Pathology: Ischaemic Heart Disease and Myocardial Infarction 1 PDF

Pathology: Ischaemic Heart Disease and Myocardial Infarction 1 Dr Sarojini Devi MB52 Blk3 Learning Outcomes Ischaemic Heart Disease 1. Define and classify ischaemic heart disease. (C3) 2. Describe the pathogenesis of ischaemic heart disease. (C2) 3. Explain the types o...

Pathology: Ischaemic Heart Disease and Myocardial Infarction 1 Dr Sarojini Devi MB52 Blk3 Learning Outcomes Ischaemic Heart Disease 1. Define and classify ischaemic heart disease. (C3) 2. Describe the pathogenesis of ischaemic heart disease. (C2) 3. Explain the types of angina pectoris. (C2) Manipal University College Malaysia 2 Learning Outcomes Myocardial Infarction 1. Describe the pathophysiology of myocardial infarction(subendocardial and transmural infarction, STEMI, non- STEMI. (C2) 3. Describe the clinical features of acute myocardial infarction. (C2) Manipal University College Malaysia 3 Anatomy of the heart Manipal University College Malaysia 4 Manipal University College Malaysia 5 Ischaemic Heart Disease (IHD) Defined as an acute or a chronic form of cardiac disability arising from imbalance between the myocardial blood supply (perfusion) and demand for oxygenated blood and nutrients Since narrowing or obstruction of the coronary arterial system is the most common cause of myocardial anoxia - the alternate term ‘coronary artery disease (CAD)’ is used synonymously with IHD IHD or CAD is the leading cause of death in most developed countries (about one-third of all deaths) and somewhat low incidence is observed in the developing countries Men develop IHD earlier than women and death rates are also slightly higher for men than for women until the menopause Manipal University College Malaysia 6 IHD - Aetiopathogenesis Invariably caused by disease affecting the coronary arteries The most prevalent being atherosclerosis accounting for more than 90% cases Other causes are responsible for less than 10% cases Three broad categories of aetiology: i. Coronary atherosclerosis ii. Superadded changes in coronary atherosclerosis iii. Non-atherosclerotic causes Manipal University College Malaysia 7 IHD – Aetiopathogenesis i) Coronary atherosclerosis i. Distribution One or more of the three major coronary arterial trunks - in decreasing frequency - anterior descending branch of the left coronary (LAD) - right coronary artery (RCA) - circumflex branch of the left coronary (CXA) ii. Location – significant myocardial ischaemia is seen with > 75% narrowing of coronary artery or its branch Area of severest involvement is about 3 to 4 cm from the coronary ostia - at or near the bifurcation of the arteries iii. Fixed atherosclerotic plaques produce gradual luminal narrowing that leads to ‘fixed’ coronary obstruction Manipal University College Malaysia 8 IHD – Aetiopathogenesis ii) Superadded changes in coronary atherosclerosis i. Acute changes in atheromatous plaques - plaque haemorrhage, fissuring, or ulceration that results in thrombosis and embolisation of atheromatous debris May be brought about by factors such as sudden coronary artery spasm, tachycardia, intraplaque haemorrhage and hypercholesterolaemia ii. Coronary artery thrombosis - initiation of thrombus occurs due to surface ulceration of fixed atheromatous plaque - causing complete luminal occlusion iii. Local platelet aggregation and coronary artery spasm Aggregated platelets release vasospasmic mediators (thromboxane A2) - probably be responsible for vasospasm in the already Manipal University College Malaysiaatherosclerotic vessel 9 IHD – Aetiopathogenesis iii) Non-atherosclerotic causes i. Vasospasm ii. Stenosis of coronary ostia - extension of syphilitic aortitis or from aortic atherosclerotic plaques encroaching on the opening iii. Arteritis - various types of inflammatory involvements of coronary arteries or small branches E.g. rheumatic arteritis, polyarteritis nodosa, thrombo-angiitis obliterans (Buerger’s disease), Takayasu’s disease, Kawasaki’s disease, tuberculosis and other bacterial infections may contribute to myocardial damage iv. Embolism - emboli originating from elsewhere in the body Manipal University College Malaysia 10 IHD – Aetiopathogenesis iii) Non-atherosclerotic causes v. Thrombotic disease - infrequent cause - from hypercoagulability of the blood such as in shock, polycythaemia vera, sickle cell anaemia and thrombotic thrombocytopenic purpura vi. Trauma - contusion of a coronary artery from penetrating injuries