Nuevas perspectivas en el tratamiento de la angina crónica estable.
Congreso de las Enfermedades Cardiovasculares 2009.
22/10/2009 Barcelona
Sociedad Española de Cardiología
EECP therapy provides an alternative treatment for refractory angina by increasing coronary perfusion pressure and reducing cardiac workload through the sequential inflation and deflation of compressive cuffs on the lower limbs. It has been shown to significantly reduce angina symptoms and improve quality of life. EECP therapy involves 35 hours of treatment over 7 weeks, with daily 1-2 hour sessions separated by rest periods. It appears to be a safe and effective option for refractory angina patients who are not candidates for revascularization.
Angina pectoris, or chest pain, is caused by a lack of oxygen to the heart muscle. There are different types of angina including stable angina and Prinzmetal's angina. Treatment goals are to reduce symptoms and prolong life. Treatment options include medications like beta blockers, calcium channel blockers, and nitrates as well as lifestyle changes and procedures like angioplasty. Exercise testing can help evaluate ischemia and risk stratify patients.
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.
Ranolazine is a new antianginal drug that represents a new class of drugs. It partially inhibits fatty acid oxidation and shifts energy production to a more efficient carbohydrate oxidation during ischemia. It also inhibits late inward sodium currents, reducing calcium overload and improving diastolic function and myocardial perfusion. Ranolazine has been shown to reduce angina frequency and improve exercise ability with no effects on blood pressure or heart rate. Its benefits and mechanisms of action were discussed along with its indications, studies, and potential role in other conditions such as diabetes and cardioplegia.
This document discusses ranolazine, a drug used to treat chronic angina. It begins by introducing chronic angina as a condition affecting many Americans. It then reviews the history of anti-anginal drugs and discusses why newer treatments are needed. The document focuses on the mechanism of action and clinical trial results of ranolazine. Ranolazine is a unique anti-anginal that acts by inhibiting fatty acid oxidation and blocking late sodium channels. Clinical trials such as MARISA, CARISA and ERICA demonstrated ranolazine's ability to reduce angina symptoms and improve exercise tolerance when added to standard anti-anginal therapies.
Treatment Options For The Chronic Stable AnginaRodolfo Rafael
This document discusses treatment options for chronic stable angina, including the metabolic agent trimetazidine. It provides an overview of angina and its epidemiology. Trimetazidine improves energy metabolism in ischemic heart tissue by inhibiting fatty acid oxidation and stimulating glucose utilization. Clinical trials show trimetazidine reduces angina symptoms and improves exercise tolerance. It may benefit patients with heart failure or diabetes by optimizing energy production and preserving heart cell function.
New pharmocological agents in the management of angina nicorandilJerin Kuruvilla
Nicorandil is a potassium channel activator used to treat angina. It works by dilating both epicardial coronary arteries through its nitrate-like properties as well as peripheral coronary arterioles through potassium channel activation. This dual mechanism of action decreases myocardial oxygen demand and increases supply. Nicorandil has been shown to be effective in treating stable and unstable angina, improving outcomes in acute myocardial infarction when administered before reperfusion, and preventing the no-reflow phenomenon during percutaneous coronary intervention. It provides cardioprotection through ischemic preconditioning with a good safety profile.
EECP therapy provides an alternative treatment for refractory angina by increasing coronary perfusion pressure and reducing cardiac workload through the sequential inflation and deflation of compressive cuffs on the lower limbs. It has been shown to significantly reduce angina symptoms and improve quality of life. EECP therapy involves 35 hours of treatment over 7 weeks, with daily 1-2 hour sessions separated by rest periods. It appears to be a safe and effective option for refractory angina patients who are not candidates for revascularization.
Angina pectoris, or chest pain, is caused by a lack of oxygen to the heart muscle. There are different types of angina including stable angina and Prinzmetal's angina. Treatment goals are to reduce symptoms and prolong life. Treatment options include medications like beta blockers, calcium channel blockers, and nitrates as well as lifestyle changes and procedures like angioplasty. Exercise testing can help evaluate ischemia and risk stratify patients.
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.
Ranolazine is a new antianginal drug that represents a new class of drugs. It partially inhibits fatty acid oxidation and shifts energy production to a more efficient carbohydrate oxidation during ischemia. It also inhibits late inward sodium currents, reducing calcium overload and improving diastolic function and myocardial perfusion. Ranolazine has been shown to reduce angina frequency and improve exercise ability with no effects on blood pressure or heart rate. Its benefits and mechanisms of action were discussed along with its indications, studies, and potential role in other conditions such as diabetes and cardioplegia.
This document discusses ranolazine, a drug used to treat chronic angina. It begins by introducing chronic angina as a condition affecting many Americans. It then reviews the history of anti-anginal drugs and discusses why newer treatments are needed. The document focuses on the mechanism of action and clinical trial results of ranolazine. Ranolazine is a unique anti-anginal that acts by inhibiting fatty acid oxidation and blocking late sodium channels. Clinical trials such as MARISA, CARISA and ERICA demonstrated ranolazine's ability to reduce angina symptoms and improve exercise tolerance when added to standard anti-anginal therapies.
