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Archive for the ‘Cardiology -Interventional -PCI’ Category

Cardiologists at confused cross roads !

Perils of  limited Intellect & Infinite greed  

When not so appropriately trained cardiologists  do Inappropriate things “use becomes misuse” . . . then, it won’t take much time for science to become total abuse. That’s what happened with the murky world of coronary stents .No surprise, it’s time to firefight the healers instead of the disease !

Now ,Comes the ORBITA study . Yes , it looks like a God sent path breaking trial that spits some harsh truths not only in cardiology, but also in behavioral ethics .Let us not work over time and hunt for any non-existing loop holes in ORBITA. Even if it has few, it can be condoned for sure as we have essentially lived out of flawed science  for too long  Injuring many Innocent hearts !

ORBITA pci vs medical mangement drsvenkatesan courage bari2d ethics in stenting auc criteria inappropriate coronary stenting placebo effect of stenting acc aha esc guidelines chronic st

Yes , its enforced premature funeral  times for a wonderful technology !

GIF Image courtesy http://www.tenor.com

Meanwhile, let us pray for a selective resurrection of  stenting in chronic coronary syndromes  and stop behaving like lesser professionals !

Postample

Extremely  sorry . . . to  all those discerning academic folks , who are looking for a true scientific review of ORBITA , please look elsewhere !

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The age old  statistics , 30 % of deaths following STEMI happen even before patients reach the hospital may still be true. But ,there is an untold story that happen regularly in the rehabilitation phase .Its ironical many  apparently stabilised STEMI patients still lose their life just before they get discharged or within 30 days .More often than not this happens in the toilet when they strain for defecation. At least a dozen deaths I have witnessed in the last few years. Of course we have resuscitated many near deaths as well.

What exactly happens to these ill-fated patients inside the toilet  ?

Straining is often an isometric exercise and prolonged strain ends up in   valsalva maneuver , a prolonged valsalva strain realistically shuts both vena cava due to raised intrathoracic  pressure .Vena caval shutdown is equivalent to asystole and imagine the chaos in the  delicately recannalised LAD when the coronary perfusion pressure nose dives (Even the  stented segment in IRA is vulnerable as distal flow restoration may take time   !)

The sudden systemic hypotension leads to  fall in coronary arterial pressure proximal  to the lesion. The normal physiological response to proximal fall would be corresponding distal fall maintaining the flow gradient . If the microvascular bed is damaged( loss of capacity to vasodilate ) this distal fall may not happen promptly .So its acute standstill of flow  across IRA ( or even Non IRA if it has a lesion )  triggering events that rapidly destabilise  unless intervened.

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hemodynamics of ffr lad valsalva 2

 

 

 

 

 

 

 

 

 

 

 

 

 

Other modes of sudden toilet deaths

*The opposite process , ie sudden spikes of blood pressure (In contrast to hypotension of  Valsalva strain ) can  occur as straining is equivalent to Isometric exercise which increase afterload .This can either cause LV failure, another episode of ACS, myocardial stretching, even tear it and result in mechanical complication.

  1. Acute LVF triggered by spikes of BP /new onset ischemic MR.
  2. Free wall rupture and tamponade.
  3. Emboli getting dislodged from LV during strain

How to anticipate and prevent these  deaths ?

  • All complicated STEMI patients should have special rehabilitation program.
  • A simple rule could be patients with persistent ST elevation with  are prone for further events.They should be flagged. (Stented / TIMI flows matters very little !)
  • Restrict all vigorous activity for minimum of one to two weeks ( I am not a believer of pre-discharge stress test even in uncomplicated MI  )
  • Use laxatives adequately.
  • Western toilets may have an hemodynamic advantage. Indian closets that require squatting which increase the venous return , ultimately it compromises coronary hemodynamics more. We don’t understand as yet ,what will happen if one perfoms a valsalva  and  squatting simultaneously.(Which will prevail over the other ?)
  • Finally toilet shouldn’t  be locked during rehabilitation for safety purposes.
  • All post STEMI pateints should have registered with emergency contact and alert service ready.

Has primary PCI has reduced the sudden deaths  in Post MI period in current era ?

I’m afraid , I can’t say a dogmatic yes . May be ,to a certain extent , However,  it has created a new subset of perfectly  stented still prone for ACS.A physiologically or pharmacologically  recannlised IRA generally heals by themself. A Stented IRA  hands over  the responsiblity of healing the injured IRA to us  .Ofcourse ,we try to do it  with lot of difficulty  .(Different versions of  confused DAPT  regimens !)

Final message 

Please note , “discharge to 30 day mortality” following STEMI   which is  upto 2 %  .It is the most neglected  and  mismanaged phase in coronary care .Toilets are definitely not a benign place for them and all the good work done by you in cath lab and CCU can be nullified in few Innocuous looking seconds !

Postample 

Is Toilet room death amounts to  negligence / mis-management  inside hospital ?

May be there is a reason for this argument. When to ambulate in complicated STEMI is a big question. ? Though we have guidelines some of the patients are reluctant to use assisted service.

I think its a calculated risk , and  there is trade off between the benefits of early ambulation and potential exertion related risk.

