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Posts Tagged ‘mitral valve prolapse’

What is the mechanism of chest pain in mitral valve prolapse syndrome ?

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , on December 17, 2011| 1 Comment »

Mechanism of chest pain in mitral valve prolapse  include

  1. Mitral valve  has pain fibers , the myxomatous degeneration  of the valve tissue generates pain .* (Not much evidence )
  2. Mitral valve stress, strain ,  stretch and bending.
  3. Mechanical stretch  of papillary muscle or LV free wall (dimple ?  ) as the mitral valve prolapse into LA.
  4. It is a central pain perception disorder .Panicky and anxiety reactions included
  5. It is not chest pain  at all it is simply a feeling of palpitation .
  6. Associated ischemic  heart disease

The commonest mechanisms  are   response  4 and 5 .

The evidence  lies in the fact ,  many of  these people  begin to complain of chest pain only after being aware this problem. MVPS is  often a  fancy entity created by cardiologists  which  unfortunately has  labeled  many of the normal  general population as cardiac patients. Barlow who described this entity  decades ago  would have never imagined  it  would be  so popular and subjected to mis-use . We have proposed a solution for this . The diagnosis of MVPS shall not be mentioned unless it is obvious  and fulfill a strict criteria . The commonest error we make is  an elongated , redundant , hyper mobile mitral leaflet   at   as  MVPS.

It is expected  ,  true MVPS must have all of the following  three criteria

  • Thickened leaflets
  • Clear prolapse of  at least one leaflet in long axis view beyond the plane  of  mitral annulus
  • At least some degree of mitral  regurgitation must be present

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Mechanisms of rheumatic mitral regurgitation

Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics, tagged , , , , , , on November 18, 2011| 1 Comment »

Mitral regurgitation is  one of  the most common lesion of rheumatic heart disease .Mechanism of MR in acute rheumatic fever is different from chronic rheumatic heart disease.

Acute Rheumatic fever

The following mechanisms contribute to MR of acute rheumatic fever

  1. Edema of leaflets (Carey Coombs murmur )
  2. Valvulitis
  3. Small verrucous  vegetations (See Image )
  4. Acute LV dilatation in fulminant cardiac failure.

* Note  : Acute rheumatic fever in its first episode can never  cause stenosis  however fulminant the fever may be  .There is no acute mitral stenosis .But ,  during recurrence and reactivation some amount of stenotic process may occur.  Still ,  recurrence and reactivation are more often related to significant MR rather than MS. ( Isolated mitral stenotic lesions  rarely  give h/o recurrent rheumatic fever )

Chronic rheumatic  heart disease

As the mitral valve gets progressively damaged  any combination of MS or MR occur .The following mechanism are involved in  the genesis of MR. (Pathology of Mitral stenosis is not discussed here)

  1. Chordal shortening, tethering , pulling , prevent proper co-optation
  2. Chordal lengthening
  3. Chordal disruption (Minor > Major )
  4. Prolapse of either AML or PML (Not both ,unlike myxamatous MVPS)
  5. Infective endocardits  of  leaflet
  6. Perforations of  leaflet
  7. Annular  dilatation
  8. Fibrosis of posteromedial/Antero-lateral   pap muscle(Rare )
  9. Left atrial pathology

* The direction and the  width of MR jet is  related to the mechanism of MR.

If there is chordal shortening due to fibrosis  of mitral valve  co -optation plane is altered . The degree of chordal shortening , pap muscle fibrosis (rare)  symmetry of chordal involvement determine the MR.

Rheumatic mitral valve prolapse

  • This could be  more common than we realise.
  • It can be true or pseudo.
  • True prolapse occur due to chordal weakening or lengthening .
  • In chordal disruption the leaflet tips usually become flail

Since rheumatic process fixes the PML first , the AML   appear to overshoot the plane of PML and   appear as prolapse.(Pseudo )

The sail like AML commonly  directs the jet posteriorly and laterally .(Murmur conducted to axilla and back )

It is rare for PML to prolapse in RHD , if  it does occur ,  it directs the jet anteriorly (murmur conducted to aortic area mimic AS !)

It is rare to see a  perfect  central jet in RHD  . presence of  Central jet is a good sign to consider mitral valve repair.

Myocardial involvement in RHD.

Even though rheumatic fever is a classical  example for  pan-carditis , it is surprising   to note (Of course fortunately !)   how  myocardium escapes in the  chronic process of RHD.

Is it really true  ,  myocardium do not get involved in chronic RHD ?

Clinical cardiologists rarely discuss this issue. Pathogists indeed have documented significant lesions within myocardium  . Involvement of left atrial myocardium and  rarely  ventricular myocardium in the sub mitral  zone  can influence the  degree of  MR

* Even in acute rheumatic fever with fulminant carditis , myocardial involvement is  disputed by many  ! . My belief is ,  there will   definitely a subset  in   both acute and  chronic  forms of   RHD   , in which myocardium  gets  involved . In our institute LV dysfunction associated with RHD occur in  up to  5 % of  RHD population .

Importance of knowing the mechanism of MR

Two aspects  appear important

1. Is there a potentially  reversible component in pathology so that we can  wait  before intervention  ?

I have seen children referred for mitral valve replacement due to severe MR  . In due course   MR regress by the time they reach the tertiary center (waiting period included ) At least one child i remember,  the MV surgery was canceled  due to spontaneous regression MR.

It was later found the MR was  more of valve inflammation than degeneration .

