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FAQs in STEMI : Why is the 3 hour gap recommended before pharmaco Invasive strategy?

Posted in acute coronary syndrome, Cardiology - Animations, Cardiology -Interventional -PCI, Cardiology -unresolved questions, cath lab tips and tricks, Infrequently asked questions in cardiology (iFAQs), open artery hypothesis, STEMI, STEMI -Managment, STEMI-Primary PCI, Thrombolysis, tagged , , , , on August 14, 2019|

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. There is something called medically( or spontaneously )stabilized ACS.  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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Critical gaps in STEMI knowledge base : What is the relationship between “Time window” and “Age”of IRA thrombus ?

Posted in cath lab tips and tricks, PCI PTCA Hardware, Primary -PCI, STEMI, STEMI -Managment, STEMI-Primary PCI, Thrombolysis, tagged , , , , on February 9, 2019|

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 

 1.Rittersma SZ,  van der Wal AC, Koch KT, Piek JJ Plaque instability frequently occurs days or weeks before occlusive coronary thrombosis: a pathological thrombectomy study in primary percutaneous coronary intervention Circulation. 2005 Mar 8;111(9):1160-5. 

 

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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Side branch sacrifice : Smart cardiologists shall do it scientifically !

Posted in Cardiology-Coronary artery disese, cath lab tips and tricks, side branch jailing, tagged , , , on June 2, 2018|

This seems to be good side branch sir, … a resident was mumbling as he was reviewing the RAO caudal test shot .Forget that diagonal man , focus your mind on main vessel , If you keep pitying these small twigs , you can never become a glorified Interventionist .I heard one of the senior consultant  was telling (rather yelling) at his assistant !

I used to wonder ,why should the fate of side branches be decided by the mercy of semi cardiac Intellectuals ?

What determines the hemodynamics after side branch jailing ?

  • Size
  • Territory
  • Myocardial viability
  • Alternate source
  • Collaterals

How do you classify side branch jailing ?

Okamura et all (Ref 3)offered a new OCT based classification based on the shape of the jail grills.

TakayukiOkamura classification of side branch jailing

JACC Cardiovascualr Interventions 2010 : Okamura  types V, T , and H jails. Implications are many both during short term as you cross , recross /rewire etc.Long term implications are largely unknown.

Does Jailing Implies flow is Interrupted  ?

This is the most critical question, We got the answer from University of Southampton in 2007 a rare and vital contribution to the knowledge base of coronary physiology. It said the struts won’t block the flow, it simply bumps on the path of blood.

You know , if the side branch ostial diameter is 2.5 mm the luminal area will be around 6sqmm. At least 1 or two struts is likely  occupy and criss cross the ostium. The issue is more than  simple compromise of side branch flow .The major concern is  the ostial jail should not be a nidus for future thrombosis that can spill over to main branch.Unfortunately there is no single meaningful study that addresses this issue of long-term patency of main vessel  in which  small side branches were jailed.(We in our department  have just started to analyse this aspect of coronary Intelligence )

Markers of significant side branch compromise.

For most of us it is not a big deal .I think there is none .There are little discussion  on new onset angina or troponin elevation after side branch jailing.

Can we Jail LCX ostium (or even LAD ostium ) during Left main PCI ?

  • Jailing a side branch can be casual or even a fashionable act , but can you do the same for left main bifurcation ?
  • It’s all about what you mean by side branch ? and the reaction time , and the useful muscle mass the branch would supply etc.
  • In emergency situations , there has been occasions one even put a stent across left main to LCX.Tackle the jailed LAD later if required.

FFR analysis of side branch jailing

Image courtesy from Bellenger 2007 Heart

Doing a FFR to assess the significance of side branch is simply a obsessive academic exercise .It is not warranted in most clinical situations. This study has taught us most side branches retain good FFR give us more confidence to sacrifice the sibling branches of main stem arteries.

Final message

Practicing cardiology in a truly professional way in cath lab can be tricky.We need to disrespect most of the side branches .Believe in your gut feeling (or your consultant’s.) If you are a sensitive scientific cardiologist do FFR pre / post procedure to the side branch .If compromised physiologically try probing the jailed struts and dilate one of them in absolute blindness , of course with a strong conviction of doing good for the science’s  sake.

A Research concept  

Long term sequelae of side branch jailing on the main branch ostia  (Please acknowledge  if some one take up this study )

References

1.

