Systemic Pathology - Heart pathology - Peters

  1. Hyaline Arteriolosclerosis
    • Chronic hemodynamic stress
    • - Endothelial cells leak plasma proteins.
    • - Smooth muscle cell matrix synthesis.
    • - Pink hyaline thickening narrows lumen
    • Causes:
    • - Hypertension
    • - Elderly persons
    • - Diabetic microangiopathy
    • - Nephrosclerosis
  2. Hyperplastic Arteriolosclerosis
    • Under severe hypertension
    • Smooth muscle proliferation, basement membrane and fibrin deposition
    • “Onion-skin lesions"
    • - Concentric, layered thickening with luminal narrowing.
    • +/ - vessel wall necrosis (necrotizing arteriolitis).
  3. Systemic Hypertension
    • Left-sided hypertensive heart disease
    • left ventricle hypertrophy, increased LV wall thickness, stiffness, and heart weight, impaired diastolic filling, minor enlarged left atrium.
    • Increased myocyte diameter (early), nuclear enlargement (late)
  4. Pulmonary Hypertension
    • Right-sided HHD, Cor pulmonale
    • Acute - following massive pulmonary embolism, right ventricular dilation.
    • Chronic - right ventricular hypertrophy AND dilation
    • Response to pressure overload
  5. Disorders Predisposing to Cor Pulmonale
    • DISEASES OF THE PULMONARY PARENCHYMA
    • DISEASES OF THE PULMONARY VESSELS
    • DISORDERS AFFECTING CHEST MOVEMENT
    • DISORDERS INDUCING PULMONARY ARTERIAL CONSTRICTION
  6. Atherosclerosis
    • Degenerative disease of large and medium sized arteries.
    • Atherosclerotic plaques - Intimal lesions protrude into and narrow the vessel lumen.
  7. Risk factors for atherosclerosis
    • NONMODIFIABLE
    • Increasing Age
    • Male gender
    • Family history
    • Genetic abnormalities
    • MODIFIABLE
    • Hyperlipidmia
    • Hypertension
    • Cigarette smoking
    • Diabetes
    • C-reactive protein
  8. Atherosclerosis Risk factors' role in endothelial injury
    hypercholesterolemia -> premature atherosclerosis; Predominant lipids in plaques, increase local O2 free radicals
  9. Endothelial Injury - Lipids
    • Oxidation of LDL occurs in the arterial wall when exposed to nitric oxide, macrophages, and some enzymes such as lipoxygenase.
    • Oxidized LDL is :
    • •Cytotoxic to endothelial cells causing
    • –dysfunction and leukocyte adhesion causing
    • –stimulation of endothelial cells and macrophages activation causing
    • –release of growth and chemotaxic factors causing
    • –smooth muscle proliferation and monocyte recruitment.
    • •ingested by macrophages which
    • –become foam cells
    • –undergo apoptosis releasing free lipids into the intima.
  10. Endothelial Injury - Hemodynamic Disturbances
    • Sites of turbulence
    • - Ostia
    • - Branch points
    • - Posterior wall of abdominal aorta
  11. Chronic Endothelial Injury
    Begins at sites of intact endothelium
  12. Endothelial Dysfunction when Injured
    • produce Chemotactic factors to attract leukocytes.
    • produce Cell surface adhesion molecule (VICAM 1) -> Leucocyte adhesion and emigration.
    • change shape -> increased permeability -> cell, platelet and lipid migrate into the intimal space.
  13. Pathogenesis of atherosclerosis
    • Monocytes migrating into the intima transform into macrophages and engulf lipoproteins including oxidized LDL -> apoptosis -> liberating free lipid
    • T lymphocytes elaborate cytokines and growth factors
  14. Smooth muscle cell recruitment and macrophage activation
    • Growth factors -> smooth muscle cell (SMC) proliferation -> extracellular matrix (collagen) synthesis -> atherosclerotic plaques stabilized, fibrofatty atheroma
    • Activated inflammatory cells -> SMC apoptosis -> increased ECM catabolism -> unstable plaques
  15. Response to injury hypothesis - atherosclerosis pathogenesis
    • Endothelial cell injury
    • Macrophage migration
    • Lipid accumulation
    • Smooth muscle proliferation
    • Role of infection
  16. Causes of injury
    • Hyperlipidemia
    • Hemodynamic turbulence
    • Hypertension
    • Smoking
    • Toxins
    • Infectious agents
    • Viruses
    • Homocysteine
  17. Infections may drive the inflammatory process
    • Herpes, cytomegalovirus, and Chlamydia pneumoniae
    • detected in atherosclerotic plaques, not normal arteries
    • Increased antibody titers to C. pneumoniae in patients
    • with severe atherosclerosis.
