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Archive for the ‘rheumatic heart disease’ Category

Significant MR is a contraindication for PTMC. However,  If MR jet is central , and mild (some times little more than mild as well ) PTMC can be safely done. The MR may not worsen .It may even disappear.

Note: Eccentric MR jets are indirect evidence for sub valvular disease. Its very likely to get worsened and may require a mitral valve replacement .

Here is patient with severe mitral stenosis, the MR is in all probability safe.

Angle of eccentricity 

One must realise , the eccentricity of a jet is not very objective .What may appear as central jet in long axis may be wall hugging in 4 chamber view. This is very important to recognise. Further , even central jets can reveal a invisible eccentricity detected only on 3D MR jet reconstruction.

One simple way to ascertain central jet is to  check whether the MR jet align in the same angle as diastolic color jets of MS into LV inflow . (Looking carefully ,the diastolic color jets also provide us info about sub-valvular disease )

More anatomical distortion in this patient 

Incidentally , this patient also had another anatomical adversary  ie ,the bulge of IAS into right atrium. This can happen two ways .Septal aneurysm or a normal septum bulging to RA due to raised mean LA pressure.

 

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Miral stenosis with Atrial fibrillation showing the changing mitral inflow jet .

 

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The radius of curvature of IAS bulge Indicates its more of septal weakness that contributes than the raised pressure. There is a small risk in these patients the IAS flap may give way during the procedure and a small ASD may be created .(Hemodynamically may not be significant though)

 

How does the MR disappear after balloon dilatation ?

If you ask this question , it means your are a thinking cardiology fellow , good.

Guess your answer. Its all about physics of  MVOs behavior  in systole and diastole . The mitral valve tissue attachment and adhesion causes not only a  diastolic narrowing but also a fixed systolic regurgitant orifice.Once you relive it the leaflets begins to co-opt normally without a systolic leaky orifice.

Final message

Though there are clear contraindications ,suitability of mitral valve for PTMC is more of a personal experience and confidence. A MR jet of grade 1  may be acceptable. A huge LA, Distorted IAS anatomy, a clot confined to LA appendage are relative contraindication only. The puncture site on IAS , minimal manipulation guide wire within LA, a gentle over the wire technique to cross mitral valve or some of the tips for success.

Never hesitate however to refer complex cases of mitral stenosis to the surgeons. Of course , you can’t insist them to do a valve preserving OMV .It is unfortunate(They have good point of argument as well)  most of the surgeons have have made Mitral valve replacement as a default modality

Post ample :

When we were cardiology fellows , we used to have a mitral valve scoring system for suitability for PTMC. Its called Wilkin’s score. Its a purely an anatomical score. (I guess still its expected in Board exams) What we need is comprehensive anatomical and physiological assessment of mitral valve. With due respects to  published literature this scoring system lacks  two  vital parameters we look before PTMC , namely the extent of commissural calcium  and degree of MR.

 

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Regurgitant  lesions of cardiac valves  are often tricky for the heart . Myocardium shows “love- hate” relationship with these  leaky valves.  Some of them are  “sort of”  stress relievers for  LV . A mild MR will make the LV comfortable in terms of wall stress. When the wall stress is reduced the contractility increases and LV EF may raise a little.Hence EF is never going to help us to assess true LV function in MR .

LV end diastolic dimension(LVEDD) is  a preload dependent  parameter .A patient with 6.5cm LV EDD  may still  have good contractility  and he may reach even a  40mm LV ESD, implying an intact LV function.

LV function should be best  assessed  in systole .(After all ,  systole is the prime function of heart) .Further , it should be assessed when the LV is  free from  influence of the all  loading  conditions of heart .  (Note : The initial part of systole  depends on after load. As the systole progresses the influence  of after-load lessens .In the pressure volume loop* , the point at which loading conditions are least operative is end systole.)

* Please realise , heart is a dynamic organ there is no true load independent point in cardiac cycle  as pressure and volume are eternally coupled.

What happens in AR ?

The same rule applies for Aortic regurgitation, but the parameters worsen little later than that of MR. For same degree of regurgitant fraction MR will require early surgery than AR.The reason for better  tolerablity of  AR  is due to largely  intact LA function and compliance till very late stages of AR.(In AR- it’s single chamber volume overload , while in MR  it’s two chambers !)