vii. Aneurysms - Extension of dissecting aneurysm of the aorta into the coronary artery or congenital, mycotic and syphilitic aneurysms may occur in coronary arteries viii. Compression - from outside by a primary or secondary tumour of the heart Manipal University College Malaysia 11 Clinical presentations of IHD Depending upon the suddenness of onset, duration, degree, location and extent of the area affected by myocardial ischaemia - the range of changes and clinical features that develop are: 1. Angina pectoris - Ischemia induced chest pain which is insufficient to cause myocyte death 2. Myocardial infarction (MI) - Ischemia is sufficient to cause cardiomyocyte death 3. Chronic IHD with congestive heart failure - Post MI- progressive cardiac decompensation which results in mechanical pump failure 4. Sudden cardiac death (SCD) - Post MI - lethal arrhythmia Manipal University College Malaysia 12 Manipal University College Malaysia 13 Angina pectoris Clinical syndrome resulting from transient ischaemia Characterised by - intermittent and recurrent attacks of sub- sternal or pre-cordial chest pain / discomfort Aggravated by an increase in the demand of the heart and relieved by a decrease in the work of the heart Caused by transient (15 seconds to 15 minutes), reversible myocardial ischaemia No cellular necrosis that defines infarction Manipal University College Malaysia 14 Chest pain in angina “Pain” is a consequence of ischaemia-induced release of adenosine, bradykinin, and other molecules that stimulate the autonomic nerves Chest pain or discomfort described as squeezing, pressure fullness or tightness in the centre of the chest. May be described as: Constricting chest pain; Pain or discomfort in the arm, neck, jaw or shoulder Pain is similar to indigestion or heartburn, feeling pressure or extreme anxiety  Women Manipal may University College not present with classic chest pain symptoms - Malaysia 15 Angina pectoris There are 3 overlapping clinical patterns of angina pectoris with some differences in their pathogenesis 1. Stable or typical angina 2. Unstable or Crescendo angina 3. Prinzmetal angina Manipal University College Malaysia 16 Stable / typical angina Most common form Characterised by attacks of pain following physical exertion or emotional excitement and is relieved by rest Due to chronic stenosing coronary Crushing /squeezing atherosclerosis (>70% coronary stenosis) pain radiating to left arm and jaw (referred pain) During the attacks, there is depression of ST Pain relieved by rest, segment in the ECG due to poor perfusion of the nitroglycerines subendocardial region of the left ventricle but there is no elevation of enzymes in the blood as there is no irreversible myocardial injury Manipal University College Malaysia 17 Unstable (Crescendo) angina Referred to as ‘pre-infarction angina’ or ‘acute coronary insufficiency’ Most serious pattern of angina Characterised by more frequent onset of pain of prolonged duration and occurring often at rest Indicative of an impending acute myocardial infarction Due to disruption of atherosclerotic plague and superimposed thrombosis, distal embolisation of thrombus and/or due to vasospasm Distinction between unstable angina and acute MI on ECG Manipal In acute MI Malaysia University College - ST segment elevation 18 Prinzmetal (variant or vasospasmic) angina Characterised by pain at rest and has no relationship with physical activity Exact pathogenesis is not known May occur due to sudden vasospasm of a coronary trunk induced by coronary atherosclerosis or due to release of humoral vasoconstrictors by mast cells in the coronary adventitia Responds promptly with vasodilators like nitroglycerine or calcium channel blockers ECG shows ST segment elevation due to transmural ischaemia Manipal University College Malaysia 19 Acute myocardial infarction Accounts for 10-25% of all deaths May virtually occur at all ages, though the incidence is higher in the elderly Males > females – lower incidence in women during reproductive period Characterised by area of coagulative necrosis of heart muscle, resulting from: A sudden, absolute or relative reduction in coronary blood supply or An acute plaque change – thrombosis or haemorrhage within or an atheromatous plaque formation Manipal University College Malaysia 20 Acute myocardial infarction: Causes 1. Coronary artery disease/ coronary heart disease Atherosclerotic change in coronary arteries seen in almost 90% cases 2. Other causes i. Increased demand - increased heart rate or hypertension ii. Reduced blood volume - with hypotension or shock iii. Reduced oxygenation - pneumonia ,congestive heart failure iv. Reduced oxygen-carrying capacity - anemia or carbon monoxide poisoning. Manipal University College Malaysia 21 Pathogenesis IHD is consequence of decreased coronary perfusion to increased myocardial demand Risk factors are similar to atherosclerosis IHD and MI occur due to 1. Fixed obstruction. ‘Fixed’ atherosclerotic occlusion of coronary arteries > 70% of lumen occluded – Stable angina > 90% of lumen occluded – Unstable angina 2. Acute plaque changes (Superimposed thrombosis and/ vasospasm.) Plaque changes and thrombosis – MI ,sudden cardiac death Manipal University College Malaysia 22 Pathogenesis of IHD and MI Acute plaque change Rupture, fissuring, ulceration Expose thrombogenic components or subendothelium Thrombosis + Haemorrhage Acute coronary syndromes Unstable angina , MI, Sudden cardiac death Manipal University College Malaysia 23 Fixed coronary obstruction causing plaque changes Large number of asymptomatic persons are at risk of a catastrophic coronary event Manipal University College Malaysia 24 Factors affecting acute plaque change 1. Intrinsic factors Plaque composition- Large atheromatous cores or thin fibrous caps 2. Extrinsic factors Physical stress on plaque Emotional stress (Adrenergic stimulation causing hypertension and vasospasm) Manipal University College Malaysia 25 Acute coronary syndrome “What it includes…” i. Unstable angina ii. Acute MI iii. Sudden cardiac death Caused by acute plaque changes Manipal University College Malaysia 26 Distribution of MI 1. Lt. anterior descending artery (40-50%) Anterior infarction Ant. wall of LV, Ant. IV septum, Apex 2. Rt. coronary artery (30-40%) Inferior infarction RV 3. Lt. circumflex artery(20%) Lateral infarction Lateral LV Manipal University College Malaysia 27 Classification of MI 1. Based on anatomic region of left ventricle that is involved: i. Anterior, posterior (inferior), lateral, septal and circumferential ii. Combination: inferolateral, anteroseptal, etc. 2. Based on degree of ventricular wall involved: i. Full thickness or transmural infarction – involves the entire thickness of the myocardium ii. Subendocardial infarction – involves the inner half or third of the myocardium 3. Based on the age of the infarction: i. Newly formed infarction – acute, recent or fresh ii. Advanced infarction – old, healed or organized Manipal University College Malaysia 28 Types of MI based on extent of ischaemia 1. Transmural infarction 2 Involves the full thickens of ventricle 2. Subendocardial infarction Limited to inner third of myocardium 1 Manipal University College Malaysia 29 Transmural Infarction Infarction involving the full thickness of ventricular wall Caused by epicardial vessel occlusion Associated with chronic atherosclerosis and thrombosis Also called STEMI (ST segment elevation MI) ECG ST segment elevation Presence of Q wave and T wave inversion Manipal University College Malaysia 30 Subendocardial Infarction Infarction limited to inner third of myocardium Also called NSTEMI (Non- ST segment elevation MI) ECG No ST segment elevation or Q wave Manipal University College Malaysia 31 Manipal University College Malaysia 32 Manipal University College Malaysia 33 Subendocardial Infarction Subendocardium is most vulnerable to” i. Hypoxia and hypoperfusion ii. Severe coronary artery disease iii. Increases in oxygen demand A narrow rim of endocardium which usually has blood diffusing in from the ventricular lumen is preserved from infarcts Manipal University College Malaysia 34  Transmural infarction( STEMI): ST segment elevation, Presence of Q wave and T wave inversion Subendocardial infarction(nonSTEMI): No University Manipal ST segment College Malaysia elevation 35 Clinical features in MI Can occur at any age ( 10% before 40years , 45% before 65years) Males > females - increase incidence in females after menopause Severe crushing substernal chest pain Radiating pain to neck, jaw, left arm, epigastrium Last several minutes to hours Referred Sweating ,Nausea pain!! Dyspnoea Pulse-feeble and weak Manipal University College Malaysia 36 References 1. Robbins and Cotran Pathologic Basis of Disease 10 th Edition 2. Underwood’s pathology: A clinical approach 7 th edition 3. Harsh Mohan’s textbook of pathology 6 th edition 4. http://library.med.utah.edu/WebPath/webpath.html Manipal University College Malaysia 37