Cardiovascular pathology II

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  • Created by: z
  • Created on: 19-03-16 20:10

Valvular heart disease

  • stenosis: filaure of valve to open completely > impedes forwards flow of blood
    • almost always has underlying valve abnormality
    • usually chronic
  • incompetence/regurgitation: fialure of valve to close completely (allows reverse flow of blood)
    • functional regurgitation: valve becomes incompetent due to dilation of ventricle
    • due either to intrinsic disease of valve cusps or damage/distortion of supporting structures (aorta, mitral valve annulus, tendinous cords, papillary muscles, ventricular free wall)
  • clinical consequences depend on:
    • which valve
    • degree of impairment
    • rate of its development
    • rate and quiality of compensatory mechanisms
  • can be unimportant (e.g. rheumatic mitral stenosis)
  • or rapidly fatal (e.g. acute aortic incompetence 2ary to destruction of valve cusp from infection)
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Valvular calcification

  • calcific aortic stenosis
  • calcification of congentially bicuspid aortic valve (50-60yro)
  • mitral annular calcification
  • due to wear and tear
    • clinically apparent in 70yr+
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Common functional valvular lesions I

  • mitral stenosis > rheumatic heart disease
    • cross reaction following GpA B-haem steptrococcal pharyngitis
    • Ft. migratory polyarthritis of lg joints, carditis, subcut nodules, rash, Sydenham chorea
    • acute RHD > pancarditis (may recur w/ susequent pharyngeal infection adding to damage)
      • endocardium > vegetations
      • myocardium > inflammatory foci w/ Aschoff bodies (rheumatic granuloma - "owl eye")
      • pericardium > pericarditis
    • chronic RHD  
      • "fish mouth/button hole" stenoses, leaflet thickening, commissural fusion and shortening, thickening and fusion of chordae tendinae
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Infective endocarditis I

  • colonisation/invasion of heart valves
  • formation of friable vegetations 
    • compris thrombotic debris and organisms
    • oft underlying tissue destruction
    • normal bacterial
  • acute IE:
    • valve previously normal
    • acute onset
    • 50% mortality 
    • lesion is necrotising, ulcerative, invasive
  • subacute IE:
    • valve usually abnormal
    • insidious onset
    • most recover
    • lesion less destructive
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Infective endocarditis II

  • predisposing factors:
    • abnormal valve: floppy mitral valve, degen calcific valvular stenosis, bicuspid aortic valve, artifical graft
    • host factors: immunosuppression, neutropenia, immunodeficiency, iatrogenic, diabetes, alcohol, IVDU
  • organisms involved:
    • A-haem streptococcus: 50-60% abnormal valve, subacute
    • S. aureus: high virulence, normla valve, IVDU
    • mouth commensals
    • staph epidermitis: prosthetic valves
  • mechanisms: seeding of blood w/ microbes e.g. dental/surgical procedure, dirty needle
    • thus give prophylactic ABx to at risk pts
  • morphology of IE:
    • aortic and mitral most commonly affected, tricuspid in IVDU (can be more than 1 valve)
    • bulky friable vegetations
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Infective endocarditis III

  • complications of IE:
    • myocardial abscess
    • valve rupture/perforation
    • systemic emboli (A/M > body esp kidney; T/P > pulmonary)
      • septic emboli
      • immune complexes
  • non-bacterial thrombotic endocarditis (sterile):
    • deposition of fibrin/platelets on valve leaflets
    • either side of heart
    • previously normal heart 
    • non-destructive but emboli risk important
    • occurs in hypercoag state (DIC, malignancy, sepsis)
  • NB artificial valves:
    • mechanical
    • bioprostheses (homograft/porcine)
    • Cx: TE (thus longterm anticoag), IE, structural deterioration
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Cardiomyopathy

"heart disease resulting from primary abnormality in the myocardium"

  • causes:
    • inflammatory
    • immunological
    • systemicmetabolic disorders
    • muscular dystrophies
    • genetic abnormalities of myocytes (energy metabolism, structural and contracile proteins)
    • idiopathic
  • 3 clinical pictures:
    • dilated cardiomyopathy (DCM, >90%)
    • hypertrophic CM (HCM/HOCM)
    • restrictive CM (RCM)
  • pattern can be: idiopathic, specifc identifiable cause, 2ary extramyocardial disease)
  • Dx by endomyocardial biopsies of RV
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Dilated cardiomyopathy

