ANGINA PECTORIS Classic angina is characterized by substernal squeezing chest pain, occurring with stress and relieved with rest or nitroglycerin. May.

Slides:



Advertisements
Similar presentations
M YOCARDIAL ISCHEMIA Prepared by: Dr. Nehad Ahmed.
Advertisements

MEDPHARM DRUGS FOR ISCHEMIC HEART DISEASE FEBRUARY 10,2110.
CASE 21 Michelle Legaspi. 65 y/o male retired teacher sought consult because of occasional chest heaviness non-radiating occuring during a moderate physical.
ANGINA PECTORIS. Angina pectoris (chest pain) is the result of myocardial ischemia caused by an imbalance between myocardial blood supply and oxygen demand.
Drugs to treat angina. I. Introduction Branching off the aorta are the coronary arteries.
Copyright © 2013, 2010 by Saunders, an imprint of Elsevier Inc. Chapter 51 Drugs for Angina Pectoris.
Chronic stable angina Dr Taban Internist & cardiologist.
Ischemic Heart Disease.  Coronary artery disease CAD is a general manifestation that dose not discriminate bet the various phases that the individual.
Management of Stable Angina Pectoris David Putnam, MD Albany Medical College.
CURRENT STATUS OF STRESS TESTING JOHN HAMATY D.O..
Coronary Artery Disease. What is coronary artery disease? A narrowing of the coronary arteries that prevents adequate blood supply to the heart muscle.
ISCHEMIC HEART DISEASE. Coronary arteries  Left coronary artery supplies:  Left ventricle  Interventricular septum  Part of right ventricle.
Modalities of Cardiac Stress Test
Ischemic heart disease
Ischemic Heart Diseases IHD
DR. HANA OMER.  ANGINA PECTORIS :is a clinical syndrome characterized by paroxysmal chest pain due to transient myocardial ischemia.  It may be occur.
This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student rotated under Nephrology Division under the supervision and administration.
 Feel better  Live longer  To improve quality of life (symptoms)  To reduce mortality  To reduce morbidity  To reduce progression of disease and.
Diagnostic Stress Testing
Stress testing Physiology: Sympathetic system activation increases: Heart rate Stroke volume Cardiac output Ventricular contractility Afterload (Vasoconstriction)
Angina and MI.
1 Dr. Zahoor Ali Shaikh. 2 CORONARY ARTERY DISEASE (CAD)  CAD is most common form of heart disease and causes premature death.  In UK, 1 in 3 men and.
Chapter 18 Agents that Dilate Blood Vessels. Copyright 2007 Thomson Delmar Learning, a division of Thomson Learning Inc. All rights reserved Coronary.
Principles of diagnsosis of ischemic heart disease Mohammad Hashemi Interventional cardiologist Department of cardiology.
EMS 353. Lectures 6 Dr. Maha Khalid physiology of pharmacology cardiovascular system.
Dr Jayachandran Thejus.  Coronary artery disease-  Block in coronary artery due to plaque or thrombus  Leads to myocardial ischemia manifested as chest.
1 ANGINA ANGINA MYOCARDIAL OXY. DEMAND >. OXY. SUPPLY. OXY. SUPPLY < SYMPTOMS – chest pain mostly relieved by taking rest, dyspnea, sweating, nausea..
Management of Stable Angina Pectoris Bushra Abdul Hadi.
Clinical case no. 22 Presenter: Lin,Huei-Hsiu (Caroline) (Caroline)