2. Bon-KwonKooMD, Hyun-JaiKang,Tae-JinYoun Physiologic Assessment of Jailed Side Branch Lesions Using Fractional Flow Reserve Journal of the American College of Cardiology Volume 46, Issue 4, 16 August 2005, Pages 633-637

3. Okamura T1, Onuma Y, García-García HM, Regar E3-Dimensional optical coherence tomography assessment of jailed side branches by bioresorbable vascular scaffolds: a proposal for classification. JACC Cardiovasc Interv. 2010 Aug;3(8):836-44

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Critical Issues in PCI :”Left” main cries foul . . . calls for “Right” thinkers ?

Posted in CABG Indications, cardiac surgery, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology wisdom, cath lab tips and tricks, tagged , , , on February 10, 2018| Leave a Comment »

Conquering  left main disease is considered as crowning glory for the Interventional cardiologists. For over three decades , CABG has remained the undisputed modality which is being challenged  today. Fortunately, the Incidence of true isolated  left main disease is  low .(If Medina bifurcation subset is excluded)

 

left main

With growing expertise , advanced hardware and Imaging ( like a 360 degree OCT fly through view ) one can virtually sit inside the left main and complete a PCI .

Still , coronary care is much . . . much  . . . more than a technology in transit !

Most importantly, these complex PCIs require rigorous maintenance protocol  with meticulous platelet knockout drugs , patient compliance and the genetic fate of drug efficacy . (Clopidogrel has since entered the final laps of inefficiency while Ticagrelor has some more time I guess !)

What is the current thinking  about  unprotected left main PCI ? Let us know it from real life experts !

For those answered , yes to  the above question please leave this page , as the following question might  trouble you much !

While competent surgeons are waiting to tackle left main by surgical means ,there are many centers which are Inclined towards  PCI though we lack long-term outcome (At least 10 years like CABG )

Why do you think this is happening ? Are you ready for another crooked poll ?!  

What exactly is left main disease ?

Some of  us also suffer from a knowledge gap and tend to think  Bifurcation lesions  and left main disease are two distinct entities .The fact of the matter is , significant subset of bifurcation lesions are Indeed either left main equivalents or true left mains ( Medina 1,1,1 would constitute > 50 % all  bifurc lesions )  If you include Invisible left main lesions in Medina ( 0,1,1 or 0,0,1 ) detected by IVUS/OCT  it might reach easily cross 90% (Scientific guess !)  Does that mean we have to think CABG even for all complex bifurcation lesions ? and reserve left main disease for isolated discrete mid shaft or ostial left main ?

Final message 

My observation (Sincere to my limited conscience !) at least in this part of the world is : Left main Interventions are  “perceived as pride” and its more related to “show of expertise” and is little to do with patient outcome.Unfortunately , cardiologists should not be blamed for it in isolation as the studies they follow are conflicted.

Forget SYNTAX/PRECOMBAT trials, the two famous studies EXCEL (Favor PCI) and NOBLE were published in 2016 made our life tough .One suggested PCI is acceptable /on par with CABG, while the  other one put CABG superior , ensuring clarity  replaced with confusion ! When we have a dispute , logic would suggest we should fall back on the status quo ie “CABG is superior” unless proved convincingly. Many sections of cardiology society failed to appreciate this.

Post PCI thoughts

*It may not be that hard to do a complex PCI . But, it’s never easier to understand current cardiology literature that is supposed to raise our intellect , which has a direct relevance to patient welfare. Note, many crucial , high stake studies  tend to play academic deceit games  with  linguistic and statistical hyperboles like Non Inferior , likely superiority , Never inferior , near equipoise , regression of hazards, virtual follow-up in  real vs trial world etc , etc !

I can only hope for a better scientific world !

Reference 

  1. Which is the best option for left main disease PCI or CABG ?  Journal of Individual wisdom and evidence based conscience : Volume 1 Chapter 1- Coronary Intellect : Pages 0 to ∞ Jan 2018.

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“Non academic” Tips and tricks in CTO – PCI : Open sesame ! , Show me your treasures !

Posted in cardiology -Therapeutics, Cath lab Hardware, cath lab tips and tricks, cto chronic total occlusion, tagged , , , , , , , , , , , , , , , , on November 27, 2017| Leave a Comment »

We know, The Mysterious Alibaba cave opens  with a voice password . . . legend  tell us it had unlimited hidden treasures. It would appear , CTOs mimic the cave in several ways. What is inside ? Should we open it ?  Can we come out safely ? Do we have any magical password in cath lab to get across the complex tissue boulders ?,   every cardiologist would love to have one !

chronic total occlusion alibaba cave corsair fileder xt pronova guideliner micro catheter asahi cart reverese cart cross boss sting ray

Dear CTO,Open Sesame . . . I have come with all the wires you love !  Please let me in !

