[HSF] Aprotinin

[Ben Bidstrup]

>Bob,
>   I would whole heartedly agree with you that Ben's opinion on  aprotinin is
>not shaped by the fees he has received.  I've met him on a  couple of
>occasions, and am convinced he is an honest man.  He and others  are 
>convinced that
>aprotinin doesn't contribute to renal failure.   That has not been my
>impression.  This will only be resolved with more  experience and 
>data collection. 
>Believe me, I'd love to use it on every  case, because I have as many problems
>with coagulopathy as most cardiac  surgeons.  Years ago, I adopted Pat Daley's
>protocol for EACA.  Ten  grams was given at induction, ten grams at
>heparinization, and 10 grams after  protamine.  I swear I didn't 
>take a single patient
>back for bleeding for 9  months.  However, I abandoned the protocol after
>watching a little lady  with 5 grafts close everything but the LIMA. 
>This happened
>as I was  closing the chest.  I crashed back on and redid the vein grafts, but
>it was  too late.  I think we are dancing on a pin with these drugs on one
>hand,  and coagulopathy on the other.
>Hal
>_______________________________________________
Hal,
You are right. There are so many things going on especially in our 
older and sicker patients. Just to name a few: they include HITT in 
various forms, F V Leyden, and now as is becoming apparent various 
polymorphisms of genes that impact on drug resistance (ASA and now 
clopidogrel).
I used to call CPB a stress test of the haemostatic system but now 
would be even more general and refer to the inflammatory system.
When our patients were young and fit, they coped, although I suspect 
a lot had the same problems we see today, but less evident.
We try more, they demand more and we push the boundaries even more.
So we look for all of these adjuncts to make not quantum leaps but 
incremental 'improvements.'
But we also have a threshold and if the outcome is less than 
favourable, we either pull back if we are clever, or in many cases, 
add even more complexity.

I often look at those huge posters one sees in labs showing a million 
little pathways in the body. They are about 6x4 feet in size. We take 
something and say well that impacts on that reaction and that will be 
good. But it doesn't take into account the many alternate pathways 
etc.
Look for example at cariporide. Lots of potential , but where has it 
gone. There are many other similar examples.
And it is not just coagulation. The kidney is very sensitive to what 
we do. Is it lack of pulsatile flow or some other causative agent 
related to what we do?
We have a long way to go to learn the answers.
If you have something that has an easily, measurable clinical effect, 
then that is a much better starting point. If agent A does X, then 
changes Y & Z are likely to be related.
But we must not give up. Maybe the chink in the DES armour is 
widening. Remember that restenosis does not kill patients, but it is 
all the other lesions we leave behind. CABG in some guise will return 
(?maybe?).

-- 
Ben Bidstrup FRACS FRCSEd FEBCTS
Consultant Cardiothoracic Surgeon