[HSF] Aortic valve

[ichfno at aol.com]

Ed;

We have a little quote we like to use when faced with this dilemma, echo schmehco! Low hct coupled with the calcification certainly contributed, but how did such a small valve area get generated, did he use Gorlin formula from the cath? See no reason why it shouldn't hold up, we use it for most of our aortic repairs in kids.

Bill 

-----Original Message-----
From: Edward Bender <ebender001 at charter.net>
Sent: May 23, 2008 5:12 AM
To: OpenHeart-L <OpenHeart-L at hsforum.com>
Subject: [HSF] Aortic valve

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.

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.  Echo on post-op day 1 showed a
peak velocity of about 2 cm/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.  Coupled with the increased mass of the leaflets,
could this account for a false positive diagnosis of AS?  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?
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.

Thanks for anyone¹s input.

Ed Bender, MD
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