    • Association with periodontal disease.
    • Possible mechanisms:
    • - Infect sites of early atheroma formation.
    • - Drive local immune responses.
    • - Add to local prothrombotic state.
  18. Fatty Streaks
    • Foamy lipid-filled macrophages infiltrate the vessel wall.
    • Multiple minute flat yellow spots coalesce into linear streaks.
    • Earliest lesions - Virtually all children > 10 years; Minimally raised, no flow disturbance
  19. Atherosclerotic Plaque
    • Gross:
    • •Yellow to grey plaques.
    • •0.3 to 1.5 cm in diameter - coalesce into masses.
    • •Patchy, eccentric, asymmetry, a result of local hemodynamics
    • •Thrombus over ulcerated plaques is red-brown.
  20. Anatomy of an atheroma
    • Necrotic lipid core - Lipid, foam cells, fibrin, thrombus, cholesterol crystal
    • Superficial fibrous cap - Smooth muscle cells, lymphocytes, collagen, elastin, proteoglycans. Neovascularization.
    • Shoulder - MPGs, T cells, and SMCs.
  21. Consequences of atherosclerotic disease
    • Major targets
    • •Large elastic arteries -aorta, carotid, and iliac arteries
    • •Large and medium-sized muscular arteries coronary and popliteal.
    • Major consequences - Myocardial Infarct, cerebral infarct, aortic aneurysms, and peripheral vascular disease - aneurysm and rupture, occlusion by thrombus, critical stenosis.
    • Outcome depends on:
    • •Size of the vessels.
    • •Stability of the plaque.
    • •Degree of degeneration of arterial wall.
  22. Vulnerable Plaques
    • More likely to rupture
    • Large areas of foam cells and extracellular lipid
    • Fibrous caps are thin or contain few smooth muscle cells - Clusters of inflammatory cells.
  23. Fibrous cap
    • continuously remodeled.
    • Collagen-synthesis versus degradation affects cap stability.
    • Plaque inflammation increases degradation and reduces synthesis of collagen, destabilizing the fibrous cap.
    • Healing plays role in the growth of atheromata
  24. Acute plaque changes
    • Rupture; fissuring; erosion; ulceration; thrombosis
    • Plaque hemorrhage - Further plaque disruption.
    • Probably common, repetitive, and often clinically silent.
  25. Atherosclerotic Stenosis
    • Severe concentric lesions- no longer respond to vasodilators.
    • Small arteries - occlude vessel lumina, compromise blood flow, and cause ischemic injury.
    • Critical stenosis - significantly limits flow, and demand begins exceeding supply. 70% fixed occlusion
    • Patients develop chest pain on exertion (stable angina).
    • Bowel ischemia; ischemic encephalopathy; intermittent claudication.
  26. Atheroembolism
    • Ruptured plaque can embolize atherosclerotic debris
    • - Distal vessel obstruction and acute thrombosis
  27. Aneurysm formation
    Atrophy of the media and loss of elastic tissue leads to weakness, dilatation rupture, thrombosis.
  28. Influences extrinsic to plaques
    • Adrenergic stimulation can increase BP and vasoconstriction, increasing stress on a plaque.
    • - Waking and rising can cause blood pressure spikes and heightened platelet reactivity - Circadian periodicity of MI.
    • – Intense emotional stress can contribute to plaque disruption - sudden death increases during disasters.
    • Vasoconstriction
    • - Compromises lumen size.
    • - Potentiates plaque disruption by increasing local mechanical forces.
    • - Vasoconstriction is stimulated by :
    • •Circulating adrenergic agonists
    • •Platelet contents released
    • •Endothelial cell dysfunction - Impaired secretion of endothelial cell relaxing factors
    • •? Inflammatory cells mediators
  29. Ischemic Heart Disease
    • Imbalance between the supply and demand for oxygenated blood.
    • Aggravated by increased in cardiac energy demand.
    • Coronary atherosclerotic lesions >90%.
