Archive for the ‘STEMI -Managment’ Category

How do you evaluate the success of thrombolysis or primary PCI  ?

If you say its coronary angiogram and the final snapshot  of  TIMI flow , you need to read further. If you thought its actually the quantum of ECG ST regression . . . great ,  you can exit this page  with credits.

CAG  may not be the gold standard in defining PCI success , it just tells you whether IRA is patent or not .Instead , the good old ECG tells you about whether  the myocardium is successfully reperfused or not .  TIMI flows are simply not good enough to identify  adequacy of  myocardial reperfusion .

By the way ,  who is telling this  ?


It appears there is only a  narrow gap between Ignorance and Knowledge !

That’s what the simple message I got  from this landmark study  published in year the 2000 in JACC by Shah.A in the thrombolytic era.The Importance of this paper  has far reaching consequences (If and only if we are  willing to accept and  understand  the concept and apply  as a whole in PCI era )

While success of thrombolysis is faith fully subjected to  the acid tests  of myocardial perfusion , primary PCI is rarely ever assessed in terms of  ST segment regression.

What is the next logical step this study should lead  us to ?  

I think I am not provocating  , . . How to  get rid of the prevailing practice of jacking up the success rate of primary PCI  ? ( Conveniently,  Ignoring the echo detected significant LV dysfunction on follow up ) Mind you, this has resulted in  creating a new crop of patient sub group called  “Angiographic success and myocardial failure”


Dear colleagues , please go thorough this article . Its from the thought leaders , Duke University ,North Carolina. I would argue the cardiology fellows to discuss this paper in detail in their  journal club as “classic paper”  till they  completely understand the conclusion .Though its  done with GUSTO 1 data  in primarily  lytic population,  its  conclusions are very much valid as an assessment tool  in reperfusion by any means.I am afraid, even 16  years after this paper  got published ,the truth has not penetrated to the targeted population within the cardiology community.

Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the “gold standard” for myocardial reperfusion assessment. Shah A1, Wagner GS, Granger CB, J Am Coll Cardiol. 2000 Mar 1;35(3):666-72.

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100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component’s  contribution in the genesis of  STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thromotic STEMI with  just a residual endothelial  erosion and hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion  seems to be biased and misunderstood scientific fact .

What happens once 100 % occlusion take place ?

Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of  tissue plasminogen system. In this aftermath  few succumb . ( Re-perfusion arrhythmia  generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus ,  and the elasticity of fibrin mesh , location of  platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3  flow !)

thrombus propgation
What happens to the natural history of thrombus in STEMI ?
Thrombus formed over the culprit lesion can follow any of the following course

  •  Can remain static
  •  Get lysed by natural or pharmacological means
  •  Progress distally (By fragmentation or by moving en-mass )
  •  Grow proximal and and involve more serious proximal side branch obstruction
  • Organise and become a CTO

Factors determining thrombus migration

The interaction between the hemodynamic  forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by  platelet vs RBC / fibrin core,  totally of obstruction,  reperfusing forces , re-exposure of raw areas and  the distal vessel integrity all matters.

While, logic would tell us,  thrombus more often migrates  distally  assisted by the direction of blood flow, an  opposite concept also seeks attention , ie since the blood flow is sluggish  in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.

(In fact, its presumed  in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to  queue up proximaly and  clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)

What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?

If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still  we don’t  know why thrombus aspiration in STEMI is not consistently useful. We also know little about  the length of the thrombotic  segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like  “cutting a slice of  butter” in some , while in few we struggle and  end up with severe no-reflow inspite of great efforts .Why ?

What is the Impact of distal collateral flow in flushing fresh thrombus ?

The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it’s soft and fail to get organised early that would help cross the lesion easily.

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Every one talks about  coronary excesses ! It happens  both  in acute and chronic  fashion , not withstanding the inappropriately  understood  . . .   appropriately  released  guidelines  on inappropriateness ! The  burden  of coronary syndromes of the humanity, I am afraid would  include these man made excess as well !

I stumbled upon two  small  “gems ” in this other wise wild dark  cardiology literature  .One from Kamaer , Netherlands and other from  Escaned from Spain.

Both  talk about a  simple and logical modality in the management of STEMI . If bulk of the STEMI events are due to coronary thrombosis just tackle it  . No more  . . . no less” Stent only , if there is tight residual lesion.

1. From Amsterdam , Holland.

krammer thrombus aspiration alone priamry poba for stemi no stent

2.This one is from Spain.These studies I am sure , only a fraction of the interventional community would have read .Reason ? We are always hijacked by the moments of glamor ! I am just sharing them .hope few are benefited

primary POBA thrombus aspiration alone for stemi no stent stemithrombus aspiration alone for stemi no stent priamry pobaThese two studies with total number of 44 patients has a potential to redefine  the entire practice pattern of acute interventional coronary care.(Of course , if only , we are ready to make sense out of it !)

But , the concept will be heavily banished by strong visible and invisible forces   for the simple reason it suggests a true possibility  of knocking  out the role of  stent from acute STEMI arena.

When I discussed with my colleagues  for a large scale study  on isolated thrombus aspiration in STEMI , they told it  is not possible for ethical reasons !

I was amused , denying such a study is biggest ethical blow to the field interventional  cardiology !

Final message

Proof of concept does not require numbers .A study with less than 50 subjects  can be far superior than multi-centre ,multi-blinded , self steered ,peer reviewed largesse ! The truth of the study lies in the core consciousness  of people who do it , not in the numbers and exotic statistical methods !.

After all , one of the greatest medical study  was  done by James Lind  (Father of RCT) who discovered vitamin c as an antidote for scurvy,  with a hand full of sailors  while they crossed the Atlantic many centuries ago !

After thought

You say , thrombus aspiration is great , Why the hell , TAPAS , INFUSE AMI, and TASTE studies  confuse us regarding thrombus aspiration  ?

Don’t blame it on thrombus aspiration .We do it perfectly . It is because of what  we do after that ! We decorate the coronary lumen finally with a piece of metal cherry  undoing all the goodness of a great pudding !

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