1. Acute coronary syndrome is defined as myocardial ischemia due to myocardial infarction (NSTEMI or STEMI) or unstable angina.
2. Unstable angina is defined as angina at rest, new onset exertional angina (<2 months), recent acceleration of angina (<2 months), or post revascularization angina.
3. The diagnosis of acute coronary syndrome is based on history, physical exam, ECG, and cardiac enzymes. Patients can then be divided into several diagnostic groups.
1. The document presents an algorithm for the assessment, treatment, and management of acute coronary syndromes, including ST-elevation myocardial infarction (STEMI) and high-risk unstable angina/non-ST-elevation MI (UA/NSTEMI).
2. It outlines the steps for EMS assessment and care, including acquiring an ECG, administering aspirin and nitroglycerin, and activating the cardiac cath lab.
3. At the hospital, it recommends further tests and treatments depending on the patient's risk level and ECG findings, with goals of door-to-balloon times under 90 minutes for STEMI and door-to-needle times under 30 minutes for fibrinolysis
This document provides guidelines for the management of chronic stable angina. It recommends comprehensive patient education on lifestyle modifications, medications, and symptoms. Medical therapy should focus on risk factor modification through statins, blood pressure control, diabetes management, and physical activity. Antiplatelet, beta-blocker, ACE inhibitor/ARB therapy are recommended. For symptom relief, beta-blockers, calcium channel blockers, or nitrates should be used. A heart team approach is advised for revascularization decisions in complex cases. CABG is recommended for significant left main coronary artery stenosis while PCI may be an alternative in selected cases.
Ischemic heart disease (IHD), also known as coronary heart disease (CHD) or coronary artery disease (CAD), is caused by a reduction of blood flow to the heart due to atherosclerosis of the coronary arteries. Risk factors include metabolic syndrome, smoking, diabetes, hypertension and high cholesterol. Symptoms range from stable angina to acute coronary syndrome (ACS). Diagnosis involves electrocardiogram (ECG), stress testing, coronary angiography and biochemical markers. Treatment depends on severity but may include lifestyle changes, medications like nitrates, beta-blockers, calcium channel blockers, statins, aspirin and revascularization procedures like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (C
This document discusses beta blockers and focuses on bisoprolol. It summarizes that:
1) Beta blockers are a class of drugs used to treat heart conditions like heart failure and hypertension, but they have diverse properties. Bisoprolol is a selective beta-1 blocker.
2) Studies show bisoprolol provides similar or better blood pressure control compared to other beta blockers like atenolol and metoprolol. It also provides superior heart rate reduction.
3) The CIBIS II trial found bisoprolol reduced all-cause mortality by 34% in heart failure patients when added to standard therapy of diuretics and ACE inhibitors.
The document discusses the management of chronic stable angina. It defines angina and stability, and outlines the typical treatment approach which includes patient education, risk factor modification through lifestyle changes and medical therapy, and consideration of revascularization. The mainstay of treatment is optimal medical therapy focusing on symptom control through anti-anginal medications like beta-blockers, calcium channel blockers, and nitrates, as well as prevention of adverse outcomes with aspirin and other drugs.
This is a power point presentation titled "Chronic Stable Angina" . For more medical power points, PDFs, ECGs, X-rays, please visit www.medicaldump.com
Coronary microvascular disease (CMVD), also known as cardiac syndrome X, can present with chest pain despite normal coronary arteries. It is classified into several types depending on whether structural heart disease is present. CMVD may be caused by abnormalities in the coronary microcirculation that lead to localized myocardial ischemia. Diagnosis involves stress tests showing ischemia without contractile abnormalities. Treatment focuses on lifestyle modification, medications like calcium channel blockers and ranolazine, and alternative therapies for pain management. In rare cases of microvascular "variant angina", coronary microvascular spasm can cause transient ST elevation resembling epicardial coronary spasm.
Non-Specific Intra-Ventricular Conduction Delay - A quick-lit-reviewSimon Daley
Non-specific intraventricular conduction delay (nsIVCD) is defined as a QRS duration over 110ms in adults without meeting criteria for right or left bundle branch block. NsIVCD can be caused by myocardial infarction, fibrosis, amyloidosis, cardiomyopathy or hypertrophy. Five studies were reviewed on the clinical significance of nsIVCD. Three of the four largest studies found that nsIVCD predicts increased mortality and cardiac risk, especially in those with or at risk of ischemic heart disease. However, one large study found no increased mortality risk in those without ischemic heart disease when adjusted for controls. There are implications for testing and management of risk factors in patients with nsIVCD.
1. The document presents an algorithm for the assessment, treatment, and management of acute coronary syndromes, including ST-elevation myocardial infarction (STEMI) and high-risk unstable angina/non-ST-elevation MI (UA/NSTEMI).
2. It outlines the steps for EMS assessment and care, including acquiring an ECG, administering aspirin and nitroglycerin, and activating the cardiac cath lab.
3. At the hospital, it recommends further tests and treatments depending on the patient's risk level and ECG findings, with goals of door-to-balloon times under 90 minutes for STEMI and door-to-needle times under 30 minutes for fibrinolysis
This document provides guidelines for the management of chronic stable angina. It recommends comprehensive patient education on lifestyle modifications, medications, and symptoms. Medical therapy should focus on risk factor modification through statins, blood pressure control, diabetes management, and physical activity. Antiplatelet, beta-blocker, ACE inhibitor/ARB therapy are recommended. For symptom relief, beta-blockers, calcium channel blockers, or nitrates should be used. A heart team approach is advised for revascularization decisions in complex cases. CABG is recommended for significant left main coronary artery stenosis while PCI may be an alternative in selected cases.
