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Heart diseases
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- 2. THE HEART NormalPathology Heart Failure: L, R Heart Disease Congenital : L R shunts, R L shunts, Obstrustive Ischemic : Angina, Infarction, Chronic Ischemia, Sudden Death Hypertensive : Left sided, Right sided Valvular : AS, MVP, Rheumatic, Infective, Non-Infective, Carcinoid, Artificial Valves Cardiomyopathy : Dilated, Hypertrophic, Restrictive, Myocarditis, Other Pericardium : Effusions, Pericarditis Tumors : Primary, Effects of Other Primaries Transplants www.freelivedoctor.com
- 3. NORMAL Features 6000L/day 250-300 grams 40% of all deaths (2x cancer) Wall thickness ~ pressure (i.e., a wall is only as thick as it has to be) LV=1.5 cm RV= 0.5 cm Atria =.2 cm Systole/Diastole Starling’s Law www.freelivedoctor.com
- 4. TERMS CARDIOMEGALY DILATATION,any chamber, or all HYPERTROPHY, and chamber, or all www.freelivedoctor.com
- 5. STRIATIONS NUCLEUS DISCSSARCOLEMMA SARC. RETIC. MITOCHONDRIA ENDOTHELIUM FIBROBLASTS GLYCOGEN A.N.P. www.freelivedoctor.com
- 6. S.A. Node AV Node Bundle of HIS L. Bundle, R. Bundle www.freelivedoctor.com
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- 8. Anterior Lateral PosteriorSeptal www.freelivedoctor.com
- 9. VALVES AV: TRICUSPIDMITRAL SEMILUNAR: PULMONIC AORTIC www.freelivedoctor.com
- 10. CARDIAC AGING www.freelivedoctor.comSigmoid-shaped ventricular septum Decreased left ventricular cavity size Increased left atrial cavity size Chambers Buckling of mitral leaflets toward the left atrium Fibrous thickening of leaflets Mitral valve annular calcific deposits Aortic valve calcific deposits Valves Atherosclerotic plaque Calcific deposits Increased cross-sectional luminal area Tortuosity Epicardial Coronary Arteries Amyloid deposits Basophilic degeneration Lipofuscin deposition Brown atrophy Increased subepicardial fat Increased mass Myocardium
- 11. CARDIAC AGING www.freelivedoctor.comAtherosclerotic plaque Elastic fragmentation and collagen accumulation Sinotubular junction calcific deposits Elongated (tortuous) thoracic aorta Dilated ascending aorta with rightward shift Aorta
- 12. BROWN ATROPHY, HEART www.freelivedoctor.com
- 13. Pathologic Pump PossibilitiesPrimary myocardial failure (MYOPATHY) Obstruction to flow (VALVE) Regurgitant flow (VALVE) Conduction disorders (CONDUCTION SYSTEM) Failure to contain blood (WALL INTEGRITY) www.freelivedoctor.com
- 14. CHF DEFINITION TRIAD1) TACHYCARDIA 2) DYSPNEA 3) EDEMA FAILURE of Frank Starling mechanism HUMORAL FACTORS Catecholamines (nor-epinephrine) Renin Angiotension Aldosterone Atrial Natriuretic Polypeptide (ANP) HYPERTROPHY and DILATATION www.freelivedoctor.com
- 15. HYPERTROPHY PRESSURE OVERLOAD(CONCENTRIC) VOLUME OVERLOAD (CHF) LVH, RVH, atrial, etc. 2X normal weight ischemia 3X normal weight HTN >3X normal weight MYOPATHY, aortic regurgitation www.freelivedoctor.com
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- 18. CHF: Autopsy FindingsCardiomegaly Chamber Dilatation Hypertrophy of myocardial fibers, BOXCAR nuclei www.freelivedoctor.com
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- 20. Left Sided FailureLow output vs. congestion Lungs pulmonary congestion and edema heart failure cells Kidneys pre-renal azotemia salt and fluid retention renin-aldosterone activation natriuretic peptides Brain: Irritability, decreased attention, stupor coma www.freelivedoctor.com
