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Contents Arteriosclerosis Atherosclerosis Contents Arteriosclerosis Tumors of blood vessels Heart failure Ischemic heart disease Sakchai Chitpakdee, M.D. Valvular heart diseases Rheumatic heart disease Infective endocarditis Myocarditis Pericardial diseases Arteriosclerosis = hardening of the arteries y Atherosclerosis ○ Large & medium size vessels y Monckeberg medial calcific sclerosis ○ Medium size vessels with tunica media calcification y Arteriolosclerosis ○ Small arteries/arterioles Atherosclerosis “intimal lesion”: atheromas or fibrofatty plaques or atheromatous plaques” Large and medium size arteries y Raised focal plaque within the intima y Core lipid (cholesterol/cholesterol esters) and a covering fibrous cap y Cells: foamy cells (macrophage/SMC), lymphocytes Atherosclerosis Complicated lesion: y Calcification y Rupture/ulceration -> atheroemboli, thrombus y Hemorrhage y Thrombosis y Aneurysmal dilation Atherosclerosis Epidemiology & risk factors: y Age: middle or later age y Sex: pre-menopause -> M > F 60s to 70s -> M = F y Genetics: familial y Hyperlipidemia: high cholesterol/TG & ↓ HDL y Hypertension y Cigarette smoking y Diabetes mellitus Atherosclerosis Clinical features & prevention Epidemiology & risk factors: Clinical features: y Elevated plasma homocysteine y Ischemic/infarction of organs y Other factors: y Atherosclerotic aneurysm ○ Competitive stressful lifestyle: type A personality Prevention: ○ Lack of exercise y Primary prevention: risk factor modification ○ Obesity y Secondary prevention: prevent recurrence of y Moderate intake of alcohol -> protective events or complications (antiplatlet drugs etc) factor Tumors Tumors Benign neoplasms: Intermediate-grade neoplasms: y Hemangioma: capillary, cavernous, pyogenic y Kaposi sarcoma granuloma y Hemangioendothelioma y Lymphangioma: simple (capillary), cavernous lymphangioma (cystic hygroma) Malignant neoplasms: y Glomus tumor, myopericytoma y Angiosarcoma y Vascular ectasia: nevus flammeus, spider y Hemangiopericytoma (benign & malignant) telangiectasia, hereditary hemorrhagic telangiectasia (osler-Weber-Rendu dis.) y Bacillary angiomatosis: B. henselae infection Hemangioma Hemangioma Pyogenic granuloma (lobular capillary) Capillary hemangioma: y Polypoid nodules of skin, gingiva, oral y Skin, subcutaneous tissue, oral cavities of head mucosa and neck, lung, liver, kidney y Bleeding, ulcerated y Strawberry type (juvenile hemangioma): 1:200 y Granuloma gravidarum: 1% pregnant newborns: fade 1-3 yr, regress by 7 yr women, pyogenic granuloma at gingiva, Cavernous hemangioma: regress after delivery y Older age, less circumscribed, deeper y No regress Lymphangioma Lymphangioma circumscriptum (capillary ymphangioma) y Subcutaneous mass of head and neck Cavernous lymphangioma y Cystic hygroma y Neck and axilla of children y Turner syndrome: neck region Vascular ectasia Kaposi sarcoma Nevus flammeus: Chronic, classic european KS y Birthmark of head and neck, flat Lymphadenopathy, African, endemic KS y Pink to purple Æ regress Transplant-associated Port-wine stain: no regress (immunosuppression-associated) KS y Trigeminal nerve Æ Sturge-Weber syndrome (ecephalotrigemina AIDS-associated KS angiomatosis), venous mass of Clinical: patchesÆ plaquesÆ nodules leptimeninges Æ seizure, hemiplegia, mental retardation Cause: HSV-8, HIV? Angiosarcoma Malignant endothelial neoplasms Skin, soft tissue, breast, liver Cause: y Breast: radiation, lymphedema y Liver: polyvinyl chloride (PVC), throrotrast y Skin: arsenic (pesticide) Heart failure Left-side heart failure Cause: IHD, HT, aortic & mitral valve CHF = congestive heart failure disease, cardiomyopathy Common end result of many forms of HD Clinical: Unable to pump blood at rate of body y Forward effect: poor organ perfusion requirement (prerenal azotemia, hypoxic Progressive deterioration of myocardial encephalopathy) contraction y Backward effect: pulmonary edema y Systolic dysfunction (dyspnea, orthopnea, PND) y Diastolic dysfunction Right-side heart failure What is Ischemic Heart Disease? Cause: pulmonary HT (cor pulmonale) Myocardial ischemia Hypertrophy of right ventricle, atrium, Imbalance btw supply (perfusion) & demand of septum Æ left-side HF oxygenated blood Clinical: Ischemia Æ ↓Oxygen y Forward effect: poor oxygenation Æ ↓ Nutrient substrates y Backward effect: organ edema, effusion Æ ↓ Metabolites removal Ischemia Æ Dysfunction of pumping Æ Abnormal heart rhythms Æ Myocardial infarction (Necrosis) Etiology of IHD Clinical manifestation 90 % Æ coronary artery Four syndromes: atherosclerosis 1. Myocardial infarction 2. Angina pectoris: variants y Atherosclerosis Æ narrow lumen 1. Stable angina Æ thrombus formation 2. Prinzmetal angina Æ coronary vasospasm 3. Unstable angina 3. Chronic