Ischemic Heart Disease Past Paper PDF

# Ischemic Heart Disease Dr. Olatunde O.Α.Ο Anatomic Pathology and Forensic Medicine Faculty of Basic Clinical Sciences. College of Medicine and Health Sciences. Afe Babalola University. ## Outline - Introduction - Epidemiology - Risk factors - Classification - Pathogenesis - Morphology - Conclus...

# Ischemic Heart Disease Dr. Olatunde O.Α.Ο Anatomic Pathology and Forensic Medicine Faculty of Basic Clinical Sciences. College of Medicine and Health Sciences. Afe Babalola University. ## Outline - Introduction - Epidemiology - Risk factors - Classification - Pathogenesis - Morphology - Conclusion ## Introduction - Ischemic heart disease (IHD) is a group of related syndromes which arise as a result of insufficient blood supply to the myocardium relative to functional demand - Imbalance between myocardial oxygen supply and demand - coronary arteries diseases (CAD) - Myocardial ischemia can result from - Vessel occlusion - Coronary atherosclerosis - Coronary emboli - Myocardial vessel inflammation - Vascular spasm - Increased myocardial demand - Myocardial hypertrophy or increased heart rate - Hypoxemia - Systemic hypotension ## Epidemiology - Ischemic heart disease (IHD) is the single leading cause of death worldwide, accounting for 11.2% of all deaths globally in 2011. - Russia, the United States of America and Ukraine account for the largest numbers of deaths - Equal incidence in white and blacks - Males are more commonly affected than pre-menopausal females | Author (Year) | Country | Population | Subjects with MI (n) | Total Subjects (N) | Prevalence of MI (%) | |-----------------------|---------------|---------------------------------------------------------------------------------|-----------------------|---------------------|------------------------| | Joubert, et al (2000) | South Africa | Patients admitted for acute stroke | 4 | 555 | 0.7% | | Ahmed, et al (2000) | Sudan | Diabetic patients who died while in hospital | 7 | 67 | 10.4% | | Sani, et al (2006) | Nigeria | Inpatients on medical ward | 22 | 5124 | 0.4% | | Seck, et al (2007) | Senegal | Emergency department patients | 52 | 77,429 | 0.1% | | Nguchu, et al (2009) | Kenya | Emergency department patients with diabetes | 10 | 400 | 2.5% | | Shavadia, et al (2012) | Kenya | Intensive care unit and step-down patients | 62 | 2156 | 2.9% | | Kolo, et al (2013) | Nigeria | Inpatients on medical ward | 14 | 6647 | 0.2% | - Maiduguri- - 0.34% of admissions - Age range 38-67 yrs - Male:female=7.5:1 - 55% were hypertensive - Ilorin - 0.21% of admissions - Age range 40-82 years (mean 55.6±12.7 yrs) - Benin - 0.4/100000 hospital admissions - Riskfactors- hypertension, hyperlipidemia, age, social class, obesity, high BMI, reduced physical exercise and significant alcohol intake ## Risk Factors - Risk factor are multiplicative rather than additive - They are classified into absolute and relative risk factor - Modifiable and non-modifiable ### Absolute risk factor - Male gender - Age - Positive family history ### Relative risk factors - Smoking - Hypertension - Diabetes mellitus - Haemostatic factor - Physical activity - Obesity - Alcohol - Other dietary factor - Personality types - Social deprivation ## Classification - IHD can present as one or more of the following overlapping clinical syndromes - Acute myocardial infarction - Angina pectoris - Chronic ischaemic heart disease with heart failure - Sudden cardiac death ## Pathogenesis - Coronary artery disease is central to the pathogenesis of ischemic heart diseases - Atherosclerosis which is a progressive inflammatory diseases of the arterial wall with lipid rich deposit (atheroma) is the main cause of ischemic heart diseases ### Early Atherosclerosis - Second to third decade of life - Site commonly are bifurcation of vessels (shear stress) - Start with any abnormal endothelia function - Binding of inflammatory cells to endothelia expressed receptor - Migration of the cell to the intima - Take up of oxidized LDL by the macrophage - Lipid laden foam cell dies leaving pool of lipid and growth factor - Migration of smooth muscle from media to intima - Formation of atheromatous plaque (asymptomatic) - A diagram illustrates early atherosclerosis with labels: - Superficial endothelial injury - Endothelial denudation - Endothelium - Deep endothelial injury - Plaque fissuring - Thrombus - Plaque core (fat deposit, foam cells, lymphocytes, phagocytes, smooth muscle cells) - Fibrous cap (smooth muscle and collagen) ### Advanced atherosclerosis - Macrophage and smooth muscle are cardinal cells in established atheroma - Smooth muscle mediate repair and cover the atheroma - Macrophage mediate inflammation - Cytokine release by macrophage degrade the smooth muscle over the plaque - Continuous exposure to stress will eventually lead to - Erosion - Fissuring - Rupture - Breach of the integrity will expose the content to blood - This trigger platelet aggregation and thrombosis that extend into the atheromatous plaque and arterial lumen - Partial or complete obstruction at the site of the lesion - Distal embolization resulting in infarct - Ischemia of the affected organ | Nomenclature and main