Treatment Options For The Chronic Stable AnginaRodolfo Rafael
This document discusses treatment options for chronic stable angina, including the metabolic agent trimetazidine. It provides an overview of angina and its epidemiology. Trimetazidine improves energy metabolism in ischemic heart tissue by inhibiting fatty acid oxidation and stimulating glucose utilization. Clinical trials show trimetazidine reduces angina symptoms and improves exercise tolerance. It may benefit patients with heart failure or diabetes by optimizing energy production and preserving heart cell function.
New pharmocological agents in the management of angina nicorandilJerin Kuruvilla
Nicorandil is a potassium channel activator used to treat angina. It works by dilating both epicardial coronary arteries through its nitrate-like properties as well as peripheral coronary arterioles through potassium channel activation. This dual mechanism of action decreases myocardial oxygen demand and increases supply. Nicorandil has been shown to be effective in treating stable and unstable angina, improving outcomes in acute myocardial infarction when administered before reperfusion, and preventing the no-reflow phenomenon during percutaneous coronary intervention. It provides cardioprotection through ischemic preconditioning with a good safety profile.
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.
Anti anginal drugs, uses, mechanism of action, adverse effectsKarun Kumar
A presentation outlining the causes of angina, mechanism of action of various anti-anginal drugs, their uses and side effects alongwith contraindications
This document discusses several newer antiarrhythmic drugs, including ranolazine, vernakalant, ivabradine, celivarone, budiodarone, and tecadenoson. It provides details on the mechanisms of action, clinical trials, efficacy, and safety profiles of these drugs. Ranolazine, vernakalant, and budiodarone have shown efficacy in cardioversion or rate control of atrial fibrillation, while ivabradine reduces heart rate without affecting contractility. Celivarone and tecadenoson are being investigated for maintaining sinus rhythm and terminating supraventricular tachycardias, respectively.
1) Despite increased awareness and treatment of hypertension over time, control rates in the US and other countries have remained low, around 30-60%.
2) Multiple studies show that intensive treatment of hypertension that aims for tighter blood pressure control provides significantly better outcomes than less tight control, reducing risks of cardiovascular events, stroke, nephropathy and other complications.
3) However, studies also found that a significant portion of patients treated for hypertension were not achieving recommended blood pressure targets due to issues like treatment inertia, failure to intensify treatment when needed, and inadequate follow up.
Anti anginal Agents /certified fixed orthodontic courses by Indian dental aca...Indian dental academy
Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients
State of the art comprehensive training-Faculty of world wide repute &Very affordable.
- A study compared the effects of glibenclamide and gliclazide, two sulphonylureas, on ischemic preconditioning (IPC) and nicorandil-induced myocardial protection in rats.
- Glibenclamide abolished the protective effects of both IPC and nicorandil, but gliclazide did not affect IPC or nicorandil-induced protection.
- Nicorandil caused a partial depolarization of mitochondrial membrane potential, an effect blocked by glibenclamide but not gliclazide. These results suggest gliclazide may allow protective effects in diabetic patients at risk of acute coronary syndromes unlike
Angina pectoris is chest pain caused by transient myocardial ischemia due to an imbalance between myocardial oxygen supply and demand. There are three main types of angina: stable angina, unstable angina, and variant angina (Prinzmetal's angina). Management of angina involves lifestyle modifications, drug treatment including nitrates, calcium channel blockers, beta blockers, and revascularization procedures for severe cases.
Phenotype specific treatment of heart failure with preserved ejectionsoumyasil
1) Heart failure with preserved ejection fraction (HFpEF) has different underlying pathophysiology compared to heart failure with reduced ejection fraction (HFrEF), involving chronic systemic inflammation and extracellular matrix remodeling rather than intra-myocardial issues as in HFrEF.
2) Due to these differences, treatments that are effective for HFrEF such as neurohormonal inhibitors have failed for HFpEF. A phenotypic approach tailored to the specific abnormalities in each patient is needed.
3) Potential phenotype-specific treatments discussed for HFpEF include diuretics, exercise training, weight loss, statins, inorganic nitrates, drugs stimulating the nitric oxide and cGMP pathway like sacubitril
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.
Role of the Renin–Angiotensin–Aldosterone System Inhibition Beyond BP Reductionmagdy elmasry
Hypertension Mediated Organ Damage : How We Prevent It?The Role Of RAAS In Cardiovascular Continuum.Changes in Arterial Diameter in Patients with Arteriosclerosis or Atherosclerosis.Not All Angiotensin-Converting Enzyme Inhibitors Are Equal.Question : ACEIs vs. ARBsIs One Class Better For Cardiovascular Diseases?BP Variability .Central BP
.
Vascular Age &
Arterial Stiffness.Achieving BP Goals.
Angina pectoris is caused by transient episodes of myocardial ischemia due to an imbalance in the myocardial oxygen supply-demand relationship. There are three main types of angina: stable angina, which is triggered by exertion and relieved by rest; unstable angina, which occurs at rest and is a medical emergency; and Prinzmetal angina, which occurs due to coronary artery spasm. Treatment strategies for angina include nitrates like nitroglycerin which relieve symptoms rapidly, calcium channel blockers which prevent calcium entry and relax blood vessels, beta blockers which reduce the heart's oxygen demand, and ranolazine which inhibits sodium channels to reduce the heart's work.
