Valvular heart disease final

VALVULAR HEART DISEASE
Dr. Nurul Anwer Shetu.MBBS

Goals and objectives
 Discuss the common etiologies of valvular stenosis and
regurgitation.
 Recognize the signs and symptoms of severe valvular
stenosis and regurgitation.
 Be able to quickly identify and treat acute mitral and
aortic regurgitation.
 Identify patients who should be referred for surgical
replacement of their valves.

Overview
 Aortic Stenosis
 Mitral Stenosis
 Aortic Regurgitation
 Acute and Chronic
 Mitral Regurgitation
 Acute and Chronic

Prevalence
 In industrialized countries, the prevalence of valvular heart disease is
estimated at 2.5%. Rheumatic heart disease still represents 22% of valvular
heart disease in Europe.
 The prevalence of secondary mitral regurgitation cannot be assessed reliably
but it seems to be a frequent disease.
 The incidence of infective endocarditis is approximately 30 cases per million
individiuals per year.. In developing countries, rheumatic heart disease remains
the leading cause of valvular heart disease. Its prevalence is high, between 20
and 30 cases per 1000 subjects when using systematic echocardiographic
screening.
 In conclusion, the temporal and geographical heterogeneity illustrates the
effect of socioeconomic status and changes in life expectancy on the frequency
and presentation of valvular heart disease..
..
Reference: 2014 Sep;30(9):962-70. doi: 10.1016/j.cjca.2014.03.022

MITRAL STENOSIS (MS)
Etiology
 Most commonly rheumatic, although history of
acute rheumatic fever is now uncommon.
 Congenital MS is an uncommon cause, observed
primarily in infants.
Reference: Harrisons manual of medicine / 17th edition/ page 678

Pathophysiology
 When the normal valve orifice area of 5 cm2 is reduced to approximately 1
cm2, severe mitral stenosis is present.
 In order that sufficient cardiac output will be maintained, the left atrial
pressure increases and left atrial hypertrophy and dilatation occur.
Consequently, pulmonary venous, pulmonary arterial and right heart
pressures also increase.
 The increase in pulmonary capillary pressure is followed by the development
of pulmonary oedema. This is partially prevented by alveolar and capillary
thickening and pulmonary arterial vasoconstriction (reactive pulmonary
hypertension).
 Pulmonary hypertension leads to right ventricular hypertrophy, dilatation and
failure. Right ventricular dilatation results in tricuspid regurgitation.
 Mitral stenosis is frequently associated with complications.
Reference: Kumar & Clark Clinical medicine/7th edition/page 760

Clinical features
Symptoms Sign
 Breathlessness (pulmonary congestion).
 Fatigue (low cardiac output).
 Oedema, ascites (right heart failure).
 Palpitation (atrial fibrillation).
 Haemoptysis (pulmonary congestion, pulmonary
embolism).
 Cough (pulmonary congestion).
 Chest pain (pulmonary hypertension).
 Thromboembolic complications (e.g. stroke,
ischaemic limb).
 Atrial fibrillation.
 Mitral facies.
 Auscultation:
 Loud first heart sound , opening snap
Mid-diastolic murmur
 Crepitations , pulmonary oedema ,
effusions (raised pulmonary capillary
pressure)
 RV heave, loud P2 (pulmonary
hypertension)
Reference: Davidsons principle of medicine/ 22nd edition/page 617

Cont…

Investigations
 ECG  Right ventricular hypertrophy: tall R waves in V1–V3.
 P mitrale or atrial fibrillation.
 Chest X-ray  Enlarged LA and appendage.
 Signs of pulmonary venous congestion.
 Echocardiography  Thickened immobile cusps.
 Reduced valve area.
 Enlarged LA.
 Reduced rate of diastolic filling of LV.

Cont.
 Doppler  Pressure gradient across mitral valve.
 Pulmonary artery pressure.
 Left ventricular function.
 Cardiac catheterisation  Coronary artery disease.
 Pulmonary artery pressure.
 Mitral stenosis and Regurgitation.

Treatment
Medical management
 This consists of anticoagulation to reduce the risk of
systemic embolism, ventricular rate control (digoxin,β-
blockers or rate-limiting calcium antagonists) in atrial
fibrillation.
 Diuretic therapy to control pulmonary congestion.
 Antibiotic prophylaxis against infective endocarditis is no
longer routinely recommended.