2. Ischaemic Heart Disease.
Ischemic Heart Disease CVS3 Hisham Alkhalidi. Ischemic Heart Disease A group of related syndromes resulting from myocardial ischemia.
Myocardial infarction My objectives are: Define MI or heart attack Identify people at risk Know pathophysiology of MI Know the sign & symptom Learn the.
Agents that Dilate Coronary Blood Vessels.  Coronary artery disease (CAD) results from atherosclerosis  Clinical symptoms caused by  narrowing of the.
BIMM118 Angina pectoris Medical term for chest pain or discomfort due to coronary heart disease. Typical angina pectoris (=“tight heart” is uncomfortable.
Silent Ischemia STABLE CAD
ANGINA PECTORIS Tb Tuberculosis Carl Matol, RN. ANGINA-to choke CLASSIC/STABLE ANGINA Due to insufficiency of O2 supply against myocardial demand Accumulated.
Antianginal drugs Angina pectoris is the severe chest pain that occurs when coronary blood flow is inadequate to supply the oxygen required by the heart.
Angina pectoris Sudden,severe,pressing chest pain starting substernal &radiate to left arm. Due to imbalance between myocardium oxygen requirement and.
1 3 rd jan 2009 Done by: Ahmed M. Aljabri Pharm.D.
Drugs used in angina pectoris
Angina pectoris Sudden, severe, pressing chest pain and radiating to the neck, jaw, back, and arms. The episodes are transient, stay between 15 sec to.
 Heart disease remains the leading cause of morbidity and mortality in industrialized nations.  40% of all deaths in the U.S.A (nearly twice the number.
MYOCARDIAL INFARCTION. CASE 1 Mr. A: 38 years old He smokes 1 pack of cigarettes per day He has no other past medical history 8 hours ago, he gets sharp.
Antianginal drugs Antidysrrhytmic drugs
Angina pectoris Sudden,severe,pressing chest pain starting substernal &radiate to left arm & neck. Due to imbalance between myocardium oxygen requirement.
Adult Echocardiography Lecture 10 Coronary Anatomy
Ischemic Heart Disease CVS3 Hisham Alkhalidi. Ischemic Heart Disease A group of related syndromes resulting from myocardial ischemia.
Prepared by Miss Fatima Hirzallah.  Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the.
Myocardial Infarction Angina Pectoris What is an MI?
Elsevier Inc. items and derived items © 2010 by Saunders, an imprint of Elsevier Inc.1 Drugs for Angina Pectoris.
Drugs for Angina Pectoris
Indication Contraindication Preparation
PHARMACOLOGY OF ANTI-ANGINAL DRUGS (ID#580) Dr. Mariam Yousif Pharmacology & Toxicology Dept. November 17 th, 2014.
1 Angina Pectoris Prepared by : Ansam Sharef Ahmad Aswad.
ISCHEMIC HEART DISEASE
CORONARY ARTERY DISEASE
Ischemic Heart Disease
CORONARY ARTERY DISEASE
Anti-Anginal Drugs.
Angina Pectoris Prepared by : Ansam Sharef Ahmad Aswad.
Angina pectoris Domina Petric, MD.
New Paradigm of Anti Anginal Therapy dr.Yerizal Karani SpPD,SpJP(K)
Nursing Management: Patients With Coronary Vascular Disorders
Anti-Anginal Drugs.
Coronary Artery Disease and Acute Coronary Syndrome
Antianginal Drugs.
Acute Coronary Syndrome (1)
Antianginal Drugs Ass. Prof. Naza M. Ali Lec 3-4 G2 21 April 2019
Drugs Used to Treat Angina Pectoris
Presentation transcript:

