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Archive for the ‘STEMI-Primary PCI’ Category

Background STEMI knowledge check : Evidence-based Ignorance

I think , It is unfortunate, In the management of STEMI , the two popular strategies of myocardial reperfusion is made to fight with each other as if they are perennial enemies for over two decades. Suddenly, someone with a rare coronary insight thought, why fight each other , they can have a friendly hug and work together. That brought the concept of pharmco -Invasive approach or strategy(PIA) backed up by STREAM, FAST-MI, and TRANSFER AMI studies.Yes, it appears to work well and devoid of all the early adverse events of pPCI. (Much to the dismay of ardent fans of Primary PCI )

*May I add one more shocker of a fact . Deep subset data mining from the above trials did show very early lysis may even act as a perfect stand-alone therapy negating the need for acutely one pharmaco Invasive PCI altogether.(Which was never published) Don’t get alarmed the concept is nothing but , the good old lysis , followed by leisure & elective Ischemia guided PCI in all uncomplicated STEMI.

Now coming to the FAQ in Cardiology Boards: Why is the time window for PIA is 3 to 24 hrs ?

The simple answer for an uncomplicated fellow is “published studies have shown benefit only in this time window. If you do PCI early (,<3h) after lysis paradoxically both bleeding and pro-thrombotic complication over the stented lesions are more common. The upper limit is 24 hrs , since by that time we lose all the potential for myocardial salvage”

End-

Larger version of the answer

(Advanced readers who are willing to get confused, may read further)

1. Lysis and immediate PCI doesn’t go well at least in trial world. (FINESSE study, by Ellis et all NEJM 2008) Though cardiologists tend to blame lysis (effect of) to Interfere with their hand skills, it can very well be the opposite. The PCI undo the true benefit of lysis. For cardiologists to accrue maximum benefit in the early time window, they need to be too fast, in the process, they accelerate and fuse adverse events of both modalities.

2. The time window 3 to 24h could simply be evidence-based empiricism. In the major STREAM trial, invasive limb happened between 6 and 16 hours only. We stretched both in the top and bottom in the time clock and made it 3 to 24 hours with other trial data.

3. One realistic reason could be this. It requires a minimum of three hours for a patient to reach a place of coronary Invasion after lysis. So one may argue its time allowance for transport .It comes in handy at times.

4 .If the patient reaches earlier, we need to delay the PCI intentionally to please the evidence based medicine. Mind you, every minute delay increases the chance of no reflow as the microvasculature goes for edematous and porous death.

5. Please note, the time window for pharmaco Invasive strategy will go for a tail spin if the initial lysis is failed. Here, we have to rush I guess. Mind you, In this situation, the evidence based blaming that early PCI increases the adverse events immediately following lysis goes topsy turvy . This is where , we should recall old studies of routine rescue PCI (without clinical criteria) rarely succeeded to correct failed thrombolysis (SWIFT trial)

6.Now, why not PCI after 24hrs? The game can be played reversed if you document ongoing Ischemia in IRA or Non IRA, one may do it . The problem arises when the flawed thought process of a cardiologist could legally justify all PCI beyond 24 h /class 3 Indication after STEMI.The argument goes like this. I think this patient has residual silent Ischemia in- spite of severe LV dysfunction (Suspicion is the justification, to which ,unfortunately no one can dispute) It only suggests open artery hypothesis is still trying to raise from the graveyard more than a decade after its near burial.

Final message

To all those energetic, evidence-based cardiac physicians, we all know coronary care is all about time. In fact, we need to be blessed much more than a sense of time. Please realise , “timely and safe intervention” for your patients could simply mean either playing the time button slow/ fast / slow or fast forward / pause or simply shutdown the cath lab, reach home early and enjoy some music or movie in your favorite streaming player.

Reference

1.Ellis SG, Tendera M, De Belder MA, FINESSE Investigators Facilitated PCI in patients with ST-elevation myocardial infarction. N Engl J Med. 2008;358(21):2205–2217. [PubMed]
2. Armstrong PW, Gershlick AH, Goldstein STREAM Investigative Team Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2013;368(15):1379–1387. [PubMed]

3. Danchin N, Puymirat E, Steg PG, T, on behalf of the FAST-MI 2005 investigators Five-year survival in patients with ST-segment-elevation myocardial infarction according to modalities of reperfusion therapy: the French Registry on Acute ST-Elevation and Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 Circulation. 2014;129(16):1629–1636. [PubMed]