- 21. Left Heart FailureSymptoms Dyspnea on exertion at rest Orthopnea redistribution of peripheral edema fluid graded by number of pillows needed Paroxysmal Nocturnal Dyspnea (PND) www.freelivedoctor.com
- 22. LEFT HeartFailure Dyspnea Orthopnea PND (Paroxysmal Nocturnal Dyspnea) Blood tinged sputum Cyanosis Elevated pulmonary “WEDGE” pressure (PCWP) www.freelivedoctor.com
- 23. Right Sided HeartFailure Etiology left heart failure cor pulmonale Symptoms and signs Liver and spleen passive congestion (nutmeg liver) congestive spleenomegaly ascites Kidneys Pleura/Pericardium pleural and pericardial effusions transudates Peripheral tissues www.freelivedoctor.com
- 24. RIGHT HeartFailu re FATIGUE “ Dependent” edema JVD Hepatomegaly (congestion) ASCITES, PLEURAL EFFUSION GI Cyanosis Increased peripheral venous pressure (CVP) www.freelivedoctor.com
- 25. HEART DISEASE CONGENITAL(CHD) ISCHEMIC (IHD) HYPERTENSIVE (HHD) VALVULAR (VHD) MYOPATHIC (MHD) www.freelivedoctor.com
- 26. CONGENITAL HEART DEFECTSFaulty embryogenesis (week 3-8) Usually MONO-morphic (i.e., SINGLE lesion) (ASD, VSD, hypo-RV, hypo-LV) May not be evident until adult life (Coarctation, ASD) Overall incidence 1% of USA births INCREASED simple early detection via non invasive methods, e.g., US, MRI, CT, etc. www.freelivedoctor.com
- 27. www.freelivedoctor.com T ricuspidatresia 1 120 T otal anomalous pulmonary venous connection 1 136 T runcus arteriosus 4 388 Transposition of great arteries 4 388 Aortic stenosis 4 396 Atrioventricular septal defect 5 492 Coarctation of aorta 5 577 T etralogy of Fallot 7 781 Patent d uctus arteriosus 8 836 Pulmonary stenosis 10 1043 Atrial septal d efect 42 4482 Ventricular septal d efect % Incidence per Million Live Births Malformation
- 28. GENETICS Gene abnormalitiesin only 10% of CHD Trisomies 21 , 13, 15, 18, XO Mutations of genes which encode for transcription factors TBX5 ASD,VSD NKX2.5 ASD Region of chromosome 22 important in heart development, 22q11.2 deletion conotruncus, branchial arch, face www.freelivedoctor.com
- 29. ENVIRONMENT RUBELLA TERATOGENSwww.freelivedoctor.com
- 30. CHD L R SHUNTS: all “D’s” in their names NO cyanosis Pulmonary hypertension SIGNIFICANT pulmonary hypertension is IRREVERSIBLE R L SHUNTS: all “T’s” in their names CYANOSIS VENOUS EMBOLI become SYSTEMIC OBSTRUCTIONS www.freelivedoctor.com
- 31. L RAS D VS D ASV D P D A NON CYANOTIC IRREVERSIBLE PULMONARY HYPERTENSION IS THE MOST FEARED CONSEQUENCE www.freelivedoctor.com
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- 33. ASD NOT patentforamen ovale Usually asymptomatic until adulthood SECUNDUM (90%): Defective fossa ovalis PRIMUM (5%): Next to AV valves, mitral cleft SINUS VENOSUS (5%): Next to SVC with anomalous pulmonary veins draining to SVC or RA www.freeliv edoc tor.com
- 34. VSD By far,most common CHD defect Only 30% are isolated Often with TETRALOGY of FALLOT 90% involve the membranous septum If muscular septum is involved, likely to have multiple holes SMALL ones often close spontaneously LARGE ones progress to pulmonary hypertension www.freelivedoctor.com
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- 36. PDA 90% isolatedHARSH, machinery-like murmur L R, possibly R L as pulmonary hypertension approaches systemic pressure Closing the defect may be life saving Keeping it open may be life saving (Prostaglandin E). Why? www.freelivedoctor.com