histology | Sequences in progression | Main growth mechanism | Earliest onset | Clinical correlation | |------------------------------------------|-------------------------|-----------------------------|-----------------|-----------------------| | Type I (initial) lesion: Isolated macrophage foam cells | I | | From first decade | Clinically silent | | Type II (fatty streak) lesion: Mainly intracellular lipid accumulation | II | Growth mainly by lipid accumulation | | Clinically silent | | Type III (intermediate) lesion: Type II changes and small extracellular lipid pools | III | | From third decade | | | Type IV (atheroma) lesion: Type II changes and core of extracellular lipid | IV | | | | | Type V (fibroatheroma) lesion: Lipid core and fibrotic layer, or multiple lipid cores and fibrotic layers, or mainly calcific, or mainly fibrotic | V | Accelerated smooth muscle and collagen increase | From fourth decade | Clinically silent or overt | | Type VI (complicated) lesion: Surface defect, haematoma-haemorrhage, thrombus | VI | Thrombosis. haematoma | | | - A diagram illustrates the stages of atherosclerosis from normal artery to critical stenosis with descriptions of the stages: - Normal artery - Fatty streak - Fibrofatty plaque - Advanced/vulnerable plaque - Aneurysm and rupture - Occlusion by thrombus - Critical stenosis - Description of the changes at each stage - Another diagram illustrates the process of atherosclerosis with labels: - Lumen - Endothelial Injury/Dysfunction - LDL - Endothelium - Intima - T cell - Internal elastic membrane - Media - Monocyte adhesion and emigration into intima - Macrophage - Cytokines (e.g., IL-1, MCP-1) - Oxidized LDL - Cytokines (e.g., interferon-y) - Lipid uptake - Growth factors - Smooth muscle cells - Extracellular matrix synthesis - Foam cells - Proliferation of smooth muscle cells - Extracellular lipids and necrotic cells - Recruitment and migration of smooth muscle cells - Normal vessel - Progressive development of atherosclerotic plaque - A diagram outlines the main stages of atherosclerosis with their main features and clinical implications - Initial lesion - Fatty streak - Intermediate lesion - Atheroma - Fibroatheroma - Complicated lesion - Main growth mechanism - Earliest onset - Clinical correlation ## Pathogenesis Ischemic Heart DX - Chronic vascular occlusion due to atherosclerosis - 70% critical luminal obstruction- is significant causing symptoms on exercise - 90% obstruction-symptoms at rest - Acute plaque change - Erosion, ulceration, hemorrhage, fissuring thrombus - May lead to acute coronary syndromes - Unstable angina, - acute MI, - sudden cardiac death - A picture of a heart with a plaque in the coronary artery ## Morphology - Gross - MIs less than 12 hours old are usually not apparent on gross examination. - However, triphenyl tetrazoliumchloride can be used if infarct preceded death by 2 to 3hours | Time from Onset | Gross finding | |-----------------|-------------------------------------------------------------------------------------------------------------| | 6-12hrs | Pallor | | 12-24hours | reddish-blue area of haemorrhage due to stagnation of blood | | 3-7days | Yellow tan and soft-neutrophils | | 10days-2weeks | Maximally yellow and soft with rim of vascularised granulation tissue | | 7weeks | Fibrous scar | | | Grossmorphologicalfindingovertime in myocardial infarction. Kumar, Abbas, Fausto, Aster. 2010. Pathological basis of disease, 8th edition,Saunders https://library.med.utah.edu/WebPath | - Pictures of different stages of heart infarctions ## Angina Pectoris - Transient (15 seconds to 15 minutes) myocardial ischemia that is insufficient to induce myocyte necrosis - Stable angina-chest discomfort precipitated by activity and relieved by rest or vasodilators - Unstable angina-discomfort/frankpain, precipitated by progressively lower levels of physical activity or even occurring at rest. Due to acute plaque change - Prinzmetal angina-caused by vaso-spasm. Unrelated to physical activity, heart rate, or blood pressure. - Diagram illustrating stable angina pectoris, unstable angina pectoris and myocardial infarction. - Stable angina pectoris: - Adventitia - Endothelium - Media - Lumen - Atherosclerotic plaque - Necrotic centre - Unstable angina pectoris: - Sub-total occlusive thrombus - Ulcerated fibrous cap - Necrotic centre - Myocardial infarction (STEM I): - Thrombus with total occlusion of the lumen - Necrotic centre ## Canadian Cardiovascular Society Functional Classification of Angina | CLASS | Characteristic | |-------|----------------------------------------------------------------------------------------------------------------------------------------------------------------------------| | Class I | No angina with ordinary activity. Angina with strenuous activity | | Class II | Angina during ordinary activity, e.g. walking up hills, walking rapidly upstairs, with mild limitation of activities | | Class III | Angina with low levels of activity, e.g. walking 50-100 yards on the flat, walking up one flight of stairs, with marked restriction of activities | | Class IV | Angina at rest or with any level of exercise | ## Myocardial Infarction - Is death