Ischemic heart disease (IHD), also known as coronary heart disease (CHD) or coronary artery disease (CAD), is caused by a reduction of blood flow to the heart due to atherosclerosis of the coronary arteries. Risk factors include metabolic syndrome, smoking, diabetes, hypertension and high cholesterol. Symptoms range from stable angina to acute coronary syndrome (ACS). Diagnosis involves electrocardiogram (ECG), stress testing, coronary angiography and biochemical markers. Treatment depends on severity but may include lifestyle changes, medications like nitrates, beta-blockers, calcium channel blockers, statins, aspirin and revascularization procedures like percutaneous coronary intervention (PCI) or coronary artery bypass grafting (C
This document discusses beta blockers and focuses on bisoprolol. It summarizes that:
1) Beta blockers are a class of drugs used to treat heart conditions like heart failure and hypertension, but they have diverse properties. Bisoprolol is a selective beta-1 blocker.
2) Studies show bisoprolol provides similar or better blood pressure control compared to other beta blockers like atenolol and metoprolol. It also provides superior heart rate reduction.
3) The CIBIS II trial found bisoprolol reduced all-cause mortality by 34% in heart failure patients when added to standard therapy of diuretics and ACE inhibitors.
The document discusses the management of chronic stable angina. It defines angina and stability, and outlines the typical treatment approach which includes patient education, risk factor modification through lifestyle changes and medical therapy, and consideration of revascularization. The mainstay of treatment is optimal medical therapy focusing on symptom control through anti-anginal medications like beta-blockers, calcium channel blockers, and nitrates, as well as prevention of adverse outcomes with aspirin and other drugs.
This is a power point presentation titled "Chronic Stable Angina" . For more medical power points, PDFs, ECGs, X-rays, please visit www.medicaldump.com
Coronary microvascular disease (CMVD), also known as cardiac syndrome X, can present with chest pain despite normal coronary arteries. It is classified into several types depending on whether structural heart disease is present. CMVD may be caused by abnormalities in the coronary microcirculation that lead to localized myocardial ischemia. Diagnosis involves stress tests showing ischemia without contractile abnormalities. Treatment focuses on lifestyle modification, medications like calcium channel blockers and ranolazine, and alternative therapies for pain management. In rare cases of microvascular "variant angina", coronary microvascular spasm can cause transient ST elevation resembling epicardial coronary spasm.
Non-Specific Intra-Ventricular Conduction Delay - A quick-lit-reviewSimon Daley
Non-specific intraventricular conduction delay (nsIVCD) is defined as a QRS duration over 110ms in adults without meeting criteria for right or left bundle branch block. NsIVCD can be caused by myocardial infarction, fibrosis, amyloidosis, cardiomyopathy or hypertrophy. Five studies were reviewed on the clinical significance of nsIVCD. Three of the four largest studies found that nsIVCD predicts increased mortality and cardiac risk, especially in those with or at risk of ischemic heart disease. However, one large study found no increased mortality risk in those without ischemic heart disease when adjusted for controls. There are implications for testing and management of risk factors in patients with nsIVCD.
MANAGEMENT OF ANTERIOR WALL MI WITH SHOCK IN A NON PCI CENTER Praveen Nagula
Cardiogenic shock is a major cause of death in AMI patients and requires immediate diagnosis and management. The document outlines the definition, causes, predictive indicators, medical and interventional management of cardiogenic shock. It recommends emergency revascularization with PCI or CABG for suitable patients irrespective of time delay from MI onset. For those unsuitable for revascularization, fibrinolytic therapy is recommended if no contraindications. Intra-aortic balloon pump can be useful for hemodynamically unstable patients while alternative devices may be considered for refractory shock.
1. Chronic coronary syndromes (CCS) refer to conditions involving atherosclerotic plaque buildup in the coronary arteries that can cause various clinical presentations depending on the dynamic nature of the disease process.
2. The most common clinical scenarios in patients with suspected or established CCS involve those with stable angina symptoms, new onset of heart failure, recent acute coronary syndrome, or asymptomatic patients more than 1 year after initial diagnosis or revascularization.
3. Evaluation and management of patients with suspected CCS involves assessing symptoms, risk factors and comorbidities, performing basic testing, estimating pre-test probability of CAD, selecting appropriate non-invasive testing to confirm diagnosis when needed, calculating risk, and determining long-
This document discusses risk stratification for patients presenting with unstable angina/NSTEMI. It defines risk stratification and outlines its benefits in guiding initial evaluation and treatment. Several common risk scores for ischemic risk (TIMI, PURSUIT, FRISC, GUSTO, GRACE) and bleeding risk (CRUSADE, ACUITY, HAS-BLED) are described. The GRACE score was found to best predict risk of death or myocardial infarction at one year. ECG patterns suggestive of ischemia and infarction are also reviewed. In conclusion, risk stratification using simple bedside scores like TIMI can categorize patients' risk, while the GRACE score further guides long-term prognosis and care
1) Coronary artery disease (CAD) is a leading cause of death worldwide. Risk factors like high blood pressure, smoking, and diabetes can increase the probability of CAD occurring within 10 years.
2) CAD results from atherosclerosis, a chronic inflammatory disease involving endothelial dysfunction and narrowing of the coronary arteries. Manifestations include angina, myocardial infarction, and sudden cardiac death.
3) Early risk stratification of patients with suspected acute coronary syndrome involves assessing anginal symptoms, ECG findings, and cardiac biomarkers to determine risk and guide initial evaluation and management.
Trimetazidine is an effective treatment for chronic stable angina. It works by shifting cardiac energy production from fatty acid oxidation to glucose oxidation, thereby reducing ischemia and improving cardiac efficiency. The document outlines the definition, grading, pathophysiology, and treatment goals for chronic stable angina. It describes the mechanisms of action and benefits of trimetazidine, including reduced angina attacks, increased exercise capacity, improved left ventricular function, and reduced mortality risk. Trimetazidine is recommended in international guidelines as an effective second-line treatment for chronic stable angina.
This document discusses several novel biomarkers for acute coronary syndrome (ACS). It describes C-reactive protein (CRP) as a marker of extensive vascular inflammation. High-sensitivity CRP levels above 10 mg/L are more predictive of outcomes in ACS patients. Soluble CD40 ligand and myoglobin are also discussed as inflammation markers. Microalbuminuria is related to endothelial dysfunction and an increased risk of cardiovascular disease. Cystatin C and metalloproteinases are associated with arterial stiffness and plaque degradation. Several microRNAs such as miR-1, miR-133 and miR-208 are described as potential biomarkers for myocardial infarction, cardiac hypertrophy, and arrhythmias.
