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Archive for the ‘Cardiology -unresolved questions’ Category

A young man aged around 40 years, had a STEMI was promptly thrombolysed in a small hospital located about 40 KM away in the suburbs of my city Chennai. They did an awesome job of saving the patient life and salvaging the myocardium.

Now begins the story . . . one of the non-medical person who is the owner of the hospital has an unfortunate working  business relationship with a frighteningly big nearby hospital  which had signed a memorandum of irresponsible understanding . It demanded any  patient who arrives in the small hospital with MI should be transferred at earliest opportunity to them.

So, an ambulance was arranged  and the patient (with a fairly well reperfused heart ) was shifted  in an emergency fashion . It reached desired destination after nicely chugging along the choked chaotic Chennai evening traffic for 45 minutes.

The guy was taken directly to cath lab through the side doors to perform a second salvage  procedure on a successfully opened IRA. Young cardiology consultants  in designer cath suite welcomed the smiling ACS patient to their posh new lab .Did few rapid radial shots, mumbled among themselves for few minutes,  decided to stent  a minimal LAD lesion for a patient who was in  zero distress with well-preserved LV function.

*The relatives of the patients were curious when they were asked sign a fresh set of consent which elaborately  mentioned about possible life risk during the procedure.

The patient’s wife  was clearly  amused and she pointed out to the superior cardiologists about  the earlier briefing by the Inferior freelance cardiologist who treated him in the previous hospital. She recalled , “I was told in confident terms  that  Initial thrombolysis  has been spectacularly  successful and bulk of the treatment is over and risk of complication has dramatically reduced”.

Then why is this distressing risk taking story again ,  she asked ?

The doctors hurriedly explained ,”this procedure is different. We are sorry to say we have no other option but to add  further risk to you” ! but , its all for your good !

Why should I ?  If the initial lysis is very successful  why do you want to meddle with it again ?

No Madam , you are ill-informed , you can’t talk like that .This is what modern  science  is all about. Leave the professional decision to us. We need to check immediately  whether the lysis is really successful .We can’t rely on the ECG.Further, true success lies in stenting the lesion as we fear the ill-fated site may close again.We are  taught to practice protocols based on standard scientific guidelines. This hospital has highest rating in-terms of quality care. That’s why we got updated ISO 2000  NABH accreditation

The women who is a soft ware engineer was smartly and  scientifically silenced in 5 minutes flat !

Post-amble :

What happened  to the patient then ? (When you fear something it happens is in’t the  Murphy’s law ?)

The apparently asymptotic and comfortable patient had uneventful PCI. A  long drug eluting  stent  was  implanted in recanalized  lesion in LAD with around 30 % narrowing that ended with an innocuous looking diagonal pinch. The procedure was uneventful , however next day he developed some fresh ECG changes and chest pain . The worried team took him for another angio found  stent was patent But , ultimately after a stressful 3 days of stay , some thing went wrong he ended up with new LV dysfunction.He got discharged fine with a caution  that , his stent needs to intensively monitored for the next 1 year since technically he had recurrent ACS !

Lessons we don’t learn from such cases.

When two procedures are done to accomplish the same aim (Reperfusion) , but with  differing success rates, expertise, time ,and unpredictable hazards , the benefits from them may not add together. There is clear knowledge deficit here. Scientific data can never provide fair answers to  these questions  as all real life cofounders can never be recreated in study population.

While we expect 1+1 to become  two in pharmaco-Invasvie strategy  ,one should realise it may end up with  either zero or even  – 2 .

1 -1 = 0

-1 + (-1)=  -2 ?

Learning cardiology from lay persons 

The patient’s shrewd wife threw this question ,

After two modes of re-perfusion done sequentially in my  husband’s  heart ,  at a total cost of Rs4.5Lakhs Why he  is  still left with significant LV dysfunction (Which was  around 40% EF.)

The query raised by the lady appeared much more crucial and logical than the ones discussed in many top-notch live interventional workshops we attend every few months!

As usual , I started mulling over the issue. There is something wrong with the way , we  understand  the pharmaco invasive approach-PIA .You go with it only if  initial pharmacological  approach has failed.

