Posts Tagged ‘low flow’

A patient with  extensive anterior STEMI  presented 18 hours  after onset of  chest pain . He  was  other wise stable and free from angina but had persistent ST elevation (5mm in V 1 to V 5 ). He had a  total occlusion of LAD  with TIMI zero  flow . He had a  tight PDA lesion  as well . A bed side echo revealed LV EF  of 50% . The septum was hypo-kinetic but did not appear severely dysfunctional .

So , it was decided to open up the LAD. The moment  LAD was opened he developed severe acute LVF  /   flash pulmonary edema   .  Even after a 30 minutes of  heart (Fire )  fighting  he could not be resuscitated .

What is the mechanism of death here ? Expert  STEMI interventionist  from core  labs  may answer this !

An acute ischemic MR with myocardial disruption was suggested . Why it  was triggered after opening the IRA ?

Three mechanisms were discussed

  1. Re-perfusion injury
  2. Collateral  damage
  3. Physiological  de-stabilisation of  Contra -Lateral lesion (Remote lesions )

Re-perfusion Injury ?  How relevant it is in cath lab ?

Is re-perfusion injury  electrical  ,  mechanical or  both ?

In this particular patient even though there was a total LAD occlusion , the segments supplied   by  the LAD  was partially functional and  it was contributing to LV  pump function.  The moment  a trickle of   flow was established  , some thing happened and the whatever  little mechanical function  his LV  had  was also interrupted  . The LV came to standstill and the patient died .

If re-perfusion Injury is  simply an   electrical  event   like VF ,  it can be resuscitated . If it is mechanical  outcome is bad ! This is not a new concept  . It is  part of the  once famous  concept called myocardial stunning . There are  lots of reasons   for stunning  to be a  clinically relevant phenomenon .Unfortunately   if any cardiologist talks about it in 2012 ,  he is at risk of  labeled  as old fashioned !

Collateral damage.

One more mechanism which we feel that  might have contributed to death here  is   the  “collateral damage” .(This is not cross fire !)

We know collaterals can be recruited within 12 hours in many STEMI patients . In some  it can even salvage  significant mass of  myocardium . The acute collaterals to LAD may be interrupted  during primary PCI . Once you poke the lesion the coronary  vascular  bed which had dilated  (as a response to total occlusion ) may react with inappropriate vasoconstriction . This raises the local hydrostatic pressure (Myocardial edema)  and further impede  the   incoming  micro collateral flow . This a very  critical time  for the myocardium  where antegrade and retrograde flow are kept in a fine balance .

Interference with remote lesion Hemodynamics .

Another possibility  is  the  opening the  LAD lesion some how  impact on remote lesional  flow as well (PDA  in this patient  )

Please remember ,

Even a transient hypo- tension can have  devastating effect in  the  hemo -dynamics   of  non IRA  territory  especially if it harbors a critical lesion !

Final message

Coming to the title question  , Is no – flow better than  slow- flow in late presenters of STEMI ?

Common sense dictates whenever  an artery is obstructed  just get rid of it.  When  it  comes to the heart it must be done in an urgent basis That is the essence of primary angioplasty  . . .  agreed . But in this  patient  I believe ,  the  common sense  was proved wrong !

Truths are always hidden.  The  science of  myocardial re-perfusion is a perfect example . We need to learn a lot still !

This I  call as  Para cardiology : Heart  facts without  evidence !

Counter point

One may argue this   is an  exceptional case  in STEMI  intervention. Don’t  hype   exceptions  and undermine the importance of a great concept ! Exceptions  and rules  are directly related to our  experience  we have accrued.  Exceptions are the great  knowledge substrates  and help  crack  medical  mysteries !

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