- 37. AVSD Associated withdefective, inadequate AV valves Can be partial, or COMPLETE (ALL 4 CHAMBERS FREELY COMMUNICATE) www.freelivedoctor.com
- 38. R LT etralogy of Fallot T ransposition of great arteries T runcus arteriosus T otal anomalous pulmonary venous connection T ricuspid atresia www.freelivedoctor.com
- 39. R LSHUNTS TETRALOGY of FALLOT most COMMON 1) VSD, large 2) OBSTRUCTION to RV flow 3) Aorta OVERRIDES the VSD 4) RVH SURVIVAL DEPENDS on SEVERITY of SUBPULMONIC STENOSIS Can be a “PINK” tetrology if pulmonic obstruction is small, but the greater the obstruction, the greater is the R L shunt www.freelivedoctor.com
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- 41. TGA (TRANSPOSITION of GREAT ARTERIES) NEEDS a SHUNT for survival PDA or PFO (65%), “unstable” shunt VSD (35%), “stable” shunt RV>LV in thickness Fatal in first few months Surgical “switching” www.freelivedoctor.com
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- 43. TRICUSPID ATRESIA HypoplasticRV Needs a shunt, ASD, VSD, or PDA High mortality www.freelivedoctor.com
- 44. Total Anomalous PulmonaryVenous Connection (TAPVC) PULMONARY VEINS do NOT go into LA, but into L. innominate v. or coronary sinus Needs a PFO or a VSD HYPOPLASTIC LA www.freelivedoctor.com
- 45. OBSTRUCTIVE CHD COARCTATIONof aorta Pulmonary stenosis/atresia Aortic stenosis/atresia www.freelivedoctor.com
- 46. COARCTATION of AORTAM>F But XO’s frequently have it INFANTILE FORM (proximal to PDA) (SERIOUS) ADULT FORM (CLOSED DUCTUS) Bicuspid aortic valve 50% of the time www.freelivedoctor.com
- 47. PULMONIC STENOSIS/ATRESIA If100% atretic, hypoplastic RV with ASD Clinical severity ~ stenosis severity www.freelivedoctor.com
- 48. AORTIC STENOSIS/ATRESIA VALVULARIf severe, hypoplastic LV fatal SUB-valvular (subaortic) Aortic wall THICK BELOW cusps SUPRA-valvular Aortic wall THICK ABOVE cusps in ascending aorta www.freelivedoctor.com
- 49. HEART DISEASE CONGENITAL(CHD) ISCHEMIC (IHD) HYPERTENSIVE (HHD) VALVULAR (VHD) MYOPATHIC (MHD) www.freelivedoctor.com
- 50. SYNDROMES of IHDAngina Pectoris: Stable, Unstable Myocardial Infarction (MI, AMI) Chronic IHD CHF (CIHD) Sudden Cardiac Death (SCD) “ Acute” Coronary Syndromes: UNSTABLE ANGINA AMI SCD www.freelivedoctor.com
- 51. IHD RISK Numberof plaques Distribution of plaques Size, structure of plaques www.freelivedoctor.com
- 52. ACUTE CORONARY SYNDROMES“ The acute coronary syndromes are frequently initiated by an unpredictable and abrupt conversion of a stable atherosclerotic plaque to an unstable and potentially life-threatening atherothrombotic lesion through superficial erosion, ulceration, fissuring, rupture, or deep hemorrhage, usually with superimposed thrombosis .” www.freelivedoctor.com
- 53. EPIDEMIOLOGY ½ milliondie of IHD yearly in USA 1 million in 1963. Why? Prevention of control controllable risk factors Earlier, better diagnostic methods PTCA, CABG, arrythmia control 90% of IHD patients have ATHEROSCLEROSIS www.freelivedoctor.com
- 54. ACUTE CORONARY SYNDROMEFACTORS ACUTE PLAQUE CHANGE ******* Inflammation Thrombus Vasoconstriction www.freelivedoctor.com
- 55. ACUTE PLAQUE CHANGERupture/Refissuring Erosion/Ulceration, exposing ECM Acute Hemorrhage NB: Plaques do NOT have to be severely stenotic to cause acute changes, i.e., 50% of AMI results from thromboses of plaques showing LESS THAN 50% stenosis www.freelivedoctor.com
