Valvular Heart Diseases

Dr. Mehzabin
Ahmed
 The normal function of cardiac valves is to prevent

retrograde flow of blood between the atria and

ventricles and between the ventricles and the aorta

or pulmonary artery. The vibration of blood as valves

close produces heart sounds.

 The first heart sound (S1) is due to the closure of the

mitral and the tricuspid valves and the second (S2)

by the closure of the aortic and the pulmonary

valves.

 A murmur is an abnormal heart sound produced by

 Valvular abnormalities

 Valvular stenosis - in which valves become thickened or

calcified and obstruct the normal flow of blood into a

chamber or vessel.

 Valvular incompetence - also called regurgitation or

insufficiency in which there is lose of the normal function

of the valves and thus fail to prevent the reflex of blood

after contraction of an individual cardiac chamber.

 Vegetations - in which the valves leaflets bear either

 Valve lesions
 Mechanical disturbances:

– Stenosis

– Regurgitation

 Vegetations:

– Infective endocarditis

– Immunological conditions- SLE- Libman-Sacks

endocarditis

– Hypercoagulable states like widespread metastatic

cancers or severe chronic infections- Marantic
 Pathological causes of valvular heart
diseases
 Congenital abnormality- due to rubella infection,
antiepileptic drugs,

 Post infarction resulting in papillary muscle dysfunction

 Post inflammatory scarring (Rheumatic heart diseases)

 Degeneration with aging

 Connective tissue disorders like Marfan’s syndrome

 Acute destruction by necrotizing inflammation

 Calcification of the valvular leaflets.

 Inflammatory disorders of the
heart valves
 Immune mediated damage causing an inflammation in
the valve cusps
 Damage due to infections as in bacterial and fungal
endocarditis
 Valves on the left are more frequently involved
 Consequences:
– Vegetations: exposure of the valve collagen results in
thrombus deposition as exophytic irregular warty
nodules
– Inflammation and thrombus formation causes
 Rheumatic fever
 An immune disorder that follows a streptococcal
tonsillitis or pharyngitis by certain strains of
streptococci particularly group A β Hemolytic
streptococci
 The antibodies that are formed against the
streptococcal antigens cross-react with the host cardiac
muscle protein.
 The disease occurs mainly in children between the ages
of 5 and 15 years.
 A systemic disorder, which in acute phase presents with
 Rheumatic Heart Diseases

 In the acute phase pancarditis is seen

 The pericarditis and myocarditis resolve without any

long term effect.

 The endocarditis (valve) damage heals by fibrosis and

thickens the valves and the chordae tendinae. The

valve leaflets may fuse in some cases causing

stenosis.
 Diagnostic criteria for Rheumatic
fever - Jone's Criteria
 Major manifestations  Minor manifestations

1) Carditis 1) Polysynovitis (flitting

2) Polyarthritis arthropathy)

3) Skin rashes (erythema 2) Arthralgia

marginatum & subcutaneous 3) Raised ESR or CRP (C-

nodules) Reactive protein)

4) Neurological symptoms 4) Prolonged PR interval on

(Sydenham's chorea) ECG

5) Fever
Diagnosis requires

 two major features or

 one major and two minor features,

 plus raised antistreptococcal antibody levels (anti

strepolysin O liter) or positive throat culture for

group A βHemolytic streptococcus

 Rheumatic heart disease
 Patients develop characteristic inflammatory lesions (Aschoff's

nodules) in various parts of the heart

i) Rheumatic Pericarditis: - Aschoff's nodules in the pericardium with

acute inflammatory exudate predominantly of serous type

ii) Rheumatic Myocarditis: - Aschoff's nodules in the myocardium are

associated with interstitial edema and mild inflammation and muscle
fiber necrosis.

iii) Rheumatic endocarditis: - Aschoff's nodules may form anywhere in

the endocardium, producing slight irregularity of the endocardial
surface. Aschoff's nodules in the valves leads to greater irregularity,
erosion of the overlying endocardium particularly at the points at
which the valves contact each other at the line of closure. In these
sites small aggregations of fibrin and platelets accumulate to form
small vegetation's. The aortic and mitral valves are most prone to
Thickened chordae Vegetations on the line of
tendinae closure of the valve
 Mitral valve diseases- Mitral
stenosis
 Rheumatic heart disease is an important cause of MS
 The long-term effects of the immune damage causes chronic
scarring of valves, by fibrosis, of the valve leaflets and
associated chordae tendinae. The valve leaflets become
thickened, fibrotic and shrunken producing mitral stenosis
 In addition rigid and immobile mitral cusps can cause
incompetence because of ineffective closure.
 Failure of the left atrium to empty through the stenosed valve
leads to left atrial hypertrophy and dilation . Back pressure
causes pulmonary hypertension and pulmonary vascular
congestion producing hemoptysis. Left heart failure develops
 Atrial fibrillation is a common complication  atrial thrombosis
Severe mitral stenosis producing a fish mouth appearance
 Mitral incompetence

 Causes are
– Chronic Rheumatic fever,
– Papillary muscle dysfunction after myocardial
infarction,
– Cusp destruction by infection and
– Floppy mitral valve syndrome.