Surgical treatment
 Mitral valve replacement
 Mitral balloon valvuloplasty.
 Criteria for mitral valvuloplasty
 Significant symptoms.
 Isolated mitral stenosis.
 No (or trivial) mitral regurgitation.
 Mobile, non-calcified valve/subvalve apparatus on echo.
 LA free of thrombus.

Reference: Harrisons principles of medicine / 19th edition/ page 1541
Cont.

MITRAL REGURGITATION (MR)
Etiology
 Rheumatic heart disease in ~33% of patients with chronic MR.
 Other causes:
 Mitral valve prolapse.
 Ischemic heart disease with papillary muscle dysfunction.
 LV dilatation of any cause.
 Mitral annular calcification.
 Hypertrophic cardiomyopathy.
 Infective endocarditis.
 Congenital.

Pathophysiology
 Regurgitation into the left atrium produces left atrial dilatation but
little increase in left atrial pressure if the regurgitation is long-
standing, as the regurgitant flow is accommodated by the large left
atrium.
 With acute mitral regurgitation the normal compliance of the left
atrium does not allow much dilatation and the left atrial pressure rises.
Thus, in acute mitral regurgitation the left atrial ‘v’ wave is greatly
increased and pulmonary venous pressure rises to produce pulmonary
oedema.
 Since a proportion of the stroke volume is regurgitated, the stroke
volume increases to maintain the forward cardiac output and the left
ventricle therefore enlarges.

Clinical features
Symptoms Signs
 Dyspnoea (pulmonary venous
congestion).
 Fatigue (low cardiac output).
 Palpitation (atrial fibrillation,
increased stroke volume).
 Oedema, ascites (right heart failure).
 Atrial fibrillation/flutter.
 Cardiomegaly: displaced hyperdynamic apex beat
 Apical pansystolic murmur ― thrill
 Soft S1, apical S3.
 Signs of pulmonary venous congestion .
 crepitations.
 pulmonary oedema & effusions
 Signs of pulmonary hypertension and right heart
failure.

Investigations
 ECG  Left atrial hypertrophy (if not
in atrial fibrillation).
 Left ventricular hypertrophy.
 Chest X-
ray
 Enlarged LA.
 Enlarged LV.
 Pulmonary venous congestion
 Pulmonary oedema (if acute).
 Doppler  Detects and quantifies
regurgitation..
 Echo  Dilated LA, LV.
 Dynamic LV (unless myocardial
dysfunction predominates).
 Structural abnormalities of mitral
valve (e.g. prolapse).
 Cardiac
catheterisation
 Dilated LA, dilated LV, mitral
regurgitation.
 Pulmonary hypertension.
 Coexisting coronary artery disease.

Cont..

Treatment
 Medical management
 Diuretics.
 Vasodilators, e.g. ACE inhibitors.
 Digoxin if atrial fibrillation is present.
 Anticoagulants if atrial fibrillation is present.

Surgical treatment
 Any evidence of progressive cardiac enlargement generally
warrants early surgical intervention by either mitral valve
repair or replacement.
 Advantages of surgical intervention are diminished in more
advanced disease.

Reference:Harrisons principles of medicine / 19th edition/ page 1545
Cont..

AORTIC STENOSIS (AS)
Etiology
 Most common cause in adults is age-related degenerative
calcific AS and is usually mild.
 Other causes are congenital (bicuspid valves) or rheumatic
(almost always associated with rheumatic mitral valve
disease).

Pathophysiology
 Obstructed left ventricular emptying leads to increased left ventricular
pressure and compensatory left ventricular hypertrophy.In turn, this results in
relative ischaemia of the left ventricular myocardium, and consequent angina,
arrhythmias and left ventricular failure.
 The obstruction to left ventricular emptying is relatively more severe on
exercise.
 Normally, exercise causes a many-fold increase in cardiac output, but when
there is severe narrowing of the aortic valve orifice the cardiac output can
hardly increase.
 Thus, the blood pressure falls, coronary ischaemia worsens, the myocardium
fails and cardiac arrhythmias develop.
 Left ventricular systolic function is typically preserved in patients with aortic
stenosis (cf. aortic regurgitation).