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- 57. INFLAMMATION Endothelial cellsrelease CAMs, selectins T-cells release TNF, IL-6, IFN-gamma to stimulate and activate endothelial cells and macrophages CRP predicts the probability of damage in angina patients www.freelivedoctor.com
- 58. THROMBUS Total occlusionPartial Embolization www.freelivedoctor.com
- 59. VASOCONSTRICTION Circulating adrenergicagonists Platelet release products Endothelially released factors, such as endothelin www.freelivedoctor.com
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- 61. www.freelivedoctor.com Often smallplatelet aggregates or thrombi and/or thromboemboli Frequent Usually severe Sudden death Widely variable, may be absent, partial/complete, or lysed Variable Variable Subendocardial myocardial infarction Occlusive Frequent Variable Transmural myocardial infarction Nonocclusive, often with thromboemboli Frequent Variable Unstable angina No No >75% Stable angina Plaque-Associated Thrombus Plaque Disruption Stenoses Syndrome Coronary Artery Pathology in Ischemic Heart Disease
- 62. ANGINA PECTORISParoxysmal (sudden) Recurrent 15 sec. 15 min. Reduced perfusion, but NO infarction THREE TYPES STABLE: relieved by rest or nitro PRINZMETAL: SPASM is main feature, responds to nitro, S-T elevation UNSTABLE (crescendo, PRE-infarction, Q-wave angina): perhaps some thrombosis, perhaps some non transmural necrosis, perhaps some embolization, but DISRUPTION of PLAQUE is universally agreed upon www.freelivedoctor.com
- 63. MYOCARDIAL INFARCTION Transmuralvs. Subendocardial (inner 1/3) DUH! EXACT SAME risk factors as atherosclerosis Most are TRANSMURAL, and MOST are caused by coronary artery occlusion In the 10% of transmural MIs NOT associated with atherosclerosis: Vasospasm Emboli UNexplained www.freelivedoctor.com
- 64. MYOCARDIAL RESPONSE www.freelivedoctor.com>1 hr Microvascular injury 20–40 min Irreversible cell injury 40 min to 10% of normal 10 min to 50% of normal ATP reduced <2 min Loss of contractility Seconds Onset of ATP depletion Time Feature
- 65. PROGRESSION OF NECROSISwww.freelivedoctor.com
- 66. RE -PERFUSION ThrombolysisPTCA CABG Reperfusion CANNOT restore necrotic or dead fibers, only reversibly injured ones REPERFUSION “INJURY” Free radicals Interleukins www.freelivedoctor.com
- 67. AMI DIAGNOSIS SYMPTOMSEKG DIAPHORESIS (10% of MIs are “SILENT” with Q-waves) CKMB gold standard enzyme Troponin-I, Troponin-T better CRP predicts risk of AMI in angina patients www.freelivedoctor.com
- 68. COMPLICATIONS Wall motionabnormalities Arrhythmias Rupture (4-5 days) Pericarditis RV infarction Infarct extension Mural thrombus Ventricular aneurysm Papillary muscle dysfunction (regurgitation) CHF www.freelivedoctor.com
- 69. CIHD, aka, ischemic“cardiomyopathy” Progress to CHF often with no pathologic or clinical evidence of localized infarction Extensive atherosclerosis No infarct H&D present www.freelivedoctor.com
- 70. SUDDEN CARDIAC DEATH350,000 in USA yearly from atherosclerosis NON-atherosclerotic sudden cardiac death includes: Congenital coronary artery disease Aortic stenosis MVP Myocarditis Cardiomyopathy (sudden death in young athletes) Pulmonary hypertension Conduction defects HTN, hypertrophy of UNKNOWN etiology www.freelivedoctor.com
