Abnormalities of the valve leaflets, the annulus, the chordae tendineae or papillary muscles, or the left ventricle
Causes of mitral regurgitation
Degenerative (myxomatous) disease
Ischemic heart disease
Rheumatic heart disease
Infectious endocarditis
Other diseases associated with mitral regurgitation
Dilated and hypertrophic cardiomyopathy
Rheumatic autoimmune diseases, e.g. systemic lupus erythematosus
Collagen diseases, e.g. Marfan's and Ehlers–Danlos syndromes
Drugs including centrally acting appetite suppressants (fenfluramine) and dopamine agonists (cabergoline)
Pathophysiology of mitral regurgitation
1. Regurgitation into the left atrium produces left atrial dilatation
2. In acute mitral regurgitation, the normal compliance of the left atrium does not allow much dilatation and the left atrial pressure rises, producing pulmonary oedema
3. 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
Carpentier classification
Uses mitral leaflet motion to divide patients into different classes according to the mechanism of regurgitation, which can be useful when considering surgical intervention
Mitral regurgitation
Can be present for many years
Cardiac dimensions greatly increased before any symptoms occur
Increased stroke volume is sensed as a palpitation
Dyspnoea and orthopnoea develop due to pulmonary venous hypertension
Fatigue and lethargy develop due to reduced cardiac output
In late stages, symptoms of right heart failure occur and lead to congestive cardiac failure
Cardiac cachexia may develop
Thromboembolism is less common than in mitral stenosis
Subacute infective endocarditis is much more common
Physical signs of uncomplicated mitral regurgitation
Laterally displaced (forceful) diffuse apex beat and a systolic thrill (if severe)
Soft first heart sound, owing to the incomplete apposition of the valve cusps and their partial closure by the time ventricular systole begins
Pansystolic murmur, owing to the occurrence of regurgitation throughout the whole of systole, being loudest at the apex but radiating widely over the precordium and into the axilla
With a floppy mitral valve there may be a mid-systolic click, which is produced by the sudden prolapse of the valve and the tensing of the chordae tendineae that occurs during systole. This may be followed by a late systolic murmur owing to some regurgitation
Prominent third heart sound, owing to the sudden rush of blood back into the dilated left ventricle in early diastole (sometimes a short mid-diastolic flow murmur may follow the third heart sound)
The signs related to atrial fibrillation, pulmonary hypertension, and left and right heart failure develop later in the disease
The onset of atrial fibrillation has a much less dramatic effect on symptoms than in mitral stenosis
Chest X-ray
Shows left atrial and left ventricular enlargement
Increase in the CTR
Valve calcification is seen
Electrocardiogram
1. Shows left atrial delay (bifid P waves)
2. Shows left ventricular hypertrophy (tall R waves in left lateral leads, deep S waves in right-sided precordial leads)
3. SV1 plus RV5 or RV6 >35 mm indicates left ventricular hypertrophy
4. Atrial fibrillation may be present
Left ventricular hypertrophy occurs in about 50% of patients with mitral regurgitation
Echocardiogram
A diagnostic test that uses ultrasound waves to create an image of the heart
Echocardiogram findings
Dilated left atrium and left ventricle
Specific features of chordal or papillary muscle rupture
Assessing severity of regurgitation using echocardiogram
1. Colour Doppler to look at jet area and size of vena contracta
2. Calculating regurgitant fraction, volume or orifice area
Ventricular function dynamics
Useful information regarding severity of condition can be obtained indirectly by observing
Transoesophageal echocardiography
Can be helpful to identify structural valve abnormalities before surgery and intraoperative TOE can aid assessment of the efficacy of valve repair
Cardiac catheterization
A diagnostic test that demonstrates a prominent left atrial systolic pressure wave and shows regurgitation of contrast injected into the left ventricle into an enlarged left atrium during systole
Treatment for mild mitral regurgitation in the absence of symptoms
1. Managed conservatively by following the patient with serial echocardiograms
2. Prophylaxis against endocarditis is discussed in Chapter 4 (see p. 87)
Evidence of progressive cardiac enlargement
Generally warrants early surgical intervention
Surgical intervention
Either mitral valve repair or replacement
Indications for surgical intervention
Symptomatic severe mitral regurgitation, left ventricular ejection fraction >30% and end-diastolic dimension of under 55 mm
Asymptomatic patients with left ventricular dysfunction (end-systolic dimension >45 mm and/or ejection fraction of under 60%)
Asymptomatic severe mitral regurgitation with preserved left ventricular function and atrial fibrillation and/or pulmonary hypertension
The advantages of surgical intervention are diminished in more advanced disease
Sudden torrential mitral regurgitation, as seen with chordal or papillary muscle rupture or infective endocarditis, necessitates emergency mitral valve replacement
Management for patients not appropriate for surgical intervention, or in whom surgery will be performed at a later date
1. Treatment with ACE inhibitors
2. Diuretics
3. Possibly anticoagulants
Percutaneous mitral valve repair (MitraClip)
Compared to cardiac surgery in the EVEREST II trial and appears effective in the short-term at reducing the severity of mitral regurgitation and providing symptomatic relief
Percutaneous mitral valve repair (MitraClip)
Appropriate in patients unsuitable for cardiac surgery
Mitral regurgitation (MR)
Abnormality or disease process that affects any one or more of the five functional components of the mitral valve apparatus (leaflets, annulus, chordae tendineae, papillary muscles, and subjacent myocardium)
Causes of acute MR
Acute myocardial infarction with papillary muscle rupture
Blunt chest wall trauma
Infective endocarditis
With acute MI, the posteromedial papillary muscle is involved much more frequently than the anterolateral papillary muscle because of its singular blood supply
Transient, acute MR can occur during periods of active ischemia and bouts of angina pectoris
Rupture of chordae tendineae can result in "acute on chronic MR" in patients with myxomatous degeneration of the valve apparatus
Causes of chronic MR
Rheumatic disease
Mitral valve prolapse
Extensive mitral annular calcification
Congenital valve defects
Hypertrophic obstructive cardiomyopathy
Dilated cardiomyopathy
Rheumatic heart disease is the cause of chronic MR in only about one-third of cases and occurs more frequently in males
Rheumatic process
Produces rigidity, deformity, and retraction of the valve cusps and commissural fusion, as well as shortening, contraction, and fusion of the chordae tendineae
MR associated with mitral valve prolapse and hypertrophic obstructive cardiomyopathy
Usually dynamic in nature
MR in hypertrophic obstructive cardiomyopathy
Occurs as a consequence of anterior papillary muscle displacement and systolic anterior motion of the anterior mitral valve leaflet into the narrowed LV outflow tract
Annular calcification is especially prevalent among patients with advanced renal disease and is commonly observed in elderly women with hypertension and diabetes
MR may occur as a congenital anomaly, most commonly as a defect of the endocardial cushions (atrioventricular cushion defects)
A cleft anterior mitral valve leaflet accompanies primum atrial septal defect