Rheumatic heart disease
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Transcript of Rheumatic heart disease
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VALVULAR HEART DISEASES
8/1/2014
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Normal heart valves
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Normal heart valves
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Valvular heart disease
• A major group of cardiac pathology affecting cardiac valves.
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Clinical consequences
1. Stenosis – failure of a valve to open completely,
obstructing forward flow.
2. Insufficiency (regurgitation ) - failure of a valve to
close completely, allowing (backflow) of blood.
Stenosis or regurgitation can occur alone or together in
the same valve.
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What is STENOSIS ? What is REGURGITATION?
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Clinical consequences
• Abnormal flow through diseased valves - produces
abnormal heart sounds (murmurs)
• severe lesions can even be palpated as thrills.
• severity - quality and timing of the murmur
(e.g., harsh systolic or soft diastolic murmurs)
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Valvular heart disease
Types
1. Congenital valvular heart diseases
2. Acquired valvular heart diseases
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Congenital valvular heart diseases
most common – bicuspid aortic valve
• neither stenotic nor incompetent through early life
• more prone to early and progressive degenerative
calcification
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Acquired valvular heart diseases
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Most Common Causes
1. AS: calcification of anatomically normal and
congenitally bicuspid aortic valves
2. AR: dilation of ascending aorta, usually related to
hypertension and aging
3. MS: rheumatic heart disease
4. MR: myxomatous degeneration (mitral valve prolapse)
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Aortic stenosis
Most common cause –
calcification of
1. anatomically normal (senile calcific aortic stenosis) and
2. congenitally bicuspid aortic valves
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Pathogenesis
• Degenerative changes due to aging process (wear and tear)
• Repetitive mechanical stresses to valves —40 million
beats/yr
• chronic injury due to hyperlipidemia, hypertension,
inflammation, atherosclerosis leads to .......
• dystrophic calcification (deposits of calcium phosphate salts)
• Normal valves - Senile calcific aortic stenosis >70 yrs
• Bicuspid valves – more stress – earlier calcification <50 yrs
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MORPHOLOGY
• heaped-up calcified masses on outflow side of cusps
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Clinical Features
• gradual narrowing of the valve orifice ( 0.5 to 1 cm2 in
severe AS ; normal, 4 cm∼ 2 )
• Left ventricular pressures - > 200 mm Hg
• Pressure overload concentric LVH
• hypertrophied myocardium -prone to ischemia and angina
• Systolic and diastolic dysfunction – CHF
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calcific aortic stenosis
Prognosis
• Asymptomative at earlier stage – excellent
• Late stage - development of angina, CHF, or syncope
poor prognosis
• without surgical intervention, 50% to 80% die within 2
to 3 years
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Most Common Causes
1. AS: calcification of anatomically normal and
congenitally bicuspid aortic valves
2. AR: dilation of ascending aorta, usually related to
hypertension and aging
3. MS: rheumatic heart disease
4. MR: myxomatous degeneration (mitral valve prolapse)
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Myxomatous Mitral Valve
• Mitral prolapse - parachute-like protrusion of value into the
left atrium
• “floppy” and prolapse— balloon back into LA during systole.
• Men = women
Two types
1. P
2. Secondary where MR due to others(e.g., IHD).
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Myxomatous Mitral Valve
Causes
1. primary myxomatous degeneration
• intrinsic defect of connective tissue synthesis or remodeling
(e.g., Marfan syndrome)
2. Secondary
• results from injury to the valve myofibroblasts, by
chronically aberrant hemodynamic forces
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Pathogenesis
Myxoid degeneration due to accumulation
of glycosaminoglycan, within the connective tissue
matrix of the valve.
many cases, degeneration limited to mitral valve
Marfan syndrome - degeneration is more extensive
and involves other heart valves.
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• Characterized by ballooning
(hooding) of the mitral
leaflets
• affected leaflets are
enlarged, thick, and rubbery
• L A - dilated due to long-
standing volume overload.
