[HSF] TR after CABG

[Tea Acuff]

Well I guess we can't blame the usual scapegoat, poor myocardial protection...can we?

tea


----- Original Message ----
From: Ani Anyanwu <anianyanwu at hotmail.com>
To: openheart-l at lists.hsforum.com
Sent: Wednesday, December 26, 2007 8:19:48 AM
Subject: RE: [HSF] TR after CABG

Don

Whatever was the final outcome in this case? I remembered it when you mentioned your 1000 anoaortic OPCABs without stroke (which I most certainly do believe) as a reminder that nothing good comes for free and inasmuch as we gain some (hopefully many) from avoiding CPB we lose some (hopefully few) - as in this case where one can argue the wrong operation [OPCAB]was done at first instance. Also noted that one of the grafts was blocked and although only one case I recall Tohru's concern about T grafts and yours and other's response that you have done hundreds and not seen these problems.

PS - as regards the cause of tricuspid regurgitation, by virtue of the findings and solution used, the cause was by definition not a congenital anomaly (as even if present was not cause of leak) but annular dilatation likely secondary to LV dysfunction, RV dysfunction or  pulmonary hypertension either of which may not necessaily have predated the OPCAB. Even the small infarct from the blocked graft which you refer you could lead to TR if in the right location. If the valve was congentially abnormal it could not be fixed with a ring (as a ring corrects only one thing - annular dilatation). Thickening and fusion suggests stenosis which patient didnt have. In retropect what do Manu and yourself think was the cause of the TR?

Ani



> From: donross at bigpond.com> Subject: Re: [HSF] TR after CABG> Date: Wed, 12 Dec 2007 15:59:40 +1100> To: OpenHeart-L at lists.hsforum.com> CC: > > Thank you all for your help and advice.> Hal, The PVI was done this way because the case was an opcab with > incidental AF and my limited experience with this method had been > good. I used to use the cryocath but it is more time consuming and > not so reliable probably because of the continuous warming of the > endothelium by normal PV blood flow. ( She is in SR now.)> Michael, I will watch for welding of the PV; it didn't occur in this > case.> > There was a recath in this case as soon as the troponin rose, > combined with a CI of less than 1.0> It showed patency if ima and T-vein graft to PLCx but no flow to the > small OM branch and I suspect there may have been a small infarct > despite normal EKG and LV ( max troponin 2.9 ?? how much troponin > generated by PVI and LA appendage resection.)> > At operation
 today I put a cannula into the IVC ( there was no SVC) > opened the RA ( beating heart ) and put a second cannula into the > coronary sinus ( #7 cuffed ET tube.. didn't need to blow up cuff ) > and got a lovely dry field.> The valve was probably congenitally abnormal with fusion of anterior > and posterior leaflets. The other leafelts were a bit thickened but > not rheumatic looking. There was obvious failure of coaptation.> The origin of the coronary sinus was 5cm from the valve with the RA > extending over the septum a bit like an Epstein's but definitely no > atrialisation of the ventricle.> > Our valve repair guru, Manu Mathur, helped me install a 28 mm > tricuspid ring and I closed a hole where the leaflets were fused.. > probably unnecessary and at the conclusion there was no TR.> > My explanation:> Some congenital TV defect with barely coapting leaflets pushed over > the hill by the high PA pressure after surgery +/- small infarct and > not able
 to correct itself when all the pressures were back to normal.> PRE OP TEE
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