by a sudden blockage or rupture of an artery in the brain, cutting off blood flow. There are two main types - ischemic (caused by clot) and hemorrhagic (caused by bleeding). Risk factors include hypertension, smoking, diabetes, heart disease, and family history. Symptoms depend on the affected brain region but may include weakness, numbness, trouble speaking, and loss of coordination. Treatment focuses on restoring blood flow, preventing further damage, and rehabilitation. Control of risk factors can help prevent strokes.
Myocardial infarction occurs when there is prolonged ischemia to the heart muscle due to reduced oxygen supply or increased oxygen demand. It is usually caused by formation of a blood clot within a coronary artery blocking blood flow. Diagnosis is made through symptoms, electrocardiogram changes, and cardiac biomarker levels. Treatment involves oxygen, aspirin, nitrates, beta blockers, fibrinolytics or percutaneous coronary intervention to restore blood flow, as well as long term medications like statins to prevent future heart attacks.
The term ischemic heart disease (IHD) describes a group of clinical syndromes characterized by myocardial ischemia, an imbalance between myocardial blood supply and demand.
Because the fundamental pathophysiologic defect in the ischemic myocardium is inadequate perfusion, ischemia is associated not only with insufficient oxygen supply, but also with reduced availability of nutrients and inadequate removal of metabolic end products.
Ischemic heart disease (IHD) caused by atherosclerosis of the epicardial vessels leading to coronary heart disease (CHD) is the main etiology of IHD.
Leading cause of death
Resulting from myocardial ischemia—an imbalance between the supply (perfusion) and demand of the heart for oxygenated blood.
90% of cases, the cause of myocardial ischemia is reduced blood flow due to obstructive atherosclerotic lesions in the coronary arteries.
IHD is often termed coronary artery disease (CAD) or coronary heart disease.
There is a long period (up to decades) of silent, slow progression of coronary lesions before symptoms appear.
IHD are only the late manifestations of coronary atherosclerosis that may have started during childhood or adolescence
Myocardial infarction, the most important form of IHD, in which ischemia causes the death of heart muscle.
Angina pectoris, in which the ischemia is of insufficient severity to cause infarction, but may be a harbinger of MI.
Chronic IHD with heart failure.
Sudden cardiac death.
The dominant cause of the IHD syndromes is insufficient coronary perfusion relative to myocardial demand, due to • Chronic, progressive atherosclerotic narrowing of the epicardial coronary arteries, and • Variable degrees of superimposed acute plaque change, thrombosis, and vasospasm
Clinical manifestations of coronary atherosclerosis are generally due to • Progressive narrowing of the lumen leading to stenosis (“fixed” obstructions) or • Acute plaque disruption with thrombosis, both of which compromise blood flow.
A fixed lesion obstructing 75% or greater of the lumen is generally required to cause symptomatic ischemia precipitated by exercise (most often manifested as chest pain, known as angina)
Obstruction of 90% of the lumen can lead to inadequate coronary blood flow even at rest.
This document provides an overview of congestive cardiac failure/heart failure. It begins with definitions and terminology. It then discusses the epidemiology, etiology, risk factors, pathogenesis, complications, signs and symptoms, diagnosis, and management of heart failure. For pathogenesis, it describes the normal cardiac function and compensatory mechanisms in heart failure, including tachycardia, fluid retention, vasoconstriction, and ventricular hypertrophy. It also discusses the neurohormonal model of heart failure and factors that can precipitate or exacerbate the condition. The document provides a comprehensive review of heart failure.
Acute coronary syndrome (ACS) refers to unstable angina and myocardial infarction and is usually caused by rupture of an atherosclerotic plaque leading to coronary artery thrombosis. It is characterized by prolonged chest pain and cardiac enzyme elevations. Diagnosis involves electrocardiogram showing ST segment changes and elevated troponin levels. Treatment focuses on reperfusion therapy, antiplatelets, anticoagulants, and lifestyle modifications to prevent future events. Prognosis depends on extent of myocardial damage, with in-hospital mortality over 10% and 5-year survival rates around 75% for those who survive the initial event.
This document provides guidance on managing medically compromised patients for oral and maxillofacial surgery. It discusses general principles like conducting late morning appointments in an upright position to minimize stress. It also reviews guidelines for specific conditions like cardiovascular diseases, including managing angina, myocardial infarction, and hypertension. For endocrine diseases, it overviews the endocrine system and managing disorders like diabetes. Throughout, it emphasizes the need for medical consultation, minimizing stress, and considering risks from things like epinephrine in local anesthesia.
This document provides objectives and content about acute myocardial infarction (AMI) or heart attack. It begins with objectives of explaining AMI and its various aspects. It then defines AMI as reduced blood flow in a coronary artery due to atherosclerosis or thrombus. It discusses the incidence, classifications, risk factors like hypertension and smoking, etiological factors, pathophysiology of plaque buildup and thrombus formation blocking blood flow. It covers clinical features like chest pain, diagnostic evaluation including ECG, cardiac enzymes and angiography. It outlines management including pharmacological treatments, angioplasty, and other surgical procedures to reopen blocked arteries and restore blood flow to the heart.
Periodontal Treatment of Medically Compromised Patients [Autosaved].pptxANIL KUMAR
The world's population is estimated to be over 7.7 billion. [1] Within this mass of humanity is a
substantial number of people who are elderly; the graying of the world's population is predicted to
produce millions of individuals with systemic medical conditions that can affect oral health and
dental treatment. The dental management of these medically compromised patients can be
problematic in terms of oral complications, dental therapy, and emergency care
This document provides information about myocardial infarction (MI) or heart attack. It defines MI as reduced blood flow in a coronary artery due to atherosclerosis or blockage. MI is a leading cause of death. Risk factors include age, family history, smoking, hypertension, high cholesterol, diabetes and stress. Signs and symptoms include chest pain and shortness of breath. Diagnosis involves ECG, cardiac enzymes and angiography. Treatment includes aspirin, nitrates, beta blockers, statins, clot-busting drugs, angioplasty and bypass surgery. Complications can include arrhythmias, heart failure and heart rupture.