- 71. AUTOPSY findings inSCD >75% narrowing of 1-3 vessels Healed infarcts 40% “ ARRHYTHMIA” is often a very convenient conclusion when no anatomic findings are present www.freelivedoctor.com
- 72. HEART DISEASE CONGENITAL(CHD) ISCHEMIC (IHD) HYPERTENSIVE (HHD) VALVULAR (VHD) MYOPATHIC (MHD) www.freelivedoctor.com
- 73. HHD (Left) DEFINITION:Hypertrophic adaptive response of the heart, which can progress: Myocardial dysfunction Cardiac dilatation CHF Sudden death www.freelivedoctor.com
- 74. NEEDED for DIAGNOSIS:LVH (LV>2.0 and/or Heart>500 gm.) HTN (>140/90) www.freelivedoctor.com
- 75. PREVALENCE: WHAT %of USA people have hypertension? www.freelivedoctor.com
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- 77. HISTOPATHOLOGY INCREASED FIBER(MYOCYTE) THICKNESS INCREASED nuclear size with increased “blockiness” (boxcar nucleus) www.freelivedoctor.com
- 78. CLINICAL EKG Summaryof LVH Criteria 1) R-I + S-III >25 mm 2) S-V1 + R-V5 >35 mm 3) ST-Ts in left leads 4) R-L >11 mm 5) LAE + other criteria Positive Criteria: 1=possible 2=probable 3=definite ATRIAL FIBRILLATION Why? CHF, cardiac dilatation, pulmonary venous congestion and dilatation www.freelivedoctor.com
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- 80. COURSE: NORMAL longevity,death from other causes Progressive IHD Progressive renal damage, hemorrhagic CVA (Which arteries?) CHF www.freelivedoctor.com
- 81. HHD (Right) = COR PULMONALE ACUTE: Massive PE CHRONIC: COPD, CRPD, Pulmonary artery disease, Chest wall motion impairment www.freelivedoctor.com
- 82. Diseases of thePulmonary Parenchyma Chronic obstructive pulmonary disease Diffuse pulmonary interstitial fibrosis Pneumoconioses Cystic fibrosis Bronchiectasis Diseases of the Pulmonary Vessels Recurrent pulmonary thromboembolism Primary pulmonary hypertension Extensive pulmonary arteritis (e.g., Wegener granulomatosis) Drug-, toxin-, or radiation-induced vascular obstruction Extensive pulmonary tumor microembolism www.freelivedoctor.com
- 83. www.freelivedoctor.com Disorders AffectingChest Movement Kyphoscoliosis Marked obesity (pickwickian syndrome) Neuromuscular diseases Disorders Inducing Pulmonary Arterial Constriction Metabolic acidosis Hypoxemia Chronic altitude sickness Obstruction to major airways Idiopathic alveolar hypoventilation
- 84. ValvularHD Opening problems:Stenosis Closing problems: Regurgitation or Incompetence www.freelivedoctor.com
- 85. 70% of allVHD AS Calcification of a deformed valve “ Senile” calcific AS Rheum, Heart Dis. MS Rheumatic Heart Disease www.freelivedoctor.com
- 86. AORTIC STENOSIS 2Xgradient pressure LVH, ischemia Cardiac decompensation, angina, CHF 50% die in 5 years if angina present 50% die in 2 years if CHF present www.freelivedoctor.com
- 87. MITRAL ANNULAR CALCIFICATIONCalcification of the mitral “skeleton” Usually NO dysfunction Regurgitation or Stenosis possible F>>M www.freelivedoctor.com
- 88. REGURGITATIONS AR RheumaticInfectious Aortic dilatations Syphilis Rheumatoid Arthritis Marfan MR MVP Infectious Fen-Phen Papillary muscles, chordae tendinae Calcification of mitral ring (annulus) www.freelivedoctor.com
- 89. Mitral Valve Prolapse(MVP) MYXOMATOUS degeneration of the mitral valve Associated with connective tissue disorders “ Floppy” valve 3% incidence, F>>M Easily seen on echocardiogram www.freelivedoctor.com
- 90. MVP: CLINICAL FEATURESUsually asymptomatic Mid-systolic “click” Holosystolic murmur if regurg present Occasional chest pain, dyspnea 97% NO untoward effects 3% Infective endocarditis, mitral insufficiency, arrythmias, sudden death www.freelivedoctor.com