Morphology
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Clinical features
• Most – asymptomatic
• minority - palpitations, dyspnea, or atypical chest pain
• Auscultation - midsystolic click, caused by abrupt
tension on valve leaflets as valve attempts to close
• diagnosis can be confirmed by echocardiography
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complications
• 3% - develop complications
(1) IE
(2) MR , sometimes with chordal rupture
(3) stroke or systemic infarct, resulting from embolism
(4) arrhythmias, both ventricular and atrial
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Complications
• pronounced hooding
of mitral leaflet with
thrombotic plaques
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Most Common Causes
1. AS: calcification of anatomically normal and
congenitally bicuspid aortic valves
2. AR: dilation of ascending aorta, usually related to
hypertension and aging
3. MS: rheumatic heart disease
4. MR: myxomatous degeneration (mitral valve prolapse)
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Rheumatic heart disease
1. cardiac manifestation of rheumatic fever.
2. Chronic rheumatic heart disease
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Acute Rheumatic Fever
• acute, immunologically mediated, multisystem
inflammatory disease 2- to 3-weeks after group A β-
hemolytic streptococcal infections (pharyngitis)
• Occurs commonly in children (4 to 9 years)
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PATHOGENESIS
• Heart valves - common antigenic sequences with GAS
bacteria (Mprotein= Glycoprotein antigen)
• GAS pharygitis - Formation of antistreptococcal Abs
• cross reacts with Cardiac myosin and Sarcolemma
• joints (Antibody against Streptococcal hyaluronic acid
cross reacts with connective tissue proteoglycans)
• Only 3% of infected patients develop rheumatic fever
depends on individual immune response
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Rheumatic Valvular Disease
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Rheumatic heart disease
• Pathological Changes Of Heart In Acute Rhumatic Fever
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Morphology
Aschoff bodies or Rheumatic granuloma
• fibrinoid necrosis surrounded by lymphocytes,
plasma cells and plump activated macrophages
(Anitschkow cells)
• pathognomonic of rheumatic carditis
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Anitschkow cells
• modified
macrophages
• nuclei that have
central caterpillar-
shaped wavy
chromatin
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Aschoff bodies or Rheumatic granuloma
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Morphology
Pancarditis:
• Diffuse inflammation and Aschoff Bodies in any of the
3 layers of heart – pericardium, myocardium,
endocardium (including valves)
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Morphology
Pancrditis
• Pericardium: “Bread and Butter” Pericarditis
• Myocardium: Myocarditis (Scattered Aschoff bodies)
• Endocardium: Fibrinoid necrosis along the lines of closure
of valves forming 1 to 2 mm vegetations (verrucae)
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“Bread and Butter” Pericarditis
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Macculum plaques
• irregular thickenings of
endocardium in left
atrium caused by
regurgitant blood flow
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Subendocardial fibrosis
Macculum plaques
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Vegetations
• vegetations (verrucae)
along the lines of
closure of valves
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Clinical Features of ARF
• Following upper airway infection with GAS
• Silent period of 2 - 3 weeks
• Sudden onset of fever, pallor, malaise, fatigue
Arthritis - occurs in 75%
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• two of five major criteria, OR
• one major criterion and two minor criteria
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Sydenham's chorea
• movement disorder
• described as 'rapid, irregular, aimless and involuntary'.
• affect the muscles in the limbs, face and trunk.
• girls > boys
• 25% - develop chronic rheumatic valve disease.
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Erythema marginatum
• occurs in < 5% of patients.
• start as red macules that
fade in the centre
• remain red at the edges
• mainly on trunk and
proximal extremities
• but not the face.
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Investigations
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Rheumatic heart disease
1. cardiac manifestation of rheumatic fever.
2. Chronic rheumatic heart disease
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Chronic rheumatic heart disease
• Develope in 50% of rheumatic carditis.
• 2/3 - women.
• history of rheumatic fever or chorea in 50%
• > 90% - mitral valve is affected
• 25% - Isolated mitral stenosis
• 40% - mixed mitral stenosis and regurgitation
• others - aortic valve , tricuspid and pulmonary valve
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Pathogenesis
• main pathological process - progressive fibrosis.
• characterized by organization of the acute
inflammation and subsequent scarring.
• Aschoff bodies are replaced by fibrous scar
• Fusion of the mitral valve commissures and shortening
of the chordae tendineae mitral stenosis
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Morphology
• Fibrous bridging across the valves and calcification create
“fishmouth” or “buttonhole” stenoses
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Major causes of death in RHD
Cardiac failure
• Bacterial Endocarditis
• Embolism
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So…………
The first step in preventing Rheumatic fever &
Rheumatic heart disease is to detect & treat
STREPTOCOCCAL PHARYNGITIS.
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Diagnosing a streptococcal pharyngitis
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you must know why ………………
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