ANGINA PECTORIS Classic angina is characterized by substernal squeezing chest pain, occurring with stress and relieved with rest or nitroglycerin. May radiate down the left arm. May be associated with nausea, vomiting, or diaphoresis.

ANGINA

STABLE ANGINA CLASSIFICATION Exertional. Variant. Anginal Equivalent Syndrome. Prinzmetal’s Angina. Syndrome-X. Silent Ischemia.

ANGINA: EXERTIONAL Coronary artery obstructions are not sufficient to result in resting myocardial ischemia. However, when myocardial demand increases, ischemia results.

ANGINA: VARIANT ANGINA Transient impairment of coronary blood supply by vasospasm or platelet aggregation. Majority of patients have an atherosclerotic plaque. Generalized arterial hypersensitivity. Long term prognosis very good.

ANGINA: ANGINAL EQUIVALENT SYNDROME Patient’s with exertional dyspnea rather than exertional chest pain. Caused by exercise induced left ventricular dysfunction.

ANGINA: PRINZMETAL’S ANGINA Spasm of a large coronary artery. Transmural ischemia. ST-Segment elevation at rest or with exercise. Not very common.

ANGINA: SYNDROME X Typical, exertional angina with positive exercise stress test. Anatomically normal coronary arteries. Reduced capacity of vasodilation in microvasculature. Long term prognosis very good. Calcium channel blockers and beta blockers effective.

ANGINA: SILENT ISCHEMIA Very common. More episodes of silent than painful ischemia in the same patient. Difficult to diagnose. Holter monitor. Exercise testing.

ANGINA: TREATMENT GOALS Feel better. Live longer.

ANGINA: PROGNOSIS Left ventricular function. Number of coronary arteries with significant stenosis. Extent of jeoporized myocardium.

STABLE ANGINA Risk stratification. Noninvasive testing. Cardiac catheterization.

STABLE ANGINA EVALUATION OF LV FUNCTION Physical exam. CXR. Echocardiogram.

STABLE ANGINA EVALUATION OF ISCHEMIA History. Baseline Electrocardiogram. Exercise Testing.

CCS ANGINA CLASSIFICATION Class II. Class III. Class IV . Angina only with extreme exertion. Angina with walking . 1 to 2 blocks. Angina with walking. 1 block. Angina with minimal activity.

STABLE ANGINA EXERCISE TESTING The goal of exercise testing is to induce a controlled, temporary ischemic state during clinical and ECG observation.

ANGINA: EXERCISE TESTING

ANGINA: EXERCISE TESTING HIGH RISK PATIENTS Significant ST-segment depression at low levels of exercise and/or heart rate<130. Fall in systolic blood pressure. Diminished exercise capacity. Complex ventricular ectopy at low level of exercise.

ECG TREADMILL TEST IN WOMEN Higher false-positive rate. Reduces procedures without loss of diagnostic accuracy. Only 30% of women need be referred for further testing.

STABLE ANGINA GUIDELINES FOR NUCLEAR TEST Diagnosis/prognosis for CAD. Non-diagnostic TEST. Abnormal resting ECG. Negative TEST with continued chest pain. Intermediate probability of disease.

STABLE ANGINA GUIDELINES FOR NUCLEAR TEST Defined CAD. Post infarct risk stratification. Risk stratification to determine need for revascularization ( viability study ).

STABLE ANGINA DIPYRIDAMOLE NUCLEAR TEST Near equivalent sensitivity/specificity with symptom-limited nuclear TEST. Most useful in patients who cannot exercise. Major contraindication is severe bronchospastic lung disease ( consider Dobutamine study ).

STABLE ANGINA STRESS ECHO Ischemia may cause wall motion abnormalities, no rise of fall in LVEF. Sensitivity/specificity same as nuclear testing. May be better in women.

STRESS ECHO VS. NUCLEAR STRESS

EXERCISE TESTING CONTRAINDICATIONS MI—impending or acute. Unstable angina. Acute myocarditis / pericarditis. Acute systemic illness. Severe aortic stenosis. Congestive heart failure. Severe hypertension. Uncontrolled cardiac arrhythmias.