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
Advances in Medical Management of Heart FailurePraveen Nagula
This document discusses recent advances in the medical management of heart failure. It begins by describing the types of heart failure and the historically available treatment options of diuretics and digoxin. It then discusses neurohormonal blockers that have been effective in reducing morbidity and mortality for HFrEF. The document reviews evidence for drugs like hydralazine/isosorbide and goes on to describe several novel drug categories and agents that may further improve heart failure treatment, such as neprilysin inhibitors, soluble guanylate cyclase stimulators, calcium sensitizers, and metabolic modulators.
presentation for drugs used to treat different types of angina pectoris : stable, unstable and vasospastic and the best for each type and side effects,
Perioperative case of myocardial ischemia and its management ZIKRULLAH MALLICK
This document describes the case of a 40-year-old male patient who experienced hypotension, bradycardia, and ST segment changes during a long orthopedic surgery, indicating possible acute coronary syndrome. Biomarkers after surgery confirmed myocardial injury. The patient was treated in the ICU and recovered. The document then reviews risk factors, mechanisms, diagnosis, and management of perioperative myocardial infarction.
This document discusses antianginal drugs used to treat angina pectoris, or chest pain caused by reduced blood flow to the heart. There are three main classes of drugs used: organic nitrates, beta-blockers, and calcium channel blockers. Organic nitrates like nitroglycerin work by dilating blood vessels to increase blood flow to the heart and reduce its workload. Beta-blockers lower the heart rate and force of contraction to decrease oxygen demand. Calcium channel blockers inhibit calcium entry into heart and blood vessel cells to relax vessels and reduce workload. Each drug class is described in more detail regarding mechanisms, effects, pharmacokinetics, uses, and side effects.
Recent advances in ischemic heart diseasessaachslides15
This document provides an overview of ischemic heart diseases and recent advances in treatment. It discusses the types of angina pectoris and myocardial infarction. Current treatment strategies include nitrates, beta blockers, calcium channel blockers, and potassium channel openers. Newer agents that are discussed include trimetazidine, ranolazine, and ivabradine which lower cardiac oxygen demand and improve symptoms of angina. Combination therapies are also used to maximize antianginal effects while minimizing side effects.
This document summarizes the drug levosimendan, which was developed as a new inotropic agent to increase contractility without the side effects of existing drugs like dobutamine. It has a triple mechanism of action: binding to cardiac troponin C to increase contractility, opening potassium channels in blood vessels to cause vasodilation, and opening mitochondrial potassium channels in cardiomyocytes for cardioprotection. Levosimendan does not increase intracellular calcium levels or oxygen consumption. It provides benefits like preconditioning and reduces remodeling, apoptosis, and inflammation in heart failure. Levosimendan was found to improve outcomes compared to dobutamine and other existing inotropic drugs.
The document discusses non-ST elevation myocardial infarction (NSTEMI), including its pathophysiology, clinical presentation, diagnostic testing, and management. NSTEMI is caused by reduced blood supply or increased oxygen demand in the heart muscle due to atherosclerotic plaque. Patients experience chest pain and may have abnormal ECG or elevated cardiac enzymes. Treatment involves aspirin, anticoagulants, reperfusion therapies like thrombolysis or angioplasty, and long-term secondary prevention including medications and lifestyle changes.
This document discusses arrhythmias and their treatment. It defines arrhythmias as abnormalities in heart rhythm that result in insufficient cardiac output. The document describes the normal physiology of cardiac rhythm controlled by the sinoatrial node. It outlines different types of arrhythmias caused by issues with pacemaker impulse formation or conduction. The mechanisms of various arrhythmias are explained including reentry circuits and abnormal pacemaking. Finally, the document discusses pharmacological treatments for arrhythmias including classes I-IV antiarrhythmic drugs that act on ion channels and membranes to normalize heart rhythm.
This document discusses the physiology of cardiac rhythm, classification of arrhythmias, and anti-arrhythmic drugs used to treat arrhythmias. It covers the phases of the cardiac action potential, mechanisms of arrhythmia production, Vaughan Williams classification of anti-arrhythmic drugs based on their effects on the action potential, and details several important anti-arrhythmic drugs including their mechanisms, uses, and potential adverse effects. The document concludes that treatment of arrhythmias depends on the type of arrhythmia and patient's condition, as anti-arrhythmic drugs are efficacious but can have serious side effects, and non-pharmacological therapies are also used.
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.
Anti anginal drugs, uses, mechanism of action, adverse effectsKarun Kumar
A presentation outlining the causes of angina, mechanism of action of various anti-anginal drugs, their uses and side effects alongwith contraindications
This document discusses several newer antiarrhythmic drugs, including ranolazine, vernakalant, ivabradine, celivarone, budiodarone, and tecadenoson. It provides details on the mechanisms of action, clinical trials, efficacy, and safety profiles of these drugs. Ranolazine, vernakalant, and budiodarone have shown efficacy in cardioversion or rate control of atrial fibrillation, while ivabradine reduces heart rate without affecting contractility. Celivarone and tecadenoson are being investigated for maintaining sinus rhythm and terminating supraventricular tachycardias, respectively.
1) Despite increased awareness and treatment of hypertension over time, control rates in the US and other countries have remained low, around 30-60%.
2) Multiple studies show that intensive treatment of hypertension that aims for tighter blood pressure control provides significantly better outcomes than less tight control, reducing risks of cardiovascular events, stroke, nephropathy and other complications.
3) However, studies also found that a significant portion of patients treated for hypertension were not achieving recommended blood pressure targets due to issues like treatment inertia, failure to intensify treatment when needed, and inadequate follow up.