This document provides information about myocardial infarction (MI) or heart attack. It defines MI as reduced blood flow in a coronary artery due to atherosclerosis or blockage. MI is a leading cause of death. Risk factors include age, family history, smoking, hypertension, high cholesterol, diabetes and stress. Signs and symptoms include chest pain and shortness of breath. Diagnosis involves ECG, cardiac enzymes and angiography. Treatment includes aspirin, nitrates, beta blockers, statins, clot-busting drugs, angioplasty and bypass surgery. Complications can include arrhythmias, heart failure and heart rupture.
Coronary artery disease (CAD) is the most common type of cardiovascular disease. It is caused by plaque buildup in the coronary arteries that supply blood to the heart. This restricts blood flow and oxygen supply to heart muscle. Symptoms include chest pain and discomfort known as angina. Diagnosis involves electrocardiograms, stress tests, imaging like angiography and echocardiograms. Treatment focuses on lifestyle changes and medications to control symptoms and risk factors as well as procedures like angioplasty and stents to open blocked arteries. High dose thiamine injections showed promise in curing CAD in one research study. Proper management can help cure angina and allow those with CAD to live long, productive lives
This document discusses cardiovascular pathology and includes the following:
1. It provides an overview and outline of topics to be covered related to heart and vascular diseases including atherosclerosis, myocardial infarction, aneurysms, and others.
2. It discusses the six principal mechanisms of heart disease including failure of the pump, obstruction to flow, regurgitant flow, shunted flow, disorders of conduction, and rupture of the heart or vessels.
3. It provides learning objectives for the presentation that cover topics like atherosclerosis, hypertension, aneurysms, congestive heart failure, and more.
This document discusses hypertensive diseases and their complications. It begins by outlining various hypertensive diseases that can affect the cerebrovascular system, eyes, heart and kidneys. It then defines hypertension and hypertensive emergencies/urgencies. The remainder of the document provides more details on specific hypertensive diseases and complications, including hypertensive encephalopathy, cerebrovascular accidents, retinopathy, left ventricular hypertrophy, coronary artery disease, cardiac arrhythmias, congestive heart failure, benign and malignant nephrosclerosis. It also discusses diagnostic criteria and management of various hypertensive conditions.
The document provides information about myocardial infarction (MI), also known as a heart attack. It defines MI as the death of heart muscle caused by a blockage of blood flow through the coronary arteries. It discusses the causes, symptoms, diagnosis, and treatment of MI. The main symptoms of MI are chest pain and shortness of breath. Diagnosis involves electrocardiograms, cardiac enzyme levels, and other cardiac tests. Treatment focuses on restoring blood flow, reducing myocardial workload, and preventing complications through medications, procedures like angioplasty, and lifestyle changes.
This document provides an overview of the management of acute stroke. It defines stroke and transient ischemic attack, and discusses the epidemiology, classification, risk factors, pathophysiology, clinical presentation, diagnosis, management, complications and prognosis of stroke. The management involves resuscitation, reperfusion therapies like thrombolysis and thrombectomy, treating complications, secondary prevention including blood pressure and diabetes control, and rehabilitation. The document emphasizes the importance of specialized stroke units and timely management to improve outcomes for patients with acute stroke.
Hemorrhagic stroke accounts for 10-15% of all strokes and is associated with higher mortality than ischemic stroke. Patients often present with headache, altered mental status, seizures, nausea/vomiting, or hypertension. The bleeding occurs directly into the brain from damaged arteries, and mortality is high, with 40-80% dying within 30 days. Risk factors include age, hypertension, amyloidosis, coagulopathies, anticoagulation, cocaine abuse, and genetic conditions. Treatment focuses on stabilizing vital signs, controlling blood pressure and seizures, and reducing intracranial pressure if elevated.
This document provides an overview of carotid artery stenosis. It discusses the anatomy of the carotid arteries and how stenosis can increase the risk of stroke by reducing blood flow to the brain. Symptoms of stenosis range from transient ischemic attacks to full strokes, depending on the location and severity of the blockage. Imaging plays a key role in detecting and evaluating carotid artery stenosis. Treatment may involve medications, lifestyle changes, or carotid endarterectomy surgery to remove plaque buildup.
Sudden cardiac death is defined as natural death from cardiac causes that occurs abruptly within one hour of the onset of symptoms. It accounts for about 50% of cardiovascular deaths with an annual incidence of 250,000 cases in the US and 7 lakh cases in India. Risk factors include increasing age, male sex, and underlying heart diseases such as coronary artery disease, cardiomyopathies, and cardiac channelopathies. Management involves cardiopulmonary resuscitation, defibrillation if ventricular fibrillation is detected, and administration of antiarrhythmic drugs. Strategies for prevention include implantable cardioverter-defibrillators, catheter ablation, antiarrhythmic medications like beta-blockers, and surgical interventions tailored to
This document discusses conjunctivitis (pink eye). It begins by defining conjunctivitis and describing common causes such as viral, bacterial, or allergic infections. The clinical presentation of conjunctivitis is then outlined, including symptoms like redness, discharge, irritation. Risk factors and methods of transmission are later reviewed. The document separates conjunctivitis into specific types (viral, bacterial, allergic) and discusses signs, common causes and treatment for each. Prevention focuses on maintaining good hygiene to avoid spreading conjunctivitis.
Chronic obstructive pulmonary disease (COPD) refers to chronic bronchitis and emphysema. It is characterized by airflow limitation caused by damage to airways and lung tissue. The most common risk factor is tobacco smoking. Symptoms include a productive cough, wheezing, and shortness of breath. A diagnosis is made based on symptoms and lung function tests. Treatment focuses on smoking cessation and medications to relieve symptoms.
This document provides an overview of asthma, including its definition, pathophysiology, clinical presentation, diagnosis, and management. It defines asthma as a chronic inflammatory disorder of the airways involving various cells. The pathophysiology involves acute and chronic inflammation from triggers like allergens. Diagnosis is based on symptoms, exam, and lung function tests showing reversible airflow obstruction. Management focuses on education, environmental control, and a stepped pharmacologic approach including bronchodilators and inhaled corticosteroids.