  30. Ischemic Heart Disease -Clinical syndromes
    • Myocardial infarction
    • Angina pectoris
    • Chronic IHD with heart failure.
    • Sudden Cardiac Death.
  31. Pathogenesis of Myocardial infarction
    • Chronic Atherosclerosis
    • > 70% occlusion -> Symptomatic ischemia precipitated by exercise.
    • 90% occlusion -> Inadequate perfusion at rest.
    • Progressive ischemia -> protective collateral vessels
    • Locations of clinically significant plaques:
    • •First several centimeters of the LAD and LCX (left circumflex)
    • •Entire RCA.
    • •Major secondary epicardial branches.
    • •Anywhere.
    • Progressive atherosclerotic narrowing -> Acute plaque change, Thrombosis, Vasospasm -> Insufficient coronary perfusion
  32. Acute coronary syndrome
    • Stable plaque abruptly converts to unstable atherothrombotic lesion.
    • •Rupture, erosion, ulceration, fissuring, hemorrhage.
    • •Superimposed thrombus occludes the affected artery.
    • •Often associated with plaque inflammation.
  33. Coronary Arterial Occlusion
    • Sudden change in an atheromatous plaque.
    • Platelets adhere to subendothelial collagen and necrotic plaque.
    • - Activate and release granules.
    • - Aggregate to form microthrombi.
    • - Vasospasm stimulated by released platelets mediators.
    • Tissue factors activate coagulation pathway, adding to thrombus.
    • Thrombus evolves to complete occlusion within minutes.
    • Some occlusions resolve due to fibrinolysis, or relaxation of spasm.
    • - 4 hours of onset of MI - 90% thrombosed
    • - 12 to 24 hours after onset - 60% thrombosed
  34. MI in Absence of Coronary Atherosclerosis
    • ~10%
    • Vasospasm with or without coronary atherosclerosis.
    • - Platelet aggregation (vasoconstrictor release)
    • - Cocaine abuse (granule release -> vasoconstriction)
    • Emboli from the left atrium
    • - Atrial fibrillation
    • - Mural thrombus
    • - Vegetations of infective endocarditis
    • - Prosthetic material
    • Emboli from the right atrium
    • - Paradoxical emboli via patent foramen ovale.
    • Disorders of small vessels (intramural) -Vasculitis.
    • Hematologic abnormalities - Sickle cell; amyloid deposition; apple-green stain.
    • Lowered systemic blood pressure (shock).
    • Inadequate myocardial “protection” during cardiac surgery.
  35. Sequential Progression of Coronary Artery Lesions
    • Normal -> atherosclerosis -> fixed coronary obstruction (FCO, typical angina) -> severe fixed coronary obstruction (SFCO, chronic ischemic heart disease)
    • FCO -> platelet aggregate -> plaque disruption (PD)
    • PD -> healing -> SFCO
    • PD -> thrombus -> mural thrombus variable obstruction (Unstable angina, subendocardial MI, sudden death)
    • PD -> thrombus -> occlusive thrombus (transmural MI, sudden death)
  36. Myocardial Response
    • Compromise of myocardial blood supply -> myocardial Ischemia, dysfunction, necrosis.
    • The early biochemical consequences:
    • - Cessation of aerobic metabolism within seconds leads to:
    • •Inadequate production of ATP
    • •Accumulation of metabolites - lactic acid
    • - Myocardial function is highly oxygen dependent.
    • •Loss of contractility within 60 seconds, which can precipitate acute heart failure long before myocardial cell death (irreversible at >30min).
  37. Ultrastructural changes
    • Within minutes of the onset of ischemia:
    • •Myofibrillar relaxation
    • •Glycogen depletion
    • •Cell and mitochondrial swelling
    • •Potentially reversible
    • Severe ischemia >20-30min -> irreversible damage
    • •Necrosis of cardiac myocytes.
    • - Disruption of sarcolemmal membrane.
    • - Intracellular macromolecules leak out of cells.
  38. Progression of Myocardial Necrosis - Location, size, and morphology depend on:
    • Location, severity, and rate of obstruction.
    • Size of perfused vascular bed
    • Duration
    • Metabolic/oxygen needs
    • Collateral blood vessels
    • Coronary arterial spasm
    • Other - heart rate, cardiac rhythm, oxygenation.
  39. Progression of myocardial necrosis after coronary artery occlusion
    • Irreversible injury occurs first in the subendocardial zone.