- A study evaluated the efficacy and safety of alirocumab in adults with homozygous familial hypercholesterolemia.
- 45 patients received alirocumab and 24 received placebo for 78 weeks.
- Alirocumab reduced LDL-C levels by 24.8% compared to placebo and was well tolerated, with adverse events similar between groups.
- Alirocumab provided clinically significant LDL-C lowering in patients with homozygous familial hypercholesterolemia.
The document discusses refractory angina, a condition where chest pain persists despite optimal medical therapy and invasive procedures. It describes various treatment options for chronic angina when standard therapies fail, including ranolazine which inhibits the late sodium current as a new potential antianginal option.
Risk stratification in UA and NSTEMI: Why and How?cardiositeindia
This document discusses risk stratification in patients with unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI). It summarizes three risk scores - the TIMI score, PURSUIT score, and GRACE score - and evaluates their ability to predict adverse cardiac outcomes at 30 days and 1 year. The study found that all three scores had fair to good predictive accuracy at 30 days, while the GRACE score was best at predicting outcomes at 1 year. Revascularization was found to provide greater benefit in higher risk patients as classified by these risk scores.
Risk stratification and medical management of stemidrranjithmp
This document discusses criteria for diagnosing myocardial infarction and risk stratification of STEMI patients. It outlines the definition of MI, criteria for acute/evolving MI, and criteria for established MI. It also discusses risk stratification tools like TIMI risk score and management of STEMI in the initial presentation, in-hospital course, and at discharge. Medical management includes oxygen, nitrates, analgesics, and beta blockers. Fibrinolytic therapy and anticoagulation are also summarized.
This document discusses coronary artery disease (CAD) and ischemic heart disease (IHD). It defines IHD as a disease of the heart muscle resulting from a lack of oxygen due to an imbalance between myocardial oxygen requirements and supply. CAD is most commonly caused by atherosclerosis. The spectrum of IHD ranges from silent ischemia to myocardial infarction and heart failure. Acute coronary syndrome (ACS) refers to the unstable spectrum of IHD and includes unstable angina and myocardial infarction. Biomarkers, imaging, and risk scores are used to stratify patients according to their risk. Medical management involves anti-ischemic therapies, antiplatelet agents, and risk factor modification.
Non st elevation myocardial infarction and unstable anginaGrerk Sutamtewagul
This document outlines the definition, pathophysiology, clinical presentation, risk stratification, and management of unstable angina and non-ST elevation myocardial infarction (NSTEMI). It defines unstable angina and NSTEMI and describes the pathophysiologic process involving plaque rupture, thrombosis, and vasoconstriction. It discusses the clinical examination, electrocardiogram, cardiac markers, and high-risk subgroups. Scoring systems like the TIMI risk score and GRACE risk score are presented to aid in risk stratification and prognostication.
emergency treatment of NSTE-ACS, STEMI,Bibhash Kumar
1. Acute coronary syndrome can present as STEMI, NSTEMI, or unstable angina. The document discusses treatment recommendations for NSTEMI.
2. The goals of treatment are immediate relief of ischemia to prevent heart attack and death. Initially patients are monitored in intermediate care and receive medications and oxygen as needed.
3. Recommendations include high intensity statins, aspirin, P2Y12 inhibitors like clopidogrel or ticagrelor, and anticoagulants like enoxaparin as initial therapies. Beta blockers and nitroglycerin are also recommended depending on patient factors.
This document discusses recent advances in the treatment of thrombotic disorders. It describes the pathophysiology of arterial and venous thrombus formation and lists various activators and inhibitors of coagulation. It then summarizes various anticoagulant, antiplatelet and thrombolytic agents and their targets, mechanisms of action, advantages and limitations. Several newer oral anticoagulants targeting factor Xa and thrombin are discussed along with their ongoing clinical trials. The document also explores newer antiplatelet agents targeting PAR-1, P2Y12 receptors and thromboxane receptors. Various investigational agents such as RNA aptamers, monoclonal antibodies and aptamers are briefly outlined.
This document provides clinical practice guidelines for the management of unstable angina/non-ST elevation myocardial infarction (UA/NSTEMI) from 2011. It outlines:
1. The diagnosis and risk stratification of UA/NSTEMI based on history, ECG changes, and cardiac biomarker levels.
2. The initial management of intermediate- and high-risk patients, which includes aspirin, clopidogrel or ticagrelor, antithrombotics, beta-blockers, statins, ACE-I/ARB, and consideration of urgent angiography for refractory or unstable cases.
3. Medical therapies and revascularization for low-, intermediate-, and high
This document summarizes evidence from major clinical trials supporting current pharmacological treatments for chronic heart failure (CHF). It discusses trials that demonstrated mortality benefits of ACE inhibitors, beta-blockers, aldosterone receptor antagonists, and hydralazine/isosorbide dinitrate combinations. Together, these trials established the current neurohormonal model of CHF and shifted focus to treatments targeting the renin-angiotensin-aldosterone system and sympathetic nervous system overactivation in CHF.
Risk stratification remains central to implement appropriate therapeutic measures for patients with NSTEMI.
The ECG provides rapid risk assessment for patients presenting with chest pain that permits their allocation to appropriate management algorithms to improve the outcomes
This document provides an overview of acute coronary syndrome (ACS). It defines ACS and describes the epidemiology in Malaysia. The pathophysiology, classification, clinical presentation and investigations are discussed for unstable angina/NSTEMI and STEMI. Management is outlined for both conditions, including medications, fibrinolytic therapy, percutaneous coronary intervention and complications. A clinical case of STEMI is then presented demonstrating diagnosis and management. The document concludes with references to Malaysian clinical practice guidelines for ACS.