- 91. RHEUMATIC Heart DiseaseFollows a group A strep infection, a few weeks later DECREASE in “developed” countries PANCARDITIS www.freelivedoctor.com
- 92. ACUTE: -Inflammation -Aschoffbodies -Anitschkow cells -Pancarditis -Vegetations on chordae tendinae at leaflet junction CHRONIC: THICKENED VALVES COMMISURAL FUSION THICK, SHORT, CHORDAE TENDINAE www.freelivedoctor.com
- 93. CLINICAL FEATURES MigratoryPolyarthritis Myocarditis Subcutaneous nodules Erythema marginatum Sydenham chorea www.freelivedoctor.com
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- 95. INFECTIOUS ENDOCARDITIS MicrobesUsually strep viridans Often Staph aureus in IVD users Enterococci HA Č EK (normal oral flora) Hemophilus influenzae Actinobacillus Cardiobacterium Eikenella Kingella Fungi, rickettsiae, chlamydia www.freelivedoctor.com
- 96. INFECTIOUS ENDOCARDITIS Acute:50% mortality (course=days) SUB -acute: LOW mortality (course=weeks) www.freelivedoctor.com
- 97. VEGETATIONS INFECTIVE >5mm NON-Infective <5mm www.freelivedoctor.com
- 98. DIAGNOSIS MAJOR Positiveblood culture(s) indicating characteristic organism or persistence of unusual organism Echocardiographic findings, including valve-related or implant-related mass or abscess, or partial separation of artificial valve New valvular regurgitation minor Predisposing heart lesion or intravenous drug use Fever Vascular lesions, including arterial petechiae, subungual/splinter hemorrhages, emboli, septic infarcts, mycotic aneurysm, intracranial hemorrhage, Janeway lesions Immunologic phenomena, including glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor Microbiologic evidence, including single culture showing uncharacteristic organism Echocardiographic findings consistent with but not diagnostic of endocarditis, including new valvular regurgitation, pericarditis www.freelivedoctor.com
- 99. www.freelivedoctor.com Splinter hemorrhages,Janeway lesions (palms, soles), Osler’s “nodes” (raised), Roth’s spots (eye)
- 100. NON-infective VEGETATIONS <5mm PE Trousseau syndrome (migratory thrombophlebitis with malignancies) s/p Swan-Ganz Libman-Saks with SLE (both sides of valve) www.freelivedoctor.com
- 101. Carcinoid Syndrome Episodicskin flushing Cramps Nausea & Vomiting Diarrhea ↑ serotonin, ↑ 5HIAA in urine FIBROUS INTIMAL THICKENING RV, Tricuspid valve, Pulmonic valve (all RIGHT side) Similar to what Fen-Phen does on the LEFT side www.freelivedoctor.com
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- 103. ARTIFICIAL VALVES MechanicalXenografts (porcine) 60% have complications within 10 years www.freelivedoctor.com
- 104. HEART DISEASE CONGENITAL(CHD) ISCHEMIC (IHD) HYPERTENSIVE (HHD) VALVULAR (VHD) MYOPATHIC (MHD) PERICARDIAL DISEASE www.freelivedoctor.com
- 105. CARDIOMYOPATHIES Inflammatory ImmunologicMetabolic Dystrophies Genetic Idiopathic DILATED (DCM) SY-stolic dysfunction HYPERTROPHIC (HCM) DIA-stolic dysfunction RESTRICTIVE (RCM) DIA-stolic dysfunction www.freelivedoctor.com
- 106. www.freelivedoctor.com Splinter hemorrhages,Janeway lesions (palms, soles), Osler’s “nodes” (raised), Roth’s spots (eye)
- 107. DILATED cardiomyopathy Chamberthickness (not just LVH) Adults Progressively declining LVEF LVEF ~ prognosis 50% die in 2 years 3 Main causes Myocarditis ETOH Adriamycin www.freelivedoctor.com