This document provides an overview of dyslipidemia (abnormal lipid levels). It defines dyslipidemia and discusses lipid transport via lipoproteins. Primary causes of dyslipidemia include genetic disorders affecting lipid metabolism. Secondary causes include diabetes, hypothyroidism, obesity, and certain medications. The document outlines the pathophysiology of lipid transport through exogenous and endogenous pathways and the roles of lipoproteins such as LDL, HDL, VLDL, and chylomicrons. Treatment aims to lower LDL and triglycerides while raising HDL through lifestyle and pharmacological interventions.
This document discusses thyroid disorders and provides information on:
- The thyroid gland, its hormones, histology, and hormone synthesis process
- Thyrotoxicosis (hyperthyroidism), including causes, symptoms, signs, diagnosis and treatment
- The differences between the thyroid hormones T3 and T4
- Classification of thyroid disorders and drugs used to treat them
This document discusses osteoporosis, including its definition, epidemiology, bone physiology, risk factors, pathophysiology, clinical presentation, diagnosis, and prevention and treatment approaches. It covers the role of vitamin D, calcium, and parathyroid hormone in bone health. It also examines the pathophysiology of postmenopausal, male, and age-related osteoporosis as well as secondary causes. Diagnostic tools and the goals of osteoporosis management are outlined. Both nonpharmacologic and pharmacologic therapy options are reviewed.
Hormone replacement therapy (HRT) involves supplemental estrogen, progesterone, and sometimes testosterone to treat symptoms of menopause. It can help reduce hot flashes, night sweats, and risks of osteoporosis and heart disease, but also increases risks of blood clots, stroke, and breast cancer. HRT regimens include continuous or intermittent combinations of estrogen and progesterone in pills, patches, or other forms for varying numbers of days per month. The benefits and risks should be considered on an individual basis.
It is a group of metabolic disorders of fat, carbohydrate and protein metabolism that results from defects in insulin secretion, insulin action (sensitivity) or both
Oral contraceptives are medications that prevent pregnancy through combinations of estrogen and progestin hormones that inhibit ovulation. They come in monophasic, biphasic, and triphasic forms that contain constant or varying levels of hormones throughout the menstrual cycle. The goal of oral contraceptive treatment is to prevent pregnancy while providing other health benefits like regularizing menstrual cycles and preventing certain cancers. They work primarily by inhibiting the hormones LH and FSH to prevent egg release and thickening cervical mucus to block sperm penetration.
Study material for Doctor of pharmacy and other medical students. Hypertension is a condition in which the force of the blood against the artery walls is too high. Approximately one billion adults or ~22% of the population of the world have hypertension. It is slightly more frequent in men, in those of low socioeconomic status, and prevalence increases with age. So it is more important to manage it as early, this includes Pharmacological as well as Non-pharmacological Management.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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
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.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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).
4. Introduction
▪ Acute coronary syndromes (ACSs), including unstable angina and
myocardial infarction (MI), are forms of coronary heart disease (CHD)
that constitute the most common cause of CVD death.
▪ The cause of an ACS is erosion or rupture of an atherosclerotic plaque
with subsequent platelet adherence, activation, aggregation, and
activation of the clotting cascade. Ultimately, a clot composed of fibrin
and platelets forms.
▪ Myocardial infarction (MI), commonly known as a heart attack,
occurs when blood flow decreases or stops to a part of the heart, causing
damage to the heart muscle.
▪ The most common symptom is chest pain or discomfort which may travel
into the shoulder, arm, back, neck, or jaw.
@Dr.Prasad Chinchole
5. ▪ Often it is in the center or left side of the chest and lasts for more than
a few minutes.
▪ The discomfort may occasionally feel like heartburn.
▪ Other symptoms may include shortness of breath, nausea, feeling faint,
a cold sweat, or feeling tired.
▪ About 30% of people have atypical symptoms.
▪ Women more often have atypical symptoms than men.
▪ Among those over 75 years old, about 5% have had an MI with little or
no history of symptoms. An MI may cause heart failure, an irregular
heartbeat, cardiogenic shock, or cardiac arrest.
@Dr.Prasad Chinchole
6. Terminology
▪ Myocardial infarction (MI) refers to tissue death (infarction) of the
heart muscle (myocardium)
▪ It is a type of acute coronary syndrome, which describes a sudden or
short-term change in symptoms related to blood flow to the heart.
▪ The phrase "heart attack" is often used non-specifically to refer to a
myocardial infarction and to sudden cardiac death.
▪ An MI is different from—but can cause—cardiac arrest, where the
heart is not contracting at all or so poorly that all vital organs cease to
function.
▪ It is also distinct from heart failure, in which the pumping action of the
heart is impaired. However, an MI may lead to heart failure
@Dr.Prasad Chinchole
7. Definition
▪ The term "myocardial infarction" focuses on the myocardium (the heart
muscle) and the changes that occur in it due to the sudden deprivation
of circulating blood.
▪ The main change is necrosis (death) of myocardial tissue.
▪ The word "infarction" comes from the Latin "infarcire" meaning "to
plug up or cram."
▪ It refers to the clogging of the artery.
@Dr.Prasad Chinchole
9. Epidemiology
▪ Myocardial infarction is a common presentation of coronary artery
disease. The World Health Organization estimated in 2004, that 12.2%
of worldwide deaths were from ischemic heart disease.
▪ Worldwide, more than 3 million people have STEMIs and 4 million
have NSTEMIs a year.
▪ STEMIs occur about twice as often in men as women.
▪ In contrast, IHD is becoming a more common cause of death in the
developing world.
▪ For example, in India, IHD had become the leading cause of death by
2004, accounting for 1.46 million deaths (14% of total deaths) and
deaths due to IHD were expected to double during 1985–2015.
@Dr.Prasad Chinchole
10. Etiology & Risk factors
1. Atherosclerotic plaques
2. Inflammation
3. Genetic
4. Decrease synthesis of nitric oxide
5. Evolution of endothelial
dysfunction
6. Atherosclerosis
7. including hypertension
8. Age
9. Male gender
10. Tobacco use
11. Diabetes Mellitus
12. Obesity
13. Dyslipidemias
14. Lack of physical activity
15. Illegal drug use
16. A history of preeclampsia
@Dr.Prasad Chinchole
12. SPECTRUM OF ACS
▪ Acute coronary syndromes (ACSs) is a term that includes all
clinical syndromes compatible with acute myocardial ischemia
resulting from an imbalance between myocardial oxygen demand
and supply.
