L45 IHD PDF

45 ISCHAEMIC HEART DISEASE ILOs By the end of this lecture, students will be able to 1. Explain the relation between partial / complete coronary artery occlusion and clinical spectrum of ischemic heart disease. 2. Discuss consequences and complications of myocardial infarction. Ischemic heart diseas...

45 ISCHAEMIC HEART DISEASE ILOs By the end of this lecture, students will be able to 1. Explain the relation between partial / complete coronary artery occlusion and clinical spectrum of ischemic heart disease. 2. Discuss consequences and complications of myocardial infarction. Ischemic heart disease (IHD) is a broad term encompassing several closely related syndromes caused by myocardial ischemia Ischaemic heart disease is the most common cause of death in the Western world. The most frequent cause of obstruction in a main coronary artery is atherosclerosis. Causes of ISCHEMIC HEART DISEASE [IHD] A. Impaired oxygen supply: 1. Coronary Narrowing (90%)  by Atherosclerotic lesion (plaque) Spasm 2. Impaired Coronary Filling (in diastole)  affected by diastolic time as in tachycardia filling pressure as in hypotension …etc 3. Impaired oxygen carrying capacity (in anaemia) B. Increase myocardial oxygen demand:  Cardiac Work:  Heart Rate workload; i.e  BP…etc. CORONARY HEART DISEASES [CHD] is either Angina or myocardial infarction depending on: Rate of progression Nature of plaque Extent of occlusion Angina pectoris Chest pain due to ischemia of heart muscle caused by obstruction or spasm of coronary arteries. Character: Constricting & tight, oppressive, crushing. Site: Starts in the center behind the sternum or on left side of the front of chest & spread out to the shoulder, arm and left side of the jaw. Due to stimulation of sympathetic and vagal afferent nerves. 1. Stable Angina (Effort angina): Due to ≥70% chronic stable stenosis Develops by exertion Resolves at rest Lasts ~5 min Insidious onset 2. Unstable angina (Crescendo angina): Due to Thrombosis in a Vulnerable plaque without complete obstruction Page 1 of 4 Occurs at rest / minimal exertion Severe / Lasting >10 min Either of: New onset (nothing for last 4–6 w) Crescendo pattern: getting > severe / prolonged / frequent than previous 3. Variant angina / Spastic angina / Prinzmetal angina: Occurs at rest Cyclic (vasospasm) due to contraction of Vascular smooth muscles Symptoms are unrelated to exertion >in younger women Myocardial infarction (MI) MI follows complete interruption of blood flow to an area of myocardium. Most commonly due to acute coronary event: rupture of an atherosclerotic plaque + thrombosis and vasospasm completely occluding the lumen of a critical major epicardial blood vessel. The infarction occurs downstream from the occluded blood vessel. Outcome of complete coronary occlusion depends on the severity and duration of flow deprivation: Within 60 seconds, severe ischemia leads to ATP depletion and loss of contractile function (but not cell death). Complete deprivation of blood flow for 20 to 30 minutes leads to irreversible myocardial injury. Patterns of infarcts: The distribution of myocardial necrosis depends on: collateral perfusion location of the occlusion within the vessel the vessel involved the duration of ischemia. A. According to occluded vessel: 1. Left anterior descending artery obstruction (50% of cases). Infarcts in the anterior wall of the left ventricle ECG changes in the anterior chest leads (V1 – V3 ). Occlusion of this artery may be a cause of sudden death. 2. Right coronary artery obstruction (30% of cases) Infarcts in inferior wall and posterior septum. The ECG changes in leads II, III and aVF. 3. Circumflex artery obstruction (20% of cases) Infarcts in lateral wall ECG changes in leads I, aVL and the lateral chest leads (V4 – V6 ). B. According to duration of ischemia: 1. Subendocardial MIs : Limited to the inner 30% to 50% of the ventricle. It is due to lysis of a thrombotic occlusion before full-thickness infarction These result in “non-ST elevation MI” NSTEMI 2. Transmural MIs Involves the full thickness of the ventricular wall) These are due to atherosclerosis and acute plaque change with thrombosis. Page 2 of 4 ST elevations “ST elevation MI” STEMI Morphology of MI: 2 weeks: Granulation tissue is replaced by fibrous tissue. 1 to 2 months: Grossly: Gray-white fibrous scar progressively fills in the defect. >2 months: Scarring is complete but can remodel with time. Clinical picture of myocardial infarction A frequent symptom is severe crushing chest pain (angina) which may have a sudden onset or may build up more slowly. Accompanying symptoms often include nausea, vomiting, sweating, pallor, breathlessness, and collapse. Examination : hypotension & bradycardia Patients may give a history of angina or non-specific chest discomfort over previous weeks At least 10% of patients, particularly the elderly, MI is painless. Investigations: MI is typically identified with characteristic ECG changes, The specific leads involved give an indication of the location and extent of the injury. a. Subendocardial MIs “non-ST elevation MI” N-STEMI NON-Q-wave AMI b. Transmural MIs ST elevations “ST elevation MI” STEMI Q-wave AMI Increases in the serum level of proteins released from the disrupted myocardial cells. The MB isoenzyme of Creatine Kinase is found in the heart. The CK-MB test is used for early confirmation of a diagnosis of MI. Troponins T and I are the gold standard for MI, (found solely in myocardial cells). Troponin T and I levels may be modestly raised with unstable angina. Complications of MI: ❖ Contractile dysfunction: systemic hypotension pulmonary edema (e.g., CHF) Cardiogenic shock: severe pump failure with loss of ≥40% left ventricular mass. It has a 70% mortality rate. ❖ Arrhythmias. Page 3 of 4 ❖ Fibrinous pericarditis (Dressler syndrome) : 2 to 3 days after an MI. ❖ Ventricular rupture (1% to 2% of transmural MIs), typically within the first 10 days (median, 4 to 5 days). ❖ Rupture of the free wall causes pericardial tamponade ❖ Septal rupture causes a left-to- right shunt with right-sided volume overload. ❖ Papillary muscle infarction (+/− rupture) and/or dysfunction causes mitral regurgitation. Poor contractility leads to: stasis Turbulence endocardial damage creation of a thrombogenic surface Mural thrombosis adjacent to a non-contractile area Can cause peripheral embolization. Extension: Infarction adjacent to existing MI. Ventricular aneurysm: due to healing of a large transmural infarct Prone to mural thrombosis. Long-term prognosis depends on: 1. Size and location of injury 2. Residual left ventricular function 3. Reperfusion: For 30 minutes after the onset of even the most severe ischemia, myocardial injury is potentially reversible. Progressive loss of viability occurs and is complete by 6 to 12 hours. Half of MI-associated deaths occur within the first hour due to arrthymia, most before reaching a hospital. References: 1. Noble, Robertson , Thomas. The Cardiovascular system, 2nd ed. Elsevier. P53, P57-59. 2. Kumar, Abbas, Aster. Robbins Basic Pathology, 10th ed. Elsevier. P408-419. Page 4 of 4