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Archive for the ‘valvular heart disease’ Category

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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Doppler Mitral Inflow velocity profile   is the key to  assess LV diastolic function . The ratio between  E and A has become most popular parameter .

In the absence of atrial contraction what shall we do ?

The answer is simple .  We have 2 D parameters of LV diastolic function.

LA dimension ( > 30 % basal dimension which is  usually >  4 cm  ) is a most specific marker of diastolic dysfunction in the absence of   mitral regurgitation or stenosis.

The only available  velocity E wave profile  can help .A short  E deceleration time in a short cycle  would suggest  significant diastolic dysfunction.High amplitude   E  wave  > 2  M/sec in the absence of MR  will suggest diastolic dysfunction .

Curiously  ,   it can be  assumed    an episode of   lone AF  per-se   ,  be an indicator of diastolic stress for the left atrium .

After all ,  why should a person all of a sudden develop an episode of AF .(Hypoxia, Ischemia ,  excluded )

Other parameters.

Mitral annular velocities / E propagation velocity   / E/E’  are other tissue Doppler parameters  can be used.

Pulmonary venous flow velocity is  largely not useful  (Since A reversal does not occur )

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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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While their cardiology colleagues are extravagantly indulging in coronary arteries   ,It is heartening to note the pediatricians our country has  silently come out with the first India specific  criteria for Acute Rheumatic fever diagnosis and management.

It was long over due . . . three cheers to them !

* It is ironical  these guidelines came in 2008,many of us are aware about the  existence  such guidelines , still  every one is after PTMC  for a full blown mitral stenosis !

http://www.indianpediatrics.net/pdf/acute_rheumatic_fever.pdf

Highlights and Summary

  • WHO criteria  of 2001 is adopted
  • ASO titre positivity alone has less value  in the diagnosis .Hence the importance of which is down graded
  • Steroids  are mandatory in all grades of carditis for 12 weeks
  • Benzathine  penicillin  should be administered weight  based and to be given  every 15 days in children less than 27 kg.

More high lights will be posted.

Secondary prophylaxis of  for Rheumatic fever

Note the Important advice regarding weight based penicillin prophylaxis.

 

//

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Who said  knowledge comes at a cost . Here is a great resource . Everything about 3D echo

A sample of   3D echo  evaluation of  mitral valve anatomy

http://www.escardio.org/communities/EAE/3d-echo-box/3d-echo-atlas/mitral-valve/Pages/normal-mitral-valve.aspx

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Cardiologists are  closing in ,  trying to capture the final frontiers. The  trans-cutaneous Aortic valve Implantation now has  a two year follow up. (NEJM March 2012  Issue) . The results are encouraging .

While two companies are fighting for the supremacy in TAVI ,   the real  threat is for the cardiac surgeons. Currently Edward  Sapiens  has an edge over Medtronic core valve as it  has a provision to redeploy or fine-tune the  final geo- position.

Reference

PARTNER 1

PARTNER 2

Medtronic core valve

Open access  article  by Martin Leon

http://www.rmmj.org.il/userimages/22/1/PublishFiles/25Article.pdf

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Here is an X-ray of classical rheumatic mitral stenois with a mitral orifice of  .8 square cm.

Why the left heart border is straight in mitral stenosis ?

It is due to 4 factors.

  1. Hypoplastic aorta
  2. LAA
  3. PA
  4. Under filled LV

Note :

  • This straightening occurs   only  in  isolated , severe forms of mitral stenosis  as it requires under filling of left  ventricle   and Aorta.
  • Significant mitral regurgitation will lift the lower end of straight line .
  • In associated aortic valve lesions especially in aortic regurgitation the straightening can not occur as LV and  Aorta continues  to be conspicuous.
  • If mitral stenosis  causes severe PAH and tricuspid regurgitation , RV  can  become  huge  and form the left heart border and distort the straight line.

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I  wonder  this  question is being  asked  over many  generations in medical schools ,  yet to be answered clearly. The traditional explanation  given is   ”  mitral valve is  kept  open wide till onset of systole and it closes with a bang due to a long excursion it has to make ”   This concept is no longer tenable and acceptable ( For the simple reason  if the valve is wide open  . . .  hemodynamically significant  mitral stenosis  cease to exist !)

There are  two major factors that determine the loudness of S1 in mitral stenosis

  1. Hemodynamic
  2. Valve structure and morphology

Mitral valve closes whenever the ventricular pressure  curve crosses above the LA mean pressure . This is the pressure crossover point (LV/LA) .

In normal persons it happens very early after the onset of  ventricular contraction  .(ie  the LV pressure has to raise only to  about 8-12mmhg . At this point the LV pressure curve has  certain  force of contraction (Dp/Dt) .Since in mitral stenosis the mean pressure is raised well above normal  (Often 20-30mmhg)  the LV pressure cross over point is slightly delayed  and more importantly occur at a higher  slope  of LV pressure curve  . Even this slight delay adds a punch in the ventricular contractility .The impact of LV contractility on mitral valve closure especially the  AML is forceful .

(Imagine the force of  impact of a  stone hitting you  from a distance of 1 meter from above ,   is different from a stone hitting you from 10 meter above   as it gains the momentum )

The second phenomenon is  probably  more important as it involves acoustics the final step in the genesis of loud  S1  .

The mitral valve need to be  not only pliable  but also the conduction properties should be intact.