One such argument by a cardiologist in a medicolegal situation goes like this. “I thought my patient’s heart  is stable enough to use toilet , it misfired , hence it is just an error of  judgment. I can’t be faulted.  Though this argument appear logical , many times it can’t hold water in court of law !”

Reference

1.Siebes M, Chamuleau SA, Meuwissen M,   Influence of hemodynamic conditions on fractional flow reserve: parametric analysis of underlying model Am J Physiol Heart Circ Physiol. 2002 Oct;283(4):H1462-70

Further reading

Cardiac rehabilitation NICE guidelines  : Myocardial infarction: cardiac rehabilitation and prevention of further cardiovascular disease 2013

 

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If human coronary artery is comparable to live wire , attempting  bifurcation (BFL) stenting is akin to tame a live snake .True BFL  (with Medina 1, 1, 1)  being the most complex of all .The fact is ,we have atleast a dozen strategies for BFL with varying loads of metal abutting the ostia ,side branch and carina.This  would essentially Imply we are still struggling with these lesions .

While current science tends to vouch PCI* for most  BFLs . . . wisdom  might whisper CABG !

Who should do complex PCI ?

Obviously,  not every interventional cardiologist can. Confidence is one thing , but , falling short of minimum standard of care is rampant in India. Newer Imaging tools, techniques are promising , unfortunately  still the gap between, knowledge , science and  reality continue to widen.

* Its true ,some expert Interventionists do a good job !

What is the simplest approach for Bifurcation lesions ?

Final message 

We have come a  long way in BFL. Still , some of the lesions can sting  like a snake ! I am sure, everyone of us would have lost sleep after a complex BFL PCI !( Praying the humble  heparin and DAPT to do the rescue act ! )

bifurcation lesions medina stenting srategies 002

How to escape this double headed threat ?

A meticulous assessment of  patient  &  lesion , mindfulness in choosing the hardware & Imaging , diligent usage of anticoagulants & DAPT and  . . . finally  willingness to listen to your own conscience ,  will ensure a gratifying result that includes abandoning the procedure !

Reference 

For everything in Bifurcation Intervention

The ultimate source : Visit the in this link  European Bifurcation  Club

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Some of the noise bites from a busy cath lab after a  mid noon angioplasty

         Oh’  that  looks bad , whats that projecting !

There is some haziness too ,

            Make sure its not a flap,

  Better to do IVUS or should I OCT ?

           Shall I  post dilate with NCB ?

Should we cover with  another stent ?

           I think we can manage with Tirofiban or Reopro 

Call the chief ! suggested a first year resident,that seemed to be the most reasonable noise bite among all .Yes, the final command came from the chief cardiologist after a 10 second glance over the workstation ,”Guys,  forget it , . . its acceptable  pinching, DAPT will take care of it , just ensure adequate ACT till night , put the next case . . .on table” !

That’s fairly common chat session in any high volume cath centres (Which ended abruptly  in this case with the chief’s uttering)

Does any body know  what the chief meant by  the term pinching ?

  • Is it the  pinch of Intimal fold ?
  • Is it pinch of plaque ?
  • Is it a flap ?
  • Is it a plaque prolapse within the strut ?
  • Or just a evaginated thrombus
  • A subintimal calcium speck ?
  • A longitudinal stent deformation?

Any one knows the histology ? Is there any natural history  study of such pinching ?

Iam afraid no one knows . But common sense tell us it can be anything  between a totally benign entity to  Imminent nidus  for an acute stent thrombosis , depending upon the patient’s destiny and physician’s luck !

How does one make a decision in such an uncertain situation ?

The decision to leave that pinching is taken by any  cardiologist  based on his past experience or  Inexperience or both. Some do IVUS/OCT , many don’t . Whatever the decision  ( empirical or scientific ) its  going to be tentative  and  outcome is any body’s guess.

Final message

Coronary arterial pinching is a dangerous cath lab slang used exclusively by expert Interventional cardiologists , often after a hurried PCI ! It may sound  innocuous .To label a protruding plaque as a “safe pinch”demands heavy courage that is an essential requirement  for a successful Interventional  cardiologist , which most of them are blessed with !

Reference 

1.No Reference as such :There is no specific study about histology of coronary pinching  .Though , IVUS and OCT data are available for various post PCI shadows , it never addresses the issue of pinching specifically as no one is clear about what they mean by it.  Hence ,we are planning to decode this long pending mystery with our own  PINCH-iVUS  study.

2.This article from Circulation Imaging  new generation IVUS could reveal  histology of pinching

f5-large

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This paper was presented as a poster (Not good enough for  oral ! ) in the just concluded CSI 2016  (Cardiological society of India ) Annual conference at Kochi, India.

 

What constitutes successful  Primary PCI ?   A proposal to include “ LV dysfunction”  as an  essential  criteria !

A  series of breakthrough technologies  in drugs , devices, techniques has revolutionised the management of STEMI in modern times.This  includes various formats of heparin , antiplatelet agents thrombolytics  and coronary interventions.Of all these, primary PCI is considered to be the greatest thing to happen in STEMI care.