Anti anginal Agents /certified fixed orthodontic courses by Indian dental aca...Indian dental academy
Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients
State of the art comprehensive training-Faculty of world wide repute &Very affordable.
- A study compared the effects of glibenclamide and gliclazide, two sulphonylureas, on ischemic preconditioning (IPC) and nicorandil-induced myocardial protection in rats.
- Glibenclamide abolished the protective effects of both IPC and nicorandil, but gliclazide did not affect IPC or nicorandil-induced protection.
- Nicorandil caused a partial depolarization of mitochondrial membrane potential, an effect blocked by glibenclamide but not gliclazide. These results suggest gliclazide may allow protective effects in diabetic patients at risk of acute coronary syndromes unlike
Angina pectoris is chest pain caused by transient myocardial ischemia due to an imbalance between myocardial oxygen supply and demand. There are three main types of angina: stable angina, unstable angina, and variant angina (Prinzmetal's angina). Management of angina involves lifestyle modifications, drug treatment including nitrates, calcium channel blockers, beta blockers, and revascularization procedures for severe cases.
Phenotype specific treatment of heart failure with preserved ejectionsoumyasil
1) Heart failure with preserved ejection fraction (HFpEF) has different underlying pathophysiology compared to heart failure with reduced ejection fraction (HFrEF), involving chronic systemic inflammation and extracellular matrix remodeling rather than intra-myocardial issues as in HFrEF.
2) Due to these differences, treatments that are effective for HFrEF such as neurohormonal inhibitors have failed for HFpEF. A phenotypic approach tailored to the specific abnormalities in each patient is needed.
3) Potential phenotype-specific treatments discussed for HFpEF include diuretics, exercise training, weight loss, statins, inorganic nitrates, drugs stimulating the nitric oxide and cGMP pathway like sacubitril
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.
Role of the Renin–Angiotensin–Aldosterone System Inhibition Beyond BP Reductionmagdy elmasry
Hypertension Mediated Organ Damage : How We Prevent It?The Role Of RAAS In Cardiovascular Continuum.Changes in Arterial Diameter in Patients with Arteriosclerosis or Atherosclerosis.Not All Angiotensin-Converting Enzyme Inhibitors Are Equal.Question : ACEIs vs. ARBsIs One Class Better For Cardiovascular Diseases?BP Variability .Central BP
.
Vascular Age &
Arterial Stiffness.Achieving BP Goals.
Angina pectoris is caused by transient episodes of myocardial ischemia due to an imbalance in the myocardial oxygen supply-demand relationship. There are three main types of angina: stable angina, which is triggered by exertion and relieved by rest; unstable angina, which occurs at rest and is a medical emergency; and Prinzmetal angina, which occurs due to coronary artery spasm. Treatment strategies for angina include nitrates like nitroglycerin which relieve symptoms rapidly, calcium channel blockers which prevent calcium entry and relax blood vessels, beta blockers which reduce the heart's oxygen demand, and ranolazine which inhibits sodium channels to reduce the heart's work.
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
Advances in Medical Management of Heart FailurePraveen Nagula
This document discusses recent advances in the medical management of heart failure. It begins by describing the types of heart failure and the historically available treatment options of diuretics and digoxin. It then discusses neurohormonal blockers that have been effective in reducing morbidity and mortality for HFrEF. The document reviews evidence for drugs like hydralazine/isosorbide and goes on to describe several novel drug categories and agents that may further improve heart failure treatment, such as neprilysin inhibitors, soluble guanylate cyclase stimulators, calcium sensitizers, and metabolic modulators.
presentation for drugs used to treat different types of angina pectoris : stable, unstable and vasospastic and the best for each type and side effects,
Perioperative case of myocardial ischemia and its management ZIKRULLAH MALLICK
This document describes the case of a 40-year-old male patient who experienced hypotension, bradycardia, and ST segment changes during a long orthopedic surgery, indicating possible acute coronary syndrome. Biomarkers after surgery confirmed myocardial injury. The patient was treated in the ICU and recovered. The document then reviews risk factors, mechanisms, diagnosis, and management of perioperative myocardial infarction.
This document discusses antianginal drugs used to treat angina pectoris, or chest pain caused by reduced blood flow to the heart. There are three main classes of drugs used: organic nitrates, beta-blockers, and calcium channel blockers. Organic nitrates like nitroglycerin work by dilating blood vessels to increase blood flow to the heart and reduce its workload. Beta-blockers lower the heart rate and force of contraction to decrease oxygen demand. Calcium channel blockers inhibit calcium entry into heart and blood vessel cells to relax vessels and reduce workload. Each drug class is described in more detail regarding mechanisms, effects, pharmacokinetics, uses, and side effects.
Recent advances in ischemic heart diseasessaachslides15
This document provides an overview of ischemic heart diseases and recent advances in treatment. It discusses the types of angina pectoris and myocardial infarction. Current treatment strategies include nitrates, beta blockers, calcium channel blockers, and potassium channel openers. Newer agents that are discussed include trimetazidine, ranolazine, and ivabradine which lower cardiac oxygen demand and improve symptoms of angina. Combination therapies are also used to maximize antianginal effects while minimizing side effects.