ACUTE CORONARY SYNDROME FOR CRITICAL CAREAbhinovKandur
The document defines acute coronary syndrome (ACS) as a group of diseases including unstable angina, myocardial infarction, and sudden cardiac death. ACS is classified into STEMI, NSTEMI, or unstable angina based on ECG and cardiac biomarker findings. The diagnosis of ACS involves taking a medical history, performing an ECG, and measuring cardiac biomarkers like troponin and CK-MB. Treatment involves pain relief medications, antiplatelet drugs, anticoagulants, and sometimes revascularization through procedures like angioplasty.
MANAGEMENT OF ANTERIOR WALL MI WITH SHOCK IN A NON PCI CENTER Praveen Nagula
Cardiogenic shock is a major cause of death in AMI patients and requires immediate diagnosis and management. The document outlines the definition, causes, predictive indicators, medical and interventional management of cardiogenic shock. It recommends emergency revascularization with PCI or CABG for suitable patients irrespective of time delay from MI onset. For those unsuitable for revascularization, fibrinolytic therapy is recommended if no contraindications. Intra-aortic balloon pump can be useful for hemodynamically unstable patients while alternative devices may be considered for refractory shock.
1. Chronic coronary syndromes (CCS) refer to conditions involving atherosclerotic plaque buildup in the coronary arteries that can cause various clinical presentations depending on the dynamic nature of the disease process.
2. The most common clinical scenarios in patients with suspected or established CCS involve those with stable angina symptoms, new onset of heart failure, recent acute coronary syndrome, or asymptomatic patients more than 1 year after initial diagnosis or revascularization.
3. Evaluation and management of patients with suspected CCS involves assessing symptoms, risk factors and comorbidities, performing basic testing, estimating pre-test probability of CAD, selecting appropriate non-invasive testing to confirm diagnosis when needed, calculating risk, and determining long-
This document discusses risk stratification for patients presenting with unstable angina/NSTEMI. It defines risk stratification and outlines its benefits in guiding initial evaluation and treatment. Several common risk scores for ischemic risk (TIMI, PURSUIT, FRISC, GUSTO, GRACE) and bleeding risk (CRUSADE, ACUITY, HAS-BLED) are described. The GRACE score was found to best predict risk of death or myocardial infarction at one year. ECG patterns suggestive of ischemia and infarction are also reviewed. In conclusion, risk stratification using simple bedside scores like TIMI can categorize patients' risk, while the GRACE score further guides long-term prognosis and care
1) Coronary artery disease (CAD) is a leading cause of death worldwide. Risk factors like high blood pressure, smoking, and diabetes can increase the probability of CAD occurring within 10 years.
2) CAD results from atherosclerosis, a chronic inflammatory disease involving endothelial dysfunction and narrowing of the coronary arteries. Manifestations include angina, myocardial infarction, and sudden cardiac death.
3) Early risk stratification of patients with suspected acute coronary syndrome involves assessing anginal symptoms, ECG findings, and cardiac biomarkers to determine risk and guide initial evaluation and management.
Trimetazidine is an effective treatment for chronic stable angina. It works by shifting cardiac energy production from fatty acid oxidation to glucose oxidation, thereby reducing ischemia and improving cardiac efficiency. The document outlines the definition, grading, pathophysiology, and treatment goals for chronic stable angina. It describes the mechanisms of action and benefits of trimetazidine, including reduced angina attacks, increased exercise capacity, improved left ventricular function, and reduced mortality risk. Trimetazidine is recommended in international guidelines as an effective second-line treatment for chronic stable angina.
This document discusses several novel biomarkers for acute coronary syndrome (ACS). It describes C-reactive protein (CRP) as a marker of extensive vascular inflammation. High-sensitivity CRP levels above 10 mg/L are more predictive of outcomes in ACS patients. Soluble CD40 ligand and myoglobin are also discussed as inflammation markers. Microalbuminuria is related to endothelial dysfunction and an increased risk of cardiovascular disease. Cystatin C and metalloproteinases are associated with arterial stiffness and plaque degradation. Several microRNAs such as miR-1, miR-133 and miR-208 are described as potential biomarkers for myocardial infarction, cardiac hypertrophy, and arrhythmias.
- A study evaluated the efficacy and safety of alirocumab in adults with homozygous familial hypercholesterolemia.
- 45 patients received alirocumab and 24 received placebo for 78 weeks.
- Alirocumab reduced LDL-C levels by 24.8% compared to placebo and was well tolerated, with adverse events similar between groups.
- Alirocumab provided clinically significant LDL-C lowering in patients with homozygous familial hypercholesterolemia.
The document discusses refractory angina, a condition where chest pain persists despite optimal medical therapy and invasive procedures. It describes various treatment options for chronic angina when standard therapies fail, including ranolazine which inhibits the late sodium current as a new potential antianginal option.
Risk stratification in UA and NSTEMI: Why and How?cardiositeindia
This document discusses risk stratification in patients with unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI). It summarizes three risk scores - the TIMI score, PURSUIT score, and GRACE score - and evaluates their ability to predict adverse cardiac outcomes at 30 days and 1 year. The study found that all three scores had fair to good predictive accuracy at 30 days, while the GRACE score was best at predicting outcomes at 1 year. Revascularization was found to provide greater benefit in higher risk patients as classified by these risk scores.
Risk stratification and medical management of stemidrranjithmp
This document discusses criteria for diagnosing myocardial infarction and risk stratification of STEMI patients. It outlines the definition of MI, criteria for acute/evolving MI, and criteria for established MI. It also discusses risk stratification tools like TIMI risk score and management of STEMI in the initial presentation, in-hospital course, and at discharge. Medical management includes oxygen, nitrates, analgesics, and beta blockers. Fibrinolytic therapy and anticoagulation are also summarized.
This document discusses coronary artery disease (CAD) and ischemic heart disease (IHD). It defines IHD as a disease of the heart muscle resulting from a lack of oxygen due to an imbalance between myocardial oxygen requirements and supply. CAD is most commonly caused by atherosclerosis. The spectrum of IHD ranges from silent ischemia to myocardial infarction and heart failure. Acute coronary syndrome (ACS) refers to the unstable spectrum of IHD and includes unstable angina and myocardial infarction. Biomarkers, imaging, and risk scores are used to stratify patients according to their risk. Medical management involves anti-ischemic therapies, antiplatelet agents, and risk factor modification.
