Mitral regurgitation

Due to the imperfect closure of the valve leaflets (cusps), part of the blood, instead of continuing its path towards the aorta, flows backwards, “regurgitating” inside the atrium.
The more the valve struggles to close, the more serious the problem becomes.

Forms of mitral valve regurgitation

Mitral regurgitation can be of organic or primary origin or of functional or secondary origin: the acute onset can be fatal for the patient

Organic mitral regurgitation

The morphological alteration of the heart valve is caused by diseases that damage its original structure: among the organic/degenerative forms of the mitral valve we can include: myxomatous degeneration (the intermediate layer of the connective tissue of the valve leaflets suffers from a modification of its extracellular matrix); fibroelastic deficiency (loss of collagenous and elastic tissue); calcifications of the mitral annulus or ring. There are then forms caused by rheumatic or bacterial endocarditis and by congenital defects - present since birth - like cleft (fissuring of the anterior valve leaflet); double orifice; parachute mitral valve (the cusps of the mitral valve are lengthened and connected to just one subvalvular papillary muscle). Finally, the ischaemic causes like fibrosis or rupture of the papillary muscle following myocardial infarction should be considered.
 
Calcification of the mitral ring occurs rather frequently in the elderly population, female first of all. The strong evidence in elderly subjects leads us to believe that this is due to the functional stress that the valve undergoes over the years. Arterial hypertension, chronic kidney failure and diabetes accelerate the process of deposition of calcium salts on the mitral ring.

Functional mitral regurgitation

In the so-called “functional or secondary” form, the mitral valve is described as normal from the anatomical viewpoint and therefore without organic lesions, though no longer suitable to perform its “job” because of the modification undergone by the geometry of the left ventricle to which it is closely connected. In reality this concept does not correspond to the truth since the leaflets (i.e. the valve cusps) are not completely whole either. In light of this it is possible to identify three main causes of functional mitral regurgitation: dilation of the mitral annulus (ring); lengthening of the chordae tendineae; dilation/malfunction of the left ventricle. 

Symptoms & Diagnosis

Symptoms

Patients with functional mitral regurgitation do not have problems until the left ventricle fails: the disease may remain silent for decades. 

Subjects with very mild or moderate regurgitation, on the other hand, show no signs of the disease for their entire life, nor does it produce any consequences. 

When, on the contrary, the mitral regurgitation is of the organic type, the onset is quite quick and sudden and the repercussions on the patient’s health very serious.

In both forms of regurgitation it is essential to not underestimate the symptoms, even when minimal. The first recommendation remains that of turning to High Specialty Cardiology Centers capable of formulating precise diagnoses on the basis of the clinical evidence and in relation to the results of the instrumental tests performed: if the disease is not dealt with properly, there is the risk of developing significant cardiorespiratory failure.

It is necessary to see your doctor when the following symptoms appear and are persistent:

  • Shortness of breath (dyspnoea), on exertion or at rest
  • Feeling of tiredness
  • Nighttime cough
  • Palpitations (fast heart beats)
  • Swollen feet and ankles
  • Chest pain

Diagnosis

A diagnosis of mitral regurgitation is reached through examination of the clinical manifestations as well as some instrumental investigations aimed at characterizing the valve defect.

For example:

  • Chest x-ray
  • Echocardiograph
  • Electrocardiogram (ECG)
  • Doppler echocardiogram
  • Doppler echocardiogram with color flow
  • Cardiac catheterization (Ventriculography, Angiography, Coronary angiography)
  • Thoracic Magnetic Resonance Imaging
  • Chest CT scan / CT coronary angiography
An electrophysiological study of the heart may also be necessary, i.e. analysis of the heart’s electrical system to identify possible arrhythmias (alterations in heart rate) linked to the disease.

Treatment

How is mitral regurgitation treated?

Patients who do not have problems - and who have been diagnosed with mild mitral valve prolapse - generally do not require any type of treatment. In the event of concomitant alteration in heart rate, confirmed by an electrocardiogram, antiarrhythmic drugs can be administered. In cases in which more severe mitral regurgitation has been identified, associated with left ventricular failure, the therapeutic indication is for surgery.
Surgery is also recommended in situations in which, in the absence of an actual “succession” of symptoms, the left ventricle is damaged by the disease in any case. The options available to the heart surgeon - possible even with minimally invasive and ultra-minimally invasive methods - are repair of the original valve (valvuloplasty) or replacement of the defective mitral valve, implanting an artificial valve in its place. 

Mitral valve repair has various “plusses”:

  • removal of the prolapsed part of the posterior leaflet of the valve and subsequent closure of the defect
  • reconstruction of the cusps with insertion of a prosthetic ring (annuloplasty) to provide additional support to the valve
  • restoration of the normal dimensions of the mitral annulus - dilated by now - with implantation of an artificial prosthesis (Cardioband)
  • elimination of the “regurgitation” (backward flow of blood) by shortening, lengthening or replacing the chordae tendineae that hold the mitral valve in the correct position (Neochord)
  • suturing of the leaflets to prevent their excessive movement and thus their physiological continence
  • creation of a double valve orifice using a metal clip (MitraClip)
  • stitching of the subvalvular papillary muscle “ruptured” after acute myocardial infarction.
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