This document summarizes the drug levosimendan, which was developed as a new inotropic agent to increase contractility without the side effects of existing drugs like dobutamine. It has a triple mechanism of action: binding to cardiac troponin C to increase contractility, opening potassium channels in blood vessels to cause vasodilation, and opening mitochondrial potassium channels in cardiomyocytes for cardioprotection. Levosimendan does not increase intracellular calcium levels or oxygen consumption. It provides benefits like preconditioning and reduces remodeling, apoptosis, and inflammation in heart failure. Levosimendan was found to improve outcomes compared to dobutamine and other existing inotropic drugs.
The document discusses non-ST elevation myocardial infarction (NSTEMI), including its pathophysiology, clinical presentation, diagnostic testing, and management. NSTEMI is caused by reduced blood supply or increased oxygen demand in the heart muscle due to atherosclerotic plaque. Patients experience chest pain and may have abnormal ECG or elevated cardiac enzymes. Treatment involves aspirin, anticoagulants, reperfusion therapies like thrombolysis or angioplasty, and long-term secondary prevention including medications and lifestyle changes.
This document discusses arrhythmias and their treatment. It defines arrhythmias as abnormalities in heart rhythm that result in insufficient cardiac output. The document describes the normal physiology of cardiac rhythm controlled by the sinoatrial node. It outlines different types of arrhythmias caused by issues with pacemaker impulse formation or conduction. The mechanisms of various arrhythmias are explained including reentry circuits and abnormal pacemaking. Finally, the document discusses pharmacological treatments for arrhythmias including classes I-IV antiarrhythmic drugs that act on ion channels and membranes to normalize heart rhythm.
This document discusses the physiology of cardiac rhythm, classification of arrhythmias, and anti-arrhythmic drugs used to treat arrhythmias. It covers the phases of the cardiac action potential, mechanisms of arrhythmia production, Vaughan Williams classification of anti-arrhythmic drugs based on their effects on the action potential, and details several important anti-arrhythmic drugs including their mechanisms, uses, and potential adverse effects. The document concludes that treatment of arrhythmias depends on the type of arrhythmia and patient's condition, as anti-arrhythmic drugs are efficacious but can have serious side effects, and non-pharmacological therapies are also used.
This document discusses antiarrhythmic drug therapy and summarizes the following key points:
- Antiarrhythmic drugs are classified into four classes based on their mechanism of action and effects on the cardiac action potential. Classes I-III work by blocking sodium, calcium or potassium channels.
- Class I drugs like quinidine and procainamide work by blocking fast sodium channels, reducing the rate of depolarization. Class II drugs like propranolol are beta blockers that reduce heart rate and conduction velocity.
- Common arrhythmias treated include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardias. Drug choice is based on the arrhythmia type
This document provides an overview of the management of hypertension, including hypertensive emergencies. It discusses the prevalence and pathophysiology of hypertension, outlines treatment goals, and reviews pharmacologic treatment options. Key points include:
1) Hypertensive emergencies require rapid blood pressure control to prevent end-organ damage, while avoiding precipitous drops in pressure.
2) Intravenous antihypertensive agents discussed include labetalol, esmolol, nicardipine, sodium nitroprusside, and fenoldopam.
3) Nicardipine is highlighted as an effective option for hypertensive emergencies due to its rapid onset, titratability, and limited
Anesthesia for children with long QT syndromecairo1957
This document discusses long QT syndrome (LQTS) in children, including causes, diagnosis, treatment, and considerations for anesthesia management. It describes how LQTS results from genetic mutations affecting cardiac ion channels, causing prolonged ventricular repolarization and risk of dangerous arrhythmias. Diagnosis involves calculating the QT interval from ECG and applying the Schwartz criteria. Treatment focuses on beta-blockers, antiarrhythmic drugs, pacemakers or ICDs. Anesthesia requires avoiding triggers of arrhythmias and prolonging the QT interval through careful drug selection and electrolyte management.
Antiarrhythmic drugs work by altering the electrophysiology of the heart. They are classified into four main classes based on their mechanisms of action: Class I drugs block sodium channels, Class II block beta-adrenergic receptors, Class III prolong the heart's repolarization, and Class IV block calcium channels. While these drugs can treat arrhythmias, they may also paradoxically cause arrhythmias due to their effects on the heart's electrical activity. Pacemakers provide an alternative treatment for arrhythmias by using implanted leads and a pulse generator to electrically stimulate the heart and maintain a normal rhythm.
This document discusses the diagnosis of peri-operative myocardial infarction. It defines peri-operative myocardial ischemia and explains why the traditional MI definition does not apply under anesthesia. The ACC criteria for diagnosing a peri-operative MI is described. The pathophysiology involves acute coronary syndrome (Type I) or oxygen supply-demand imbalance (Type II). Diagnostic tools include electrocardiography, cardiac enzymes, echocardiography, nuclear imaging techniques and cardiac MRI/CT. Early recognition can help prevent morbidity and mortality through pharmacological interventions.
The document discusses several topics related to acute coronary syndrome including cardiogenic shock, acute myocardial infarction, congestive heart failure, and arrhythmias. It provides definitions and pathophysiology of cardiogenic shock, acute coronary syndrome, and discusses management strategies including use of inotropes, vasopressors, intra-aortic balloon pump counterpulsation, and revascularization. It also discusses definitions and management of acute coronary syndromes including unstable angina and myocardial infarction and the role of antiplatelet and anticoagulation therapies.