Of Course ,there is one more modality possible ie Pharmaco -Angio strategy where in, you look at the coronary anatomy and take a call ! This sounds good , the only issue is taking a right call ! My experience suggests wrong calls are the rule and  exceptions are rare. Then a whole new issue erupts about all those non IRA lesions

Final message

So till we have gain complete self-control over our evolved ignorance and evolving knowledge , it is better to follow this proposed  funny new ACS algorithm called “Pharmaco -non invasive” approach (PNIA)  in asymptomatic ACS patients  who have had apparently successful lysis.

*Please note, Incidentally  PNIA actually  refers to simple good old traditional stand alone thrombolysis.

Counter point

No one can deny Interventional cardiology carries a risk of untoward effects.Don’t blow this out of proportion. Do you know, how many lives have been saved by routine Pharmaco -Invasive approach ?

I am not sure , my experience may be limited.Let me ask the readers. Is routine PIA is warranted in all asymptomatic , successfully lysed STEMIs ?

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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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Bernoulli principle states  that , when a high pressure jet (Air, Water, blood etc ) moves over a conduit,  the pressure exerted by the jet on its sides (Lateral wall) reduces . The velocity gain is equal to pressure drop .This is why we take velocity as a rough guide to pressure gradient and the sacred formula in doppler echocardiography 4V2 came in to vogue . (Incidentally, Bernoulli principle shares the same principle when aircrafts  lifts from runway at its peak speed as the pressure above the wings   drops to zero or negative  and the plane lifts up.)

Please note , the pressure should drop both above and below the aircraft by Bernoulli principle .But, the engine and wings are arranged in such a way , the air speed below the aircraft is slower and hence the pressure is high below and low above and the lift occurs promptly at take of velocity. Imagine , how the valve leaflets in heart is subjected to lift and drag forces every time the blood gushes with high velocity flows.This is also the reason for the Pulsus bisferiens, SAM in HOCM, Coanda effect in supra valvular stenosis, and any post stenotic dilatation.

 

In Echocardiography the Bernoulli equation is modified.

In clinical doppler echocardiography, we have liberally simplified the original Bernoulli equation by ignoring the the proximal sub valvular velocity V1 . Further , two more components in the equation is also amputated  for our convenience ! (Flow acceleration and the viscous friction) .This is the reason we tend to err many times  especially in outflow tract gradients and prosthetic valve gradients .

Pressure recovery phenomenon.

This  is another  hemodynamic lacunae in clinical echocardiography. We know, thepeak velocity of blood is attained  just distal to site of  obstruction. As the distal velocity beyond the obstruction begins to fall, the pressure tends to recover corresponding to the loss of velocity. This happens to certain distance beyond the obstruction. Since continuous wave doppler measures the pressure in its entire axis of alignment , it  is likely to pick more pressure samples  from the recovered areas and net result is, it measures more than the true difference in gradient across the valve.The phenomenon is most relevant in assessment of Aortic stenosis and results in over estimation of severity of stenosis.

How much can be the overestimation ?

It can be up to 30 % or even more.Especially in prosthetic Aortic valves.

How to recognise it and overcome it ?

  1. First of all,  recognise such a hemodynamic phenomenon  exists and the sacred 4v square can be a myth !
  2. Never go with gradient alone in diagnosing valve stenosis. Look for 2D features also.This is more vital when you suspect acute valve obstruction.
  3. Always add the proximal sub valvular velocity (V1 ) in your Bernoulli equation .It need to be subtracted.
  4. The effect of heart rate on pressure recovery has not been properly studied.(The impact of which  could be vital and hence too many false prosthetic emergencies could be avoided, as cardiologists tend to rely mostly on gradient than anatomical diagnosis of valve obstruction like visualising thrombus or struck leaflet by TEE or fluro.

Does this phenomenon happen with cath gradient ?(Generally it’s more pronounced in doppler echo )

Yes, It does happen in cath lab also , as its related to physics of flow. It can be minimised if we can use two simultaneous catheters ,one in LV  and the other Aortic catheter placed very close to the leaflets.

pressure recovery in aortic stenosis animation

Click below for an Animated version

pressure recovery phenomenon in aortic stenosis 005

Note the pressure recovers from P 2 to P3

Reference

Pressure recovery phenomenon in doppler echocardiography

pressure recovery phenomenon doppler echocardiography

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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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