▪ In contrast to stable angina, an ACS results primarily from
diminished myocardial blood flow secondary to an occlusive or
partially occlusive coronary artery thrombus.
▪ ACSs are classified according to electrocardiographic (ECG)
changes into STE ACS, also called STEMI, and NSTE ACS, which
includes NSTE MI and unstable angina
@Dr.Prasad Chinchole
19. COMPLICATIONS
▪ it is important for clinicians to recognize complications of MI because
they are associated with increased mortality.
▪ The most serious complication is cardiogenic shock, which occurs in
approximately 5% to 6% of patients presenting with STEMI and in less
than 2% of those presenting with NSTE ACS.
▪ Other complications that may result from MI are heart failure, valvular
dysfunction, ventricular and atrial tachyarrhythmias, bradycardia, heart
block, pericarditis, stroke secondary to LV thrombus embolization,
venous thromboembolism, and LV free-wall rupture.
▪ More than 25% of MI patients die, presumably of ventricular
fibrillation, prior to reaching the hospital.
@Dr.Prasad Chinchole
21. Signs and Symptoms
CLINICAL PRESENTATION
Symptoms
▪ The classic symptom of ACS is
midline anterior chest discomfort.
Accompanying symptoms may
include arm, back or jaw pain,
nausea, vomiting, or shortness of
breath.
▪ Patients less likely to present with
classic symptoms include elderly
patients, diabetic patients, and
women.
Signs
▪ No signs are classic for ACS.
▪ However, patients with ACS may
present with signs of acute heart
failure, including jugular venous
distension, rales, and S3 sound on
auscultation.
▪ Patients may present with
arrhythmias and therefore may
have tachycardia, bradycardia, or
heart block.
@Dr.Prasad Chinchole
24. Diagnosis
1. SYMPTOMS AND PHYSICAL EXAMINATION FINDINGS
▪ The classic symptom of an ACS is midline anterior anginal chest
discomfort, most often at rest, severe new-onset angina, or increasing
angina at least 20 minutes in duration.
▪ The chest discomfort may radiate to the shoulder, down the left arm,
to the back, or to the jaw.
▪ Associated symptoms that may accompany chest discomfort include
nausea, vomiting, diaphoresis, and shortness of breath.
@Dr.Prasad Chinchole
25. ▪ Typically, patients with STE ACS present with unremitting chest
discomfort.
▪ Patients with NSTE ACS may present with (1) rest angina, (2) new
onset (<2 months) angina, or (3) angina that increases in frequency,
duration, or intensity. All healthcare professionals should review these
warning symptoms with patients at high risk for CHD.
▪ On physical examination, no specific features are indicative of ACS.
@Dr.Prasad Chinchole
26. 2. TWELVE-LEAD ECG
▪ Key features of a 12-lead ECG identify and risk stratify patients with an
ACS.
▪ Within 10 minutes of a patient presenting to an emergency department with
symptoms of ischemic chest discomfort, a 12-lead ECG should be obtained
and interpreted.
▪ Key findings on review of a 12-lead ECG indicating myocardial ischemia
or MI are ST-segment elevation, ST-segment depression, and T-wave
inversion.
▪ ST-segment and/or T-wave changes in contiguous leads help to identify the
location of the coronary artery that is the cause of the ischemia or
infarction.
@Dr.Prasad Chinchole
27. ▪ In addition, the appearance of a new left bundle-branch block
accompanied by chest discomfort is highly specific for acute MI.
▪ Approximately 65% of patients diagnosed with MI present with STE
on ECG; the remainder have ST-segment depression, T-wave inversion,
or in some instances, no ECG changes.
▪ Some parts of the heart are more “electrically silent” than others, and
myocardial ischemia may not be detected on surface ECG.
▪ Therefore, it is important to review findings from the ECG in
conjunction with biochemical markers of myocardial necrosis.
@Dr.Prasad Chinchole
29. 3. BIOCHEMICAL MARKERS
▪ Biochemical markers of myocardial cell death are important for confirming
the diagnosis of MI.
▪ These are termed positive biochemical markers for MI.
▪ Although troponins and CK MB appear in the blood within 6 hours of
infarction, troponins stay elevated in the blood for up to 10 days, whereas
CK MB returns to normal values within 48 hours.
▪ Therefore, if a patient is admitted with elevated troponin and CK MB
concentrations and several days later experiences recurrent chest discomfort,
the troponin will be less sensitive for detecting new myocardial damage
because the level still is elevated from the earlier event.
@Dr.Prasad Chinchole
30. ▪ If early re-infarction is suspected, CK MB concentration determination
is the preferred diagnostic test.
▪ Biochemical markers, such as troponin measurements, that are below
the detectable limit of hospital laboratories are termed negative, and the
diagnosis of MI is excluded.
▪ CK MB normal Value 5 to 25 IU/L.
▪ Troponin normal Value less than 0.01 ng/mL.
@Dr.Prasad Chinchole
32. RISK STRATIFICATION
▪ Patient signs and symptoms, medical history, ECG, and troponin or CK MB
determinations are used to stratify patients as having low, medium, or high
risk of death or MI or likelihood of not responding to pharmacotherapy and
requiring urgent coronary angiography and Percutaneous coronary
intervention PCI.
▪ The ACC/AHA defines a target time to initiate reperfusion treatment for
STEMI within 30 minutes of hospital presentation for fibrinolytics and within
no more than 90 minutes from resentation for primary PCI.
▪ Approximately 83% of eligible patients presenting to the hospital with
STEMI underwent reperfusion therapy; 62% of the patients were treated with
primary PCI, 17% fibrinolysis alone, 1% fibrinolysis followed by immediate
PCI, and 2% immediate CABG surgery.
