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Archive for the ‘PCI PTCA Hardware’ Category

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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Cullotte is a trouser worn by 18th century French aristocrats.Now,in 21st century French interventional  cardiologists  found a striking similarity  of cullotte with  two stent strategy in bifurcation lesion .

Though this technique is in vogue for more than a decade , it has not been popular due to  perceived complexity .

It is making a come back in recent years , as we begin to negotiate bifurcation lesions with better expertise and hardware.

7  steps  in Culotte technique (From NORDIC study )

  1. Wiring  both main and side branch .

  2. Pre-dilatation of  main branch  and/or side branch,( Optional)

  3. Stenting of main branch

  4. Rewiring  side branch  through main branch stent strut,

  5. Stenting of side branch  through  main branch stent,(Now main branch is jailed by side branch stent

  6. Recross main branch  through struts of SB.

  7. Procedure completed with  final kissing balloon dilatation

culotte technique  stenting ptca pci 004

culotte technique  stenting ptca pci

culotte technique  stenting ptca pci 002

Reference

http://heart.bmj.com/content/90/6/713.full.pdf+html

NORDIC CULOTTE TECHNIQUE FOR BIFURCATION STENTING

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  1. The concept of  FFR is based on pressure gradient  alone.In any hydraulic model (Both biological and non biological systems ) pressure difference  is the least   important parameter  that determines flow.
  2. FFR  is unphysiological  as hyperemia   is  artificially induced one .(Adenosine  is not the only parameter that determines it !)
  3. Serial obstructions and branch point hemodynamics are  conveniently ignored.
  4. Reproducibility  remains a big question mark .
  5. On safety  issues  FFR  is a suspect.( Often times , it  requires expertise comparable to  that of a  complex  PCI !) .Beware , the FFR unit has stiff catheter system and is an additional health hazard .  I have witnessed   atleast two cases  where  insignificant lesions were  made significant by  FFR related Injury .
  6. And  now the  knock out punch ,  ! Probably the most vital  issue for which FFR should be banished * , it is not taking into account of vulnerabilty of a plaque .( An FFR > .9 with a hanging , eccentric , mid LAD lesion was left alone by one of the  academically up to date ,  evidence  based interventional cardiologist!  )
           (*If perfomed  in isolation without IVUS/OCT  )
I am still wondering how this concept came into cardiologist domain and into the cath lab .It should have  never been let out of theoretical physics labs !
Final message
The best way to assess physiological significance of an anatomical obstruction is  to  do  exercise  stress test .
If  the lesion is  able to sustain good exercise capacity , it  can be deemed physiological unimportant.
While , this is an explicit  proof  in single vessel disease  ,  even  in   multivessel  CAD ,   EST  is   a  collective  measure of  coronary  reserve flow .( Something like instantaneous equivalent of virtual  multivessel  FFR  )
Moderated After thought
FFR is a highly specialized theoretical  tool , that has very limited role in cath lab .
The two major practical (Non academic)  use of FFR   is to shun away  those   internet fed ,  annoying, pseudo  intellectual patients ,  who constantly ask for  angioplasty  for  obliviously insignificant lesions !
FFR comes very handy  to  bail out  cardiologists at  times of distress   ! (To escape  from the wrath of our patients   after a sub optimal &  technically inferior   PCIs   and   in  the  long term confabulations  in   restenosis  after stenting !  )

//

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Soft skills in pPCI 

Experience  would tell  us only about 70-80 % of STEMI are truly eligible for a  good  quality pPCI .(Multivessel CAD, Complex bifurcation lesion, difficulty in identifying IRA, No IRA-sapsms , complete spontaneous reperfusion )  The remaining 20-30 %  should , logically  be included in the failed pPCI category .This fact is largely concealed in the literature .

Beware of huge thrombus load in every patient with STEMI .The  contribution of  mechanical occlusion  vs thrombus  (in the total occlusion )  is the single most important factor in determining the intervention strategy.