Final message

LVEDD is not used in assessing MR  as it is a pre-load dependent parameter that will not reflect true myocardial  function /dysfunction. LV ESD is fairly accurate  measure of LV systolic function minus all loading factors .

Watch out  for next topic

Vasodilator therapy in MR and AR : How is it different ?

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No procedure is  impossible in medicine    . . . but it should be useful for the patient !
Where will you ablate ? What is the purpose ?
The much  hyped*  ablation of pulmonary vein  is never going to help in rheumatic heart since  arrhythmia focus occurs at  random . How can you  locate a   focus of AF over a  huge , scarred  left atrium  ? ( which looks like a lunar surface  sprinkled with a rocky terrain ! )
Gross specimen
                                      Note the huge , scarred LA .It would
                                      be a wild guess to locate the true focus
                                      of AF . (Image source : http://www.e-heart.org)
So , the other option was disconnecting atria electrically . In the past  surgeons advocated  linear  or multiple incisions as in Maze and  Corridor procedure  after mitral commissurotomy .This  helped to a certain extent , still effective , organised atrial contraction was not restored in many.
Now , some electrophysiologists tried to do the same with catheters without much benefit.* Please realise , pulmonary vein ablation even in lone and ischemic AF is struggling  with a concept collision !
Can Right atrial focus trigger and  sustain  AF in RHD ?
Autopsy studies reveal tricuspid valve scarring in 33%  of all RHD .Since RHD is a diffuse process , RA lesions can  be very well be the focus .  It is not an easy task to identify the real culprit focus. So ,concentrating  LA  for ablation may end up in futility.
There are only few studies available on RF ablation in RHD  .This one from Istanbul ,Turkey  and it  does not favor it as recurrence rate is still significant .
rf ablation in rheumatic atrial fibrillation
Final message
Approach  to AF in RHD  : Opening up the mitral valve (or replacing it )  and controlling ventricular rate  with beta /calcium blocker along with  adequate  oral  anti-coagulation substantially reduce the risk of embolic events .One may never need to contemplate restoring sinus rhythm  in rheumatic atrial fibrillation.

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The pericarditis  of acute rheumatic fever is not a true infective pericarditis.It is more of inflammation .It is primarily  T cell mediated  reaction . Neutrophils rarely take part  in this inflammation and hence  no significant  exudation . Hence , there is less  sticky and adhesive molecules inside the pericardial space .The most inflamed layer is epicardium which a nothing but visceral  pericardium .This layer lacks the tensile strength to constrict the underlying myocardium.

why rheumatic pericarditis does not go for constrictionFor constriction to occur the fibrinous  ( thick ) layer of pericardium need to be involved . In rheumatic fever  even though it is  pancarditis ,  fibrous layer is not  involved. Further the inflammatory gradient is thought to spread from within  (Unlike tuberculosis )

Note :  In chronic tuberculous pericarditis,  diffuse inflammatory process  invade from the exterior surface . Very often ,  one can not differentiate  layers. In extreme cases even myocardium and pericardium can not be separated .

Summary

The peri-cardial effusion of acute rheumatic fever

  1. Is transient ,non infective and resolving (Unlike valvular inflammation !)
  2. Less of neutrophil activation  (Less adhesion)
  3. It does not involve the thick , tensile  fibrous layer of pericardium hence lacks the contractile force .

Other lingering  questions

1.How common is tamponade  in acute rheumatic fever ?

2.How important is the mass of the effusion (Viz  a Viz  Intra pericardial pressure !) in causing tamponade ?

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Rheumatic fever and RHD is still a major cause for  cardio vascular morbidity and mortality in India .It seems , improving quality of life  has little  impact on the incidence .(We could realise  this as  we sit in the cardiology OPD of a 200 year old hospital !) There is no country wide data on the true prevalence .  Our understanding of rheumatic heart disease is based on isolated  studies on localized populations .

Of late , cardiology   resources  in our country is diverted towards  much glamorous CAD the poor continue to  suffer with  RHD.

Just Imagine many   hospitals indulge in 1000s of PTCA every year  but hardly do  a  hand full of PTMCs.