    • Extended ischemia - progresses to transmural infarct.
  40. Dominant
    • The coronary artery that perfuses the posterior 1/3 of the septum
    • •Right coronary - Right dominant
    • •Left circumflex artery - Left dominant.
  41. areas of perfusion and resulting zones of damage in hypo-perfusion of each of the main coronary arteries.
    • LCX (15-20% MI)
    • -> Left ventricle lateral wall
    • RCA (30-40% MI)
    • -> Right ventricular free wall
    • -> Posterior basal LV wall
    • LAD (40-50% MI)
    • -> Apex
    • -> Anterior LV wall
    • -> Anterior 2/3 of the septum
    • Global hypotension -> circumferential subendocardial MI
    • Small intramural vessel occlusions -> microinfarcts
    • RCA -> Posterior 1/3 ventricular septum In Right Dominant Circulation (80%)
    • LCX -> Posterior 1/3 ventricular septum In left Dominant Circulation (20%)
  42. Microscopic changes after MI
    • 4–12 hr
    • - Contraction bands
    • - Myocytolysis
    • - Wavy fibers
    • - Also early coagulative necrosis, edema, and hemorrhage.
    • 12-24 hr
    • - Gross: Reddish blue discoloration, stagnated blood.
    • - Micro: Coagulative necrosis (dead cell, architecture intact, nuclei disappear); contraction bands; edema; hemorrhage; eosinophilia; pyknosis; early neutrophilic infiltrate.
    • 1-3 days
    • - Gross : Mottling with softening yellow-tan infarct center
    • - Micro: Coagulative necrosis, loss of nuclei and
    • striations; brisk interstitial neutrophilic infiltrate.
    • 7-14 days
    • - Gross: Maximally yellow-tan; Depressed red-tan-gray infarct borders.
    • - Micro: Phagocytosis of dead cells by MPG; Fibrovascular granulation tissue at margins; Early collagen deposition.
    • 2 weeks - 2 mos
    • - Gross: Gray-white scar, progresses from border
    • to center.
    • - Micro: Increasing collagen deposition, with decreasing cellularity; collagenous scar.
  43. Infarct Extension
    • Infarct extends beyond original borders.
    • Causes of Infarct extension
    • •Retrograde propagation of a thrombus.
    • •Proximal vasospasm.
    • •Impaired contractility causes insufficient flow through stenoses.
    • •Microemboli.
    • •Arrhythmia.
  44. Infarct Modification by Reperfusion
    • Rescue – Goal: Restore myocardial blood flow as rapidly as possible by reperfusion.
    • Within 20 minutes of the onset of ischemia may prevent necrosis.
    • Gross: Reperfused infarcts - hemorrhagic due to vascular injury.
    • Micro : Contraction bands; Myocytolysis.
  45. Complications Following Acute MI
    • Contractile dysfunction - Heart failure -shock
    • Arrhythmias
    • RV infarction - Acute right-sided heart failure
    • Infarct extension
    • Infarct expansion – like a balloon
    • Weakening of necrotic muscle allows stretching, thinning, and dilation of the infarct region.
    • Papillary muscle dysfunction/rupture – Post infarct mitral regurg.
    • Progressive late heart failure
    • Myocardial rupture
  46. Complications of MI -Myocardial rupture
    • Necrotic myocardium – soft and weak - Usually rapidly fatal.
    • - 3 to 7 days after MI ; mean 4 to 5 days.
    • - Risk factors: > 60, female, hypertension.
    • Ventricular free wall - hemopericardium and cardiac tamponade
    • - Most common site: antero-lateral wall, midventricular level
    • Rupture of the ventricular septum - acute VSD and L-R shunt
  47. Pericarditis
    • Early: Underlying myocardial inflammation -> fibrinous pericarditis
    • Late: Dressler's syndrome - Several weeks or months post-MI - autoimmune.
  48. Mural Thrombus
    • Abnormal contractility and endocardial damage
    • - Potential thromboembolism.
  49. Ventricular aneurysm
    • True aneurysms bounded by scarred myocardium
    • Large transmural infarcts with early expansion.
    • Paradoxically bulges during systole.
    • Complications - mural thrombus; arrhythmias; heart failure.
  50. Sudden Cardiac Death
    • Unexpected cardiac death without symptomatic heart disease or early after symptom onset.