@Dr.Prasad Chinchole
34. Management
A. DESIRED OUTCOMES
▪ The short-term goals of treatment for the ACS patient are as follows:
1. Early restoration of blood flow to the infarct-related artery to prevent
infarct expansion (in the case of MI) or prevent complete occlusion and
MI (in unstable angina)
2. Prevention of death and other complications
3. Prevention of coronary artery reocclusion
4. Relief of ischemic chest discomfort
5. Maintenance of normoglycemia
@Dr.Prasad Chinchole
35. GENERAL APPROACH TO TREATMENT
▪ General treatment measures for all STE ACSs and high- and
intermediate-risk NSTE ACS patients include admission to hospital,
oxygen administration (if oxygen saturation is low, i.e., <90%).
▪ Continuous multilead ST-segment monitoring for arrhythmias and
ischemia, glycemic control, frequent measurement of vital signs,
bedrest for 12 hours in hemodynamically stable patients, avoidance of
Valsalva maneuver (prescribe stool softeners routinely), and pain relief.
▪ If these test results are negative, the patient may be admitted to a
general medical floor with ECG telemetry monitoring for ischemic
changes and arrhythmias, undergo a noninvasive stress test, or be
discharged from the emergency department.
@Dr.Prasad Chinchole
36. NONPHARMACOLOGIC THERAPY
▪ Either fibrinolysis or immediate primary PCI is the treatment of choice
for reestablishing coronary artery blood flow in patients with STE ACS
when the patient presents within 3 hours of symptom onset and both
options are available at the institution.
▪ For primary PCI, the patient is taken from the emergency department
to the cardiac catheterization laboratory and undergoes coronary
angiography with either balloon angioplasty or placement of a bare-
metal or drug-eluting intracoronary stent.
▪ Compliance—give careful advice about disease, treatment, and self
help strategies
▪ Diet—ensure adequate general nutrition and, in obese patients, weight
reduction
@Dr.Prasad Chinchole
37. ▪ Salt—advise patients to avoid high salt content foods and not to add salt
(particularly in severe cases of congestive heart failure)
▪ Fluid—urge overloaded patients and those with severe congestive heart
failure to restrict their fluid intake
▪ Alcohol—advise moderate alcohol consumption (abstinence in alcohol
related cardiomyopathy)
▪ Smoking—avoid smoking (adverse effects on coronary disease, adverse
haemodynamic effects)
▪ Exercise—regular exercise should be encouraged
▪ Vaccination—patients should consider influenza and pneumococcal
vaccinations
▪ Contraceptive advice
@Dr.Prasad Chinchole
38. Commonly consumed processed foods that have a
high sodium content
▪ Cheese
▪ Sausages
▪ Crisps, salted peanuts
▪ Milk and white chocolate
▪ Tinned soup and tinned vegetables
▪ Ham, bacon, tinned meat (eg. corned beef)
▪ Tinned fish (eg. sardines, salmon, tuna)
▪ Smoked fish
@Dr.Prasad Chinchole
40. ▪ According to the ACC/AHA STE ACS practice guidelines, early
pharmacotherapy of STE ACS should include intranasal oxygen (if
oxygen saturation is <90%), sublingual (SL) nitroglycerin (NTG),
aspirin, a β-blocker, unfractionated heparin (UFH) or enoxaparin, and
fibrinolysis in eligible candidates.
▪ Morphine is administered to patients with refractory angina as an
analgesic and a venodilator that lowers preload.
▪ These agents should be administered early, while the patient is still in
the emergency department. An ACE inhibitor should be started within
24 hours of presentation, particularly in patients with LVEF ≤40%,
signs of heart failure, or an anterior wall MI, in the absence of
contraindications.
41. ▪ Intravenous (IV) NTG and β-blockers should be administered to
selected patients without contraindications.
▪ Dosing and contraindications for SL and IV NTG, aspirin, β-blockers,
UFH, enoxaparin, ACE inhibitors, and fibrinolytics are
42.
43.
44.
45.
46.
47.
48.
49.
50. Fibrinolytic Therapy
▪ Fibrinolytic drug, also called thrombolytic drug, any agent that is
capable of stimulating the dissolution of a blood clot (thrombus).
▪ Fibrinolytic drugs work by activating the so-called fibrinolytic
pathway.
▪ This distinguishes them from the anticoagulant drugs (coumarin
derivatives and heparin), which prevent the formation of blood clots by
suppressing the synthesis or function of various clotting factors that are
normally present in the blood.
▪ Administration of a fibrinolytic agent is indicated in patients with STE
ACS who present to the hospital within 12 hours of onset of chest
discomfort and have at least 1 mm of STE in two or more contiguous
ECG leads or a new left bundle-branch block.
51. ▪ Fibrinolytic therapy also should be considered in patients presenting
within 12–24 hours of onset of chest discomfort and have persistent
symptoms of ischemia and at least 1 mm of STE in two or more
contiguous leads.
▪ Because administration of fibrinolytics results in clot lysis, patients at
high risk for major bleeding, including those with ICH, have either
relative or absolute contraindications.
▪ Patients presenting with an absolute contraindication likely will not
receive fibrinolytic therapy, and primary PCI is preferred.
▪ Fibrinolytic therapy is controversial in patients older than 75 years.
▪ Stroke rates also grow in number with increasing patient age.
55. Adverse Drug Reactions
▪ Non-cardiogenic pulmonary edema.
▪ Hypotension.
▪ Fever and shivering.
▪ History of cerebrovascular hemorrhage at any time.
▪ Nonhemorrhagic stroke or other cerebrovascular event within the past year.
▪ Marked hypertension ( reliably determined systolic arterial pressure >180
mmHg and/or a diastolic pressure >110 mmHg) at any time during
presentation.
▪ Suspicion of aortic dissection.
▪ Active internal bleeding (excluding menses).
56. Relative contraindications to thrombolytic therapy
▪ Current use of anticoagulats (INR 2).
▪ A recent (<2 weeks) invasive or surgical procedure or prolonged (10
min) cardiopulmonaty resuscitation .
▪ Known bleeding diathesis.
▪ Pregnancy.
▪ Hemorrhagic ophthalmic condition.
▪ Active peptic ulcer disease.
▪ History of severe hypertension that is currently adequately controlled
57. Aspirin
▪ Based on several randomized trials, aspirin has become the preferred
antiplatelet agent for treatment of all ACSs.
▪ Early aspirin administration to all patients without contraindications
within the first 24 hours of hospital admission is a quality care
indicator.