Clinical features
 Signs  Ejection systolic murmur
 Slow-rising carotid pulse
 Thrusting apex beat (LV pressure overload)
 Narrow pulse pressure
 Signs of pulmonary venous congestion (e.g.crepitations)
 Symptoms  Mild or moderate stenosis usually asymptomatic
 Exertional dyspnoea
 Angina
 Exertional syncope
 Sudden death
 Episodes of acute pulmonary oedema

Cont..

Investigations
ECG • Left ventricular hypertrophy (usually).
• Left bundle branch block.
Chest X-ray May be normal; sometimes enlarged LV and dilated ascending aorta on PA
view, calcified valve on lateral view.
Echocardiography • Calcified valve with restricted opening, hypertrophied LV .
Doppler Measurement of severity of stenosis.
• Detection of associated aortic regurgitation.
Cardiac
catheterisation
Mainly to identify associated coronary artery disease.
• May be used to measure gradient between LV and aorta.

Treatment
 Avoid strenuous activity in severe AS, even in asymptomatic phase.
 Treat heart failure in standard fashion but use vasodilators with
caution in patients with advanced disease.
 Valve replacement is indicated in adults with symptoms resulting from
AS and hemodynamic evidence of severe obstruction. Operation
should be carried out before frank failure has developed.

Cont..

Aortic regurgitation
Etiology
 Rheumatic etiology is common, especially if rheumatic
mitral disease present.
 May also be due to,
 infective endocarditis
 Syphilis
 aortic dissection or aortic dilatation due to cystic medial necrosis.
 Three-fourths of patients are males.

Pathophysiology
 Aortic regurgitation is reflux of blood from the aorta through the aortic
valve into the left ventricle during diastole.
 If net cardiac output is to be maintained, the total volume of blood
pumped into the aorta must increase, and consequently the left
ventricular size must enlarge. Because of the aortic run off during
diastole, diastolic blood pressure falls and coronary perfusion is
decreased.
 In addition, the larger left ventricular size is mechanically less
efficient so that the demand for oxygen is greater and cardiac
ischaemia develops.

Clinical features
Symptoms
Mild to moderate aortic regurgitation
• Often asymptomatic.
• Awareness of heart beat, ‘palpitations’.
Severe aortic regurgitation
• Breathlessness.
• Angina.
Signs
Pulses
• Large-volume or ‘collapsing’ pulse.
• Low diastolic and increased pulse pressure.
• Bounding peripheral pulses.
• Capillary pulsation in nail beds: Quincke’s sign.
• Femoral bruit (‘pistol shot’): Duroziez’s sign.
• Head nodding with pulse: de Musset’s sign.
Murmurs.
• Early diastolic murmur.
• Systolic murmur (increased stroke volume).
• Austin Flint murmur (soft mid-diastolic).
Other signs
• Displaced, heaving apex beat (volume overload).
• Pre-systolic impulse.
• Fourth heart sound.
• Crepitations (pulmonary venous congestion).

Investigations
ECG  Initially normal, later left ventricular hypertrophy .
 T-wave inversion
Chest X-ray  Cardiac dilatation, maybe aortic dilatation
 Features of left heart failure
Echocardiography  Dilated LV
 Hyperdynamic LV
 Doppler detects reflux
 Fluttering anterior mitral
 leaflet
Cardiac
catheterisation
 Dilated LV
 Aortic regurgitation
 Dilated aortic root

Treatment
 Underlying cause of aortic regurgitation (e.g. syphilitic aortitis or
infective endocarditis) may require specific treatment.
 The treatment of aortic regurgitation usually requires aortic valve
replacement but the timing of surgery is critical.Because symptoms do not
develop until the myocardium fails.
 Both mechanical prostheses and tissue valves are used.Tissue valves are
preferred in the elderly and when anticoagulants must be avoided, but are
contraindicated in children and young adults.
 Antibiotic prophylaxis against infective endocarditis is sometimes
necessary if a prosthetic valve replacement has been performed.

Cont..

Valvular heart disease final

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Destacado

Destacado (20)

Similar a Valvular heart disease final

Similar a Valvular heart disease final (20)

Último

Último (20)

Valvular heart disease final