Valvular Disease_Fishbein

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jlyip89
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257396
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Valvular Disease_Fishbein
Updated:
2014-01-19 18:04:16
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Valvular Disease
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systems 1
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Systems: Fishbein Lecture 2.5
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  1. Heart Valves

    - function
    - what happens when valves are deformed?
    • • Valves are important in maintenance of
    • unidirectional blood flow

    • • Deformed valves produce significant
    • hemodynamic disturbance on cardiac chambers
  2. Valvular stenosis

    - what is it?
    - effects
    - aka valve obstruction

    Increased resistance to blood flow results in increased pressure in emptying chamber

    –Cardiac chambers adapt by concentric hypertrophy
  3. Valvular regurgitation

    - what is it?
    - effects?
    – incompetence: valves don't close all the way

    - Blood flows back into emptying chamber resulting in volume overload

    –Cardiac chambers adapt by eccentric hypertrophy
  4. Major Causes of acquired valve disease
    • 1. aortic stenosis
    • 2. aortic regurgitation
    • 3. mitral stenosis
    • 4. mitral regurgitation
  5. SENILE CALCIFIC AORTIC STENOSIS
    •Degenerative & calcific valvular disease due to progressive & advanced age-related “wear & tear” of normal aortic valves

    •Patients over 65, often in 80s & 90s

    •Increasing incidence of aortic stenosis due to rising age of population

    •Functional valve area diminished resulting in obstruction to outflow (pressure overload)
  6. SENILE CALCIFIC AORTIC STENOSIS: Gross Findings
    • –Heaped-up calcified masses at bases of aortic cusps protruding through outflow surfaces into sinus of Valsalva & preventing opening of cusps

    –No commissural fusion

    –Usually normal mitral valve
  7. CALCIFIC STENOSIS OF CONGENITAL BICUSPID AORTIC VALVE
    • Congenital bicuspid aortic valve occurs with
    • estimated frequency of ~1.0 – 2.0% of live births

    Instead of having 3 leaflets, valves have 2

    •Predisposed to progressive degenerative calcification

    •Calcific aortic stenosis in congenitally bicuspid valves usually occurs before age 65
  8. CALCIFIC STENOSIS OF CONGENITAL BICUSPID AORTIC VALVE:

    Gross Findings
    • - Only 2 functional cusps, usually of unequal
    • size

    –Midline raphe of larger cusp due to incomplete separation during development

    Raphe = major site of calcific deposits
  9. ACUTE RHEUMATIC FEVER

    what is it?
    sequela?
    incidence and mortality?
    •Immune-mediated, multisystem inflammatory disorder occurring 2-4 wks after group A streptococcal pharyngitis in about 3% of pts

    •Most important sequela of RF = chronic valvular deformities, esp. mitral stenosis

    • •Incidence & mortality of RF declined
    • significantly in many parts of the world

    Improved socioeconomic conditions

    Rapid diagnosis & treatment of streptococcal pharyngitis

    –Unexplained decrease in virulence of group A streptococcus
  10. DIAGNOSIS OF ACUTE RHEUMATIC FEVER
    Diagnosis established via Jones criteria

    –Evidence of preceding infection with group A streptococcus

    + 2 major criteria (or)

    +1 major and 2 minor criteria
  11. ACUTE RHEUMATIC FEVER: gross findings
    • Fibrinous pericarditis

    –Small, irregular warty vegetations along lines of closure

    McCallum plaques = irregular endocardial thickenings usually in left atrium
  12. ACUTE RHEUMATIC FEVER:

    Aschoff body
    –Most distinctive lesion of acute rheumatic fever

    –Can be found in all layers of heart = pancarditis

    –Foci of necrotic collagen surrounded by lymphocytes, plasma cells, & Anitschkow cells
  13. Acute Rheumatic Fever:

    - Anitschkow cells
    Pathognomonic for RF

    Plump macrophages with abundant cytoplasm, central round-to-ovoid nuclei with central, slender, wavy chromatin
  14. Chronic RHEUMATIC HEART DISEASE
    • <10% acute RF cases progress to chronic RHD w/ latent period of 20-30 yrs bf symptoms appear

    •Chronic RHD most frequent cause of mitral stenosis (99% cases)
  15. CHRONIC RHEUMATIC HEART DISEASE: Gross Findings
    • Valvular deformities
    • –Fibrous thickening of leaflets

    Commissural fusion & shortening (“fish mouth” deformity)

