CTSNET READER COMMENTS

Dear Lishan
Thanks for your comments, and I hope you are well.  The progress you review
was mentioned at the AATS symposium.  But from what was reported there and from your
analysis, I must conclude that the electrical activation of the ventricle and the
pathoanatomy of the heart are irrelevant if you just install the proper eponymous ring.
This may be proven correct, but my contrarian brain says it's too simple minded and
mechanical.  I would be comforted to know these details in the patients who were
successfully treated because I can easily imagine such success in certain IMR patients,
but not so easily in others.  For instance in the patient I described with an entirely
dead posterior wall, you could say that he had a tethered posterior leaflet, but I
would cut the back of his heart out and replace his mitral from within the open LV.  No
matter what you do, could his prognosis be the same as a patient with a severely
ischemic but living posterior wall that can be revascularized? 

 By the  way, why do
some of these rings have a funny bump in them?   Warm regards!  VG

Vince,

As always, I enjoyed your comments, particulary your willingness to be
provocative.

I think you make an excellent point in highlighting the contribution of
ventricular dyschrony and its eletrical component in the pathophysiology (and potential
treatment) of "ischemic" MR. (Ed - I agree that the term is a misnomer, I personally
think we should call it post-infarction MR, but I suspect we are stuck with IMR).
There is a lot of evidence in the cardiology literature, some of it overstated, that
BiV pacing alone can improve "functional MR".

However, I would respectfully disagree
with some of your intial statements on the pathophysiology of ischemic MR and the
success rate of currently available treatments.  I have recently done an exhaustive
overview of the ischemic MR literature for the STS Workforce on Evidence Based Surgery.
Over the past 10 years there has been an enormous literature both in animals and in
patients, most recently using pretty sophisticated 3D echo analysis, that has really
enhanced our understanding of the mechanisms of IMR.  They have coalesced into a
relatively clear picture focusing on specific patterns of papillary muscle displacement
secondary to post-MI LV remodeling (not always just the posterior wall or the
posteromed PM) leading to leaflet restriction, tenting and ultimately loss of
coaptation.

I think the greatest myth about IMR is that currently available treatments
fail because they only address the annulus and IMR is a "ventricular problem" (which of
course it is).  The clinical literature on CABG/annuloplasty is thoroughly muddled
because many of the early series used a variety of non-remodeling rings, did not
consistently downsize the AP diameter, etc.  Hence rash of reports 3 or 4 years ago
showing high rates of residual MR, recurrent MR and ongoing negative LV remodeling,
etc.

However, more recent studies (eg Dion, et al), that rigorously apply aggressively
downsized, remodeling (rigid), complete annuloplasty rings show significantly better
outcomes - residual/recurrent MR rates <10%, good mid/late functional status and clear
evidence of sustained reverse LV remodeling.  The one early report on the IMR ring
(Daimon), whose primary feature is aggressive downsizing of the AP diameter with
overcorrection at P3, is really quite good.  Residual MR rate of 3% and solid echo
evidence of decreased tenting.

Of course, this by no means implies that we shouldnt be
searching for improved techniques and tools to treat IMR, particulary at the LV level
and in an off-pump or endovascular setting.  I just think it is important to
acknowledge that a carefully downsized, rigid annuloplasty works pretty well.

Lishan

I read and very much agree with your thoughts.  I would like to add one more aspect to
your crusade.  I believe the term ischemic MR is inaccurate and should be changed to
"ischemia induced" MR.  The mitral valve is not ischemic, with the exception of the
papillary muscle which a ventricular component, the mitral valve has no blood supply.
The terms degenerative MR, myxomatous MR and rheumatic MR describe changes directly to
the structure of the mitral valve. The term "ischemia induced" accurately reflects the
concepts you are promoting.