4. Cantor WJ, Fitchett D, Borgundvaag B, TRANSFER-AMI Trial Investigators Routine early angioplasty after fibrinolysis for acute myocardial infarction. N Engl J Med. 2009;360(26):2705–2718.. [PubMed]
5.. Bonnefoy E, Steg PG, Boutitie F, , CAPTIM Investigators Comparison of primary angioplasty and pre-hospital fibrinolysis in acute myocardial infarction (CAPTIM) trial: a 5-year follow-up. Eur Heart J. 2009;30(13):1598–1606. . [PubMed]

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Cardiologists are grappling with at least  half a dozen time windows  in the management of STEMI. (It can be combinations of any of the following :Symptom – DAPT Loading – Door – Needle /Balloon-Sheath, wire crossing etc ) Time windows are Important in choosing the right (or no)modality of re-perfusion . Though superiority of  primary PCI  is thought to be established in academic community , it  may not be in real world. Published studies that suggest pPCI is superior to lysis at any time window  still lack good evidence.

Why is this long drawn confusion  ? 

One of the important determinant of outcome in STEMI , is the thrombus organisation (hardening )time . Some how we have assumed PCI can tackle hardened thrombus  much better than lysis (In fact the outcome in late PCI is as bad or good as lysis in terms of true myocardial reperfusion in this population.This fact will not be visible in scientific data that’s read superficially .One has  to  mine deep for the truth) (Claeys MJ,. . Arch Intern Med. 2011;171(6):544–549)

Two more virtual pathological Time windows.

While we are preoccupied with certain time windows in STEMI  ,may I suggest  two more  Invisible pathological windows. I don’t know , whether these are presumptive theoretical stuff ,  but understanding these time windows will sharpen our decision-making skills in STEMI.

1.Symptom to  ATO time (Acute total occlusion) 

ery gets occluded(ATO ).This is truly Invisible time window .( Pre-Infarction angina  to Infarct time ) Taking the last episode of most Intense pain need not refer to beginning of ATO / Infarct pain. (ACS being as dynamic process in a 24 hour time span an angina  can even be post Infarct angina!)

2. ATO to thrombus organising (hardening) time

It is obvious time is primary factor that correlates with thrombus organisation. But there is much more to it. It’s not the fibrin organisation alone that makes a thrombus hard. ATO gets reinforced by plaque and tissue material ( like steel rods  inside cement) In other words no one really knows  when does the thrombotic process begin or end  and  hardens thereafter. But we know for certain is  tackling a hard thrombus is difficult for both modalities currently we have lysis and PCI*

.(Almost forgot the third modality,  yes its humble drug heparin(.It can do wonders little slow though , Slowness doesn’t matter beyond 24 hrs is it not ?) Now there can be a role for Warfarin also to get rid of chronic IRA thrombus (Moon JY, N The role of oral anticoagulant therapy in patients with acute coronary syndrome. Ther Adv Hematol. 2017;8(12):353-366.)

There are excellent studies that correlated time window to thrombus hardness.At least in  50%  IRAs with time  window less than 12 hrs have thrombus age more than 24 hours Some of the thrombus material aspirated has been shown to be many days old (Kramer et al PLoS One. 2009;4(6):e5817)

Image source : Miranda C.A. Kramer Relationship of Thrombus Healing to Underlying Plaque Morphology in Sudden Coronary Death Volume 55, Issue 2, January 2010

How to arrive at the age of the thrombus  ?

It’s a difficult task to guess the age of thrombus with help  symptom onset and ECG .  There  can be 50 %  error as discussed earlier.

Is coronary angiogram helpful ?

There is no good clue to differentiate fresh from old thrombus by just looking at angio shot. Some experts are able do it (Guess it ?)

Poke and feel with guidewire  : This is probably the best way to tell whether thrombus is fresh or old (Still not fool proof ) Most of us do this in STEMI . All is well if guide wire cuts through  smoothly and nice flow is established.(What we call guide wire angioplasty) Procedure is completed with or without a stent ( &residual lesion) .This is the most gratifying and desirable outcome of primary PCI. (Note : Hardness of thrombus can be overcome stiff wires and force.That doesn’t make it a fresh clot ! This is where we may end up with No-reflow)

nrcardio.2016.38-f4

Image courtesy : Karim D. Mahmoud & Felix Zijlstra Nature Reviews Cardiology volume 13, pages 418–428 (2016) Various forms of thrombus aspirated during primary PCI.