  • characterised by:
    • cardiac hypertrophy, dilation, contracatile dysfunction
  • results in CCF
  • causes: idiopthic (most), alcohol, peripartum, genetic (OX phos, B ox FFA, dystrophin), myocarditis, haemochromatosis, chronic anaemia, drugs (doxorubicin, adriamycin), sacroidosis
  • gross morphology:
    • heavy heart (2-3x norm), large and flabby
    • dilation of all chambers, pos 2ary mitral/tricuspid regurg
    • mural thrombi (> TE risk)
    • normal coronary arteries
  • histology: hypertrophied fibres, attenuated/stretched fibres, interstitial and endocardial fibrosis
  • any age (20-60)
  • slowly progressive CCF, 50% mortality in 2 years (from CCF, arrythmias)
  • EF 25% (norm= 50-65%)
  • Rx - cardiac transplant
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Hypertrophic cardiomyopathy

  • charactarised by:
    • myocardial hypertrophy > abnormal diastolic filling
    • 1/3 intermittent LV outflow obstruction
  • gross morphology:
    • massive myocardial hypertrophy, NO ventricular dilatation
    • assymetrical septal hypertrophy (NB 10% symmetrical)
  • histology:
    • extensive myocyte hypertrophy
    • myocyte disarray
    • interstitial fibrosis
  • 50% genetic, 50% sporadic
  • genetic: AD w/ variable penetrance, mutations in 4 genes that encode contractile proteins
    • B-myosin heavy chain, cardiac troponin T, A-tropomyosin, myosin-binding protein C
  • angina, AF, CCF, ventricular arrythmias, sudden death
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Myocarditis

  • causes:
    • infection (esp. viral) > most common
    • immune
      • post-viral
      • post-streptococcal (RHF)
      • SLE
      • drug hypersensitivity (methyldopa, sulphonamides)
      • transplant rejection
    • sarcoidosis
  • clinical features:
    • asymptomatic
      • DCM years later (e.g. w/ CMV)
      • arrythmias
      • acute heart failure (e.g. in rejection)
      • sudden death 
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Pericardial disease

  • pericardial effusion- transudate/exudate
  • haemopericardium: cardiac tamponade post-MI/traumatic perforation/ruptured aortic dissection
  • purulent pericarditis - pus
  • pericarditis
    • 2ary to cardiac disease, thoracic or systemic disorders or metastases
      • infections: virus, B, Tb, fungi
      • immune: RF, SLE, scleroderma, post-MI (Dressler syndrome), hypersensitivity reaction
      • misc: MI, uraemia, post-cardiac surgery, neoplasia, trauma, radiation
    • types:
      • serous, fibrinous, purulent/suppurative, haemorrhagic, caseous
    • outcome:
      • reabsorbed, resolved
      • organise > obliterate pericardial space
      • +/- constrictive pericarditis: heart suurounded by fibrous scar limits filling thus SV/CO
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Neoplasms

  • 2ary - in 5% of pt who die from ca
    • most commonly melanoma or mediastinal primary
  • primary - rare
    • myxoma
      • most common primary tumour
      • 90% in atria (majority LA) = atrial myxoma
      • morphologically can be:
        • sessile: firmly immobile, attached like a limpet
        • pedunculated (more common): attached on a stalk
          • can swing into valve: 'ball-valve obstruction'
      • can injure valve
      • embolisation risk
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Congenital heart disease

  • 'abnormalities of herat or great vessels at birth'
  • right to left shunt
    • pulmonary to systemic, thus less oxygenated > cyanosis= 'cyanotic congenital HD'
      • tetralogy of Fallot
      • transposition of great rteries
      • persistent truncus arteriosus
      • tricuspid atresia
      • total anomalous pulmonary venous connection
    • can get paradoxycal embolus as veins > systemic
  • left to right shunt
    • systemic > pulmonary thus incr pulm flow > pulm HTN 
      • intially reversible, later will reverse to RtL w/ pr gradient (Eisenmengers syndrome)
      • ASD, VSD (most common CHD). AV septal defect
      • PDA (b/w pulm art and desc aorta)
  • obstructive: due to abnormal narrowing of chamber/valve/vessel e.g. coarctation of aorta
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Vasculitis

  • cause:
    • immune
      • immune-complex, ANCA (antineutrophil cytoplasmic antibodies), direct ab mediated, cell mediated, IBD, paraneoplastic
    • infectious
    • unknown
      • giant cell (temporal) arteritis (most common)
      • Takayasu arteritis (granulomatous vasculitis w/ huge intimal fibrosis and vascular narrowing)
      • polyarteritis nodosa (characterised by necrotising lesions in middle sized vessels)
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Common functional valvular lesions II

  • mitral incompetence > floppy mitral valve, myxomatous degeneration, mitral valve prolapse
    • floppy mitral stenosis: common
    • one or both mitral leaflets enlarhed, hooded, redundant > prolapse into RA in systole
    • usually incidental finding, v rarely can cause sudden death
  • aortic stenosis > calcification of normal/congentially bicuspid valves
  • aortic incompetence > dilation of ascending aorta related to HTN and age
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