How our cath  lab resources  are used   across the breadth and length of country needs some introspection (Currently , I believe we have about 750   labs ) .I think there should  be a binding legislation  in every cath lab .For every 10 PTCAs done   at least one PTMC must be done to heal the poor .( Like the Air-craft license  .You can’t fly only the lucrative metro sector is given only if IT  services less developed areas )

In this scenario ,  it is a pleasant  surprise  to find a  wonderful review article on RHD from the two pioneers ,  in lesser known medical journal IJMR  .

Review article rheumatic fever  Indian journal of medical researchEspecially heartening  is  the fact ,  it is a collective effort  from two  distant  regions of India ( Kochi from down south and  New Delhi In the north) . While politicians keep the divide , it is a great  work  of the authors , which  would help  youngsters  who  would like  to go on a national mission on eradication of RHD. .

Reference

http://www.icmr.nic.in/ijmr/2013/april/centenary%20review%20article.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840767/#CIT12

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A 32 year old unmarried female with rheumatic heart disease   presented with class  3 dyspnea . She had severe mitral  stenosis with significant calcification , subvalvular fusion , and  a LA appendage clot . She had an aortic valve  which showed mild to moderate AR*  was  and  mild  Aortic stenosis ( Peak  Aoric gradient 30mmhg ).LV diastolic dimension was 40mm and systolic 26 mm .LA was huge 48 X 56 mm  EF was 66 % .

* The patient was having three echo reports done in various parts of the state ranging from mild  to severe  AR . I did the echo myself and I  was convinced  ,  it can at best termed as Mild AR . Let us take it as moderate AR for discussion  

To my surprise  , this patient  was   being planned for double valve replacement . (MVR  and AVR ) .

I agreed with MVR since the valve was completely  damaged and neither PTMC or mitral valve repair  is possible.

However  , I was taken aback   , how can  one  plan for a  AVR for mild aortic valve disease ? I  asked the surgeon  ?

The answer was even more a shocker to me .

Since we are  opening the chest for MVR it is better to replace Aortic valve as well . Since  repeat surgery can be avoided .

The surgeon seemed to be very much convinced about this argument .

I asked him ,   is the mortality /morbidity due to DVR is too high  to take a risk .

The LV dimension is absolutely  normal (In fact it is less than normal !)  so  the AR is definitely not significant .

The surgeon was in no mood to leave me . He argued ,  Since the mitral stenosis is severe , the AR is  probably underestimated .   ” We have quiet a few experience of AR worsening after MVR” ? he asserted !

I still fail to  understand  the reasoning of the surgeon .

How is that ,  indication for AVR could vary if it is  accompanied by  mitral valve disease . If the same patient has  isolated moderate AR  AVR is  forbidden  . Poor patient !

By the way , we have problems with our patients as well .I recall an event ,   a  disappointed  patient’s  spouse  arguing  with his the doctor for not fulfilling his Initial  promise of  replacing two valves . We are living in difficult times , I agreed with the surgeon !

Do we have  alternate solutions ?

  1. Assess on table after MVR by TEE if the AR seems worsen proceed with  AVR .
  2. Modern technology might answer .Let us dream  TAVR for rheumatic valve . . . not too far ?

*Transcutananeous Aortic vale replacement .

Final message

Cardiologists and cardiac surgeons should take extra care before finalizing a decision on DVR in any combined valve disease. It may seem  easier to replace two valves . Please spend few moments silently and think about these young men and women  . Valve replacements are  not like replacing  worn tires of your car.  Do not  burden the heart with multiple artificial valves without a real need for it !

The rate of progression of Aortic valve disease following MVR  can be slower than we think . With surgical techniques and  expertise   improving every year ,   repeat aortic surgery may be done safely in selected few ,  in case it becomes necessary !

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Rheumatic valvulits , Valvular inflammation and edema  is the traditional answer .A detailed Echocardiographic study from All India Institute of medical sciences New Delhi  ,India  which was published in circulation 1996 answers this question most authentically .

From a meticulous  Echocardiographic  study of about 70 patients  (with both first and recurrent episodes of carditis ) the following findings were observed.

After reading this article one should be able to answer variety of  questions in RHD  such as

  • How common is MVPS in RHD ?
  • How often MR dissapear with Aspirin etc ?
  • Echocardiographic correlates  for care -coombs murmur ?

Reference

http://circ.ahajournals.org/content/94/1/73/T5.expansion.html

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