This document summarizes key aspects of cardiac function and disorders of cardiac rhythm and conduction. It describes the anatomy and function of the cardiac conduction system, including the sinoatrial node, atrioventricular node, and Purkinje fibers. It discusses the phases of the cardiac action potential and how disorders can disrupt normal rhythm. Treatment options covered include medications that affect sodium, calcium, potassium channels or conduction, as well as non-pharmacological approaches like cardioversion, defibrillation, and ablation.
The document discusses common arrhythmias seen in emergency settings, including bradycardia and tachycardia. It covers the classification, mechanisms, diagnosis and treatment of various arrhythmias like sinus bradycardia, heart blocks, supraventricular tachycardia, ventricular tachycardia and fibrillation. Diagnostic tests mentioned include 12-lead ECG, exercise stress testing, Holter monitoring and implanted cardiac monitors. Treatment depends on the type of arrhythmia and includes atropine, pacing, cardioversion, defibrillation and drugs.
This document discusses antiarrhythmic drugs and their classification and mechanisms of action. It begins by defining arrhythmia and describing the normal cardiac conduction pathway and rhythm. It then classifies antiarrhythmic drugs according to the Vaughan-Williams classification system into Classes I-IV based on their effects on cardiac ion channels and action potentials. Class I drugs are sodium channel blockers and are further divided into IA, IB and IC subgroups based on their binding properties and effects on cardiac tissue. Representative drugs from each subclass are described in detail including their mechanisms of action, uses, dosages and adverse effects.
This document discusses anti-arrhythmic drugs, describing the physiology of normal cardiac rhythm, mechanisms of arrhythmias, classification of anti-arrhythmic drugs, and important drugs including their mechanisms and characteristics. It covers drugs like lidocaine, flecainide, amiodarone, adenosine, verapamil and digoxin; their uses in treating arrhythmias; potential adverse effects; and non-pharmacological treatments. Management of arrhythmias involves assessing the patient and diagnosing the type of arrhythmia to determine appropriate acute or prophylactic treatment.
SQTS is a heart condition characterized by a short QT interval on electrocardiogram. It is usually hereditary and caused by genetic mutations affecting ion channels. SQTS increases the risk of life-threatening arrhythmias and cardiac arrest, which are commonly the first clinical presentation. Diagnosis is based on a QT interval ≤340 ms and confirmed by genetic testing or family history. Implantable cardioverter defibrillator is the definitive treatment, while quinidine may be used in young patients who cannot receive an ICD or as an alternative to prevent arrhythmias.
Aritmia pada Hiperkalemia dan Hipokalemia serta LQTS.pptxShaoranAulia1
This document discusses long QT syndrome (LQTS), a genetic disorder characterized by a prolonged QT interval on electrocardiogram that can cause dangerous arrhythmias like torsade de pointes. It describes the genetic causes and clinical features of LQTS, including presentations like unexplained syncope. Triggering factors like exercise and emotions are discussed. The pathophysiology involving early and delayed afterdepolarizations is explained. Diagnosis, risk stratification, and management including lifestyle changes, beta blockers, pacemakers, and ICDs are summarized.
Electrophysiology of Heart & Drugs Affecting Renin Angiotensin System Monika Bhardwaj
The document discusses cardiac electrophysiology and the renin-angiotensin system. It describes how cardiac myocytes in the sinoatrial and atrioventricular nodes can generate impulses, and how these impulses propagate through specialized conducting tissue. It also details the actions of angiotensin II, including its effects on vasoconstriction, sodium reabsorption, and aldosterone secretion. Common drugs for manipulating the renin-angiotensin system are also summarized, such as ACE inhibitors like lisinopril and angiotensin receptor blockers like losartan.
This document discusses heart arrhythmias and how anti-arrhythmic drugs work to treat them. It provides details on:
1) The electrophysiology of normal heart contraction and how disturbances can cause arrhythmias.
2) Classification systems for anti-arrhythmic drugs based on their mechanisms of action, such as blocking specific ion channels.
3) How different classes of drugs can alter properties like conduction velocity, refractoriness, and automaticity to restore normal rhythm or prevent dangerous arrhythmias.
Reverse Takotsubo Cardiomyopathy Following General AnaesthesiaPremier Publishers
Reverse takotsubo cardiomyopathy(r-TTC) is a rare condition in which regional wall motion abnormalities affect the basal segments of left ventricle in absence of significant coronary artery disease. The Diagnosis is established by characteristic echocardiographic findings, clinical manifestations, and laboratory features. In this report we demonstrate a case of general anaesthesia induced cardiomyopathy in 21 years old female.
Pharmacotherapy of Cardiac arrhythmiasDrSnehaDange
This document provides an overview of pharmacotherapy for cardiac arrhythmias. It discusses the normal conduction pathway in the heart and mechanisms of arrhythmogenesis. Cardiac arrhythmias are classified and characteristics of different types are described including extrasystoles, supraventricular tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia and ventricular fibrillation. Antiarrhythmic drugs are classified according to the Vaughan Williams system with details provided on mechanisms and examples for Class IA, IB, IC, II, III and IV drugs.
