[HSF] Aortic valve

[Rwmfglycar at aol.com]

In a message dated 5/22/2008 11:09:51 P.M. Eastern Daylight Time,  
ebender001 at charter.net writes:

A couple  of days ago I was referred a 79 year old male with  myelodysplastic
problems, along with easy fatigability, class 3 heart  failure symptoms and a
loud murmur at the aortic area.  The  cardiologist did an echo in his office
which showed aortic stenosis  (indexed valve area of 0.4 cm2)  He did a right
and left heart cath  revealing trivial coronary disease, and mildly elevated
PA pressures.   He did not feel the need to cross the valve since this was so
obviously a  stenotic aortic vaalve.  He did, however do a TEE confirming AS.
His  office echo purported to also show severe PI.  TEE did not show  this.
Do you see where I am going with this case?

I operated on him  2 days ago (minimally invasive approach).  The valve was
tri-leaflet,  with easy mobility of the leaflets into a wide open position.
Annulus was  about 22 - 23 mm, and there was no  LVOTO by direct inspection
or  intra-operative TEE.  There was however a very large amount of heaped  up
calcium on the left coronary leaf, and lesser amounts on the other  two
leaflets with no restriction of motion.It is very  difficult to feel how much 
force  is needed to open a thick leaflet using  your fingers and a forceps. I 
have made artificial valves with different  thicknesses  of pericardium and 
shown significant differences in  obstruction to flow between thick and thin. 
Leaflets with blobs of calcium on  their downstream cupped sides cannot bend 
into a fully open  position.  I suspect that if the echo had shown a short axis 
view  across the open valve then planimetry would have shown a reduced orifice 
area.  

I could not justify replacing this valve, so I pealed all the  calcium off
the leaflets.  This was easy, but left a very thin area on  the majority of
the left leaflet, so I sutured in a piece of gluteraldehyde  treated
pericardium to bolster the thinned leaflet. Smart move. I have seen a leaflet 
(mitral) pop a hole at one  year after excessive thinning. (Do you know  what 
the thickness of the pericardium was?) Echo on post-op day 1  showed a
peak velocity of about 2 m/sec. Which  translates into about a 16-20 mm
gradient with trace AI.

My question  to the valve experts are:
1. His pre-op Hct was 24. Certainly anemia would have put the cardiac output 
up and turned  a small gradient into a big one. Coupled with the increased 
mass  of the leaflets,
could this account for a false positive diagnosis of AS?  I would not call it 
"false positive" but rather ask the  question was it significant? Was there 
left  ventricular hypertrophy?  Does a slower
opening time  (assuming increased inertia to get the valve open)  cause  an
artificially elevated transvalvar gradient? 
2. What do you think the  durability of such a repair might be?  Is the
experience with patches  to the perforated leaflet secondary to endocarditis
applicable to calcific  degeneration pathology? Why not? I would trust the  
patch. But note that in 11 patients in whom I did aortic  decalcification, all 
had recalcified or died by 10 years.
3. I  will not get into the behavior and practice standards questions
regarding  the complete workup of potential AS.  Most new cardiologists I
know  have learned this lesson. I will. There is absolutely NO justification 
for not getting  LV  and aortic pressures and a cardiac output in a case like 
this. It would  have been easy to get across the valve and would have provided 
more valuable  data than the TEE.



Thanks for anyone¹s input.

Ed Bender,  MD
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