▪ The antiplatelet effects of aspirin are mediated by inhibition of
thromboxane A2 synthesis through irreversible inhibition of platelet
cyclooxygenase- 1 (COX-1).
▪ Following administration of a non–enteric-coated formulation, aspirin
rapidly (<10 minutes) inhibits thromboxane A2 production in the
platelets.
58. ▪ Aspirin also has anti-inflammatory actions, which decrease C-reactive
protein and may contribute to its effectiveness in ACS.
▪ In patients experiencing an ACS, an initial dose equal to greater than
160 mg nonenteric aspirin is necessary to achieve rapid platelet
inhibition.
▪ This first dose can be chewed in order to achieve high blood
concentrations and rapid platelet inhibition.
▪ Current data suggest that although an initial dose of 160 to 325 mg is
required, long-term therapy with doses of 75 to 150 mg daily are as
effective as higher doses and, therefore,48 a daily maintenance dose of
75 to 160 mg is recommended in most patients to inhibit the 10% of
the total platelet pool that is regenerated daily.
59. MOA ADR
▪ Abdominal or Stomach Pain, Cramping, or
Burning, Black, Tarry Stools, Bloody or Cloudy
Urine.
▪ Change In Consciousness, Chest Pain or
Discomfort, Confusion, Constipation.
▪ Decreased Frequency or Amount of Urine,
Diarrhea.
▪ Difficult Breathing, Drowsiness, Fainting, Fast
Breathing.
61. Thienopyridines
▪ Although aspirin is effective in the setting of ACS, it is a relatively
weak platelet inhibitor that blocks platelet aggregation through only
one pathway.
▪ The thienopyridines clopidogrel and ticlopidine are antiplatelet agents
that mediate their antiplatelet effects through a blockade of ADP
P2Y12 receptors on platelets.
▪ Because ticlopidine is associated with the occurrence of neutropenia
that requires frequent monitoring of the complete blood count during
the first 3 months of use.
▪ Clopidogrel is the preferred thienopyridine for ACS and PCI patients.
64. Contraindications
▪ Increased risk of bleeding (i.e. frequent falls, gastrointestinal bleeds)
▪ History of hematological disease
▪ Severe liver disease
▪ History of allergic reaction to ticlopidine or any thienopyridine drug
such as clopidogrel
▪ Because of the increased risk of bleeding, patients taking ticlopidine
should discontinue the medication 10–14 days before surgery.
▪ Pregnancy and lactation
66. GP IIb/IIIa Receptor Inhibitors
▪ Abciximab is a first-line GP IIb/IIIa receptor inhibitor for patients
undergoing primary PCI who have not received fibrinolytics.
▪ It should not be administered for medical management of patients with
STE ACS who will not be undergoing PCI.
▪ Abciximab, in combination with aspirin, a thienopyridine, and UFH
reduced mortality and reinfarction without increasing the risk of major
bleeding.
67. MOA
GP IIb/IIIa receptor inhibitors block the final
common pathway of platelet aggregation,
namely, cross-linking of platelets by fibrinogen
bridges between the GP IIb/IIIa receptors on
the platelet surface.
68. ADR
▪ allergic reaction
▪ headache, back pain, nausea/vomiting
▪ dizziness/lightheadness/ fainting, and
▪ pain at the injection site.
69. Dose
GP IIb/IIIa Receptor
Inhibitors
Recommended Dose Duration of Therapy
Abciximab Bolus: 0.25mg/kg
Continuous: 0.125mg/kg/min
Continue 12h post
procedure
Tirofiban Bolus: 0.25mg/kg
Continuous: 0.125mg/kg/min
Continue 12-18h post
procedure
Eptifibatide Bolus: 180mcg/kg × 2 bolus
dose
Continuous: 2mcg/kg/min
71. 1. Indirect Thrombin Inhibitors (Heparin)
▪ UFH, administered as an IV bolus followed by a continuous infusion, is
a first-line anticoagulant for treatment of patients with STE ACS, both
for medical therapy and for patients undergoing PCI.
▪ UFH binds to antithrombin and then inhibits the activity of clotting
factors Xa and IIa (thrombin).
▪ Anticoagulant therapy should be initiated in the emergency
department and continued for at least 48 hours in selected patients
who will be bridged over to receive chronic warfarin anticoagulation
following acute MI.
▪ If a patient undergoes PCI, UFH is discontinued immediately afterthe
procedure.
72. ▪ For more than 40 years UFH has been the traditional anticoagulant
administered to patients with STE ACS for prevention of infarct
artery reocclusion.
▪ Other beneficial effects of anticoagulation in patients with ACS are
prevention of cardioembolic stroke and venous thromboembolism.
▪ LMWH, because their composition is mostly short saccharide
chain lengths, they preferentially inhibit factor Xa over factor IIa,
which requires larger chain lengths for binding and inhibition.
▪ Although the bleeding rates were increased in patients older than
75 years compared to younger patients.
73. ▪ Fondaparinux is an indirect-acting specific inhibitor of factor Xa
that has recently been studied in the setting of STE ACS.
▪ Unlike UFH and LMWHs, fondaparinux does not cause heparin-
induced thrombocytopenia.
75. ADR
▪ A possible side effect of anticoagulants is excessive bleeding (haemorrhage),
because these medicines increase the time it takes for blood clots to form.
▪ Excessive bleeding
Signs of excessive bleeding can include:
Passing blood in your urine, passing blood when you poo or having black poo
Severe bruising, prolonged nosebleeds (lasting longer than 10 minutes)
Bleeding gums, vomiting blood or coughing up blood
Sudden severe back pain, difficulty breathing or chest pain
In women, heavy or increased bleeding during your periods, or any other
bleeding from your vagina
76. ▪ Diarrhoea or Constipation
▪ Feeling and being sick
▪ Indigestion
▪ Dizziness
▪ Headaches
▪ Rashes
▪ Itchy Skin
▪ Hair Loss
▪ Jaundice
78. Fondaparinux 2.5 mg SC OD 5mg (<50kg), 7.5mg (50-100),
10mg (>100kg) SC OD
0.25 s.c. once day
79. 2. Direct Thrombin Inhibitors
Direct thrombin inhibitors (DTIs) are a class of medication that act
as anticoagulants (delaying blood clotting) by directly inhibiting
the enzyme thrombin (factor II).