When poke test fails  . . . be ready for a long haul or quit

Thrombus is not a single aged mass of blood. It has lawyers of clot with different maturity  ( like shells over earth ).Hence poking has its own side effects too.Some of it can be violent.When  deeper layers of old thrombus is exposed to fresh blood it can create fresh  cycle of clot activation.( Ofcourse we fight it out with DAPT and heparin) Winner of this fight can never be predicted. To conquer the thrombus or quit is directly linked to the cardiologist wisdom.

What about OCT/IVUS ?

They could help us to assess the morphology of thrombus and give  us Indirect clues about the age of thrombus. Some of the experts say they use it efficiently . My opinion is it adds more glamour than true enlightenment .(Mind you , we need to  cross , clear and flush the vessel to complete OCT. The fact that we are able to complete OCT in STEMI settimg would mean  thrombus is  fresh .In that way it may be useful but without a true purpose.)

Thrombus aspirate analysis : Its more scientific way of arriving at the age of thrombus (Any one want to do carbon dating on this ?) , This again lacks practical use as we need to assess  the thrombus age before poking to avoid subsequent complications. It is also not clear whether thrombus in STEMI is more of RBC and fibrin and net platelet content can’t be quantified.This especially true in stuttering ACS where NSTEMI is threatening to become STEMI or vice versa. (Platelets love to hug each other at high shear force , RBCs do the opposite )

Is the Consistency of the thrombus uniform ?

Here comes the importance of the length of the thrombotic segment. It’s estimated the length of the thrombus segment can be anywhere between 1 cm to entire length of the coronary artery distal to the site of occlusion .The initial proximal part may be soft as its directly exposed to DAPT and heparin.The distal thrombus is flushed only with collateral or a trickle of flow from anti-grade .So ,very likely the distal thrombus is harder than proximal.

How does DAPT loading and subsequent heparin interfere with thrombus organisation ?

Loading DAPT has a definite impact and prevents hardening.(But, one issue is it shouldn’t have been happened before administration)

What is the natural history of organised hard thrombus in IRA ?

  • It transforms  into a CTO.(Many of us believe this is dominant theme)
  • Late total recannalisation – 20% by 30 days
  • Partial recannalisation  (More than 20 % ?)
  • Since wide-spread use of predischarge PCI , true natural history is masked.

Final message

Taming STEMI with pPCI  is not always  a time sensitive emergency procedure . It’s important to recall STEMI patients can harbour thrombus with different maturity .We know STEMI can occur even in  patient with chronic thrombotic process also (even a CTO) . This is proven by a simple fact people walk in 3 days after MI casually. Further, during pPCI both early and late arrivals have equal difficulty though they carry different set of problems tackling the IRA.

If we really  believe principles of coronary care is aimed at tackling coronary thrombosis , wisdom  lies in  judicious use of both CCU and Cath lab facilities .Never hesitate to rush back the patient to CCU for a quick lysis (Or Intra coronary) and avoid the potentially prolonged  battle against huge mass of hard thrombus.

Reference 

 

Post-ample : A quote 

Importance of  early arrival of STEMI patient to nearest hospital is huge , not because of the possibility getting an emergent PCI . Rather, it is  due to fact that simply reaching the nearest coronary care center dramatically reduce the mortality.(My guess is , this mortality benefit should be more than Lysis/pPCI put together)

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It was 1912 , Titanic had just sank off the Atlantic . When the world attention was elsewhere , An unassuming young Dr.Herrick J.B silently working in his Michigan lab inquisitively proposed thrombus occluding the coronary artery is the chief culprit in acute myocardial Infarction.It took seven more decades when Davis et all from Glasgow .UK. proved it by doing dramatic angiographic studies soon after STEMI in year 1979.

Now, even after 100 years , we, the confused cardiologists debate endlessly in glamorous global conclaves in exotic locales whether to aspirate these humble looking thrombus, threatening to damage the myocardium with every passing moment !

Why is this controversy ?

My answer

I am failing to understand the concept and the answer is elusive .While every one agrees that thrombus is true culprit, in bulk of the STEMI , still we are not authorised (In an assertive fashion ) either to lyse as first choice or to aspirate as second choice.

It seems vital, thrombus must be tackled vigorously by any means. Drugs,lytics,(Intravenous or Intra-coronary.) by micro and rheolytic catheters .Only documented, flow limiting complex mechanical lesions must be stented. If we are convinced tackling thrombus by mechanical means is problematic (As studies would suggest ) lysis should prevail over aspiration as a routine measure by default isn’t ?

