Download VALVULAR HEART DISEASE

VALVULAR HEART DISEASE
Learning objectives
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Describe the etiology and clinical symptoms of acute rheumatic
fever.
Describe the pathology and natural history of acute rheumatic fever
and rheumatic heart disease.
Describe an Aschoff body.
Describe which parts of the heart are affected in acute rheumatic
fever.
Describe the long-term consequences of rheumatic fever.
Describe the pathology and natural history of chronic rheumatic
heart disease, and know which valves are most often involved.
Describe the pathology of postrheumatic mitral stenosis.
Enlist the components of vegetation.
Rheumatic fever and
Rheumatic heart disease
Rheumatic fever
 Rheumatic fever is an acute immunologically
mediated multisystem inflammatory disease that
occurs a few weeks following an episode of group A
streptococcal pharyngitis.
 Acute rheumatic carditis, during active phase
 May progress to Chronic rheumatic heart disease.
Etiopathogenesis
 Acute rheumatic fever is a hypersensitivity
reaction induced by group A streptococci.
 Antibodies against M proteins of certain strains
of streptococci cross react with antigens in heart,
joints and other tissues.
 Genetic susceptibility is suggested
 Autoimmune response to self antigens also
suggested.
 Chronic sequelae are a result of progressive
fibrosis (healing process) and blood turbulance
in valvular areas
Pathogenesis
CROSS REACTIONS
vegetations
Aschoff body,
myocardium
Fibrinous
pericarditis
Morphology
ACUTE RH. FEVER-- Pancarditis
 Pericarditis- serofibrinous/ Bread and butter
type
 Myocarditis  Aschoff bodies
 Endocarditis 
Verrucous vegetations (1-2mm) at lines of closure of
valves
 Fibrinoid necrosis along cusps and teninous cords
 MacCallum plaques in left atrium (Sub endocardial
thickenings due to regurgitant jets)
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vegetations
Aschoff body,
myocardium
Fibrinous
pericarditis
Carditis
Aschoff bodies
Aschoff/ Anitschow cells
Aschoff giant cell
Chronic disease
rheumatic mitral valve,
rheumatic aortic stenosis
With fused commisures
Morphology of chronic RHD
 Mitral valve is most often affected with rheumatic
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heart disease, followed by mitral and aortic together,
then aortic alone, then mitral, aortic, and tricuspid
together.
Mitral stenosis (99% cases)
Fishmouth/ buttonhole stenosis
Microscopy
Fibrosis/ scarring
Neovascularization
 Mitral valve as seen from
above in the left atrium.
 Typical "fish mouth"
shape with chronic
rheumatic scarring.
 Mitral valve is most often
affected with rheumatic
heart disease, followed by
mitral and aortic together,
then aortic alone, then
mitral, aortic, and
tricuspid together.
Clinical features of ARF
The major clinical manifestations of ARF:
 migratory polyarthritis
 carditis,
 subcutaneous nodules,
 erythema marginatum, and
 Sydenham chorea.
Minor manifestations of ARF:
 Fever, arthralgias, Increased blood levels of acute phase
reactants etc.
DIAGNOSIS
Jones criteria:
 Evidence of preceding group A strept. Infection
 Presence of two major or one major and two minor
manifestations
Clinical features of ARF
 Age: 5-15 but may be in adults
 Time: 10 days to 6wks after pharyngitis
 3% of pts effected
 Prognosis of 1st attack good.
Clinical features of chronic rheumatic
carditis
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Valvular disease and its sequelae (yrs later)
Murmurs
Cardiac hypertrophy, dilatation, heart failure
Arrythmias esp Atrial fibrillation
Thromboembolic complications
Infective endocarditis
 In the dilated atrium
with a stenotic mitral
valve, the blood
stagnates. Hence,
stasis is a factor in
thrombogenesis..
Infective endocarditis
 Infection of heart valve or mural endocardium by a
microbe leading to formation of bulky friable
vegetations and destruction of underlying tissue.
 Vegetations are composed of thrombotic debris and
organisms
Classification
 Acute
 Virulent organism
 Normal valve
 Necrotizing ulcerative, invasive infection
 Maybe fatal
 Subacute
 Less virulent organism
 Damaged valve
 Treatable with antibiotics
Etiopathogenesis
ORGANISMS
Most cases are bacterial although chlamydiae and
ricketia also implicated
 Damaged valves: Strept. Viridans (50-60%)
 Normal/ damaged: Staph. Aureus (10-20%)
 I/V drug abusers: Staph. Aureus Prosthetic valves:
Staph epidermidis
 Others are enterococci, HACEK
 Culture negative: 10%
Etiopathogenesis
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PREDISPOSED VALVES
RHD (previously)
Myxomatous mitral valve
Degenerative calcific valvular stenosis
Prosthetic valves
HOST FACTORS
Immunodeficiency, immunosupression
Malignancy
Diabetes
Alcohol
I/V drug abuse
Clinical features
Splinter hgs
Petechiae
Osler’s nodes
Janeway lesions
Diagnosis
morphology
 The more virulent
bacteria causing the acute
bacterial form of infective
endocarditis can lead to
serious destruction, as
shown here in the aortic
valve. Irregular reddish
tan vegetations overlie
valve cusps that are being
destroyed. Portions of the
vegetation can break off
and become septic emboli.
 Here is a valve with
infective endocarditis. The
blue bacterial colonies on
the lower left are
extending into the pink
connective tissue of the
valve. Valves are relatively
avascular, so high dose
antibiotic therapy is
needed to eradicate the
infection.