Deploying a stent in a poorly  prepared (debrided of thrombus  ) lesion confers  further continuous  risk of a STEMI .Stents smartly jail  even large thrombus against the coronary vessels and they release it into the lumen in a controlled fashion  and prolong  the  acute coronary  risk phases

If thrombus aspiration  does a neat job and establishes a good   flow , if the   lumen  appear   good , think twice or even thrice before deploying a stent .It is akin to stent a  zero % lesion and we know it is foolish to do that at any stretch of imagination .(Stenting has never been proven to convert a vulnerable ulcerated lesion into stable one )

IVUS, OCT are not the answer in the above situations  as we are dealing with  emergency coronary  fire fighting !

Of course the intensive anti-platelet   protocols , will take care of  potential after effects of the intra coronary contact sport we play  !    . But . . . there is a limit for every thing. So spend as little time as possible when attempting catheter based reperfusion during STEMI.

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Japanese are the pioneers in CTO reopening .(I understand they do less   CABG surgeries  for  religious reasons ) CTO is the ultimate test for cardiologist patience .  it may  take  hours to open up a CTO (or even to abandon it .)  Here is a  success prediction tool from Japan .

cto score success in chronic total occlusion

j cto score  sheet

Source courtesy  : JACC: Cardiovascular Interventions Volume 4, Issue 2, February 2011

Reference

http://www.sciencedirect.com/science/article/pii/S193687981000912X

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Dear Cardiologist , can you spare a minute  extra  in cath  lab   . . . and give many happy years for your patients !

clock

PCI  (Fondly  called PTCA)  made  a  humble  beginning from  a Zürich hospital in 1977 . In 4 decades  it has become the staple diet  of most cardiologists ,   of course bulk of our patients benefit from that . When Gruentzig introduced the concept stent was never in the picture .Now stents have become mandatory in all most all PCI (We have gone one stop ahead (probably in  the  wrong direction !)  and given a cult status  to  drug electing stent .

Now we enjoy our work  with countless tools and techniques in our coronary automobile shop .

Suddenly  . . .   0ne primitive ,  common sense based question  is  asked !

How many seconds are required to optimally dilate and deploy the coronary stent ?

This  debate is   thrown out  live into  cath lab  . . .  by this simple and elegant study from the prestigious CCI journal.

cci journal ptca pci balooln inflation time

Highlights

  • 105 patients, 150 lesions , Three different stents were used
  • Cypher Select (55%)  , Xience V (30.%), Taxus Liberté (15.%)
  • Three  balloon inflation timing
  • 5, 15, 25 seconds
  • Complex lesion (B2) formed 26 %

balloon inflation time pci ptca

 

This paper concludes ,  duration of stent balloon inflation has a significant impact on stent expansion. Stent deployment for >25 sec is recommended.

It again keeps the vital answer  to our guess !  Can we inflate it for 60 seconds  ?  After all 60 /120 seconds both  are greater than 25 sec is isn’t ?

Final message

This seemingly simple paper  conveys a  strong  message  .

Time is every thing , . . . we have to be fast . . . where we need to  (Time is muscle)  and we have to be slow where we  need to*  .  It has rekindled  the  basic senses  of  our  supposedly advanced brains !

I agree  . . . every minute of cardiologist’s life is precious  as  “Time is  also  Wealth”  , still few minutes of caution and   patience  in cath lab can make world of good for our patients !

* The most important determinant of cath lab complications ,   is lack of patience on the part of cardiologist .Next only comes , expertise , adequacy of hardware  etc . Surprisingly , patient factors  come in the bottom of the list in most non emergency interventions.

Reference

http://onlinelibrary.wiley.com/doi/10.1002/ccd.23343/abstract

Further questions ?

  1. Can post dilatation be as  efficacious   as that of  stent- balloon  dilatation ?
  2. In difficult lesions  , the sum of  “Pre  / Per / Post”  balloon dilatation  gives  us net inflation  time(NIT)  Does it  add any sense to our understanding of optimal stent deployment  ?

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