Valvular Heart Disease

Learning Outcomes
Describe the various valve disorders

Understand the difference between stenosis and

regurgitation
Enumerate various congenital, inflammatory and
degenerative valve disease
Understand the etiology, pathogenesis, pathology
and complications of degenerative calcific aortic
stenosis

Normal Valves
1. Unidirectional blood flow.
2. Anatomical dimensions & Functional aspects
3. Differences between the semilunar and
Atrio-ventricular (A-V) valves.
Valve competency
Depends on:
Annulus
Leaflets
Cords
Papillary muscles
Ventricular wall
Layers - Ventricularis, spongiosa, fibrosa

Valvular heart disease

Impose hemodynamic burden by causing
(i) obstruction (stenosis)
(ii) regurgitation (incompetence)
Lesions of tricuspid and pulmonic valves less common than
those of mitral and aortic
Increase susceptibility to infective endocarditis

Causes of Valvular heart disease

Calcific Aortic Stenosis
Mitral Valve Prolapse
Rheumatic Fever
Nonbacterial Thrombotic Endocarditis
Infective Endocarditis
Prosthetic Cardiac Valves

Types of Valvular heart disease

Stenosis, insufficiency (regurgitation) or both.
Stenosis: failure of a valve to open completely, thereby
impeding forward flow.
Insufficiency, regurgitation, incompetence: failure of a
valve to close completely, thereby allowing reversed flow.
Abnormalities can be pure or mixed.

Valvular dysfunction
Dysfunction may affect a single valve ( isolated) or
multiple valves (combined), sudden or delayed
Depending on degree, duration, and cause valvular
stenosis or insufficiency often produces secondary
changes in the heart, blood vessels, and other organs.
Functional regurgitation is incompetence due to
dilation of ventricle, aortic, pulmonary arteries.

VHD - congenital or acquired.

Acquired stenoses of mitral and aortic valves: 2/3rd of all valve
lesions.
Congenital:
aortic stenosis (supravalvular, valvular and subvalvular)
pulmonary stenosis.
Acquired (different causes)
Occurs in isolation or in association with other heart diseases.
Primary valvular diseases
VHD stenosis/ insufficiency
Valvular stenosis:
Almost always is due to a primary cuspal abnormality and is
virtually always a chronic process.
Valvular insufficiency: Results from either intrinsic disease of the
valve cusps or damage to or distortion of the supporting
structures.

Acquired heart valve disease

Mitral valve diseases

1. Mitral stenosis
post inflammatory scarring (RHD).

2. Mitral regurgitation
A. abnormalities of leaflets and commissures:
post inflammatory scarring.
infective endocarditis.
mitral valve prolapse.
B. Abnormalities of tensor apparatus
rupture of papillary muscle.
papillary muscle dysfunction (fibrosis).
rupture of chordae tendineae.
C. Abnormalities of left ventricular cavity and/ or annulus
Lt ventricular enlargement
(myocarditis,congestive cardiomyopathy)
Calcification of mitral ring.

Acquired heart valve disease

Aortic valve diseases
1. Aortic stenosis:
Post inflammatory scarring (RHD)
senile calcific aortic stenosis
calcification of congenitally deformed valve
2. Aortic regurgitation
Aortic disease
Intrinsic valvular disease
post inflammatory scarring(RHD) degenerative aortic dilation
syphilitic aortitis
infective endocarditis
ankylosing spondylitis
rheumatoid arthritis
Marfan syndrome

Calcific aortic stenosis

Calcific aortic stenosis:
Most frequent. Congenital or acquired

Fibrosis of valve cusps with calcification (heaped up mass)

Rigid Valves sclerosis: asymptomatic (discovered
incidentally).
No fusion of aortic valve leaflets (seen in RHD)
Degenerative calcific aortic stenosis.

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Clinical features - calcific AS

Usually asymptomatic until the 7th or the 8th decadewhen it arises in a previously normal valve.
Angina pectoris (due to reduced aortic outflow).
Syncope (due to poor perfusion of the brain).
Congestive heart failure (later stages).
In 2%, arise in congenitally bicuspid aortic valves.

Valve area approx 0.5-1 sq cm

Clinical features
Abnormal configuration
Excessive haemodynamic stress
Greater wear and tear
Early degenerative changes.
Clinical course
- In congenital cases, lesions become manifested 10-20 years
earlier than degenerative calcific aortic stenosis.
- Left ventricular hypertrophy
- Untreated- death within 3 to 4 years- due to CHF or
arrhythmia.
- Surgical valve replacement is ideal management.
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Other causes of Aortic stenosis:

Severe atherosclerosis.

Endocarditis

Ochronosis.

Hypertension

Rheumatic fever

Marfan's syndrome

SLE.

Aortic dissection

Fabrys disease - LSD.

Injury resulting from
radiation.
Pagets disease of bone

Ankylosing spondylitis
Reiter's syndrome
Syphilis
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Rx
Hospitalization required for severe symptoms.

Diuretics, digoxin, activity restriction.

Surgical repair or replacement of aortic valve.
Prognosis: curable with surgical repair. The person
may become symptom-free unless complications
develop.

Complications: stable angina, heart failure, aortic

regurgitation, pulmonary oedema, endocarditis
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Bicuspid valve with calcification

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Mitral valve prolapse

Myxomatous degeneration of mitral valve.
3 % of adults in USA, young women, 20-40.
Complication of Marfan syndrome or similar connective
tissue disorders.

Accumulation of loose ground substance within the leaflets

and chordae of the mitral valve, causes valve to become
floppy and incompetent during systole

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MVP Morphology
Mitral valve cusps: soft, enlarged
Hooding of leaflets enlarged, redundant, thick, rubbery,
floppy.
Causes a ballooning of the valve leaflets into the left atrium
during systole prolapse
Chordae tendineae- elongated, fragile, may rupture in
severe cases as a result, one or both cusps billow or
prolapse into the atrium during ventricular systole.
Annular dilation;
Valve leaflets fibrous thickening & calcification, thrombi,
Clinical features : Mostly asymptomatic. Palpitations,
fatigue, or atypical chest pain.
Mid systolic click with late systolic murmur

MR Stages
MVP responsible for 45% of cases of MR.
Acute Stage spontaneous chordae tendineae
rupture
sudden volume overload
increased left ventricular filling pressures
transfer of blood to the left atrium during systole
elevated left atrial pressures, transmitted to the lungs
acute pulmonary oedema and dyspnoea.

Clinical features MR
Tolerated for many years. Initially angina-type pain,
dyspnoea & fatigue - rapidly progress to orthopnea &
paroxysmal nocturnal dyspnoea.
In those with MVP, palpitations and atypical chest pain.
High-pitched systolic murmur

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Complications of MR/ MVP

Acute pulmonary oedema

Cardiogenic shock
Atrial fibrillation with embolization
Susceptible to endocarditis.
Myocardial infarction
Mitral insufficiency in MVP
Congestive heart failure
Cerebral infarction /systemic infarction (from
embolism of thrombi found in the left atrium)
Sudden death (due to ventricular arrhythmia)

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Annular calcification

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