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

https://www.ncbi.nlm.nih.gov/pubmed/24986049

https://www.ncbi.nlm.nih.gov/pubmed/24986049

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…


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. 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.


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 managementDiuretics.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 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).


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..


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.


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 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).


Cont..


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


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..

Healthcare

Valvular heart disease final