    –Thickening & fusion of chordae tendinae

    –Neovascularization

    Mitral valve almost always abnormal

    65-70% MV involved alone

    –25% both MV & AV involved
  16. Mitral Valve Prolapse

    - prevalence
    - sequela
    •Most common valve defect involving >3% of adults in US, most often young women

    •Most common indication for mitral valve replacement

    •Usually incidental finding on physical exam; however, ~3% pts have serious sequelae

    –Infective endocarditis

    –Mitral regurgitation

    –Systemic embolization

    –Arrhythmias
  17. Mitral Valve Prolapse: Gross Findings
    –Intercordal ballooning of mitral leaflets – often enlarged, redundant, thick, rubbery

    –Elongated, thinned, & occasionally ruptured chordae tendinae

    –Annular dilatation

    –Commissural fusion is absent
  18. Mitral Valve Prolapse: histopathology
    Attenuation of fibrosa layer

    –Marked accumulation of myxomatous material in spongiosa layer
  19. INFECTIVE ENDOCARDITIS

    what are the 2 types?
    • 1. acute infective endocarditis
    • 2. subacute infective endocarditis
  20. Acute Infective Endocarditis
    –Destructive, fulminant infection with highly virulent organism (e.g. S. aureus)

    –Frequently on previously normal heart valve

    Death occurs within days - wks of >50% pts despite antibiotics & surgery
  21. subacute infective endocarditis
    – Less destructive, insidious infection by low virulence organism with protracted clinical course (e.g. S. viridans)

    –Usually affects deformed heart valves

    –Most pts recover after appropriate antibiotic therapy
  22. Infective endocarditis
    • •Pts with underlying congenital or acquired
    • defects are at increased risk (regurgitant > stenotic valves)

    AV & MV most common sites of involvement

    TV involvement seen in IV drug users

    Complications:

    –Septic embolization

    –Sudden death

    –Ring abscess

    –Pyogenic myocarditis

    –Valvular insufficiency
  23. Infective endocarditis:

    Pathological Findings
    –Friable, bulky, & potentially destructive vegetations containing fibrin, inflammatory cells, & organisms on valves

    SBE vegetations have granulation tissue at bases suggesting chronicity

    Chronic inflammation, fibrosis, & calcification may be present with time
  24. NONBACTERIAL THROMBOTIC (MARANTIC) ENDOCARDITIS
    •Commonly present in patients with hypercoagulable state with systemic activation of coagulation such as DIC

    May be related to:

    –Underlying malignancy: Affects people who are dying of other causes

    –Other debilitating diseases (severe burns, sepsis)

    Embolization may occur
  25. Nonbacterial thrombotic endocarditis

    - gross pathology
    - histopathology
    Gross pathology:

    –Small, sterile, nondestructive, loosely adherent single or multiple vegetations along line of closure

    • Histopathology
    • –Composed of bland thrombus without inflammation or induced valve damage
  26. PERICARDITIS
    • Inflammation of visceral & parietal
    • linings of heart

    •Usually secondary to various cardiac diseases, thoracic or systemic disorders, metastases from neoplasms, or surgical procedures on heart

    •Primary pericarditis unusual & almost always of viral origin
  27. Pericaditis: causes
    • -infectious agents that usually come in
    • through the lungs

    -Immunologically mediated

    -Ideopathic (viruses)
  28. 3 Types of Pericarditis
    • 1. serous pericarditis
    • 2. hemorrhagic pericardits
    • 3. caseous pericarditis
    • 4. finbrinous pericarditis
  29. Serous pericarditis
    –Usually due to noninfectious inflammatory conditions (RF, SLE, scleroderma, tumors,uremia)

    –Scant inflammatory infiltrate comprised of PMNs, lymphocytes, & macrophages on pericardial surface
  30. Hemorrhagic pericarditis
    • Blood mixed with fibrinous or suppurative
    • effusion

    –Most commonly caused by malignancy, bacterial infection, underlying bleeding diathesis, TB, and after cardiac surgery
  31. Caseous pericarditis
    –Most commonly TB

    –Rare, but most frequent antecedent of fibrocalcific constrictive pericarditis
  32. FIBRINOUS PERICARDITIS
    Most frequent type of pericarditis

    •Composted of serous fluid admixed with fibrinous exudate

    Common causes:

    –Myocardial infarction (heart attack)

    –Post-pericariotomy syndrome (Dressler syndrome)

    –Uremia

    –Radiation

    –Collagen vascular diseases

    –Rheumatic fever

    –Trauma

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