Acoustic principles state that even a speck of calcium in the AML  can dampen the sound that is generated  by leaflet motion.

(Try touching a speaker cone while it is playing  .The sound immediately drops and dampens.)

Similarly for S1 to be loud  the valve should pliable without any significant calcification or extreme rigidity or subvalvular  fusion .)

It is important to realize the PML  contributes less to the intensity of S1 . Hence even if some calcium present in PML it won’t  affect the intensity of S1

Other important factors that affect the intensity of S1 include

  • LV function ( Onset of LV dysfunction elevates LVEDP reduces the net gradient across mitral valve )
  • Presence of  mitral regurgitation .
  • Aortic valve disease (Especially AR )
  • Heart rate
  • Rarely associated Tricuspid stenosis make T 1 component of S 1 louder

Final message

The loud S 1 is due to both physiological and anatomical factors  of mitral valve   .The condition of valve may be  more important  for the simple reason , whatever be the hemodynamic  predispoistion  for loud S1 ,  the  prevailing  valve morphology  has a potential to nullify it !

Acknowledement

The image modified from  http://www.texasheart.org

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By statistics cardiomegaly   often implies  ventricular enlargement (especially left ventricular) .Right ventricle generally do not enlarge the  CT ratio until late stages .

More important  is the impact of right atrial enlargement on the CT ratio. Here was a  patient referred to echo lab for evaluation of cardiomegaly

The x-ray chest  was suggesting a definite LV enlargement.  To my surprise  the LV was perfectly  measuring a normal dimension .

The right atrium was huge and measuring  more than 5 cms . This increased the CTR.

The following illustration  tries to create echo equivalent of transverse CT diameter by rotating apical 4 chamber view by 90 degrees.

The right and left atrium was significantly dilated . This patient had atrial fibrillation and the atrial enlargement was due to chronic AF.

Final message

Cardimegaly in  X- ray chest do not  necessarily  mean ventricular enlargement.

Pure atrio-megaly  especially right atrial enlargement can dramatically increase the CT ratio.

This is not a big  discovery , still fellows need   to reinforce  this fact  , as  mistakes are most often committed in well  known things !

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Clinical sense

  • First and fore most  dictum  is  not  every  prosthetic valve obstruction  is  thrombotic (Most cardiologists are tuned to think that way )
  • Pannus, Mechanical failure  and  vegetations can increase the gradient across prosthetic valve.
  • If the clinical presentation is acute (< 48 hours ) it is  more likely to be a thrombotic event .
  • History of  recent discontinuation of oral anticoagulants /sub optimal INR will favor thrombosis.

A meticulous Echocardiography is vital (TEE though gives more information in an emergency TEE is suffice )

  • Thrombolysis is to be considered in all .
  • For right sided prosthetic obstruction thrombolysis is the  initial modality of choice.
  • For left sided valve thrombosis   surgery is the preferred option .However a trial of  thrombolysis for 24 hours may be tried .
  • For a high risk mobile thrombus , thromolysis is contrandicated.

The success rate is less with Mitral than Aortic valve  . Success depend upon more on the  location / Freshness of thrombus than the type of the lytic agent used.

Is there a time window for prosthetic valve thrombolysis ?

Thrombus organisation takes 2 weeks at- least.Hence , it better not to attempt thrombolysis in documented late prosthetic valve thrombosis.

Thrombolysis of left-sided valves has inherent risk of  stroke .

Heparin controversy

Simultaneous usage of heparin along with streptokinase or TPA is  perceived as risky (No good evidence for this perception )It is logical to expect even as the thrombus  lyses the clot lots of pro-coagulant debri  are released . Concomitant usage of heparin  will definitely help accelerate thrombus dissolution. (I am glad  Joseph S   Alpert also feels the same ! )

Assessing successful  thrombolysis

  • Can be a tough task .
  • Relying purely on gradient is vested with risk of huge error.
  • In a patient with shock or LV dysfunction gradients are not reliable as low flow status masks the gradient.
  • A accelerated thrombolytic  protocol 15lakhs streptokinsae in 60 minute may be tries in unstable patient .
  • It is wiser to rapidly asses for clinical improvement in high risk subsets  and refer the  patient for early surgery .

Surgery

Prohibitive mortality reported in many centres.

It need to be remembered no surgeon will operate on a  sick patient in  shock  exposed to  cocktail of heparin and streptokinase.

Valve replacement is required in most case. Simple valve debridement  (servicing the  valve ) and releasing  discs  from the  sticky thrombus is  also possible in an occasional patient.( Do not ask reference for this !)

Reference (Surprisingly most of the good papers in the topic appeared  in JACC)

http://content.onlinejacc.org/cgi/reprint/41/4/653.pdf

http://content.onlinejacc.org/cgi/reprint/41/4/659.pdf

http://content.onlinejacc.org/cgi/reprint/35/7/1881.pdf

http://content.onlinejacc.org/cgi/reprint/35/7/1874.pdf

After thought

I have not seen a single case of acute prothetic valve thrombosis involving Starr Edwards valve  in the  last  20 years of  of clinical cardiology practice.

Is it true   . . . the new age valves  with more mechanical stress points  are proving more injurious to our patients. Our  pursuit  towards a  perfect artificial  valve need some introspection .

Read a related article in my site :  Who killed Starr Edwards valve ?

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