Non st elevation myocardial infarction and unstable anginaGrerk Sutamtewagul
This document outlines the definition, pathophysiology, clinical presentation, risk stratification, and management of unstable angina and non-ST elevation myocardial infarction (NSTEMI). It defines unstable angina and NSTEMI and describes the pathophysiologic process involving plaque rupture, thrombosis, and vasoconstriction. It discusses the clinical examination, electrocardiogram, cardiac markers, and high-risk subgroups. Scoring systems like the TIMI risk score and GRACE risk score are presented to aid in risk stratification and prognostication.
emergency treatment of NSTE-ACS, STEMI,Bibhash Kumar
1. Acute coronary syndrome can present as STEMI, NSTEMI, or unstable angina. The document discusses treatment recommendations for NSTEMI.
2. The goals of treatment are immediate relief of ischemia to prevent heart attack and death. Initially patients are monitored in intermediate care and receive medications and oxygen as needed.
3. Recommendations include high intensity statins, aspirin, P2Y12 inhibitors like clopidogrel or ticagrelor, and anticoagulants like enoxaparin as initial therapies. Beta blockers and nitroglycerin are also recommended depending on patient factors.
This document discusses recent advances in the treatment of thrombotic disorders. It describes the pathophysiology of arterial and venous thrombus formation and lists various activators and inhibitors of coagulation. It then summarizes various anticoagulant, antiplatelet and thrombolytic agents and their targets, mechanisms of action, advantages and limitations. Several newer oral anticoagulants targeting factor Xa and thrombin are discussed along with their ongoing clinical trials. The document also explores newer antiplatelet agents targeting PAR-1, P2Y12 receptors and thromboxane receptors. Various investigational agents such as RNA aptamers, monoclonal antibodies and aptamers are briefly outlined.
This document provides clinical practice guidelines for the management of unstable angina/non-ST elevation myocardial infarction (UA/NSTEMI) from 2011. It outlines:
1. The diagnosis and risk stratification of UA/NSTEMI based on history, ECG changes, and cardiac biomarker levels.
2. The initial management of intermediate- and high-risk patients, which includes aspirin, clopidogrel or ticagrelor, antithrombotics, beta-blockers, statins, ACE-I/ARB, and consideration of urgent angiography for refractory or unstable cases.
3. Medical therapies and revascularization for low-, intermediate-, and high
This document summarizes evidence from major clinical trials supporting current pharmacological treatments for chronic heart failure (CHF). It discusses trials that demonstrated mortality benefits of ACE inhibitors, beta-blockers, aldosterone receptor antagonists, and hydralazine/isosorbide dinitrate combinations. Together, these trials established the current neurohormonal model of CHF and shifted focus to treatments targeting the renin-angiotensin-aldosterone system and sympathetic nervous system overactivation in CHF.
Risk stratification remains central to implement appropriate therapeutic measures for patients with NSTEMI.
The ECG provides rapid risk assessment for patients presenting with chest pain that permits their allocation to appropriate management algorithms to improve the outcomes
This document provides an overview of acute coronary syndrome (ACS). It defines ACS and describes the epidemiology in Malaysia. The pathophysiology, classification, clinical presentation and investigations are discussed for unstable angina/NSTEMI and STEMI. Management is outlined for both conditions, including medications, fibrinolytic therapy, percutaneous coronary intervention and complications. A clinical case of STEMI is then presented demonstrating diagnosis and management. The document concludes with references to Malaysian clinical practice guidelines for ACS.
ACUTE CORONARY SYNDROME FOR CRITICAL CAREAbhinovKandur
The document defines acute coronary syndrome (ACS) as a group of diseases including unstable angina, myocardial infarction, and sudden cardiac death. ACS is classified into STEMI, NSTEMI, or unstable angina based on ECG and cardiac biomarker findings. The diagnosis of ACS involves taking a medical history, performing an ECG, and measuring cardiac biomarkers like troponin and CK-MB. Treatment involves pain relief medications, antiplatelet drugs, anticoagulants, and sometimes revascularization through procedures like angioplasty.
Acute Coronary Syndrome (ACS) refers to a spectrum of conditions caused by reduced blood flow in the coronary arteries. This can range from Unstable Angina to Non-ST-elevation Myocardial Infarction (NSTEMI) and ST-elevation Myocardial Infarction (STEMI). ACS is diagnosed based on symptoms, electrocardiogram (ECG) changes, and elevated cardiac biomarkers. Prompt treatment is important and may include medications, angioplasty, or bypass surgery depending on the severity and location of the blockage. Secondary prevention focuses on lifestyle changes and medications to prevent future cardiac events.
This document discusses acute coronary syndrome and thrombolytic therapy for STEMI. It defines ACS as a spectrum ranging from unstable angina to STEMI depending on the degree of coronary occlusion. For STEMI, the goals of early management are pain relief, early reperfusion, and treating complications to minimize heart muscle loss. Thrombolytic therapy with drugs like streptokinase or tenecteplase is recommended if initiated within 12 hours of symptoms to restore blood flow. Factors that indicate successful reperfusion and guidelines for concomitant medications, complications, and contraindications to thrombolysis are also summarized.
This document discusses acute coronary syndrome (ACS) and non-ST-segment elevation acute coronary syndrome (NSTE-ACS). It defines unstable angina (UA) and non-ST elevation myocardial infarction (NSTEMI) and covers their clinical presentation, diagnostic criteria, laboratory investigation, and management. The key goals of diagnosis and treatment for NSTE-ACS patients are to recognize or exclude myocardial infarction, detect resting ischemia, and identify coronary artery obstruction. Treatment involves anti-ischemic, antithrombotic medications and consideration of coronary revascularization.
This document discusses the treatment of a 60-year-old male presenting with 30 minutes of chest pain. Key details include:
- The patient has risk factors of hypertension and diabetes.