of cardiac muscle due to prolonged severe ischemia - 10% of myocardial infarcts occur in people younger than age 40, and 45% occur in people younger than age 65. - Pathogenesis due to - Coronary Arterial Occlusion-90% - Vasospasm - Emboli - Ischemia with out detectable coronary atherosclerosis and thrombosis - Vasculitis,SCD,amyloidosis,shock,vasculardissection - Diagram of heart with coronary arteries and their branches. - Right coronary artery - Marginal artery - Left coronary artery - Circumflex branch - Anterior interventricular branch - Posterior interventricular branch - Blood supply to the heart - LAD branch of the left coronary artery supplies - Apex of the heart, - The anterior wall of the left ventricle, - The anterior two-thirds of the ventricular septum. - RCA supplies - Entire right ventricular free wall, - The posterobasal wall of the left ventricle, - The posterior third of the ventricular septum, - LCX-only the lateral wall of the left ventricle. - The frequencies of involvement of the arteries - Left anterior descending coronary artery-40% to 50% - Right coronary artery-30% to 40% - Left circumflex coronary artery-15% to 20% - Patterns of infarct - Transmural-combination of chronic coronary atherosclerosis, acute plaque change, and superimposed thrombosis within epicardial vessel - Sub-endocardial-coronary thrombus that becomes lysed before myocardial necrosis extends across the full thickness of the wall. - Multi focal micro-infarction-pathology in smaller intramural Vessels e.g vasospasm from cocaine - The morphologic features depend on - The location, severity, and rate of development of coronary obstructions - The size of the vascular bed perfused by the obstructed vessels - The duration of the occlusion - The metabolic and oxygen needs of the myocardium at risk - The extent of collateral blood vessels - The presence, site, and severity of coronary arterial spasm - Other factors, such as heart rate, cardiac rhythm, and blood oxygenation ## Morphology - Gross - MIs less than 12 hours old are usually not apparent on gross examination. - However, triphenyl tetrazoliumchloride can be used if infarct preceded death by 2 to 3hours, | Time from Onset | Gross finding | |-----------------|-------------------------------------------------------------------------------------------------------------| | 6-12hrs | Pallor | | 12-24hours | reddish-blue area of haemorrhage due to stagnation of blood | | 3-7days | Yellow tan and soft-neutrophils | | 10days-2weeks | Maximally yellow and soft with rim of vascularised granulation tissue | | 7weeks | Fibrous scar | - More pictures of different stages of heart infarctions. - Pictures of different microscopic stages of heart infarctions. - Microscopic features of myocardial infarction and its repair. - A.One-day- old infarct showing coagulative necrosis and wavy fibers. - B.Dense polymorphonuclear leukocytic infiltrate in area of acute myocardial infarction of 3 to 4 days' duration. - C. Nearly complete removal of necrotic myocytes by phagocytosis (approximately 7 to 10 days). - Complications include: - Contractile dysfunction - Arrhythmias and conduction defects, with possible "sudden death" - Extension of infarction, or re-infarction - Congestive heart failure - Cardiogenic shock - Pericarditis - Mural thrombosis - Myocardial wall rupture - Papillary muscle rupture - Ventricular aneurysm formation - Schematic for the causes and outcomes of ischemic heart disease (IHD) - Myocardial ischemia - Acute plaque change; coronary artery thrombosis - Myocardial ischemia of increased severity and duration - Mycardial infarction with muscle loss and arrhythmias - Infarct healing - Ventricular remodeling - Hypertrophy, dilation of viable muscle - Chronic ischemic heart disease (IHD) - Congestive heart failure - Sudden cardiac death ## Conclusion - IHD is a leading cause of mortality and morbidity worldwide - Syndromes are overlapping - Acute MIs are difficult to detect at autopsy without special dyes - Incidence can be reduced with lifestyle changes ## References 1. Anjorin CO, Buba F and Ene AC, 2005. Myocardial Infarction at the University of MaiduguriTeaching Hospital, Northeastern Nigeria: A Long-term Review. Journal of Medical Sciences.2005;5:358-362 2. Hertz JT, Reardon JM, Rodrigues CG, de Andrade L, Limkakeng AT, et al. Acute Myocardial InfarctioninSub-SaharanAfrica:TheNeedforData.PLOSONE.2014;9(5):e96688. https://doi.org/10.1371/journal.pone.0096688 3. Kolo PM, Fasae AJ, Aigbe IF, Ogunmodede JA, Omotosho AB. Changing trend in the incidenceofmyocardialinfarctionamongmedicaladmissionsinIlorin, north-centralNigeria.NigerPostgrad MedJ.2013Mar;20(1):5-8 4. Joseph VA. Frequency and Pattern of Acute Myocardial Infarction in the University of BeninTeaching Hospital, Nigeria. NigerMedPrac.2009;55(6) 5. Nowbar, Alexandra N. et al. 2014 Global geographic analysis of mortality from ischaemicheart disease by country, age and income: Statistics from World Health Organisation andUnited Nations.International Journal ofCardiology. 2014;174(2):293-298 6. Kumar, Abbas, Fausto, Aster. 2010. Pathological basis of disease, 8th edition,Saunders ## Cardiac Tumour - Text on the page: CARDIAC TUMOUR