- 108. Path: 4 chamberdilatation Hypertrophy Interstitial Fibrosis DCM www.freelivedoctor.com
- 109. Arrhythmogenic Right VentricularCardiomyopathy (Arrhythmogenic Right Ventricular Dysplasia) This is an uncommon dilated cardiomyopathy predominantly RIGHT ventricle. So is NAXOS syndrome. www.freelivedoctor.com
- 110. HYPERTROPHIC cardiomyopathyAlso called IHSS, (Idiopathic Hypertrophic Subaortic Stenosis) GENETIC defects involving: Beta-myosin heavy chain Troponin T Alpha-tropomyosin Myosin binding protein C PATHOLOGY: Massive hypertrophy, Asymmetric septum, DISARRAY of myocytes, INTERSTITIAL fibrosis CLINICAL: ↓chamber volume, ↓SV, ↓ diastolic filling www.freelivedoctor.com
- 111. RESTRICTIVE cardiomyopathy(idiopathic) ↓ ventricular compliance Chiefly affects DIASTOLE NORMAL chamber size and wall thickness THREE similar diseases affecting predominantly the SUBENDOCARDIAL area: Endomyocardial Fibrosis (African children) Loeffler Endomyocarditis (eosinophilic leukemia) Endocardial Fibroelastosis (infants) www.freelivedoctor.com
- 112. MYOCARDITIS INFLAMMATION ofMYOCARDIUM Chiefly microbial COXACKIE A & B , CMV, HIV Trypanosoma cruzi (Chagas dis.), 80% Trichinosis Toxoplasmosis Lyme disease (5%) Diphtheria IMMUNE: Post-viral, rheumatic, SLE, drug hypersensitivity alpha-methyl dopa, sulfas www.freelivedoctor.com
- 113. LYMPHOCYTIC INFILTRATESare the USUAL pattern of ALL myocarditis, but eosinophils, giant cells, and even trypanosomes can be seen occasionally www.freelivedoctor.com
- 114. OTHER Myocarditides AdriamycinCyclophosphamide Catecholamines (Pheochromocytomas) Amyloid, systemic or primary cardiac Congo red stain: green birefringence with polarization Amyloid, aging Congo red stain: green birefringence with polarization Hemochromatosis (Prussian Blue) BOTH HYPER-, HYPO- -thyroidism www.freelivedoctor.com
- 115. PERICARDIUM Normally 30-50ml clear serous fluid Visceral (epicardium) Parietal (Fibrous pericardium) PERICARDIAL EFFUSIONS TAMPONADE Ruptured MI Traumatic perforation Infective endocarditis Ruptured aortic dissection www.freelivedoctor.com
- 116. PERICARDITIS SEROUS :Rheum. Fever (RF), SLE, scleroderma, tumors, uremia FIBRINOUS : MI (Dressler), uremia, radiation, RF, SLE, s/p open heart surgery PURULENT : infective, bacterial HEMORRHAGIC : Malignancy, TB CASEOUS : TB CHRONIC : (ADHESIVE, CONSTRICTIVE ) www.freelivedoctor.com
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- 118. TUMORS 90% benign“mesenchymal”, i.e., stromal MYXOMAS ( LEFT ATRIUM MOST COMMON) FIBROMAS LIPOMAS FIBROELASTOMAS RHABDOMYOMA (Most common cardiac tumor in children) 10% SARCOMAS www.freelivedoctor.com
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- 120. Cardiac effects ofNON-cardiac tumors Direct Consequences of Tumor Pericardial and myocardial metastases Large vessel obstruction Pulmonary tumor emboli Indirect Consequences of Tumor (Complications of Circulating Mediators) Nonbacterial thrombotic endocarditis (NBTE) Carcinoid heart disease Pheochromocytoma-associated heart disease Myeloma-associated amyloidosis Effects of Tumor Therapy Chemotherapy Radiation therapy www.freelivedoctor.com
- 121. CARDIAC TRANSPLANT PATHOLOGYMost patients are on immunosuppressives 5 year survival >60% www.freelivedoctor.com
- 122. CARDIAC TRANSPLANT PATHOLOGYwww.freelivedoctor.com
Editor's Notes
- #3 This is the chapter outline.