- An EKG shows signs of a possible heart attack. Troponin levels are elevated.
- The document discusses guidelines for diagnosing and treating heart attacks, including medications, invasive procedures, and conservative management strategies based on risk factors. Initial treatment includes oxygen, aspirin, nitroglycerin, and monitoring of vital signs and cardiac markers.
Kaplan Cardiac Anesthesia
Braunwald Textbook Of Cardiovascular Medicine
Fundamentals Of Cardiology For USMLE
Hensley Martin Practical Approach To Cardiac Anesthesia
WWW
Early and effective treatment of patients with acute coronary syndrome saves lives. Lot of progress has been made in last few years in understanding patho-physiology and management of these patients.
Acute coronary syndrome in emergency departmentrigomontejo
This document discusses acute coronary syndrome, including unstable angina, NSTEMI, and STEMI. It outlines the risk factors, symptoms, diagnosis, and management of these conditions. For STEMI specifically, it describes evaluating patients for fibrinolysis or PCI based on time of presentation, contraindications, and cardiac status. Key treatments discussed include aspirin, oxygen, nitrates, beta blockers, ACE inhibitors, and anti-platelet medications to reduce mortality and complications from myocardial infarction.
- The document provides guidelines for the management of acute coronary syndrome (ACS), including definitions, risk stratification, diagnostic criteria, treatment protocols for STEMI, NSTEMI/UA, and secondary prevention strategies.
- It outlines the pathophysiology of ACS as resulting from atherosclerotic plaque rupture and thrombus formation, and differentiates between STEMI, NSTEMI, and UA based on ECG changes and cardiac biomarker levels.
- Initial management involves optimal medical therapy, while risk stratification determines whether conservative treatment or an invasive strategy including angiography and revascularization is most appropriate for intermediate-to-high risk NSTEMI/
1. The document discusses the management of acute coronary syndrome (ACS), including risk stratification, reperfusion therapy options like fibrinolysis and percutaneous coronary intervention (PCI), and antithrombotic and antiplatelet therapies.
2. It highlights the importance of rapid reperfusion through fibrinolysis or PCI to restore blood flow and reduce mortality. PCI is generally preferred over fibrinolysis when it can be performed quickly by an experienced center.
3. Antiplatelet therapies with aspirin and clopidogrel are recommended, along with anticoagulants like unfractionated heparin or low molecular weight heparin to prevent clotting in ACS patients.
This document discusses the management of coronary artery disease and acute coronary syndrome. It begins with the anatomy of the heart and coronary blood vessels. It then defines acute coronary syndrome as unstable angina or myocardial infarction caused by plaque rupture and thrombosis. Risk factors for coronary artery disease are outlined. The diagnostic approach involves assessing symptoms, signs, electrocardiogram changes and cardiac biomarker levels. Treatment focuses on reopening the blocked vessel with medications, fibrinolytics or percutaneous coronary intervention. Chronic stable angina from established coronary artery disease is also discussed.
1. ST elevation myocardial infarction (STEMI) occurs when there is ST elevation or new left bundle branch block on ECG due to acute coronary artery occlusion.
2. Diagnosis is based on symptoms, elevated cardiac biomarkers, and ECG changes showing ST elevation. Treatment involves stabilization, pain control, and reperfusion therapy.
3. Prognosis depends on factors like age, previous MI history, infarct location and size, and presence of heart failure or hypotension. Early reperfusion, beta-blockers, ACE inhibitors and risk factor modification can limit damage.
Stable angina is chest pain caused by plaque buildup in the coronary arteries that reduces blood flow during physical exertion. Unstable angina involves chest pain at rest that is a sign that plaques are rupturing. A STEMI occurs when a plaque rupture causes a complete blockage, lacking oxygen to heart muscle. Diagnosis involves EKG, cardiac enzymes, and angiography. Treatment focuses on lifestyle changes, medications, and procedures to restore blood flow and prevent future events. Stress testing helps evaluate risk and guide management.
Acute coronary syndromes (ACS) include unstable angina and myocardial infarction, which are forms of coronary heart disease caused by reduced blood flow due to plaque rupture and clot formation in the coronary arteries. The document discusses the epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and treatment of ACS. It provides details on evaluating patients using biomarkers, ECG, risk scores, restoring blood flow through procedures like PCI or fibrinolysis, and employing antiplatelet and anticoagulant medications in the early treatment of ACS.
A 75-year-old diabetic male presented with chest pain and other symptoms of acute coronary syndrome. The most probable diagnosis is myocardial infarction. Relevant investigations include ECG, biochemical markers like CK-MB and troponin, and echocardiogram. Management involves medical therapy in emergency, possible fibrinolysis or PCI, and long term preventative treatment. Complications can include heart failure, cardiogenic shock, arrhythmias if not properly managed.
ا.د/شريف مختار
Acute coronary syndrome management
المحاضرة التي قدمت يوم الاربعاء 9 ابريل 2014 في دار الحكمة بالقاهرة
من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب
و ضمن موديول الطوارئ و التخدير و العناية المركزة
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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).
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
2. Non-ST Elevation Acute
Coronary Syndrom- NSTE ACS
Unstable Angina
Non-ST elevation MI
ST Elevation Myocardial Infarct
STMI
Stable Angina
Class1
Class2
Class3
Class 4
3.
