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Transcript
Cardiovascular Pathology (modification of Dr. Veinot’s presentation) Michel Dionne MD FRCPC for John P. Veinot MD FRCPC Professor of Pathology University of Ottawa Pathology and Laboratory Medicine Ottawa Hospital You may only access and use this PowerPoint presentation for educational purposes. You may not post this presentation online or distribute it without the permission of the author. Overview Atherosclerosis Aneurysms Ischemic heart disease Cardiomyopathies Valvular heart disease Hypertension Figure 4-4 Leading causes of death, number and percentage of deaths, Canada, 1999 Respiratory (22,026) 10% Other IHD (21,693) 10% AMI (20,926) 9.5% Other (33,240) 15% Diabetes (6,137) 3% Infectious Diseases (2,583) 1% All Cardiovascular Cerebrovascular Disease Disease (15,409) (78,942) 7% 36% Other CVD (20,914) 9.5% Cancer (62,606) 29% Accidents/ Poisoning/ Violence (13,996) 6% Total Number of Deaths: 219,530 Cardiovascular (ICD-9 390-459); Respiratory (ICD-9 460-519); Diabetes (ICD-9 250); Cancer (ICD-9 140-239); Infectious Diseases (ICD-9 001-139); Accidents/Poisonings/Violence (ICD-9 E800-E999) Source: Health Canada, using data from Mortality File, Statistics Canada The Growing Burden of Heart Disease and Stroke in Canada 2003 CVS Anatomy 101 Endothelium muscular artery intima media adventitia Aorta Media of aorta – an elastic artery Atherosclerosis Disease of large and medium sized arteries (elastic and muscular), particularly: – aorta, iliac, coronary, popliteal, carotid, circle of Willis Develop intimal lesions called atheromas or atheromatous plaques which: – protrude into the lumen resulting in stenosis (narrowing of lumen) and possibly occlusion (lumen blocked) – can weaken the underlying media, possibly leading to aneurysm formation Atherosclerosis - risk factors Age Male gender Family history/ genetics Hyperlipidemia – high LDL – low HDL Hypertension Smoking Diabetes Other: physical inactivity, diet, obesity etc. Atherosclerosis - pathogenesis Chronic endothelial injury* resulting in endothelial dysfunction – increased permeability – increased adhesion of leukocytes (monocytes and lymphocytes) and platelets – accumulation of lipids in intima Migration of monocytes into intima leading to formation of foam cells (lipid-laden macrophages) Release of cytokines and growth factors result in smooth muscle cell migration into intima, proliferation of smooth muscle cells, deposition of extracellular matrix (e.g. collagen) * From hemodynamic forces, hyperlipidemia, HTN, smoking etc. From: Robbins and Cotran Pathologic Basis of Disease, 8th Edition Aorta – fatty streaks Aorta – fibrofatty/atheromatous plaques Aorta – complicated plaques Aortic arch vessels – advanced plaques causing severe stenosis Coronary artery Atheromatous material – foam cells (lipid laden macrophages) and cholesterol clefts From: Robbins and Cotran Pathologic Basis of Disease, 8th Edition Atherosclerosis - complications Calcification Plaque hemorrhage and rupture Plaque erosion/ulceration Thrombosis Embolization of atheromatous material (atheroemboli) Aneurysm formation and rupture Renal infarct from embolization Atherosclerosis major consequences Symptomatic disease most often affects the heart, brain, kidneys and lower extremities – Heart: angina and myocardial infarction – Brain: cerebral infarction (stroke) – Aorta (particularly abdominal): » Aneurysms » Stenosis of ostia of major branches leading to visceral ischemia – Lower extremities: peripheral vascular (arterial) disease – claudication, gangrene Aneurysm - definition a localized abnormal dilatation of a vessel Aneurysm types Atherosclerotic aneurysms are the most common, but there are other types! Aneurysms - complications Stasis of blood Thrombosis obstruction embolism Mass effect Rupture Abdominal Aortic Aneurysm (AAA) thrombus Aneurysm rupture blood lumen thrombus tear vessel wall AAA rupture Hemorrhage into surrounding tissue Dissecting “aneurysm” Coronary artery aneurysms secondary to vasculitis (inflammation of blood vessels) SVC Left lung Aorta Left atrium Pericardium Right lung Right atrium Left ventricle Right ventricle Left atrium Right atrium Left ventricle Right ventricle Interventricular septum Coronary artery anatomy http://www.drchander.com/diagnoseCAD.html Coronary artery atherosclerosis affects the epicardial arteries; tends to be more pronounced in the proximal portion of these vessels can involve 1, 2 or all 3 of the main vessels +/- their large branches if degree of obstruction is significant, can result in angina (pain from myocardial ischemia) an atherosclerotic plaque can become unstable (acute plaque lesion): – intraplaque hemorrhage – plaque rupture or erosion resulting in thrombosis