[HSF] Tricuspid repair w/pulmonary hypertension

[ICHFNO at aol.com]

Interesting situation with a number of opinions about the etiology of the  
patients demise. Now, I have not done an adult Mital/Coronary/Tricuspid in more  
than 15 years, but I am a little confused about why one would think that  
repairing a regurgitant Tricuspid valve would be one of the major issues in this  
patients death. Let's look at severe Ebstein's for starters; there are those  
with severe Carpentier Class C or Class D that do not do well when you 
perform a  repair, the RV distends, contractility is poor, if not absent and the CVP 
 skyrockets, what is the bailout, why a bidirectional Glenn, that does not  
improve RV contractility, it volume off-loads the RV. The majority of the  
myocardium is atrialized ventricle and its contractile contribution to RV  
function is limited in the early post bypass period. 
 
Another point, what is irreversable pulmonary hypertension? 
(_http://ats.ctsnetjournals.org/cgi/content/full/79/1/21_ 
(http://ats.ctsnetjournals.org/cgi/content/full/79/1/21) )  or (Ann Thorac Surg 2005;79:21-28)
You are all aware that irreversable previously meant that those who  received 
oxygen provocation at cath and did not show a decrease in PAp or PVR of  at 
least 20% were considered irreversable. But oxygen is no longer the gold  
standard. Pulmonary vascular reactivity can and should be assessed with other  
agents, NO, inhaled prostacyclin, Tracleer, Sildenafil and others, before one  
states that it is irreversable. We have operated on 32 year old patients with  
PVR after oxygen provocation of more than 20 Wood units, and yes they survived  
and guess what, the PAp after operation acutely were upwards of 100% systemic. 
 If the RV is well protected and has been "seeing" a PAp of 90% systemic 
before  operation in a chronic situation then correcting the coronary 
insufficiency and  the tricuspid insufficiency in the face of a repaired mitral with 
minimal  regurg, then it will not fail. Stumble maybe, especially if the clamp time 
is  long and the protection has been sub-optimal, but fail, not likely. This 
is Just  My Humble Opinion
 
An option would have been to create an ASD with a " surgically created  
patent foramen ovale", a patch with a fenestration and a flap valve on the LA  
side, so that when the RV recovered and the CVP dropped the flap valve would  
close and there would be no residual ASD for the interventionalists to  close. 
 
We have operated on over 150 kids/children/adults with VSD's and severe  PHT 
with PVR's elevated to levels that most surgeons would deny surgery to  the 
patient. On the basis of historical data 50% of our patients should be dead  
now, however as you can see from the KM survival curves more than 80% are still  
alive.
 
Long clamp time and inadequate protection are more likely the culprits, not  
a competent tricuspid valve.
 
Bill

William M  Novick MD
Paul Nemir Jr., MD Professor
International Child Health and  Surgery
University of Tennessee Health Sciences Center
Founder and Medical  Director
International Children's Heart  Foundation

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