    • Ischemic heart disease in most cases.
    • Lethal arrhythmia – Usual cause - asystole, V-fibrillation
    • •Acute myocardial ischemia -> electromechanical cardiac instability of myocardium distant from the conduction system.
    • •Arrythmogenic foci - often adjacent to scars of old MIs.
  51. Heritable conditions associated with SCD
    • Anatomic abnormalities
    • •Congenital anomalies
    • •Hypertrophic cardiomyopathy
    • •Mitral valve prolapse
    • Primary electrical disorders
    • •Heritable arrhythmias - Channelopathies - Mutations in genes of ion channel function.
  52. Morphology SCD
    • •Marked coronary atherosclerosis -80% to 90%
    • •Nonatherosclerotic origin -10% to 20%
    • •Acute plaque disruption -50%
    • •Acute MI - diagnostic changes 25%
    • •Myocardial ischemia–induced irritability -> malignant ventricular arrhythmias.
    • - Scars of previous infarcts and subendocardial myocyte vacuolization indicate severe chronic ischemia is common.
  53. Valvular Heart Disease
    • Presentations - Stenosis, insufficiency or both.
    • Clinical consequences vary depending on:
    • •Valve involved
    • •Degree of impairment
    • •Rate of development
    • •Rate and quality of compensatory mechanisms
  54. Calcific Aortic Stenosis
    • Most common of all valvular abnormalities.
    • • Normal valves -70-90 y/o; Bicuspid valves- 50-70 y/o
    • Wear and tear degeneration causes dystrophic and passive accumulation of calcium salt hydroxyapatite.
    • • Hyperlipidemia, hypertension, inflammation play a role.
    • Valve injury in CAS differs from atherosclerosis
  55. Calcific Aortic Stenosis - Morphology
    • Heaped-up calcified masses on cusps prevent opening.
    • Begins in the valvular fibrosa, near the margins of attachment.
    • Ultimately protrudes into the sinuses of Valsalva.
    • Commissural fusion is not usually seen.
    • Microscopic – Fibrosis; calcification; lipid deposits. Layered valve architecture (fibrosa is on the top/aortic side) is largely preserved.
    • Gradual narrowing of the valve orifice - Valve area: Severe aortic stenosis - 0.5-1 cm2 (normal - 4cm2 )
    • Concentric LVH due to increasing pressure gradient - Hypertrophied myocardium tends to be ischemic.
  56. CAS - Onset of symptoms heralds decompensation and poor prognosis.
    • Without valve replacement:
    • • 50% with angina will die within 5 years.
    • • 50% with CHF will die within 2 years.
  57. Calcific Stenosis of Congenitally Bicuspid Aortic Valve
    • Most frequent congenital cardiovascular malformation -1%
    • Late complications: AS or AR; infective endocarditis; aortic dilation and/or dissection; cusp prolapse.
    • Structural abnormalities of the aortic wall commonly accompany BAV.
    • Mitral valve is generally normal.
  58. Calcific Stenosis of Congenitally Bicuspid Aortic Valve
    • The raphe is a major site of calcific deposits.
    • Less frequently-cusps of equal size and raphe is absent.
    • Acquired Bicuspid deformity (RVD) have a fused commissure.
  59. Calcification of Mitral Annulus (skip)
    • Degenerative calcific deposits in the mitral annulus.
    • • Most common: women > 60, mitral valve prolapse and elevated left ventricular pressure.
    • • Generally does not affect valve function.
    • • Uncommonly leads to regurgitation; stenosis; arrhythmias, thromboemboli and infective endocarditis.
    • Gross: 2–5 mm irregular, hard nodules behind leaflets.
  60. Mitral Valve Prolapse - Myxomatous Degeneration of the Mitral Valve
    • One or both mitral valve leaflets are floppy and prolapse into the left atrium during systole.
    • 3% of adults in the United States.
    • Commonly an incidental finding on physical examination, particularly young women.
    • aka mid systolic click.
    • 3% develop one of four serious complications:
    • - Infective endocarditis.
    • - Mitral insufficiency +/- chordal rupture.
    • - Stroke or systemic infarct - embolism of leaflet thrombi.
    • - Arrhythmias - both ventricular and atrial.
  61. Mitral Valve Prolapse - Gross findings:
    • Interchordal ballooning of the mitral leaflets - Hooding
    • Leaflets - enlarged, thickened, redundant, and rubbery.