Indication

“CTOs are never an emergency  . . .but please realise  we can very easily create one  while resuscitating a dead snake  ! 

Don’t think hard on evidence , then , you may not do a single case of CTO in your life .Forget all those pessimistic trials like OAT,COAT, etc and the recent ones DECISION-CTO. Ignore all guidelines. Ask your patient, and his insurance company , if they are willing , reserve the cath lab and get ready.

Pre-procedure  planning

Spend at least a hour to analyse the CTO Imagery one day prior and create n action plan.

Keep knowledgeable staff for assisting , but never ask for fellow colleagues help because it hurts our ego !  Cardiac surgeon’s back up is a welcome addition even if it’s on paper.

If possible , try to ask the patient genuinely ,what is his symptom at least once !  before starting the procedure. 

Timing of the procedure.

Don’t post a CTO patient  either on a busy Monday morning  or lazy Friday afternoon.

Hardware Inventory

The wires ,catheters, the balloons form the essential tool box .There is more than a  handful of coronary automobile companies manufacture this .It is all about metallurgy , knowledge of wires, catheters , and tip thickness, (Bullet shaped as in Asahi ) , slipping , hydrophophic or philic,  polymer coating , trackability, pushability , memory etc etc.

Guide wire tip morphology is as Important as the  Lesion characteristics !

Analysis of the lesion (Probably most important)

Unlike conventional PCI we have no initial target.We need to poke first and find the target next ! Distal vessel status  is most important ( Careful review of retrograde filling  through collaterals could give more information than CT angiograms .Calcification, diffuse disease can be a real hurdle)

Lesion morphology

Softness of lesion has to be felt (Requires good wire which has sensor (Paccinian corpuscles and Merckle disc ideal ?) I guess the cortical tactile feel is as vital as the  intervention expertise .I know at least one diabetic colleague of mine who finds it difficult  to cross a CTO  and admits he never found it easy to feel  the lesion through the wires . Autonomic dysfunction ?)

Operator  expertise

(Note: These are like reading  swimming guidelines , you can’t learn in the shores reading books ! you have to plunge !)

Many techniques are proposed .Sequential approach (Ironically experts are licensed to use  specialized wired wires directly .Beginners  are advised to go with non specialized hardware and escalate step by step) Some centers are blessed with new age weapons like cross Boss and sting ray that confront the lesions in multiple frontiers. (Carpet bombing?)

CTO playground. : Its essentially a coronary contact sport with expert septal surfing , tunnelling, knuckling , kneeling , bending . Of course , It  can end up in a gratifying win in few , still most of us tend to play this game without a goal (post !) Source of the Image : Unknown Due credits to the creator.

They are basically about poking the head of the lesion and trying to cross an occluded vessel  millimeter  by mm towards the presumed distal vessel in an Imaginary trajectory. Proximal cap, central core ,the blind tunnel , distal capsule and exit points each must be successfully conquered.

CTO crossing is  the ultimate capacity of the operator to realise and feel the position of the wires in true lumen and their confidence levels in their conviction!

Multiple wires up to three are used some times to poke the lesion two of them are used to shut the false tracks and the other one is expected to enter the true lumen (Looks too good on theory !) . These are referred to in as many terms like parallel wire see-saw , CART ,Reverse CART etc .Retrograde techniques do help us but has no magic solutions.The lumen contrast , guide wire tip movement and its  side branch entry  would help.

Tacking complication :Always anticipate , it’s not negative mind set to look for it  !

Keep pericardiocentesis kit , covered stents , micro  snares and other retrieval devices ready in cart. Your support staff should be well versed with what is happening around them. Some of  the dye leaks and stains are safe .They imply minor perforations that form  sealed hematomas  (The plane of perforations also matters. myocardial (ab-pericardial ) leaks are well tolerated .Distal perforations are also safe as long as CTO is not opened ) Online echocardiography should be readily available to monitor  pericardial space leak.

When bleed into pericardial space is life threatening , A comical, but life saving option is to close the artery and restore the CTO  its original state and come out of the lab quietly ! 

Newer Imaging guidance : Can be useful , still may not matter much  when considering the interventional acumen .

CTO PCI : Time as therapeutic end point.

