Lec 4-Ischemic Heart Disease PDF

Ischemic heart disease  Ischemia is defined as inadequate blood supply to a local area due to narrowing of the blood vessels supplying this area. Ischemia means that an organ (e.g., the heart) is not getting enough blood and oxygen. When the blood flow to the heart muscle is completely blo...

Ischemic heart disease  Ischemia is defined as inadequate blood supply to a local area due to narrowing of the blood vessels supplying this area. Ischemia means that an organ (e.g., the heart) is not getting enough blood and oxygen. When the blood flow to the heart muscle is completely blocked, the heart muscle cells die (infarction), which is termed a heart attack or myocardial infarction (MI). What is the difference between myocardial ischemia and myocardial infarction? Ischemia denotes diminished volume of perfusion, while infarction is the cellular response to lack of perfusion.  Ischemic heart disease Also known as Coronary Artery Disease (CAD). Ischemic heart disease (IHD) is a condition in which there is an inadequate supply of blood and oxygen to a portion of the myocardium. Imbalance between myocardial oxygen supply and demand. Caused mainly by atherosclerosis (common cause) It includes: - Angina - Myocardial infarction - Heart failure & arrhythmias  Pathophysiology of Ischemic Heart Disease Although the narrowing can be caused by a blood clot or by constriction of the blood vessel, most often it is caused by buildup of plaque, called atherosclerosis. Atherosclerosis is nearly gradual progressive disorder & leading to plaque formation. Plaques cause narrowing of coronary arteries. Stable plaque causes predictable angina. Unstable plaque ruptures, activating clotting (coagulation) system & thrombus formation, that impairs coronary blood flow causing unstable angina or myocardial infarction (MI). MI heals with scarring, causing impairing contractility & increasing stiffness leading to heart failure (acute/chronic). Ischemic areas & scars are prone to cause ventricular arrhythmias leading to sudden death.  Aetiology of Ischemic Heart Disease I- Decreased Myocardial Oxygen Supply. II- Increased Myocardial Oxygen Demand. I-Decreased Myocardial Oxygen Supply (causes): 1- Decreased quantity of coronary blood: A- coronary artery disease Atherosclerosis Spasm Vasculitis e.g. polyarteritis nodosa. Cornoary osteal stenosis e.g. syphilis , calcification. Congenital anomalies. B- low cardiac output states especially Valvular stenosis especially aortic stenosis. Pulmonary hypertension 2- Decreased quality of coronary blood. Hypoxia Severe anaemia II-Increased Myocardial Oxygen Demand (Causes) Occurring in conditions resulting in marked increase of : - Heart rate. - contractility. - afterload (resistance to ejection). - preload (filling pressure). As in the following conditions: - Severe stress (physical, mental) - Hypertension, aortic stenosis. - Hyperdynamic states e.g. thyrotoxicosis  Risk factors of IHD Non modifiable risk factors Modifiable risk factors Contributing risk factors Non modifiable risk factors Positive family history of CAD Old age Gender (men develop CAD at earlier age than women) Modifiable risk factors Cigarette smoking , tobacco use. Hypertension Diabetes mellitus Obesity Sedentary life style Physical inactivity Hyperlipidemia Contributing risk factors Psychological tension ) stress, anxiety, depression.etc) Menopause Oral contraceptive pills Type A personality: time urgency, aggression behavior, impatience, frustrations. Classification (Types) of Ischemic Heart Disease I- Pathological Types of Ischemic Heart Disease II- Clinical Types of Ischemic Heart Disease  Pathological Types of Ischemic Heart Disease There are three main types of ischemic heart disease: (1) Obstructive coronary artery disease. (2) Non-obstructive coronary artery disease. (3) Coronary microvascular disease. Coronary artery disease affects the large arteries on the surface of the heart and many people have both obstructive and non-obstructive forms of this disease. Coronary microvascular disease affects the tiny arteries in the heart muscle. It may occur with or without coronary artery disease  Obstructive coronary artery disease occurs when plaque builds up in the large arteries, causing them to narrow gradually. This reduces the supply of oxygen-rich blood to the heart. Obstructive coronary artery disease means the heart’s arteries are more than 50 percent blocked. The blood flow may eventually be completely blocked in one or more of the three large coronary arteries  In non-obstructive coronary artery disease, the large arteries are narrowed by plaque, but not as much as they are in obstructive disease. It is diagnosed if imaging studies show less than 50 percent obstruction of the heart’s large arteries caused by plaque