    • Tendinous cords - elongated and thinned
    • Annulus may be dilated.
    • May involve tricuspid, aortic, or pulmonary valves
    • Secondary changes (skip):
    • • Fibrous thickening of the valve leaflets.
    • • Linear fibrous thickening of the LV endocardial surface.
    • • Thickening of the mural endocardium of the LV or LA.
    • • Thrombi on the atrial surfaces.
    • • Focal calcifications at base of the posterior mitral leaflet.
  62. Myxomatous degeneration of the mitral valve - Microscopic findings:
    • • Attenuation of the collagenous fibrosa layer of the valve.
    • • Marked thickening of the spongiosa layer.
    • • Deposition of mucoid “myxomatous” material
    • • Can occur secondary to regurgitation of other etiologies.
  63. Pathogenesis – Mitral valve prolapse
    • Cause unknown in most cases.
    • Associated with heritable disorders of connective tissue - Marfan Syndrome.
    • • Defects in FBN-1 alter cell-matrix interactions and dysregulate TGF-β signaling.
    • • Excess TGF-β can cause laxity and myxomatous change.
    • • Can be prevented by inhibitors of TGF-β
    • Autosomal-dominant forms of MVP have been mapped to other genetic loci.
  64. Rheumatic fever and Rheumatic heart disease
    • Rheumatic fever - acute, immunologically mediated, multisystem inflammatory disease that occurs a few weeks post group A streptococcal pharyngitis.
    • • RF rarely follows streptococci infections at other sites.
    • • Acute rheumatic carditis is common during the active phase of RF and may progress to chronic rheumatic heart disease (RHD), and deforming fibrotic valvular disease - the only cause of mitral stenosis.
  65. Rhumatic Heart Disease - Clinical findings
    • Migratory polyarthritis
    • Pancarditis
    • Subcutaneous nodule
    • Erythema marginatum
    • Sydenham chorea
  66. Acute Rheumatic Carditis - Morphology
    • Inflammation and Aschoff bodies - any layer of the heart.
    • Pericarditis, myocarditis, or endocarditis - PANCARDITIS
    • Verrucae
  67. Aschoff bodies
    • granuloma lesions
    • Anitschkow (catepillar) cells (Collections of the histiocyte variants) with wavy ribbon-like chromatin; lymphocytes, plasma cells and MPGs.
  68. Acute Rhumatic Fever - Verrucae
    • Small (1-2mm) vegetations overly necrotic foci along lines of closure.
    • Fibrinoid necrosis within the cusps or along chordae.
  69. Chronic Rhumatic Heart Disease
    • Mitral valve - Virtually always involved.
    • • Alone 65% to 70%; With aortic valve 25%.
    • • Pulmonary valve - rare
  70. Chronic Rhumatic Heart Disease - Morphology
    • Gross Findings:
    • - Leaflet thickening; Commissural fusion.
    • - Shortening, thickening and fusion of chorde.
    • Micro:
    • - Mitral leaflets
    • • Organization of acute inflammation.
    • • Diffuse fibrosis and neovascularization.
    • • Obliteration of leaflet architecture.
  71. Mitral stenosis
    • Diffuse fibrous thickening and distortion of valve leaflets.
    • Fibrous bridging of valvular commissures with calcification.
    • Fish mouth or buttonhole stenoses.
    • Left atrium progressively dilates.
    • May harbor mural thrombi in appendage or on the wall which can then embolize.
    • Long-standing pulmonary congestion leads to:
    • • Pulmonary hypertensive changes.
    • • RV hypertrophy.
  72. Rheumatic Aortic Stenosis
    • Cusps thickened and distorted.
    • Commissures fused.
    • Less than 10% of cases of acquired aortic stenosis.
  73. Infective Endocarditis
    • Organisms colonize or invade heart valves or endocardium.
    • • Vegetations of thrombotic debris and organisms often with destruction of the underlying cardiac tissues.
    • Bacterial infections >> Fungi and other microorganism classes
    • • The aorta, aneurysm sacs, other blood vessels, and prosthetic devices can also become infected.
  74. Infective Endocarditis - Pathogenesis
    • Predisposing factors: Cardiac and vascular abnormalities
    • • Mitral valve prolapse
    • • Calcific valvular stenosis
    • • Bicuspid AV
    • • Artificial valves
    • • Congenital defects
    • • Rheumatic HD
    • Risk can be lowered with antibiotic prophylaxis.