*It’s a been quite a while , the world cardiology community has made it appear thrombolysing a patient who is otherwise eligible for primary PCI ! a “coronary crime*” Ofcourse , I must say , I proudly commit that crime with rewarding results in many MI patients.

*In fact , I would think not promoting or delaying prompt lysis should qualify for the definition.

In the management of STEMI, prehospital lysis followed by a Intensive care in a good coronary care center is best modality.

This doesn’t mean in-hospital lysis is banished. Yes, STEMI is a cardiac emergency , but triaging STEMI patients must be done by scientific means (STEMI risk score) as well with accumulated wisdom .Rush only true emergencies into cath lab. (A best estimate is about 20 % of all STEMI) If we are not able to decide which STEMI will require prompt PCI , it would Imply we need to go back and do once more the basics postings in coronary care of resident days !

An angry counter from a young Interventionist

Only God can tell whether a given patient with STEMI will (or will not) derive maximum benefit from pPCI. We are not yet trained to make that decision by looking at patient and his ECG.So my logic is all STEMIs are equal. I will continue to do emergency angioplasty in all STEMI patients . I expect them blindly to accept all the potential complications arising out of poking the thrombotic milieu in those low risk patients who might have done well with thrombolysis.

Never afraid of challenges. It is like going to war. Casualties are bound to happen.We have enough technology , Imaging , expertise, to tackle all those complex lesions we encounter during primary PCI especially in elderly comorbid patients. We can even do a triple vessel angioplasty , left main etc. Only Yesterday I posted in my nonstop whatsapp group , where I did a dramatic acute angled bifurcation angioplasty for a stable STEMI patient that required a iFR guided jailed side branch assessment and 3d OCT transmitting stunning snaps of fresh thrombus, ending with a semi culotte procedure.The patient is doing well with a Impella 2.5 device and a high frequency ventilator support and my anesthetist has promised me to wean him soon ! I must actually thank his Glo-Health plus Insurance company for clearing the procedure.

An Important tip for complex lesions during STEMI

We need to know there is always a saving grace , if for some reason we couldn’t accomplish PCI due to complexities of the lesion with multiple IRA mimickers. We can always sheepishly thrombolyse these patients inside cath lab . . . a modality just few minutes ago would have been ridiculed with all our vigor to convince the anxious family for a costly Invasive procedure !

Reference

3. Herrick Original paper . https://jamanetwork.com/

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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  ?

knowledge-2

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”

Reference.

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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A STEMI patient arrives late after 48 hours with chest pain .There is  persistent ST elevation.

What is the likely mechanism of this chest pain ?

  • Index infarct pain continuing . . .
  • Post infarct Angina-IRA territory
  • Re-infarction following intermittent re-perfusion  and re-occlusion
  • Remote  ischemia from a branch of IRA
  • Ischemia from a possible  non IRA lesion in a multivessel CAD

If this patient  comes to a non PCI eligible centre. Will you lyse him  ?

If post infarct angina is  unstable angina  . Isn’t  thrombolysis  contraindicated in UA  ?

How to differentiate Post Infarct Angina from Re-Infarction ?

A very tricky issue indeed.

Unless fresh ST elevation with fresh enzyme peak is documented these entities  cannot be differentiated.

(Even  fresh ST elevation can be related to infarct expansion ,stretch or early acute remodeling.Fresh enzyme  release or new peak  may not represent new infarct always .It can be due to intermittent re-perfusion of IRA .It may  simply represent a  enzyme  flush from the index infarct zone)

What is the practical , realistic , (Unscientific !)  solution  ?

Why break our head ? Never bother to differentiate PIA   from Reinfarction  etc . Let  it  be any thing . Do a emergency CAG .Stent  whichever  lesion looks good  for the same . Of course , make sure he has enough insurance coverage .

 

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We know  streptokinase  is a non fibrin specific   agent that   results in systemic lytic state and hence more chance of bleeding.

TPA is fibrin specific  and it  will act only on fibrin  bound to clot , hence systemic bleeding risk should be less.

However , in real world , it is well  documented  stroke risk with TPA is consistently more than streptokinase .(It varies between .0.3-.5% with streptokinase , 0.7-to 1%  with TPA)

How do you explain this apparent  paradox ?

Possible explanations.

  1. The fibrin selectivity pf TPA is not absolute* .
  2. The lytic power of  TPA is more hence stroke is more likely.
  3. The FDP* released by TPA can trigger a systemic lytic state
  4. In the  post TPA protocol   heparin  is  mandatory and  this  contribute to stroke risk.