buildup. This condition can also be caused by disease or injury to the lining of the large arteries, affecting the arteries’ ability to expand in response to physical, chemical, or electrical signals that normally would stimulate more blood flow to the heart. Damage to the inner walls of the coronary arteries can cause them to spasm, leading to temporarily decreased blood flow to the heart  Coronary microvascular disease affects the heart’s smallest arteries. Coronary microvascular disease can happen either alone or with obstructive or non-obstructive coronary artery disease or other heart diseases. This type of heart disease most often occurs when molecular changes in the microvascular system—the tiny blood vessels—of the heart prevent normal blood flow through the small arteries  Clinical Types of Ischemic Heart Disease I- Angina : Stable angina (Angina Pectoris) Unstable angina Variant angina (Prinzmetal angina) Intractable angina (refractory angina): Severe. Silent ischemia: in diabetes mellitus. II- Myocardial infarction (MI).  Presentation of ischemic heart disease A- Asymptomatic: Silent myocardial ischemia B- Symptomatic: 1- Chest pain. 2- Other presentations: ( with or without chest pain). - Heart failure - Arrhythmias - Syncope - Sudden death  What is angina? Angina is a chest pain occurs due to transient inadequacy of blood and oxygen supply to the myocardium (myocardial ischemia) leads to imbalance between oxygen demand & oxygen supply.  Angina pectoris is chest pain or discomfort that occurs when the heart muscle does not get enough blood. Angina pectoris is chest pain resulting from myocardial ischemia (inadequate blood supply) to the myocardium.  Pathogenesis of angina pain Myocardial ischemia develops when coronary blood flow becomes inadequate to meet myocardial oxygen demand. This causes myocardial cells to switch from aerobic to anaerobic metabolism. How? Due to myocardial ischemia, the myocardial tissues are deprived of oxygen and nutrients for the aerobic metabolism. As a result there is inclusion of anaerobic metabolism which leads to accumulation of metabolites ( e.g. lactate, pyruvate) in cardiac muscle. These metabolites stimulate myocardial nerve endings (nerve fibers) which discharge impulses along sympathetic fibers to upper thoracic segments of the spinal cord resulting in pain in the corresponding dermatomes. And all this leads to cardiac chest pain of angina pectoris. Clinical Types of angina Stable angina = angina pectoris= classic angina Unstable angina Refractory angina Variant angina Intractable angina: Severe. Silent ischemia: Diabetes mellitus.  Chest pain of stable angina (angina pectoris) Site: retrosternal, precordial or central chest pain. Radiation: left shoulder, medial aspect of left forearm & hand, neck, lower jaw, epigastrium, right shoulder and back. Character: compressing, constricting or in the form of discomfort, tightness, heaviness. Precipitation: muscular exercise, emotional stress, heavy meal, cold atmosphere or high altitudes, excessive smoking, sexual intercourse. Relief: by rest, sublingual nitrates. Duration: Typically lasting 5-10 minutes. Associated symptoms: Dyspnea, palpitation, sense of fear of death ( angor animi), sweating, dizziness & fainting, nausea & vomiting.  Angina Pectoris (Stable Angina) It is the commonest type. It is characterized by classic anginal chest pain (mentioned before) : 1- retrosternal constricting discomfort radiating to left arm, neck, jaw. 2- Provoked by physical exertion, especially after meals and in cold, windy weather or by anger or excitement, and 3-Relieved (usually within minutes)with rest or sublingual nitroglycerin. Typical angina: all three features. Atypical angina: two out of the three. Non anginal chest pain: one or less of these features.  Unstable angina Unstable (preinfarction=crescendo): Caused by an almost complete blockage of the coronary arteries. deterioration (24hs) in previous stable angina with symptoms frequently occurring at rest (acute coronary syndrome). Unstable angina is a form of acute coronary syndrome, is defined as angina pectoris that changes or worsens. Increased episodes in frequency and in severity. Usually lasts longer than classic angina. usually lasting more than 10 minutes Chest pain occurring at rest. angina with an increase in duration, frequency or severity of pain (crescendo angina).  Variant angina (Prinzmetal angina, vasospastic angina) occurs without provocation, usually at rest, as a result of coronary artery spasm. Angina at rest & not precipitated by increased myocardial oxygen demand i.e. not after exercise or stress. It is most probably due to coronary spasm. It is usually associated with ST segment elevation. Coronary angiography may be normal.  