CTO is not an endless game with out time frame .In my opinion it shouldn’t cross 45 minutes each as in a  soccer  game with a brief  strategic time out and of course with liberal use of ,yellow and red cards

Future directions

Japanese are the ones who pioneered  CTO Interventions . We expect more Innovations ! Is it the forward looking IVUS ? It is akin to tunneling for underground metro train with GPS guiding .If you can mark the proximal and distal  points , rest will be be taken care by mortised self tunneling catheters from Robotic arms steered by sophisticated algorithms.

Final  message

CTO PCI remains a real Interventional challenge. We are often double blinded  in both directions (antegrade as well as retrograde ). Needs much effort ,time, hardware and most importantly a non fatigued mind and body. The benefits we get may vary  between  gratifying to outright mediocre .Of course , it surely satisfies operator ego and express pride and courage !

Is crossing and stenting  a CTO  synonymous with true success ?

Yes it is , for the cardiologist and  the hospital  . . . I’m not sure about it for the patient !

In this  sense , CTOs  mimic the mysterious Alibaba cave that tempts us with Imaginary treasures but can trap us with a wrong password !

Post-Ample

* Who should CTO PCI  ?

I have seen  young , enthusiastic cardiologists with Immature support staff attempting CTO in remote sub- urban settings ! Though patience and expertise are essential ingredients, some amount of organised training and hardwares make CTO PCI safe and effective. Enthusiasm and affordability alone can’t be an Indication for this complex set of coronary lesions.

Reference 

 

I still wonder why  this vital paper was never published , it was just presented in the Annual ACC conference March 2017

http://www.eurocto.eu/

 http://www.cct.gr.jp/

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What is the difference between “under-expansion & mal-apposition” of coronary stent ?

Posted in Cardiology -unresolved questions, cath lab tips and tricks, tagged , , , , on March 31, 2017| Leave a Comment »

Improper or technically deficient stent deployment is a major factor for post stent events .Few terminologies are used in assessing stent deployment.

Under expanded stent (UES) 

A stent is not fully  expanded to the desired or to its specified diameter.

This is often due to inadequate balloon pressure during inflation .

Many times its technical and It requires post dilatation.

Under-deployed stent is  often  due to a struts hitting a  hard surface or calcium .

What is mal-apposed stent  ? (MPS)

It’s a fine gap between the vessel wall and the stent.

It can be observed immediate or late. Immediate is usually due undersizing of stent.

Intermediate or late malapposition  can be due to many  reasons

  1. Due to dissolution of thrombus in the  vessel stent interface
  2. Positive vessel remodelling creating new gap between vessel wall  and stent remodeling
  3. Vessel wall regaining vasomotion and  ? ( Is it the culprit with bio vascular scaffold)
  4. Stent rejection hypersensitivity and inflammatory reaction is a rare possibility.

What is the acceptable mal-apposition ?

No stent deployment is perfect . Mal-apposition can be focal confined to one or two struts or can be diffuse . (Branch vessel are naturally malapposed)Doing a routine OCT /IVUS is inviting trouble as no cardiologist can sleep in  comfort even after a reasonably good procedure.So we have created a safe  dead space with a width of 200 micron as an acceptable mal-apposition  (As if , the 7 micron RBCs and 2 micron  platelets can’t  get trapped in this dead space)

Is routine post-dilatation the  answer for all  mal-appostion?

Not really , still It is most logical step. Liberal post-dilatation  can be a problem as it may increase plaque prolapse and may re-release or dislodge  the  thrombus trapped during the initial expansion and triggering a no- reflow.

Undersizing vs underexpanded stent

Selecting a smaller stent for a given vessel diameter is another common error that result in MPS. This again can be tackled(Though not ideal)  by high pressure inflations.

under-expanded-stent-vs-malapposition-post-dilatationstent-malapposition-vs-underexpansion-mal-apposition-under-expansion-ivus-oct
 under-expanded-stent-vs-malapposition-post-dilatation-200-microns

under-expanded-stent-vs-malapposition

Is self expanding stent best option for preventing mal-apposition ?

May be.It has more radial strength, and it is expected to take care of the current and possible  future gaps of created by positive remodeling.

Other stent related issues 

  • Plaque prolapse
  • Stent edge dissection
  • Longitudinal miss
  • Stent fatigue and fracture

Final message 

UES and MPS , though discussed separately by cardiologists , from the patient point of view , the difference is  camouflaged in technical semantics since both carry risk significant risk of recurrent ACS or restenosis .It has become fashionable to believe one needs to  be worried more about visible UES than invisible MPS.