The document discusses ischaemic heart disease (IHD). It is a leading cause of death worldwide. IHD occurs when there is an imbalance between the supply of oxygen and demand of the heart muscle, leading to ischemia. The main causes are atherosclerosis, thrombosis, or reduced blood flow. Biomarkers like troponin and CK are important for diagnosing acute coronary syndromes. Endothelial dysfunction and oxidative stress play key roles in the development of atherosclerosis and IHD. Atherothrombosis, characterized by sudden plaque rupture and thrombus formation, is the underlying pathological process.
La Sociedad Española de Cardiología (SEC) es una organización científica sin ánimo de lucro con la misión de reducir el impacto adverso de las enfermedades cardiovasculares y promover una mejor salud cardiovascular en la ciudadanía.
Ponencia presentada por la Dra. Marisol Bravo Amaro en el CardioTV Live ‘Debatiendo estrategias actuales para la reducción de eventos CV tras síndrome coronario agudo reciente’, realizado el 21 de mayo de 2024 en la Casa del Corazón
Ponencia presentada por el Dr. Armando Oterino Manzanas en el CardioTV Live ‘Debatiendo estrategias actuales para la reducción de eventos CV tras síndrome coronario agudo reciente’, realizado el 21 de mayo de 2024 en la Casa del Corazón
Ponencia presentada por la Dra. Miriam Martín Toro en el CardioTV Live ‘Debatiendo estrategias actuales para la reducción de eventos CV tras síndrome coronario agudo reciente’, realizado el 21 de mayo de 2024 en la Casa del Corazón
Ponencia presentada por los Dres. M.ª Dolores Mesa Rubio, Javier Mora Robles, Margarita Reina Sánchez, M.ª José Castillo Moraga y José Luis Bianchi Llave en el CardioTV Focus, publicado el 25 de abril de 2024 en la Casa del Corazón (Madrid).
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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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.
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1. Nu evas perspectivas en el tratamiento de la angin a crónica estable Juan Tamargo Departamento de Farmacología, Facultad de Medicina Universidad Complutense, Madrid. Spain
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4. New mechanistic approaches to myocardial ischemia Sinus node inhibition (IVABRADINE) Late I Na inhibition (Ranolazine) Rho kinase inhibition (fasudil) Metabolic modulation (trimetazidine) Preconditioning (nicorandil) O H 3 C O H 3 C O N CH 3 O CH 3 O CH 3 O O NO 2 H N N N N O N CH 3 H CH 3 CH 3 O O H N SO 2 NH N O OH CH 3 CH 3 OCH 3 H N N N O
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6. -50 -50 50 0 mV -50 -50 pA I f I f I CaT I CaL I K Potenciales de acción registrados en el nodo SA (A) y en miocitos ventriculares (B) PU PDM
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8. Cardiopatía Isquémica Inhibir la -oxidación de los ácidos grasos, aumentar la oxidación de la glucosa Trimetazidina Oxfenicina Etoxomir Perhexilina S-15176
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11. Coraboeuf et al. Am J Physiol 1979;236:H561-H567 “ They shortening was due to a TTX-sensitive Na + current flowing during the plateau of the action potential” “ This current flows through a small proportion of Na+ channels with no inactivation mechanism (or inactivation different from normal), e.g. the late I na Tetrodotoxin prolongs the APD in Purkinje fibers at concentrations lower than those at which it inhibited the I Na 1: control. 2: TTX (0.03 M) Late I Na
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13. Gating modes in cardiac Na + channels (Nav1.5 subunit) expressed in HEK cells Late I Na results from two types of channel activity: scattered late openings and burst openings Undrovinas et al. J Mol Cell Cardiol 2002; 34:1477-1489
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16. Murphy E. et al. Physiology 2008;23:115-123 2008 Representative changes in Na, Ca, Mg, ATP, PCr, and pH during ischemia
17. A pathological paradigm NaCh inactivation failure Ischemia Ca 2+ Overload late I Na Na + i NCX
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20. Transmural heterogeneity of late I Na Late I Na is more prominent in M and Purkinje cells Zygmunt et al. Am J Physiol 2001;281:H689-H697 Pathological Iate I Na increases the dispersion of ventricular repolarization, may trigger early afterdepolarizations and lead to reentrant excitation Endo M cell Epi ECG
21. Consequences of increasing the late I Na Leading to QT prolon ga tion, EADs and beat-to-beat variation in APD Song et al. J Cardiovasc Pharmacol 2004; Maltsev et al. Eur J Heart Fail 2007 Human failing heart Cardiac myocytes exposed to ATX-II