*What happens o fibrin degradation products (FDP) levels after TPA ?

FDP levels do increase after TPA  .This peaks at 1 hour after lysis.it Correlates well with risk of stroke.(Ho CH, Wang infarction.Thrombosis Research ).

Reference

This is an excellent review with analysis from 14 studies with total of 142 907 patients with thrombolysis

A meta  analysis of thrombolytic agents streptokinase vs tpa tnktpa  stroke risk fibrin slectivity

Ho CH, Wang SP Serial thrombolysis-related changes after thrombolytic therapy with TPA in patients with acute myocardial infarction.Thrombosis Research

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Pharmaco Invasive approach (PIA)  is the new mantra in the management of ACS.It simply means the intention to do PCI   should always  be the  driving force in every STEMI patient , whether the Initial lysis is successful or failed .

This concept is exclusively created  for centers where there is no cath lab (This would include  hospitals  with  inactive labs ,  cardiologist  team  who lack required expertise !)

What to do after lysis ?

  • If  the initial lysis has failed  “Rush” them  for an emergency  PCI.
  • If  Initial lysis is successful  “Send”  them for PCI in a  less emergent manner.

Generally the  time window for PIA is 3-24 hours.  In failed lysis  technically it could be as early as 1 hour as that is the time to assess the efficacy of initial lysis. (Of-course the theoretical transfer  time to be added )

Why the 3 hour period for PIA ?

We know routine   facilitated-PCI(f-PCI)  with various combinations of  fibrinolytics  and 2b -3a antagonists is a failed concept. (FINNESS )

One of  the primary reason for f-PCI to fail is , the  very narrow time window  between drug and balloon which somehow  end up in more hazard  (Needle -Balloon window)  .

If they are very close the harm is likely to be more ,still they have to be closer if lysis has failed .(This is the reason many old studies had depressing results with even with the  concept  of rescue PCI !)

Lytic agents and PCI  even though we assume to compliment each other real world evidence indicate they share a love hate relationship .

 

Beware, PIA is one form of facilitated  PCI.

If we agree routine  f-PCI is a failed concept we are in for real trouble. PIA indeed may  masquerade as f-PCI  if  you combine lytic and PCI in sequential fashion in a hurry !

My point of view is is a  successfully lysed STEMI should not be rushed to cath lab .If  he  some how reach the  cath lab ultra fast manner , it behaves like a  f-PCI and he is going  to harmed more !  by the current evidence base  isn’t ?

If the  inital lysis was successful , with a  less complex anatomy, it is  possible your PCI  that is going make the lesion more vulnerable.

(The other  issue is tied with flawed human instinct. One can’t stop with CAG in a PIA* .Interventional  cardiologists rarely have the courage to leave a well recannalised IRA  without PCI.)

**Still , you need to facilitate the PCI in complex intervention in  true rescue situation.That’s were we require the collective wisdom.

Assumptions galore in ACS

We have difficulty in  identifying true success and failure of lysis .Vagueness with which we make decisions  in CCUs and cath labs  , is exemplified by the following facts. Post thrombolysis , 40%  patients with persistent ST elevation are asymptomatic and 30 % of all those with complete  ST regression , still have occluded IRA.

We are also uncertain when do  the muscle  truly  die after a STEMI ! It is 6 hours in some, 12 in many, 24h  in few , 36 h in a lucky ones .The role  of collaterals, intermittent patency , individual variation  resistance to myocardial hypoxia injury cannot be  be quantified .

Final message

  • The importance of Needle to Balloon  time (NBT) time in PIA  is to be strongly emphasized.
  • This time can vary between 1-24 hours .But practically it will start from 3 hours .
  • The irony is , we have conflicting  engagement with time in PIA. We have to  strive for both narrowing as well as intentionally  prolonging this time window .
  • It has to be narrowed in true rescue situations and   optimally prolonged (Or is it indefinitely ! ) in non rescue situations !

After thought

Can we do pharmaco-Invasive approach(PIA)  in PCI capable center ?

  • Even in PCI capable centre one may get struck in proceeding with anticipated primary PCI for various reasons . If delay is anticipated we  have to fall back on thrombolysis .This we call as  unscheduled  or bail out  phamaco Invasive strategy .
  • Intentional PIA   in a PCI capable hospital for all low risk MI is also a viable and option .Never think  primary lysis   for STEMI  even if we  have lab ready is serious medial crime . After all , pPCI has a very  marginal benefits in if any in all low risk STEMI!

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