4. Acute coronary syndrome is defined as
myocardial ischemia due to myocardial
infarction (NSTEMI or STEMI) or unstable angina
Unstable angina is defined as angina at rest,
new onset exertional angina (<2 months),
recent acceleration of angina (<2 months), or
post revascularization angina
6. Dx of acute coronary syndrome is based on history,
physical exam, ECG, cardiac enzymes
Patients can then be divided into several groups
Non-cardiac chest pain (i.e., Gastrointestinal,
musculoskeletal, pulmonary embolus)
Stable angina
Unstable angina
Myocardial infarction (STEMI or NSTEMI)
Other cardiac causes of chest pain (i.e., aortic dissection,
pericarditis)
8. Plaque rupture and subsequent formation of thrombus
– this can be either occlusive or non-occlusive (STEMI,
NSTEMI, USA)
Vasospasm such as that seen in Prinzmetal’s angina,
cocaine use (STEMI, NSTEMI, USA)
Progression of obstructive coronary atherosclerotic
disease (USA)
In-stent thrombosis (early post PCI)
In-stent restenosis (late post PCI
Poor surgical technique (post CABG)
9. Acute coronary syndromes can also be due to
secondary causes
Thyrotoxicosis
Anemia
Tachycardia
Hypotension
Hypoxemia
Aterial inflammation (infection, arteritis)
15. In the absence of abnormal findings on physical exam,
ECG, or enzymes, the pre-test probability of acute
coronary syndrome must be determined by the
clinician
A good history is crucial (is the chest pain typical or
atypical; what are the associated symptoms)
Determination of risk factors is also crucial (male, age
>55, smoking, DM, HTN, FamHx, hyperlipidemia,
known CAD)
16. Aspirin is an antiplatelet agent that initiates the
irreversible inhibition of cyclooxygenase,
thereby preventing platelet production of
thromboxane A2 and decreasing platelet
aggregation
Administration of ASA in ACS reduces cardiac
endpoints
17. Aspirin should be given in a dose of 75-325
mg/day to all patients with ACS unless there is a
contraindication (in which case, clopidogrel
should be given)
18. Clopidogrel is a potent antiplatelet agent
It should be administered to all patients who
cannot take ASA
The CURE trial suggests a benefit to adding
Clopidogrel to ASA/Heparin in patients going for
PCI
Give 300 mg loading dose followed by 75
mg/day
19. Clopidogrel should be administered to patients who
cannot take ASA because of hypersensitivity or
gastrointestinal intolerance
In hospitalized patients in whom an early,
noninterventional approach is planned, clopidogrel
should be added to ASA as soon as possible on
admission and administered for at least 1 month and
up to 9 months. Do not use clopidogrel if there is any
possibility patient may be candidate for CABG
20. Nitroglycerin is considered a cornerstone of anti-
anginal therapy, despite little objective evidence for its
benefit
Benefit is thought to occur via reduction in myocardial
O2 demand secondary to venodilation induced
reduction in preload as well as coronary vasodilation
and afterload reduction
Titrate to relief of chest pain; chest pain = death of
myocardial cells
No documented mortality benefit
21. Beta Blockers reduce myocardial oxygen
demand by reducing heart rate, contractility,
and ventricular wall tension
Administration of beta blockers in ACS reduces
cardiac endpoints
22. Intravenous beta blockers should be used
initially in all patients (without contraindication)
followed by oral beta blockers with the goal
being decrease in heart rate to 60 beats per
minute
A combination of beta blockers and nitrates can
be viewed as first line therapy in all patients
with ACS
23. Heparin (unfractionated heparin or UFH) has
traditionally been the mainstay of therapy in
acute coronary syndromes as its efficacy has
been documented in several large, randomized
trials
24. More recent studies indicate that low molecular
weight heparin is also effective in the reduction
of end points such as myocardial infarction or
death
Some studies report that LMWH, when used in
combination with ASA, may be superior to
continuous infusion of Heparin
25. All patients with acute coronary syndromes
should be treated with a combination of ASA
(325 mg/day) and heparin (bolus followed by
continuous infusion with goal of PTT 1-2.5X
control) or ASA and low molecular weight
heparin unless one of the drugs is
contraindicated
26. The best documented mechanism by which
these agents act is to reduce ventricular
remodeling over days to weeks after myocardial
damage. However, there is data that a mortality
benefit exists when these agents are used early
in the course of ACS
Administration of ACE-I in ACS reduces cardiac
endpoints
27. ACE-I should be administered to all patients in
the first 24 hours of ACS provided hypotension
and other clear cut contraindications are absent
28. Statins may be of benefit in ACS
Possible mechanisms include plaque
stabilization, reversal of endothelial
dysfunction, decreased thrombogenicity, and
reduction of inflammation
29. Age >65 yrs
Daily ASA Therapy (>7 days prior to event)
Symptoms of Unstable Angina
Documented CAD (stenosis > 50%)
3 or more traditional cardiac risk factors
Elevated cardiac enzymes
ECG changes
30. Score of 3 or less = low risk
Score of 4-5 = intermediate risk (use IIBIIIA)
Score of 6-7 = high risk (use IIBIIIA)
31. In the setting of STEMI primary PCI is associated
with better outcomes than thrombolysis
Emergent PCI is also indicated in the setting of a
new LBBB
32. PAMI (PTCA vs. thrombolysis)
Netherlands Trials (PTCA vs. thrombolysis)
GUSTO IIB (PTCA vs. thrombolysis)
DANAMI-2 (stenting vs. thrombolysis)
STAT (stenting vs. thrombolysis)
33. Primary PCI is indicated as an alternative to
thrombolysis when the following criteria are met:
STEMI or new LBBB
Can undergo PCI within 12 hours of the onset of symptoms
The MD doing the intervention does more than 75 PCI’s/yr
The procedure is done in a center that does more than 200
PCI’s/yr and has surgical backup
34. Good History and Physical (note time and
duration of symptoms)
Careful evaluation of ECG (compare to previous
when possible)
Check Cardiac Enzymes
Monitor on Telemetry
Oxygen
35. ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
+/- Statin
+/- Clopidogrel (don’t give if CABG is a possibility)
+/- IIBIIIA inhibitors (based on TIMI risk score)
36. ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
+/-Clopidogrel (based on possibility of CABG)
IIBIIIA
+/- Statin
Activate the Cath Lab!!!