ischemic heart disease Others: hypertrophy, hypovolemia, 4. Sudden cardiac death hypoxemia,↑ heart rate Clinical manifestation Role of fixed coronary obstruction At least 75 % reduction of cross- Stable plaque Æ Unstable plaque sectional area (insufficient compensatory Stable angina Æ Acute coronary vasolidation) syndromes At least 90 % reduction Æ ischemia at rest Acute coronary syndromes: Atherosclerosis type IV-VI unstable angina, acute MI, and Affected location: proximal (LAD, LCX), sudden death entire (RCA) Role of acute plaque change Acute plaque change/disruption: y Hemorrhage into atheroma Æ ↑ volume y Rupture or fissuring Æ Thrombosis y Erosion or ulceration Æ Thrombosis A = Plaque rupture B = Thrombus over plaque rupture C = Massive plaque rupture with thrombus Angina pectoris Angina pectoris Paroxysmal and usually recurrent attacks of Stable angina: substernal or precordial chest discomfort caused by y Most common, and predictable transient (15 sec to 15 min) myocardial ischemia y Reduction of coronary perfusion by chronic that falls short of inducing cellular necrosis (infarct) stenosing coronary atherosclerosis Three patterns: y Pain brought by physical excertion, emotional y Stable or typical angina stress, heat or cold fever, anemia etc y Prinzmetal or variant angina y Pain relieved by rest (decreased demand) or y Unstable or crescendo or accelerating or nitroglycerin (vasodilator) preinfarction angina y Monitoring ECG: ST segment depression or elevation or T-wave inversion Angina pectoris Angina pectoris Prinzmetal variant angina: Unstable angina: y Uncommon, and unpredictable y Angina occurring with increasing frequency, y Occur at rest not related to physical and emotional precipitated with less effort, often occurs at exertion rest and tends to be prolonged duration y Coronary artery vasospasm y Most induced by disruption of atherosclerotic plaque with partial thrombosis and possibly y Atherosclerosis-induced hypercontractility, embolization or vasospasm vasospastic chemicals secretion by mast cells and abnormal calcium influx y Harbinger of subsequent acute MI y Response well to calcium-channel blockers and y Thrombus labile and lasts 20 to 30 minutes nitroglycerin y 10 to 15% total occlusion Å collateral vessel y ECG: elevation of ST-segment Myocardial infarction Myocardial infarction Necrosis of myocardium Transmural (Q-wave) infarction Prolonged period of ischemia at rest lasting > y Full or nearly full thickness necrosis 20 min, unresponsive to NTG y Acute plaque change + completely obstructive Ischemic ECG change and positive cardiac thrombosis (fixed and persist > 1 hour) enzymes y ECG: ST segment elevation Æ Q wave Subendocardial (Non-Q-wave) infarction 25 % silent: old age, diabetics y 1/3 to ½ inner ventricle thickness necrosis Subendocardial VS Transmural infarction y Incomplete obstructive thrombosis (>30-40 min) y Non-Q-wave VS Q-wave infarction y ¼ complete obstruction + collateral supply y ECG: ST segment elevation Æ Non-Q-wave Morphological change Almost all transmural MI involve at least a portion of left ventricle Coronary arteries and MI site: y LAD (40-50%) -> ant wall of LV, apex, ant portion of ventricular septum y RCA (30-40%) -> inf-post wall of LV, post portion of ventricular septum, RV (inf-post) y LCX (10-20%) -> lateral wall LV except apex 1 day 3 to 4 days 7 to 10 days 3 weeks Evolution of morphology change Cardiac enzymes Time Morphology change 0 - ½ hours Ultrastructural change (EM) Released enzymes after myocardial cell 2 – 3 hours Triphenyltetrazolium chloride dye: dead: noninfarct area Æ brick-red, infarcted Æ unstained y Myoglobin 4 – 24 hours Gross: dark mottling area, y Troponin (TnI and TnT) Histology: hemorrhage and necrosis y Creatine kinase (total CK and CK-MB) 1 – 7 days Gross: yellow-tan mottling, reddish border Histology: neutrophils and macrophages y LDH (LDH1, LDH2) 7 – 14 days Gross: red-tan margin Histology: macrophages and granulation tissue 2 – 8 weeks Gross: gray-white scar Histology: collagen deposition > 2 months Scarring complete Cardiac enzymes Consequences and complications 7x Myoglobin 6x Total CK 50 % AMI Æ dead Half of dead occur within 1 hour (VF) 5x In-hospital death rate 30% Æ 10-13 % 4x 75 % develop one or more complications LDH 3x y Contractile dysfunction Æ cardiogenic shock 10 – 15 % of AMI and 70 % mortality rate 2x CK-MB Troponin I y Arrhythmias Æ sudden death Upper limit of normal serum level of normal limit Upper 1x bradycardia, tachycardia, VPC, VT, VF asystole 0 20 40 60 80 100 120 140 160 Hours from onset of infarction Consequences and complications Consequences and complications Ventricular aneurysm Æ thrombus, Myocardial rupture: arrhythmias, heart failure, rupture y Ventricular free wall Æ cardiac
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