- #6 This is a section from “Shotgun Histology”, in other words, the terms on the left describe the entire myocardium. Atrial natriuretic peptide (ANP), atrial natriuretic factor (ANF), atrial natriuretic hormone (ANH), or atriopeptin, is a powerful vasodilator, and a protein (polypeptide) hormone secreted by heart muscle cells. It is involved in the homeostatic control of body water, sodium, potassium and fat (adipose tissue). It is released by muscle cells in the upper chambers (atria) of the heart (atrial myocytes), in response to high blood pressure. ANP acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressure.
- #7 The specialized myocytes of the heart’s conduction system, running sub-endocardially, have this unique appearance.
- #8 Whichever artery winds up supplying the posterior interventricular septum is said to be “DOMINANT”
- #9 The myocardial perfusion is a good test of coronary artery and myocardial function.
- #11 These features are seen so commonly in autopsies of elderly people no matter what they died from. Also keep in mind that most people who do not die ACUTELY, die in cardiac failure.
- #12 One very key philosophical question is whether atherosclerosis is part of aging or not. We can leave that for the philosophers.
- #13 The pigment which accumulates with age is called lipofucsin, and caused the heart to appear “browner” than normal. This is called “brown” atrophy of the heart.
- #14 This is the same analogy as the “straw” we talked about in the last chapter on blood vessels. You can classify cardiac diseases functionally into these 5 “pump” categories, like we had only 2 categories with the blood vessels described as straws or conduits.
- #16 Very FEW hearts of elderly people at autopsy weigh the normal 250-300 gm. Atherosclerotic or CHF hearts weigh twice as much, hypertensive hearts weight three times as much, and cardiomyopathic hearts often weigh more.
- #18 A good general diagram.
- #20 Note that not only is the FIBER thick, but so are the nuclei. Note squaring off of the nuclei, so called “BOXCAR” effect.
- #23 Can you understand why all of these findings can be related to LEFT sided heart failure? Ans: YES, primarily PULMONARY.
- #25 Can you understand why all of these findings can be related to RIGHT sided heart failure? Ans: YES, primarily STSTEMIC.
- #26 Does this look like it covers all bases? Ans: YES
- #28 Do the NAMES of these congenital heart conditions adequately describe the pathology? Ans: YES Why have I highlighted the “D”s and the “T”s? Ans: D = L shunt, T= R L shunt (cyanosis, or “blue” babies).
- #33 LEFT to RIGHT SHUNTS, NON-cyanotic
- #39 All the R L congenital shunts are CYANOTIC, and have T’s in their names.
- #41 CLASSICAL “TETROLOGY” of FALLOT: 1) VSD, large 2) OBSTRUCTION to RV flow 3) Aorta OVERRIDES the VSD 4) RVH
- #57 CHRONIC plaque PLUS acute thrombosis = Acute coronary syndromes.
- #66 Why does the necrosis spread from the endocardium to the pericardium (i.e., epicardium)?
- #74 A chamber wall is only as thick as it has to be, i.e., more pressure more thickness
- #79 Answer: owing to left atrial enlargement
- #81 Answer: lenticulostriate in basal ganglia most susceptible to hypertensive CVA
- #82 As the alveoli EXPAND in COPD, the arterioles NARROW!
- #83 A reasonably logical way of looking at COR PULMONALE, or RIGHT HEART FAILURE
- #85 Why do BOTH stenosis and regurgitation cause hypertrophy of the chamber proximal to the valve?
- #94 A GREAT classical sydenham chorea (St. Vitus “Dance”) can be seen at www.youtube.com/watch?v=RnxqqW_nH0k
- #98 Vegetations: 1) rheumatoid = small, 2) infectious = big, 3) lupus ( Libman-Saks) = BOTH sides
- #99 Another diagram which shows “quantification” of a diagnosis
- #100 Splinter hemorrhages, Janeway lesions (palms, soles), Osler’s “nodes” (raised), Roth’s spots (eye)
- #106 Note the three FUNCTIONAL classes on the RIGHT
- #107 A “restrictive” cardiomyopathy is a wall which is NOT thickened or dilated necessarily, but RIGID in diastolic relaxation.
- #118 The “bread and butter” pericarditis is classically and most often described in uremia or pericardial infections. What is the exudate? Ans: Fibrin