acute plaque lesions can result in an “acute coronary syndrome” (unstable angina, myocardial infarct) Myocardial infarct terminology Recent MI - about 24 hours old Contraction band necrosis Recent MI - about 3 days old Recent MI - interstitial infiltrate of neutrophils Recent MI - 5-7 days old Recent MI - 7-10 days old “Sick” myocytes bordering the infarct Phagocytosis of dead cells at margin of infarct Residual necrotic myocytes Remote myocardial infarcts Transmural rupture Infarct rupture and tamponade Papillary muscle rupture Left ventricle aneurysm Ischemic heart disease interventions Non-surgical Surgical thrombolysis PTCA / stenting atherectomy rotablation Coronary Artery Bypass Grafting (CABG) – typically using saphenous vein grafts and/or internal thoracic arteries endarterectomy Atherectomy device PTCA balloon Angiogram pre/post PTCA Aortic valve - normal Mitral valve - normal Aortic stenosis - causes Aortic stenosis causing LVH Mitral stenosis - rheumatic Floppy mitral valve - mitral valve prolapse (MVP) Hypertension PRIMARY (ESSENTIAL) – Genetic and environmental factors – Defects in sodium homeostasis, vascular smooth muscle structure, regulation of vascular tone SECONDARY – renal disease – vascular disease – endocrinopathies – drugs – neurogenic etc… Reno-vascular hypertension Hypertension - complications enhance other diseases (risk factor) small vessel changes – scarring/sclerosis – microaneurysms large vessel changes – ectasia / aneurysms / aortic regurgitation – dissection vessel rupture cardiac hypertrophy etc… Arteriolo-nephrosclerosis Brain hypertensive bleed Hypertensive brain stem bleed LVH (look familiar?) Cardiomyopathy - definition Heterogenous group of diseases of the myocardium associated with mechanical or electrical dysfunction that usually (but not invariably) exhibit inappropriate ventricular hypertrophy or dilation and are due to a variety of causes that frequently are genetic. Cardiomyopathies are either confined to the heart or are part of generalized systemic disorders often leading to cardiovascular death or progressive heart failure related disability. Circulation 2006 113:1807-1816 Cardiomyopathy types (clinical/functional/morphologic patterns) Dilated (DCM) – 90% Hypertrophic (HCM) Restrictive Primary cardiomyopathy (confined to the heart) - etiology Genetic – e.g. HCM, ARVC, mitochondrial defects, channelopathies (e.g. LQTS) Acquired – e.g. due to myocarditis (inflammation of the myocardium) Mixed Idiopathic Secondary cardiomyopathy (part of generalized systemic disorder) – examples of etiologies Amyloidosis Hemochromatosis Sarcoidosis Medication/Toxin induced - e.g. cancer chemotherapy, alcoholism Autoimmune diseases - e.g. SLE, rheumatoid arthritis Infections Endocrine disorders - e.g. hypothyroidism Neuromuscular diseases - e.g. muscular dystrophies Storage diseases - e.g. glycogen storage disease Nutritional deficiencies - e.g. thiamine Primary dilated cardiomyopathy Primary myocardial abnormality NO SIGNIFICANT: – – – – coronary artery disease valve disease systemic arterial hypertension systemic disorder, history of toxin exposure etc. Non-specific myocardial degenerative changes DCM - clinical presentation Progressive heart failure – systolic dysfunction – 4 chamber dilatation – hypokinesis Arrhythmias Thromboembolism Sudden death Familial (genetic) DCM About 30 % of DCM Often asymptomatic LV dilatation at detection - minority progress Examples: – muscular dystrophy – mitochondrial defects - maternal inheritance – inherited metabolic disorders Cardiomyopathy – genetic abnormalities Dilated - cytoskeletal elements largely affected dystrophin - X-linked, some muscular dystrophies lamin desmin actin etc… mitochondrial genes Hypertrophic - contractile elements affected (sarcomeric genes) myosin troponin tropomyosin myosin binding protein C etc… Viral myocarditis and DCM Enteroviral protease cleaves dystrophin Disrupted dystrophin / sarcoglycan complex Similar to primary genetic defects found in DCM Hypertrophic cardiomyopathy a genetic disease; autosomal dominant, variable penetrance phenotype variations even with same mutation - ? environmental influences myocardial hypertrophy (thickened myocardium) diastolic dysfunction sub-aortic obstruction sudden death (60% of deaths are sudden) Hypertrophic cardiomyopathy Disproportionate thickening of the interventricular septum Myocyte disarray and hypertrophy and interstitial fibrosis HCM - diastolic dysfunction ventricular hypertrophy myocyte disarray interstitial fibrosis myocardial microinfarcts Cardiomyopathy - summary Gross and histopathologic findings are nonspecific but may be diagnostic Most require clinicopathological correlation Many mimics and secondary diseases Molecular diagnosis / genetics developing