The success of primary PCI is currently defined as diameter stenosis less than 30% and TIMI 3 flow on final angiography without procedural complication. True success of reperfusion essentially lies  in the salvage of myocardium and in the prevention of LV dysfunction. In real world scenario we often find a paradox , ie Inspite of  successful pPCI by current definition a subset of patients suffer from significant  LV dysfunction. Surprisingly, LV dysfunction has  never been included in the definition of successful primary PCI .

success-of-primary-pci

In this context we did a reversed cohort  study  of patients with significant LV dysfunction (<40%) following primary PCI to find out possible factors contributing to LV dysfunction.10 patients who had LV dysfunction inspite of successful primary PCI were the subjects of the study. Patients with late PCI  beyond 12  hours were excluded .Echocardioraphy had been done at discharge and 2 weeks after the procedure to assess LV function.

TIMI  3  flow  has been  documented in all  patients at the time of primary PCI.6 patients had undergone pPCI within 6 hours.4 had it by 12 hours. 7 patients had a smooth , fast  pPCI as described by standard protocol.Of these,  2 patients had LV dysfunction inspite of TIMI 3 flow established early.7 patients 3 had complex angioplasty with no reflow managed subsequently.One had deferred stenting after 4 days for IRA.Non IRA lesion were also  tackled in two.

We also confirmed  there is no linear no correlation  between TIMI flow and  subsequent LV function .This becomes vital as time and again we are seeing PCI reports with successful TIMI 3 flow only to find  weeks later  thinned scarred ventricle. Time to reperfuse with anticipated and unanticipated procedural delay  was also  a critical  factor.

However, its clear the  incidence of significant LV dysfunction inspite of  timely, and apparently smooth  PCI is real .Why this happens is beyond the current reasoning. A scientific basis for  individual myocardial sensitivity to ischemic time is yet to be found. (Dynamic host dependent time window ?)

Meanwhile , It seems prudent , we should awake to a harsh reality of practicing coronary care  with a seemingly incomplete criteria for success of pPCI . Its proposed,  an  acceptable levels of  “LV dysfunction at discharge ” (It could be > 50 %) as an essential criteria  to define the success of pPCI  .Custodians of STEMI care should  immediately rectify this glaring omission. This will dramatically impact the current  outcome analysis of STEMI and help Improve the quality of care.

Conference bulletins

dr-venkatesan-e-poster

E-PosterPresentationSat10thDec csi cohin 2016

Session – Preview 

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Originally used in early 1990s,  self expanding coronary stents (Wall stent from Boston scientific )  subsequently lost interest because of delivery related issues. Many feel , it makes cardiologist judgment tentative and delivery system prevail over our hand skills. It is possible stents can longitudinally jump with high radial force making a geographical miss more likely.While it could be true with any technique till we master it, one should recall ,most endo-vascular work other than coronary still involve self expandable techniques.

Balloon expandable  stent is ruling the PCI field  for more than 2 decades. There has been recent surge of interest in the self expanding  technique and it could make a great difference in the PCI arena provided we take the proper cues.

Self expanding stents have some unique advantage

  • It has  high radial force.
  • Approximation with lesion is best
  • It tends to take the shape of the vessel than any other stent
  • Since the mal-opposition and gap between stent and vessel wall is minimal stent thrombosis is theoretically is  lower.

Where is self expanding stent useful ?

  • Ectatic and very irregular lesions
  • Bifurcation lesions where multi dimensional vessels with different shaped ostia converge.
  • Eccentric lesions (Non calcified) may be benefited by self expanding stents
  • Self expanding covered self (Is it available >)  may be the best bet for perforations and for thrombus  to be plastied against the wall.
  • In some small vessels PCI
  • Finally it may have a  role in primary PCI (APPOSITION 1 to 5 )

What are the self expanding stents available ?

  1.  Devax system   ( 2003)
  2.  Stentys
  3.  Radius (Boston scientific)
  4. Capella Sideguard.
  5. Cardiomind Sparrow
  6. vProtect luminal shield.

Final message

For some reason , self expanding stents were not tested widely  and  large scale data is not available. However ,  they are unique modalities in metal delivery and must be mastered and many patient subsets will be benefited by it. They are not obsolete yet, APPOSITION 5 study will answer some of the issues.

Reference

1. Agostoni P, Verheye S. Novel self-expanding stent system for enhanced provisional bifurcation stenting: examination by StentBoost and intravascular ultrasound. Catheter Cardiovasc Interv 2009;73:481
2.Jsselmuiden A, Verheye S. First report on the use of a novel self-expandable stent for treatment of ST elevation myocardial infarction. Catheter Cardiovasc Interv 2009;74:850
3.Verheye S1, Grube E, Ramcharitar S, Schofer JJ,.First-in-man (FIM) study of the Stentys bifurcation stent–30 days results.

EuroIntervention. 2009 Mar;4(5):566-71
4. van Geuns  R.-J., Tamburino  C., Fajadet  J.,  Self-expanding versus balloon-expandable stents in acute myocardial infarction: results from the APPOSITION II study: Self-expanding stents in ST-segment elevatation myocardial infarctiion. J Am Coll Cardiol Intv. 2012;5:1209-1219.

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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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