 In most cases regurgitation develops slowly and

results in left ventricular enlargement and dilation
of left atrium. Progressive left sided cardiac failure
 Mitral valve prolapse -Floppy valve
syndrome
 Myxoid degeneration of mitral valve, the valve leaflet
bulges upward into the atrium during systole;
 The valve incompetence is due to hypermobility of the
leaflet.
 It is most common in women and presents in young
adulthood.
 In some cases there is a family history
 The posterior leaflet is most commonly affected
 Rupture of one of the chordae tendinae results in
Floppy valve
 Aortic valve diseases
 Aortic stenosis is most commonly due to calcification of a
congenital bicuspid aortic valve, post inflammatory scarring
after rheumatic fever or senile calcific degeneration.
 Severe calcific disease produces rigid cusps  aortic stenosis.
 This causes progressive and left ventricular hypertrophy.
 Most elderly patients with calcific aortic valve disease have
pure aortic stenosis,
 In rheumatic heart disease there is some aortic incompetence
and involvement of the mitral valves.
 The pathological process responsible for calcification of the
aortic valve, largely a disorder of elderly is unknown.
 Approximately 1% of the population have a bicuspid aortic
valve, these valves are particularly liable to calcification,
sometimes at a relatively young age
 Calcific areas in a previously
normal valve

Calcific areas in a bicuspid

valve
 Infective Endocarditis
 Infection of the endocardium and the heart valves.
 There are two broad groups of cases.

1) Patients with a structural abnormality of heart valves or by

congenital cardiac defects - are predisposed to infection .

The infective organisms responsible are of low

pathogenicity and are derived from normal commensal
organisms of skin, mouth, urinary tract and gut.

The main underlying abnormalities in these groups are

congenital bicuspid aortic valves, post-inflammatory
scarring, mitral valve prolapse syndrome and artificial
2) Infection of normal valves accounts for remaining cases of

endocarditis, in contrast to the first group infection is with

pathogenic organism that directly invades the valve and cause

rapid destruction. The disease is predisposed by condition that

promote the entry of pathogenic organisms into the blood.

 It is common in IV drug abuses, after open heart surgery and

following septicemia.
Large friable vegetations-
Infective endocarditis
 Clinical picture
 Acute infective endocarditis is
– due to virulent organism e.g. staphylococcus aureus
– can occur in previously normal heart valves.
– The proliferation of the bacteria results in necrosis and
destruction of valve leaflets and acute disturbance of valve
function leading to acute cardiac failure.
– The disease is rapidly progressive and often fatal.
 Subacute bacterial endocarditis
– generally occurs on structurally abnormal valves.
– The causative organisms are poorly virulent, and proliferate
slowly forming thrombotic vegetation and gradual valve
destruction, the thrombi can embolise.
– Many of the effects seen in this pattern of infection are
through immunological phenomena and generation of
cytokines from persisting low grade infection
 Diagnosis of infective endocraditis
– Blood culture to isolate the organism & Echocardiogram
 Effects/ Consequences
i)  Small emboli of infected thrombotic material enter the
systemic circulation, producing infarcts in many organs,
particularly brain, spleen and kidneys

ii)  Gradual destruction of the valves lead to valve incompetence

with cardiac failure

iii) Immune complexes against the antigens in infecting

organisms are trapped in small vessels, causing skin
petechiae and microhaemorrhages in the retina, skin around
the nail beds and glomerulonephritis

iv) Cytokine generation from the grade infection leads to

systemic features of fever, weight loss and malaise
Wart like Large friable Small bland Medium sized
vegetations vegetations vegetations vegetations on
both sides of the
valve leaflets
 Artificial valves
Replacement of damaged cardiac valves with prosthesis has now
become a common and often life saving mode of therapy. Artificial
valves are of two categories:-
i) Mechanical prostheses are various rigid, mobile occluders
composed of non physiologic biomaterials
ii)Tissue valves are bioprostheses that consist of chemically treated
animal tissue, especially porcine aortic valve tissue, these valves
are flexible and function some what like natural semi lunar
valves.
Complications of artificial valves :-
 i) Thrombosis / thromboembolism
 ii) Prosthetic valve endocarditis
 iii)Structural deterioration tear, fracture, calcification
 iv)Hemolytic induced by high blood shear
At the end of the lesson on Valvular heart
diseases , the student should be able to:
 List the major causes of Valvular heart
diseases.
 Define rheumatic fever & infective
endocarditis (IE).
 Explain the pathogenesis of rheumatic
fever.
 List the ‘Jones’ criteria for diagnosing
rheumatic fever.
 List the factors, which predispose to IE.
 List the clinical features of IE.
 List the cardiac / extra cardiac
complications of IE.