45. 1. Evidence of myocardial necrosis: cardiac biomarker values (preferably
cardiac troponin [cTn]) and with at least one of the following
. Symptoms of ischemia
. New or presumed new significant ST-T changes or new LBBB
. Development of pathologic Q waves on ECG
. Imaging evidence of new loss of viable myocardium or new regional wall
motion abnormality
. Identification of an intracoronary thrombus by angiography or autopsy
. Cardiac death with symptoms suggestive of myocardial ischemia and
presumed new ischemic ECG changes of new LBBB, but death occurred
before cardiac biomarkers were obtained or before cardiac biomarker
values would be increased
. Percutaneous coronary intervention (PCI)-related MI is arbitrarily de有
ned by elevation of cTn val ues (>5 x 99th percentile U RL) in patients with
nor
mal 七as巳line val ues (王99th percentile URL) or a rise of cTn val ues
46. Criteria for Prior Myocardial l nfarction
Any one of the fol lowing criteria meets the diagnosis for prior
MI
. Pathologic Q waves with or without 5ym仁tom5 in the ab5巳
nce of nonischemlc caU5巴5
. I maging evidence of a region of 1055 of viable myocardium
that i5 thinned
and fails to contract, in the absence of a noni5chemic cause.
. Pathologic 有ndings of a prior M
47. Type 1: Sponta neous Myocardial lnfarction
Type 2: Myocardial l nfarction Secondary to an Ischemic Imbalance
Type 3: Myocardial l nfarction Resulting in Death When Biomarker
Values Are Unavailable
Type 4a: Myocardia川 nfarction Related to Percutaneous Coronary
Intervention (PCI)
Type 4b: Myocardial lnfarction Related to Stent Thrombosis
Type 5: Myocardial l nfarction Related to Coronary Artery Bypass
Grafting (CABG)
62. Syndrome Stenoses
Plaque
Disruption Plaque-Associated Thrombus
Stable angina >75% No No
Unstable angina Variable Frequent Non-occlusive
Transmural MI Variable Frequent Occlusive
Subendocardial
MI
Variable Variable Widely variable
Sudden death severe Frequent Often small
63. Ischemic Heart Disease
Angina Pectoris
Chest discomfort = prolonged, recurrent, different qualities
Cause = transient myocardial ischemia( seconds to minutes)
Patterns
Stable = 75% vessel block, transient ( <15 minutes),
aggravated by exertion, relived by rest & Nitroglycerin
(VD)
Prinzmetal = coronary spasm, episodic, Typical EKG
change – ST elevation, Relived by VD but not rest
Unstable = 90% vessel block or Acute plaque change (
superimposed thrombus), prolonged ( >15 min.), not relived
by rest, VD, Pre-infarction Angina
64. Transmural
Full thickness
Superimposed thrombus in
atherosclerosis
Focal damage
Sub-endocardial
Inner 1/3 to half of
ventricular wall
Decreased circulating blood
volume( shock, Hypotension,
Lysed thrombus)
Circumferential
65. Ischemic Heart Disease
MI= Also called Heart attack
Incidence = disease of old
elderly (45% in 65 yrs. old)
young ( 10% in 40yrs. Old),
Sex = Male > Female
Ethnic = same in African & American
Risk factors
Major modifiable- DM, HTN, Smoking,
Hypercholesterolemia
HRT for Postmenopausal females – will not protect
the heart
66. Ischemic Heart Disease
MI
Pathogenesis
Coronary vessel occlusion
Atherosclerosis with thrombus = MC cause ( 90% cases)
Others = vasospasm (10%)
Most important mechanism = dynamic changes in
the plaque (rather than plaque size),
Plaque disruption PLTS aggregation thrombus
and VC (happens in minutes)
Irreversible changes = after 30 minutes of ischemia
ATP < 10% of normal
Mechanism of cell death = necrosis ( Coagulative)
68. Ischemic Heart Disease
MI -Morphology
light microscopy
First 12 hrs. after MI – no change
Up to 3 days = Coagulative necrosis, neutrophils
1-2 weeks = Granulation tissue
≥ 3 weeks = fine scar
≥ 2 months = dense scar
EM – membrane disruption and Mitochondrial densities
Special stain = TTC ( Triphenyl Tetrazolium chloride),
Detects and stains Mahogany brown with Lactate dehydrogenase
Unstained area = infarction
Mahogany brown = viable
White, glistening= scar
Most common and nonspecific change in ischemia = sub-
endocardial myocyte vacuolization
72. Ischemic Heart Disease
MI = Clinical
Silent MI = DM, Elderly, Cardiac transplantation
recipients,
Typical features = Rapid, weak pulse and sweating
profusely (diaphoretic), Dyspnea, chest pain
Lab=
Diagnostic
Best markers = Troponins ( T & I), both sensitive and
cardio – specific
Next best – CK-MB
Predictive
CRP- >3mg/l – highest risk
73. Ischemic Heart Disease
MI –Complications
In 75% of Patients with MI
Poor prognosis in = elderly, females, DM, old case of MI, Anterior
wall infarct – worst, posterior –worse, Inferior wall – best
1. Arrhythmia = Ventr. Fibrillation – MC arrhythmia lead to
sudden death in MI patients, before they reach hospital
2. pump failure – LVF, cariogenic shock, if >LV wall infarcts,
lead to death ( 70% of hospitalized MI patients)
3.Ventricular rupture = Free or lateral LV wall – MC site, later
cause false aneurysm,
4.True aneurysm = rupture is very rare
5.Pericarditis = Dressler’s syndrome ( Late MI complication)
6.Recurrence
74. Ischemic Heart Disease
Sudden cardiac death = unexpected death in one hour due
to cardiac causes with or without clinical symptoms
Cause – Atherosclerosis ( 90%), others (10%)
Romano- Ward syndrome – Long Q-T syndrome
( K+, Na+ channel defects)
Mechanism- Most likely due to arrhythmias ( VF)
Patients – young athletes, with Pul. HTN, IHD
Morphology
Prominent finding – increased heart mass
Vacuolations in Sub – endocardial myocardium
75. Ischemic Heart Disease
Chronic IHD = also called ischemic cardiomyopathy
Patients = post heart transplant receipts, previous MI or
CABG pts
Cause =compromised ventricular function
Morphology =vacuoles, Myocyte Hypertrophy
Diagnosis= by exclusion
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