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PROGRESSION OF MVP

 

 

This is a topic that comes up many times in email lists.  I think most people are worried that MVP is going to progress to the point where surgery is required, or worse, lead to death.  There have been some studies done on this question, so I will try to shed some light on this issue.

     MVP is believed to deteriorate slowly, in the absence of infective endocarditis. This is why protection by way of antibiotic prophylactic is so important.  The infection can thus be prevented, as well as further valvular deterioration which, can lead to immediate or future cardiac enlargement and failure.

De Robert Jeresaty outlined five stages in the progression of prolapse:

  • silent prolapse

  • MSC without a murmur (mid-systolic click)

  • MSC and LSM         (late-systolic murmur)

  • PSM    (the result of infective endocarditis, gradual deterioration and chordal rupture)(pan-systolic murmur)

  • severe regurgitation, floppy valve and heart failure.

 

 

A long term study done in Netherlands, Department of Cardiology, University of Amsterdam, of 300 patients with Mitral valve prolapse.  There were 136 male and 164 females ranging in age 10 to 87, mean age 42.2. The follow up was an average of 6.1 years (range 6 months to 20 years).

  •     2 patients died of non-cardiac causes

  • 153 patients stayed clinically stable

  •   27 patients got supraventricular tachycardia, readily controlled with medication.

  •   20 patients got mitral regurgitation but remained asymptomatic.

100 patients developed serious complications.

  •     3 patents died suddenly, most likely due to ventricular fibrillation

  •   56 patients developed ventricular tachycardia, all managed successfully with medication

  •   18 patients developed infective endocarditis, of which 4 died during treatment and 6 needed replacement surgery.

  •    8 patients suffer form severe mitral regurgitation that will require surgery in the near future.

28 patients went through mitral valve operations due to progressive regurgitation.

 

     A study done by AJ Kolibash, Department of Internal Medicine, Ohio State University Hospitals, states that MVP is a very common entity, frequently associated with mild mitral regurgitation.  This usually manifests in the third or fourth decade of ones life.  Severe regurgitation is much less frequently seen and usually occurs in patients over aged 50.  There is very little information available as to the progression from mild to severe regurgitation. 

    This study include 86 patients, mean age of 60 years with cardiac symptoms and severe  mitral regurgitation.  Mitral valve replacement was performed on 75 patients.  80 patients had a pre-existing heart murmur first detected at  average age of 34. Patients were asymptomatic for an average of 25 years at which time clinical symptoms first appeared.  After symptoms appeared, mitral valve surgery was necessary in most patients within one year.  This rapid deterioration could partially be attributed to ruptured chordae in 39 (51%) or atrial fibrillation in 48 (56%). Additionally, 13 patients had  a history of documented infective endocarditis.  The study concludes that mild mitral regurgitation due to MVP and myxomatous mitral valves is a progressive disease in some patients with MVP.

 

     Another study done, was a 40 year follow up of prolapsing mitral valve by Chapman DW, Department of Cardiology, Baylor College of Medicine, Houston Texas.  The end result of the study states that about one quarter of prolapsing mitral valve cases progress, with increasing mitral insufficiency and increasing enlargement of the left atrium and left ventricle, which at times leads to congestive heart failure.  Coronary artery disease may occur with the severity commensurate with the patient's age group.  About three quarter of patients with prolapsing mitral valve syndrome lead normal lives.

 

     A heart murmur was detected in a man while he was in high school and Mitral valve prolapse detected at 23 years of age. No symptoms were present till aged 44 when he noted palpitation on exercise.  Upon testing, they noted severe mitral regurgitation and performed mitral valve replacement surgery.  At surgery they noted billowing of both leaflets with torn chordae, and  a large mitral valve orifice. Relatively slow progression of the billowing mitral leaflet syndrome did not cause apparent symptoms of heart failure in this patient.

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