Investigations ECG Echocardiography Radionuclide studies Coronary arteriography ECG Resting ECG: - In between the attacks it is usually normal. - During pain it may show evidence of ischemia: 1- St segment changes: depression (horizontal or downsloping) or elevation in variant angina. 2- T wave changes: inverted, flat or peaked. 3- Different types of arrhythmias. Exercise ECG: - may show evidence of ischemia during exercise, - ST segment depression (horizontal or downsloping). - ventricular arrhythmias, - typical angina chest pain during test. Ambulatory ECG: for the diagnosis of variant angina. Echocardiography: may show regional wall motion abnormalities dyskinesia or akinesia during rest or induced by exercise. Radionuclide study: using Thallium201 or Technitium 99m. Ischemia appears as a filling defect (cold spot) induced by exercise or dobutamine & test disappear after rest.  Coronary arteriography Indications: Intractable angina not responding to medical treatment. Indicated when non-invasive tests have failed to establish the cause of atypical chest pain. Unstable angina. Post-infarction angina. Recurrent chest pain of unknown origin in which all other investigations are normal. Now it is performed in all patients who are candidates for coronary revascularization. Benefits: It provides detailed information about the number, site & severity of obstructive lesions. Principles of treatment Increase oxygen supply or reduce oxygen demand of the myocardium: Reduce heart rate. Reduce preload. Reduce afterload. Improve coronary blood flow.  Stroke volume is the amount of the blood pumped by ventricle with each beat. COP = HR x SV Stroke volume is affected by : - Contractility strength of cardiac muscle - Preload - Afterload  Preload = volume of blood received by the heart. Basically, preload is stretch. The amount of the volume being returned to the heart. preload is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand. It is the amount of ventricular stretch at the end of diastole. Some people remember this by using analogy of a balloon – blow air into the balloon and it stretches; the more air you blow in, the greater the stretch.  Afterload = pressure or resistance the heart has to overcome to eject blood. Afterload is squeeze. The amount of resistance that the heart has to overcome in order to eject blood. Afterload is the pressure the heart must work against to eject blood during systole (ventricular contraction).... As aortic/pulmonary pressure increases, the afterload on the left/right ventricle increase respectively. It is known as the systemic vascular resistance. It is the amount of resistance the heart must overcome to open the aortic valve and push the blood volume out into the systemic circulation. If you think about balloon analogy; afterload is represented by the knot at the end of the balloon. To get the air out, the balloon must work against that knot.  Treatment I- General measures (risk factor modification). II- Exercise program III- Medical treatment (Anti-angina drugs) IV- Coronary revascularization V- Treatment of angina attack  General Measures (1) Avoidance of conditions precipitating angina pain e.g. Severe exertion. Emotional stress. (2) Control of risk factors of atherosclerosis: e.g. Smoking Obesity Hypertension Hyperlipidemia (3) Control of aggravating factors of myocardial ischemia: e.g. Anaemia Hypoxia Thyrotoxicosis.  Exercise program Benefits: Reduction of the heart rate and blood pressure especially with stress. Improvement of skeletal muscle action resulting in increase of effort tolerance. May increase collateral coronary blood flow. Decrease platelet aggregation. Increase fibrinolytic activity. Precautions: The exercise should be regular, gradual and dynamic (e.g walking 30 minutes 3 days in the week). It should be stopped short of producing pain or tachycardia more than 110- 120/min.  Medical treatment (Anti-angina drugs) Nitrates Beta-blockers Calcium channel blockers Anticoagulant: - Anti-platelets - Heparin Potassium channel activators  Coronary Revascularization Indications: 1- Improvement of survival in patient with: Disease of left main coronary, left anterior descending or three-vessel disease. Post-infarction ischemia. 2- Intractable angina not responding to medical treatment.  Coronary Revascularization Procedures: 1-Percutaneous coronary intervention (PCI) which includes: Percutaneous transmural coronary angioplasty (PTCA). Coronary stenting. 2- surgery: Coronary artery bypass graft (CABG) using internal mammary artery or saphenous vein graft.  Treatment of angina attack Complete rest. Nitroglycerine 0.5 mg or isosorbide dinitrate 5mg sublingually. If the pain is not relieved after the use of 2-3 tablets , the patient should be immediately transferred to hospital & evaluated for the possibility of myocardial infarction.