Some are in clinical use, while others are undergoing clinical
development.
Several members of the class are expected to replace heparin (and
derivatives) and warfarin in various clinical scenarios.
Bivalent DTIs enjoy limited use in circumstances where heparin would
be indicated such as the acute coronary syndrome ("unstable angina"),
but cannot be used. As they are administered by injection
(intravenous, intramuscular or subcutaneous), they are less suitable for
long-term treatment.
82. 3. Vitamin K Epoxide reductase inhibitors or Vit. K
Antagonist
▪ Vitamin K antagonists (VKA) are a group of substances that
reduce blood clotting by reducing the action of vitamin K.
▪ They are used as anticoagulant medications in the prevention
of thrombosis, and in pest control, as rodenticides.
▪ deplete the active form of the vitamin by inhibiting the enzyme vitamin
K epoxide reductase and thus the recycling of the inactive vitamin K
epoxide back to the active reduced form of vitamin K.
83. 1. Coumarins Derivatives
The most commonly used VKA is warfarin.
Others, Coumatetralyl, Phenprocoumon etc.
2. Indandiones
Pindone, chlorophacinone, and diphacinone are used as rodenticides.
Anisindione, fluindione, and phenindione are oral anticoagulant
medicines with actions similar to warfarin.
84. Nitrates
▪ Nitrates promote the release of nitric oxide from the endothelium, which
results in venous and arterial vasodilation at higher doses.
▪ Venodilation lowers preload and myocardial oxygen demand.
▪ Arterial vasodilation may lower blood pressure, thus reducing myocardial
oxygen demand.
▪ One SL NTG tablet (0.4 mg) should be administered every 5 minutes for
up to three doses to relieve myocardial ischemia.
▪ IV NTG is indicated in patients with ACS who do not have a
contraindication and who have persistent ischemic symptoms, heart failure,
or uncontrolled blood pressure.
▪ It should be continued for approximately 24 hours after ischemia is
relieved
85. ▪ The most significant adverse effects of nitrates are tachycardia,
flushing, headache, and hypotension.
▪ Nitrate administration is contraindicated in patients who have received
oral phosphodiesterase- 5 inhibitors, such as sildenafil and vardenafil,
within the past 24 hours and tadalafil within the past 48 hours.
86. β-Blockers
▪ Aβ-blocker should be administered early in the care of patients with
STE ACS and continued indefinitely.
▪ In ACS, the benefit of β-blockers results mainly from the competitive
blockade of β1-adrenergic receptors located on the myocardium.
▪ β1-blockade produces a reduction in heart rate, myocardial
contractility, and blood pressure, decreasing myocardial oxygen
demand.
▪ In addition, the reduction in heart rate increases diastolic time, thus
improving ventricular filling and coronary artery perfusion.
▪ β-blockers reduce the risk for recurrent ischemic, infarct size, risk of
reinfarction, and occurrence of ventricular arrhythmias in the hours and
days following MI.
87. ▪ The most serious side effects of β-blocker administration early in ACS
are hypotension, acute heart failure, bradycardia, and heart block.
▪ In patients in whom a major concern exists regarding a possible
intolerance to β-blockers, such as patients with bronchospastic
pulmonary disease, a short-acting β-blocker, such as metoprolol or
esmolol, initially should be administered IV.
▪ β-Blockers are continued indefinitely
88. Calcium Channel Blockers
▪ Administration of calcium channel blockers in the setting of STE ACS is reserved for
patients who have contraindications to β-blockers and is given for relief of ischemic
symptoms.
▪ Calcium channel blockers inhibit calcium influx into myocardial and vascular smooth
muscle cells, causing vasodilation.
▪ Although all calcium channel blockers produce coronary vasodilation and decrease
blood pressure, other effects are more heterogeneous between agents.
▪ Verapamil, diltiazem, and first-generation dihydropyridines also should be avoided in
patients with decompensated heart failure or LV dysfunction because these drugs can
worsen heart failure and potentially increase mortality secondary to their negative
inotropic effects.
91. ▪ In general, early pharmacotherapy for NSTE ACS is similar to that for
STE ACS with three exceptions:
1. Fibrinolytic therapy is not administered.
2. GP IIb/IIIa receptor blockers are administered to high-risk patients.
3. There are no standard quality performance measures for patients with
NSTE ACS with unstable angina (not diagnosed with MI).
▪ According to the ACC/AHA NSTE ACS practice guidelines, early
pharmacotherapy for NSTE ACS should include intranasal oxygen (if
oxygen saturation is <90%), SL NTG, aspirin, an oral β- blocker (IV β-
blocker optional), and an anticoagulant (UFH, LMWH [enoxaparin],
fondaparinux, or bivalirudin).
92. ▪ Morphine is also administered to patients with refractory angina,
as described previously in Early Pharmacotherapy for STE ACS.
▪ IV NTG should be administered in selected patients without
contraindications.
93.
94. SECONDARY PREVENTION FOLLOWING MI
▪ The long-term goals following MI are as follow:
1. Control modifiable CHD risk factors
2. Prevent development of systolic heart failure
3. Prevent recurrent MI and stroke
4. Prevent death, including sudden cardiac death
▪ Pharmacotherapy that has been proven to decrease mortality, heart
failure, reinfarction, or stroke should be initiated prior to hospital
discharge for secondary prevention.
95. ▪ Guidelines from the ACC/AHA suggest that following MI from either STE or NSTE
ACS, patients should receive indefinite treatment with aspirin, a β-blocker, and an ACE
inhibitor.
▪ All patients should receive SL NTG or lingual spray and instructions for use in case of
recurrent ischemic chest discomfort.
▪ Clopidogrel should be considered for most patients, but the duration of therapy is
individualized according to the type of ACS.
▪ Newer therapies include eplerenone, an aldosterone antagonist for heart failure.
▪ For all ACS patients, treatment and control of modifiable risk factors, such as
hypertension, dyslipidemia, and diabetes mellitus, are essential.
▪ Most patients with CHD will require drug therapy for dyslipidemia, usually with a
statin
96. Aspirin
▪ Aspirin decreases the risk of death, recurrent MI, and stroke following MI.
