The percentage of valves coming to surgery which arerheumatic is now below 50% in many series. Regurgitationcan result from:
Dilatation of the valve ring
Damage, retraction or perforation of the valve cusps
Damage to the subvalvular apparatus (chordae, papillarymuscle, or the ventricular muscle to which thepapillary muscles attach).Non-rheumatic causes of mitral regurgitation are:
Heart failure. Dilatation of the left ventricle will produce’functional mitral regurgitation’ owing to dilatation of the valve ring and a shift in the attachments of the chordae tendinae. This may disappear as the ventricle shrinks with treatment, but may become a permanent feature
. Myocardial infarction. Papillary muscle dysfunction canarise as a result of inferior myocardial infarction, producinga characteristic type of mitral regurgitation whichis usually not severe. In contrast, infarction complicatedby rupture of the papillary muscle produces catastrophicregurgitation, and is usually fatal unless repairedurgently.
Degenerative changes. These are often seen in mitral valves at surgery. The pathogenesis is not fully understood,as degenerative changes can occur in rheumaticvalves or others known to be mildly incompetent for along period.
Rupture of the smaller chordae tendinae can occur slowlyand progressively, causing increasing mitral regurgitation.Acute chordal rupture of a major trunk causes suddensevere mitral regurgitation.Other causes In mitral valve prolapse there is prolapse of a mitral valve cusp late in systole, often from a degree of ‘redundancy’ inthe length of the chordae tendinae. It may be a feature ofMarfan’s syndrome and osteogenesis imperfecta. Elderly patients often develop a minor degree of mitral regurgitationfrom calcification of the valve ring. This produces acharacteristic wheezy systolic murmur. Endocarditis may make even a trivial degree of regurgitation more severe,and acute endocarditis can rapidly destroy a normal valve.There is a degree of mitral regurgitation in most cases of hypertrophic obstructive cardiomyopathy. Congenital forms of mitral regurgitation include cleftcusps in AV canal defects and endocardial cushion defectsin association with ostium primum atrial septal defects. Sharp (stabbing) and blunt (steering-wheel injury)trauma to the precordium, acromegaly and Libman-Sacksendocarditis in systemic lupus erythematosus (SLE) are other rare causes.
Symptoms and pathophysiology
Chronic The symptoms of chronic mitral regurgitation are essentially the same as those of mitral stenosis, but severe pulmonary hypertension is less common with pure mitral regurgitation. The slowly progressive regurgitation is accommodatedby a gradual increase in size of the left ventricle,which ejects the blood into a slowly enlarging and compliant left atrium and pulmonary venous vasculature. Up to 80% of the left ventricular stroke volume may be regurgitant in severe cases, and the left ventricular stroke volume can exceed 250 mL. Symptoms in chronic mitralregurgitation usually develop when the left ventriclebegins to suffer deterioration and end-diastolic pressurerises. Usually, systolic function and ejection fraction are well maintained, because the left ventricle is ejecting largely into a low impedance outflow. The symptoms of leftheart failure, AF and pulmonary hypertension are the same as for mitral stenosis.
In acute mitral regurgitation, e.g. complicating acute MI or due to rupture of chordae tendinae, a small left ventricleis regurgitating into a small uncompliant left atrium.This produces a very high pressure pulse or v wave in the left atrium, which may reach 60 mmHg. Left atrial pressure rapidly exceeds that needed to produce pulmonary oedema.The low forward output may precipitate tachycardia,which makes the regurgitation worse. Acute mitral regurgitation thus usually presents with severe pulmonary oedema.
Uncomplicated pure mitral regurgitation, if trivial, hasonly auscultatory signs. However, if the regurgitationis more severe, the left ventricular volume load becomes clinically evident by a hyperactive left ventricle with displacement of the cardiac apex down and laterally. Enlargement of the left atrium in systole may be felt as aparasternal heave. In severe regurgitation the pulse may become small and rather jerky from a shortened ejectiontime. Severe regurgitation is evident on auscultation by the presence of a third heart sound and short mid-diastolic murmur, produced by the greatly enhanced forward flow through the mitral valve during diastole.The pansystolic murmur of rheumatic mitral regurgitation,or other types of regurgitation with a central jet, isbest heard at the apex of the heart and may be louder with the patient tipped to the left. Other types of mitral regurgitation- including the late systolic murmur of the floppy valve syndrome – may be best heard at the left sternaledge, and are often not pansystolic in character.
Differential diagnosis from trivial aortic stenosis and ventricularseptal defect can therefore be difficult, and requires noninvasive tests such as echocardiography and Doppler ultrasound,or even cardiac catheterization.
Trivial regurgitation is very well tolerated and requiresonly endocarditis prophylaxis. Moderately severe mitral regurgitation can be well tolerated for years, but the patient may slowly come to accept a diminishing exercise tolerance. The timing of valve replacement can be difficult.Worsening left ventricular function is an indication, as the procedure carries more risk when left ventricular functionis poor. Severe regurgitation and acute regurgitation merit early valve replacement. Repair of regurgitant valves isincreasingly advocated in anatomically suitable cases.