22. Abnormal Late I Na Prolongs APD (QTc), induced EADs and delayed relaxation Na + in out Na + Channel Na v 1.5 Sodium Current Action Potential 0 Late I Na 0 (Upstroke) 1 2 (Plateau) 3 4 Peak Normal 0 Late I Na Peak Abnormal Q S T Q S T Twitch Phasic Phasic Tonic EAD DAD
23. Late I Na is involved in the Long QTS * Andersen—Tawil Syndrome ** Timothy Syndrome 1505-1507 Late I Na SNTA1, -1 Syntrophin LQT12 I Ks AKAP9, Yotiao LQT11 Late I Na SCN4B, NavB4 LQT10 Late I Na CAV3, Caveolin-3 LQT9 I Ca CACNA1C, Ca v 1.2 LQT8** I K1 KCNJ2, Kir2.1 LQT7* I Kr KCN2, MiRP1 LQT6 I Ks KCNE1, minK LQT5 Ca i , Late I Na ? KCNH2, HERG LQT4 Late I Na KCNQ1, KvLQT1 LQT3 I Kr KCNH2, HERG LQT2 I Ks KCNQ1, KvLQT1 LQT1 Channel Gene 50 ms 5 pA Normal 50 ms Enhanced ( KPQ) I NaL I NaL
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25. Ranolazine selectively inhibits the late I Na Late I Na Peak I Na abnormal Ranolazine Control Δ IC 50 = 38-fold A. Ventricular Myocytes from Canine Failing Hearts 50 0 100 % Inhibition Peak IC 50 = 244 µM late IC 50 = 6.5 µM 1E-3 0.01 0.1 1 10 100 Concentration of Ranolazine (mM) Rajamani S., et al., Eur Heart J 207;28: 400 (abstract) ACE que no se controla con otros antianginosos, o en pacientes que no pueden tomar estos medicamentos. O OH CH 3 CH 3 OCH 3 H N N N O
26. Ranolazine: mechanism of action Hasenfuss G, Maier LS. Clin Res Cardiol 2008;97:222-26 Maier LS. Cardiol Clin 2008;26:603-14. Ischemia ↑ Late I Na Na + overload Ca ++ overload Mechanical dysfunction ↑ Diastolic tension ↓ Contractility Electrical dysfunction Arrhythmias O2 supply & demand ↑ ATP consumption ↓ ATP formation NCX NCX: sodium-calcium exchanger Ranolazine
27. Ranolazine reduces Na + and Ca 2+ overload induced by ATX-II in rabbit myocytes Sossalla S et al. J Mol Cell Cardiol 2008; 45: 32-43. 0 10 20 30 * End-diastolic pressure (mmHg) 40 * P<0.05 Control Ranolazine Na + overload Diastolic [Ca 2+ ] i
28. Ranolazine reduces the increase in diastolic tension in LV trabeculae from human failing heart Sossalla S et al.. J Mol Cell Cardiol 2008; 45: 32-43.
29. Ranolazine: Key Clinical Trials ROLE N=746 Chronic angina Chaitman BR, et al. JAMA. 2004;291:309-316. Stone PH, et al. J Am Coll Cardiol. 2006;48:566-575. Morrow DA, et al. JAMA. 2007;297:1775-1783. J Am Coll Cardiol 2004;43:1375– 82 CARISA N=823 Chronic angina Ranolazine vs placebo on top of standard therapy ERICA N=565 Chronic angina Ranolazine vs placebo on top of amlodipine 10mg MERLIN TIMI-36 N=6560 Non-STE ACS Ranolazine vs placebo on top of standard care MARISA N=191 Chronic angina Ranolazine vs placebo Total patients enrolled = 8,139
30. CARISA Efficacy Change from baseline (sec) Peak Trough *** ** ** *** ** * * * * * 50 100 150 Exercise duration Time to angina Time to 1-mm ST-depression Exercise duration Time to angina Time to 1-mm ST-depression Placebo Ranolazine 750 mg b.i.d. Ranolazine 1,000 mg b.i.d. n = 791, ITT/LOCF; LS means ± SE. *p<0.05; **p 0.01 ***p 0.001 vs placebo ITT: Intent To Treat LOCF: Last Observation Carried Forward Chaitman BR, et al. JAMA 2004;291:309-16.
31. MERLIN TIMI-36 trial CV Death, MI, or Recurrent Ischaemia (% at 12 months) 0 10 20 30 0 180 360 540 Days from randomisation HR 0.92 (95% CI 0.83 to 1.02) P=0.11 Ranolazine 21.8% (n=3,279) Placebo 23.5% (n=3,281) Recurrent Ischemia (%) Days from Randomization Ranolazine 17.3% (N=3,279) Placebo 20.0% (N=3,281) HR 0.87 (95% CI 0.76 to 0.99) P =0.030 0.00 0.05 0.10 0.15 0.20 0.25 0 180 360 540 Percentage (%) p=0.048 p=0.005 p=0.002 8.1 16.4 21.1 5.6 12.5 16.5 0 5 10 15 20 25 Worsening Angina New anti- anginal therapy Reccurrent Ischemia Placebo n = 1,776) Ranolazine n = 1,789)
32. Rate of tachyarrhythmias detected on cECG monitoring after Non-ST-segment MI Scirica et al. Circulation 2007;116:1647-1652.
33. Scirica et al. Circulation 2007 Morrow, D. A. et al. Circulation 2009 Cahnege in HbA1c and estimated risk of recurrent ischemia at 1 year in patients allocated to ranolazine vs placebo stratified by diabetes status 0.48% reduction (P = 0.008 Ranolazine 750 mg bid vs placebo
The I f current drives the diastolic depolarization slope, thereby increasing or decreasing the slope. Therefore, it becomes clear, looking at this diagram, that any drug able to increase the intensity of the I f current would increase the diastolic depolarization slope, and that any drugs able to inhibit the I f current would slow the diastolic depolarization slope. So, the I f current drives the diastolic depolarization slope, the frequency of action potentials, and thus the heart rate.
Analysis of the safety and tolerability from the three major trials of the short-term use of ranolazine – at doses ranging from 500 mg bid to 1000 mg bid – confirmed that the incidence of adverse events was dose-related and that the most common adverse events were constipation and dizziness.