VALVULAR HEART DISEASE Dr. Nurul Anwer Shetu.MBBS
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 valve disease
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 featuresSymptoms 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…
Reference: Kumar & Clark Clinical medicine/7th edition/page 761
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.
Reference: Davidsons principle of medicine/ 22nd edition/page 617
Cont.
Reference: Davidsons principle of medicine/ 22nd edition/page 617
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.
Reference: Davidsons principle of medicine/ 22nd edition/page 618
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: Davidsons principle of medicine/ 22nd edition/page 618
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. Reference: Harrisons manual of medicine / 17th edition/ page 678
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.Reference: Kumar & Clark Clinical medicine/7th edition/page 763
Clinical featuresSymptoms 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.
Reference: Davidsons principle of medicine/ 22nd edition/page 618
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.
Reference: Davidsons principle of medicine/ 22nd edition/page 618
Cont..
Reference: Kumar & Clark Clinical medicine/7th edition/page 761
Treatment
Medical managementDiuretics.Vasodilators, e.g. ACE inhibitors.Digoxin if atrial fibrillation is present.Anticoagulants if atrial fibrillation is present.
Reference: Davidsons principle of medicine/ 22nd edition/page 620
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: Kumar & Clark Clinical medicine/7th edition/page 764
Reference:Harrisons principles of medicine / 19th edition/ page 1545
Cont..
Aortic valve disease
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).
Reference: Harrisons manual of medicine / 17th edition/ page 680
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).
Reference: Kumar & Clark Clinical medicine/7th edition/page 763
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
Reference: Davidsons principle of medicine/ 22nd edition/page 620
Cont..
Reference: Kumar & Clark Clinical medicine/7th edition/page 765
InvestigationsECG • 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.
Reference: Davidsons principle of medicine/ 22nd edition/page 621
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.
Reference: Harrisons manual of medicine / 17th edition/ page 681
Reference:Harrisons principles of medicine / 19th edition/ page 1533
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.
Reference: Harrisons manual of medicine / 17th edition/ page 680
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.
Reference: Kumar & Clark Clinical medicine/7th edition/page 767
Clinical featuresSymptoms
Mild to moderate aortic regurgitation• Often asymptomatic.• Awareness of heart beat, ‘palpitations’.Severe aortic regurgitation• Breathlessness.• Angina.
SignsPulses• 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).
Reference: Davidsons principle of medicine/ 22nd edition/page 623
Cont..
Reference: Kumar & Clark Clinical medicine/7th edition/page 765
InvestigationsECG 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
Reference: Davidsons principle of medicine/ 22nd edition/page 624
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.
Reference: Kumar & Clark Clinical medicine/7th edition/page 767
Reference:Harrisons principles of medicine / 19th edition/ page 1537
Cont..