    • Source of the organism:
    • • Infection elsewhere
    • • Dental or surgical procedure
    • • Contaminated needle (IVD)
    • • Trivial breaks in the epithelial barriers of gut, oral cavity, or skin.
  75. Acute Bacterial Endocarditis
    • Rapildy progressive.
    • Highly destructive.
    • • Highly virulent organisms - Staph Aureus (10-20% of cases overall)
    • • Typically infects previously normal heart or deformed valves, IV drug abuser
  76. Subacute Bacterial Endocarditis
    • More insidious protracted course.
    • Less destructive to underlying valves.
    • • Less virulent organisms – Strep Viridans (50% to 60% of all cases)
    • • Infects deformed valves.
  77. Infective Endocarditis – Other causative organisms
    • Enterococci and HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella)
    • Prosthetic valve endocarditis - coagulase-negative staphylococci
    • Gram-negative bacilli and fungi.
    • Culture-negative endocarditis -10% to 15% of all cases, still infective
  78. Morphology - Infective Endocarditis
    • Gross: Friable, bulky destructive vegetations on the heart valves; single or multiple; one or more valves.
    • sub acute vegetations - less valve destruction than acute.
    • Microscopic findings:
    • - Vegetations - fibrin, inflammatory cells, and organisms. Underlying tissues show granulation tissue, fibrosis, calcification, and chronic
    • inflammation.
    • - Emboli containing bacteria can cause abscesses at sites where the emboli lodge -> Septic infarcts or mycotic aneurysms
  79. Nonbacterial Thrombotic Endocarditis / Marantic endocarditis - Predisposing conditions:
    • • Debilitated patients; cancer or sepsis - marantic endocarditis.
    • • Systemic hypercoagulable state.
    • • Association with mucinous adenocarcinomas - Procoagulant effects
    • • Trousseau syndrome of migratory thrombophlebitis - pancreatic
    • • Endocardial trauma: Indwelling catheter
    • • Track along Swan-Ganz PA catheters
    • Gross:
    • - Small sterile thrombi on the leaflets of the cardiac valves.
    • - 1 mm to 5 mm, single or multiple.
    • - Along the line of closure of leaflets or cusps.
    • Micro: Fibrin thrombi loosely attached to underlying valve.
    • Not invasive; no inflammation.
    • • Local effect usually unimportant.
    • • +/- Systemic emboli – Produce infarcts in the brain, heart, or elsewhere.
  80. Endocarditis of SLE - Libman-Sacks Endocarditis
    • Gross findings:
    • Mitral and tricuspid valves
    • • 1–4 mm, single or multiple, pink, warty, sterile vegetations.
    • • Undersurfaces of the AV valves; endocardium; chordae.
    • Microcopic findings:
    • • Fibrinous vegetations.
    • • +/- Valvulitis with fibrinoid necrosis of the valve substance
    • • +/- Hematoxylin bodies - degenerated nuclear material due to antinuclear Abs
    • Fibrosis and deformities can resemble CRHD and require surgery.
  81. Vegetative Endocarditis
    • RHD - rheumatic, at the cusps
    • NBTE - nonbacterial thrombotic, sterile
    • IE - infective, destructive
    • LSE - SLE, undersurface
  82. Carcinoid Heart Disease
    • 50% of pts. with carcinoid syndrome.
    • Elaboration of bioactive products by carcinoid tumors - Products are degraded in the liver.
    • Tricuspid insufficiency +/- pulmonary valve insufficiency.
    • Right sided stenosis.
    • Tends to spare left heart because products are also broken down in the lung.
    • Left-sided valvular disease – Right to left shunting; lung tumor; Serotonergic drugs.
  83. Carcinoid Heart Disease – Gross findings
    • Firm, plaque-like endocardial fibrous thickenings.
    • Inside surfaces of the right cardiac chambers.
    • Tricuspid and pulmonary valves.
    • Occasionally involve IVC & PA.
  84. Carcinoid Heart Disease – Microscopic findings
    • • Plaque-like thickenings.
    • • Smooth muscle cells and sparse collagen fibers.
    • • Acid mucopolysaccharide-rich matrix.
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Systemic Pathology - Heart pathology - Peters
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Systemic Pathology - Heart pathology Dr. Peters
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