▪ The clinical value of aspirin in secondary prevention of ACS and other
vascular diseases was demonstrated in a large number of clinical trials.
▪ The risk of major bleeding from chronic aspirin therapy is approximately
2% and is dose related. (Dose related)
▪ After an initial dose of 325 mg, chronic therapy with aspirin should be 75 to
81 mg once daily.
▪ AHA/ACC recommend 162–325 mg of aspirin once daily for at least 30
days
▪ To minimize the risk of bleeding combinations should be avoided unless the
combination is clinically indicated.
97. Thienopyridines
▪ For patients with NSTE ACS, clopidogrel decreases the risk of
developing death, MI, or stroke.
▪ The benefit derives primarily from reducing the rate of MI.
▪ Most patients with NSTE ACS should receive clopidogrel, in addition
to aspirin, for up to 12 months.
▪ The most common adverse effects in patients receiving clopidogrel are
rash (5%) and gastrointestinal upset (3%).
98. Anticoagulation
▪ Warfarin should be considered in selected patients following an ACS,
including patients with an LV thrombus, patients demonstrating
extensive ventricular wall-motion abnormalities on cardiac
echocardiogram, and patients with a history of thromboembolic disease
or chronic atrial fibrillation.
99. β-Blockers, Nitrates, and Calcium
Channel Blockers
▪ Current treatment guidelines recommend that, following an ACS, patients
should receive a β-blocker indefinitely, whether or not they have residual
symptoms of angina.
▪ benefit from β-blockers appears to be maintained for at least 6 years
following an MI.
▪ β-blockers should be avoided in patients with decompensated heart failure
from LV systolic dysfunction complicating an MI.
▪ All patients should be prescribed short-acting SL NTG or lingual NTG spray
to relieve any anginal symptoms when necessary and should be instructed on
its use.
▪ Chronic long-acting nitrate therapy has not been shown to reduce CHD
events following MI.
100. ACE Inhibitors and Angiotensin
Receptor Blockers
▪ ACE inhibitors should be initiated in all patients following MI to
reduce mortality, decrease reinfarction, and prevent development of
heart failure.
▪ The benefit of ACE inhibitors in patients with MI most likely derives
from their ability to prevent cardiac remodeling.
▪ Other proposed mechanisms include improvement in endothelial
function, reduction in atrial and ventricular arrhythmias, and promotion
of angiogenesis, leading to a reduction in ischemic events.
▪ The largest reduction in mortality is observed for patients with LV
dysfunction (low LVEF) or heart failure symptoms.
101. ▪ Many patients cannot tolerate chronic ACE inhibitor therapy secondary
to adverse effects.
▪ However, trials have documented that the angiotensin receptor blockers
candesartan and valsartan improve clinical outcomes in patients with
heart failure.
▪ Although some data have suggested that aspirin use may decrease the
benefits of ACE inhibitor treatment, a systematic review of more than
20,000 patients demonstrated that ACE inhibitors improve outcome
irrespective of treatment with aspirin.
102. Aldosterone Antagonists
▪ Administration of an aldosterone antagonist, either eplerenone or
spironolactone, should be considered within the first 2 weeks following
MI in all patients already receiving an ACE inhibitor who have EF
≤40% and either heart failure symptoms or a diagnosis of diabetes
mellitus to reduce mortality.
▪ Aldosterone plays an important role in heart failure and MI because it
promotes vascular and myocardial fibrosis, endothelial dysfunction,
hypertension, LV hypertrophy, sodium retention, potassium and
magnesium loss, and arrhythmias.
103. Lipid-Lowering Agents
▪ The benefits of statins in patients with CAD for the prevention of total
mortality, cardiovascular mortality, and stroke.
▪ dietary counseling, LDL <100 mg/dL.
▪ A fibrate or niacin should be considered in selective patients with a low
high-density lipoprotein (HDL) cholesterol concentration (<40 mg/dL)
and/or a high triglyceride level (>200 mg/dL).
▪ use of gemfibrozil (600 mg twice daily) significantly decreased the risk
of nonfatal MI or death from coronary causes.
▪ Due to the increased risk of myopathy, gemfibrozil is not
recommended in patients receiving a statin.
104. Fish Oils (Marine-Derived ω-3 Fatty Acids)
▪ Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are ω-3
polyunsaturated fatty acids that are most abundant in fatty fish such as
sardines, salmon, and mackerel.
▪ Although the exact mechanism responsible for the beneficial effects of
ω-3 fatty acids has not been clearly elucidated, potential mechanisms
include triglyceride-lowering effects, antithrombotic effects,
retardation in the progression of atherosclerosis, endothelial relaxation,
mild antihypertensive effects, and reduction in ventricular arrhythmias.
▪ Adverse effects from fish oils include fishy after taste, nausea, and
diarrhea.
105. Other Modifiable Risk Factors
▪ Smoking cessation, control of hypertension, weight loss, and tight
glucose control for patients with diabetes mellitus, in addition to
treatment of dyslipidemia, are important treatments for secondary
prevention of CHD events.
▪ All patients with CAD should receive annual influenza vaccination.
▪ Hypertension should be strictly controlled to a target blood pressure
<130/80 and even lower, and to <120/80 in patients with LV
dysfunction according to recently published guidelines from AHA.
▪ Patients who are overweight should be educated on the importance of
regular exercise, healthy eating habits, and of reaching and maintaining
an ideal weight.
106. ▪ diabetics have up to a fourfold increased risk of mortality compared
with non-diabetics, the importance of tight glucose control, as well as
other CHD risk factor modification, cannot be understated.
109. EVALUATION OF THERAPEUTIC OUTCOMES
The monitoring parameters for efficacy of non-pharmacologic and
pharmacotherapy for both STE and NSTE ACS are similar:
Relief of ischemic discomfort
Return of ECG changes to baseline
Absence or resolution of heart failure signs
110. References
1)Joseph. T. Dipiro, Pharmacotherapy: A pathophysiologic approach, seventh
edition
2)Eric. T. Herfindal, Textbook of Therapeutics : Drug and Disease
Management, Eight edition
3) Roger Walker, Clinical Pharmacy And Therapeutics, Fourth Edition