Reference

2. Lotta Francesco Prati, Enrico Romagnoli, Laura Gatto, Alessio La Manna,Clinical Impact of Suboptimal Stenting and Residual Intrastent Plaque/Thrombus Protrusion in Patients With Acute Coronary SyndromeThe CLI-OPCI ACS Substudy CIRCINTERVENTIONS.115.003726

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Ignorance based cardiology : I guess this question will bother you . . . Which is the side branch for Left main ? 

Posted in Cardiology -unresolved questions, cath lab tips and tricks, tagged , , , , , , , , , , , on March 19, 2017| Leave a Comment »

Bifurcation  angioplasty is a  newly conquered(Or not yet !)  target  for Interventional cardiologists.We have come a long way  in planning  interventions  for left main  with state of the art  hardware, expertise and  image assistance .However , every  classification , approach, strategy  for BFL talks about tackling the main and  side branches meticulously.

Still . . . one question  is not answered clearly is  . . .

A mini MCQ.

Answer: Open for contribution.

My inference

*It all depends upon the Indication and Individual arterial ischemic burden. In ACS, if  LAD territory is infarcted and beyond 24 hours.LAD becomes a  side kick to the vital LCX which supplies  the remaining life sustaining myocardium which includes the critical basal segments.

Final message 

Since , the risks involved in the interventions of  left main and its bifurcation is inherently linked  with , what exactly we mean (and do ! ) to the side branch .Its mandatory we spare few intellectual moments before our hands invade the coronary battle zone.

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Anatomical basis of self sealing coronary dissection flaps : An Illustration

Posted in cath lab tips and tricks, Dissection coronary, tagged , , , , , , on November 4, 2015|

There is something to understand in the movement of dissection flaps with reference to incoming coronary blood flow.Why some dissections dangerously escalate and totally occlude within moments while some others seal spontaneously ? Though uncommon ,  retrograde dissections has some unique hemo–anatomical property .

dissection flaps antegrade vs retrograde

 

 

 

benign dissection no flow limiting self sealing

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Forward looking IVUS : A catheter with a camera on its leading edge !

Posted in cath lab tips and tricks, ivus, Newer technology, tagged , , , , on February 22, 2015| 2 Comments »

Cardiologists do magic inside the human coronary artery , that too in a  live beating heart , unlike the surgeons.Blocks are removed , holes are closed, valves are inserted ,  scars are burnt, new electrical connections  are laid .They do this with relative blind vision with good degree of success. Still, as we aim for more precise interventions we require excellent imaging  modalities to assist us.

In  PCI of CTO(Chronic total occlusion)   the critical element to know  is  the morphology of the  tissue plane , what  exactly  we burrow ?  as we navigate  through complex, often hard shapeless tortuous tissue tunnels  . Our patients will be  surprised to know we are currently doing this with our eyes shut. If only we have a camera guide in the tip of the wire it give us tremendous advantage .

CTO pathology

The CTO morphology .Image source : Kenichi Sakakura ,Eur Heart J. 2014 Jul 1;35(25):1683-93.

The exiting IVUS technology can only look sideways . Now a new vision is added by annular array of transducer at tip with CMOS sensor .The technology is just coming out it would be  use for us in the near future .

Anatomy of the forward looking ultrasonic eye

ivus forward loooking cto intervention

Reference

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What to do with this curious 90% LAD obstruction ?

Posted in Cardiology -Interventional -PCI, Cardiology -unresolved questions, cath lab tips and tricks, tagged , , , , on January 24, 2015| Leave a Comment »

A patient with near 90% LAD disease who had a significant TMT/EST positivity with no clinical angina  was  subjected to FFR by a scientific  cardiac physician. Since FFR was recorded as  .9 , he was adviced against a stent and sent home with drugs.

Now , in the  physiological assessment of a coronary lesion ,  which one you are going to trust , TMT positivity or FFR ?

FFR  measures trans-lesional pressure drop  by creating a artificial exercise physiology  in a particular coronary bed by injecting just one of coronary vasodilators  namely Adenosine. FFR assessment can never be considered truely  physiological .There has been huge discrepancy in the amount , rate and route of administration and the hyperemic response to Adenosine.

Final message

In a single vessel disease population , if TMT is positive the lesion is to be taken as significant, irrespective of FFR.(Provided Anemia and other systemic factors are excluded )

*Read this and get ready to get  confused further , single vessel disease with TMT positivity  doesn’t mean medical management is never an option .OMT ,(optimal medical therapy ) even though a battered concept is not yet dead for SVD !

 

 

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