* Always think about the possibility of reversible rheumatic MR  in every severe isolated  MR in children (Do not apply this rule in adults or in combined MS or MR  )  Do a ESR, ASO and start an  intensive anti inflammatory therapy  , aspirin with strict penicillin prophylaxis .With this  one can definitely postpone the surgery  in few cases  and  may avoid it altogether !

2. Surgical implication

If we could delineate  the  exact pathology of MR   it will facilitate  the   repair . Annular  reduction and  neo  chordae  etc . Of course ,the surgery could be  very  difficult in scarred mitral valves ,  Dr Sampath kumar *of AIIMS  New delhi , India  would  feel other wise !

*A pioneer in mitral valve repair in chronic  RHD (See reference 2 )

Questions  that need  answers

How is balloon/Surgery  related injury different from rheumatic process ?

Why is  rheumatic  mitral vale  prone for bacterial infection ?

What is the relationship  between  extent of  aortic valve involvement and  degree of mitral valve involvement in RHD ?

Reference

1.http://circ.ahajournals.org/content/94/1/73.full?sid=10599470-3563-4c38-b688-c5fc8c032f96

2. http://icvts.ctsnetjournals.org/cgi/reprint/5/4/356

Books

There two popular books exclusively  for cardiac pathology

1.Silver

2. Renu Virmani

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Mitral valve prolapse : Finally . . . facts are trying to prevail over fiction !

Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics, tagged , , , , , on March 12, 2011| 4 Comments »

 

Ever since  Barlow reported  this entity , mitral valve prolapse was made  a fascinating disease of  the heart . Cardiologist’s honeymoon with this disorder lasted  for too long   . . .  four  decades ?. It is probably the most  common valvular disease physicians diagnose .The importance of which was  exaggerated  and at one point of time  the term was  getting  abused.

So the criterias  were made strict in later decades . Now unless MR is present along  with valve thickening MVPS should not be diagnosed.

Clinical presentation

  • Atypical chest pain
  • Palpitation
  • VPDS
  • Asymptomatic pre excitation
  • Anxiety state  including  panic attacks (More common after informing the patient about MVPS.) 

 

Here is Monograph with excellent Images.I think this is available  free with Google Books. 

 

MVPS -Auscultation

Classical finding is mid systolic click with late systolic murmur.

But in reality,   It can present with  any of the following

  • Early -mid systolic click,   with  murmur
  • Only murmur
  • Only click
  • No click,  no murmur -Only Echo evidence of MVPS
  • Clinical Click  but no MVPS in echo*

The timing of click and murmur depends on the LV volume and the contractile force.Status of pap muscle is also important.There are studies which  show dehydration can induce MVPS and hydration corrects it  .One can guess the anatomical importance of this entity.

Currently myxamatous  valves with clear prolapse with at least  grade 1 MR (Not the often reported trivial MR !) only be labelled as MVPS.All other  forms increase patient  anxiety , lead to unnecessary echocardiogram and of course promotes   physician    affluence !

*Chordal clicks

This was first described by Reid .A redundant  lengthy chrordae  folds unfolds  making a noise. Mitral valve as such may not  prolapse into LA and hence echocardiogram would be normal.

Origin of chest pain in MVPS

It is still a mystery  out there regarding the origin of chest pain in MVPS.

It is thought to be a  mechanical pain from any of the following

  • Valve
  • Chordae
  • Myocardial stretch
  • Ischemic unlikely

*currently it is  believed  to be a pain perception problem at cortical level.

ECG

  • Non specific T wave inversions in inferior and lateral  leads common
  • Early repolarization patterns are common
  • WPW has a  rare association

TMT

False positives excercise stress tests are  reported  often .

Echo

  • Echo  is to be primarily blamed for the  rampant diagnosis of this entity .
  • In deserving patients Echo is vital to define valve anatomy and MR assessment.
  • TEE will help us the exactly identify  culprit  scallops (Commonly P2 A2)  and facilitate the surgeon during repair.

Coronary angiogram

Many of the MVPS patients end up in inappropriate CAGs ( Decent term for guideline violation !).As a rule  , almost all will have normal coronary angiogram.

Incidence of  Ventricular arrhythmias

VPDs can be common in MVPS. ( Myocardial /Pap muscle Stretch induced ?)

Sudden cardiac death is no more common than general population .So no worries .

IE prophylaxis

Generally not required unless significant MR present

Management

Most( 99.9%) will require no treatment . Only reassurance .This , if properly done shall be a one time process.There are many young persons  who report to the physicians  periodically to get reassured (Each time  spending 500 Rs !) This is called reassurance failure .Here , the  physician needs  to be urgently  changed.

Many times , parents , spouse and relatives  will  require more  counselling  than the victim  of mvps !

Few with progressive MR will need close monitoring  (Eg Associated Marfan )

Tall,  thin individuals will require aortic size monitoring as well.

Highly anxious persons will do well with beta blockers. Panicky individuals require sedatives as well.

Very severe MR needs surgery .Surgeons   are encouraged  to repair a  myxamatous valve than to replace it .

Secondary MVPS

(MVPS in association with other structural disease  like Ischemic, RHD, Infective endocarditis are important pathological entities that need to be discussed separately )

Final message

MVPS is a benign disorder (Rather it can be called as  a variation in mitral valve morphology  ).  Only  In  a  fraction of  population it  can take a true  pathological course. Cardiologist and physicians should  disseminate this message widely to their draining population.Unfortunately  in the current state of affairs , MVPS  seem to be  less dangerous for human community than the  events  that   follow  the  misplaced diagnosis of this entity. In the name of health awareness  huge costs , time and resources are wasted in dealing with this almost  . . .non entity !

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