STABLE ANGINA NON-INVASIVE EVALUATION Non disabling Angina Resting LV Functions LV dysfunction Normal LV function Coronary Angiography Stress Test High Risk Low Risk Coronary Angiography Medical Therapy Stable Recurrent Angina Medical Therapy Coronary Angiography

CARDIAC CATHETERIZATION INDICATIONS Suspicion of multi-vessel CAD Determine if CABG/PTCA feasible Rule out CAD in patients with persistent/disabling chest pain and equivocal/normal noninvasive testing

RISK FACTOR MODIFICATION Hypertension Smoking Dyslipidemia Diabetes Mellitus Obesity Stress Homocysteine

STABLE ANGINA TREATMENT OPTIONS AAaaaaa Angina Treatment Option Percutaneous Intervention AAaaaaa AAaaaaa Medicine AAaaaaa CABG

STABLE ANGINA MEDICAL TREATMENT Beta-blockers Calcium channel blockers Nitrates Aspirin Statins ? ACE inhibitors

STABLE ANGINA CONSIDERATIONS WHEN CHOOSING A DRUG Effect on myocardium Effect on cardiac conduction system Effect on coronary/systemic arteries Effect on venous capitance system Circadian rhytm

BETA-BLOCKERS Decrease myocardial oxygen consumption Blunt exercise response Beta-one drugs have theoretical advantage Try to avoid drugs with intrinsic sympathomimetic activity First line therapy in all patients with angina if possible

BETA-BLOCKERS

BETA BLOCKERS SIDE EFFECTS Bronchospasm Diminished exercise capacity Negative inotropy Sexual dysfunction Bradyarrhythmia Masking of hypoglycemia Increased claudication Hair loss

BETA BLOCKERS COMMON AVAILABLE AGENTS Propranolol Atenolol Metoprolol Nadolol Timolol

CALCIUM CHANNEL BLOCKERS MECHANISMS OF ACTION Arterial dilation/after-load reduction Coronary arterial vasodilation Prevention of coronary vasoconstriction Enhancement of coronary collateral flow Improved subendocardial perfusion Slowing of heart rate with diltiazem, verapamil

CALCIUM CHANNEL BLOCKERS MECHANISMS OF ACTION

CALCIUM CHANNEL BLOCKERS MECHANISMS OF ACTION

CALCIUM CHANNEL BLOCKERS SIDE EFFECTS Palpitations Headache Ankle edema Gingival hyperplasia

CALCIUM CHANNEL BLOCKERS AVAILABLE AGENTS Verapamil Diltiazem Nifedipine Nicardipine Amlodipine Felodipine Nisoldipine Bepridil

NITRATES MECHANISMS OF ACTION Nitric oxide has been identified as endothelium-derived relaxing factor Organic nitrates are therapeutic precursors of endothelium-derived relaxing factor

NITRATES MECHANISMS OF ACTION Venous vasodilation/pre-load reduction Arterial dilation/after-load reduction Coronary arterial vasodilation Prevention of coronary vasoconstriction Enhancement of coronary collateral flow Antiplatelet and antithrombotic effects

NITRATES REDUCING TOLERANCE Smaller doses Less frequent dosing Avoidance of long-acting formulations unless a prolonged nitrate-free interval is provided Build-in a nitrate-free interval o 8-12 hours

NITRATES SIDE EFFECTS Headache Flushing Palpitations Tolerance

NITRATES COMMON AVAILABLE AGENTS Isorbide dinitrate Isorbide mononitrate Long-acting transdermal patches Nitroglycerin SL

STABLE ANGINA TREATMENT OPTIONS CABG PTCA

STABLE ANGINA: 1-VESSEL CAD THERAPEUTIC STRATEGIES Initiate pharmacologic treatment A. Nearly half of patients will become asymptomatic PTCA preferred alternative if medical therapy does not relieve angina or causes adverse effects

STABLE ANGINA: 2-VESSEL CAD THERAPEUTIC STRATEGIES Initial medical management in patients with mild ischemic symptoms and normal LV function Revascularization in patients who fail medical therapy Selection of PTCA vs. CABG depends on coronary anatomy, LV function, need for complete revascularization, and patient preference

STABLE ANGINA: 3-VESSEL CAD THERAPEUTIC STRATEGIES CABG in patients with left-main disease or 3-vessel CAD and decreased LVEF PTCA or medical management an alternative in patients with 3-vessel CAD, mild symptoms, and preserved LVEF