Archive for the ‘Cardiology -unresolved questions’ Category

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.


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 !


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 !”


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 !


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 !


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


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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.



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.


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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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Critical multivessel CAD is commonly confronted by cardiologists .These patients either receive multivessel stenting, CABG, with or without optimal medical management(OMT) !

CABG is always done with intention of  complete revasularisation  for all significant lesions. Comprehensive  multivessel PCI though feasible is not practiced widely.Considering the diffuse nature of CAD no treatment is complete except probably intensive medical management.

As of now , addressing only one (or two ) critical lesions in a triple vessel disease by PCI though appear attractive and logical is considered unscientific.Guidelines are not clear in answering the issue.


In a triple vessel disease with a critical LAD lesion,  

Shall we do PCI for LAD and medical management for lesions in RCA or LCX  ?

How about this coronary wisdom  “While medical therapy can take care of less tighter lesions , only critical lesions need catheter based Intervention”

In fact, in STEMI setting we do apply this logic of  targeting one lesion (IRA) at a time. Why not in chronic coronary setting ? There are significant  pros and cons for this approach.While, most 0f us will go with the logical herd,an unique  paper by Mineok  asks us to think again(American Heart Journal, 2016-09-01, 157-165)

How do you define the completeness of revascularization? Is it not emprical ?

We know medical management has well documented advantages in chronic CAD. while multivessel stenting has its own hazards.Hence limiting the time spent within the coronary artery and reducing total stent length should be one of our important goals.

A mini quiz  . . .

How often you have left a fairly significant lesion (attending only the critical lesions )  in your practice ?

What do you think will happen to those non critical lesions  in the long run  ?

Do you believe earnestly drugs can take care of these lesions ?

Forget the science . Whats your experience and  gut feeling ? 

Do you agree , even surgeons do not always do a complete revascularisation either intentionally or for technical reasons ?

Finally ,why we are still  hesitant to call intensive medical therapy as a  “Revascularisation  equivalent”  inspite of valid proof for improved functional class, symptom relief , regression of atherosclerois , collateral preservation and improved microcirculaion.

Final message 

I would say , the science of coronary revascularisation in chronic CAD is stranded at a confused cross road even after three decades of aggressively grown interventional cardiology .At any given point of time medical  management can give a tough fight to catheter  based intervention in most stable IHD.

Hybrid therapy doesn’t always mean combination of PCI and CABG. Judicious mix of PCI and medical therapy is also  a hybrid modality that can bring CAD burden effectively in a meaningful fashion with less metal load.   If you can convert a critical triple vessel disease to non critical DVD or SVD with a single stent it should be welcomed without prejudice. 

With a section of cardiac scientists are in hot pursuit for a completely  bi0reabsorbable stents , let us adopt this “Minimalistic PCI approach” in multivessel CAD, till the time  we reach the “dream the end point” of modern coronary care , ie to  get rid of stent altogether by biological cure for atherosclerosis.


1.Mineok chang, Jung MinAhn, Nayoung  complete versus incomplete revascularization in patients with multivessel coronary artery disease treated with drug-eluting stents Kim,American Heart Journal, 2016-09-01, 157-165,

 2.Tamburino C, Angiolillo DJ, Capranzano P, et al: Complete versus incomplete revascularization in patients with multivessel disease undergoing percutaneous coronary intervention with drug-eluting stents. Catheter Cardiovasc Interv 2008; 72: pp. 448-456

3.Wu C, Dyer AM, King SB, et al: Impact of incomplete revascularization on long-term mortality after coronary stenting. Circ Cardiovasc Interv 2011; 4: pp. 413-421

4.Gao Z, Xu B, Yang YJ, et al: Long-term outcomes of complete versus incomplete revascularization after drug-eluting stent implantation in patients with multivessel coronary disease. Catheter Cardiovasc Interv 2013; 82: pp. 343-349

5.Ong ATL,Serruys PW. Complete revascularization: coronary artery bypass graft surgery versus percutaneous coronary intervention. Circulation. 2006; 114: 249255

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Less than a century ago an easy chair  was enough to manage this most important medical emergency of mankind. Of course, at that time mortality of STEMI was estimated to be around 30%.We have since pushed the in-hospital death rate down to less than 10 %  and its around 5-8% currently.(*The lifeless chairs were able to save 70 lives is a different story!)

Heparin , thrombolytic agents, critical coronary care has helped us to achieve this , of course It must be admitted primary PCI also played a small role (at best 1 % ) in our fight against this number one killer.

Now, why not combine  both lysis and PCI ?

The concept of PIA (Pharmaco Invasive approach) came into vogue  primarily for two reasons.

1.If thrombolysis and  pPCI are powerful strategies by individual merits why not combine both and achieve double the benefit ?

2. Since pPCI is going to be a logistical nightmare in most points of care and we can’t afford to lose time . So, let us lyse first and consider PCI later !

Unfortunately medical science is not math .One plus one in medicine is rarely two !

Though , it looks attractive , Pharmaco invasive approach  has its own troubles.Fortunately , most of them are man-made, few are beyond our knowledge though.

Following general rules  may help us

  • STEMI  should ideally managed by early thrombolysis (or PCI) in all deserving patients.
  • Don’t wait for PCI if you think , there will be delay or reduced expertise and poor track record of the center in this modality.
  • Pharmaco invasive  therapy is not a default in all STEMI .Do good quality , monitored  lysis , (Not necessarily new generation thrombolytic .(I prefer one hour sustained thrombolytic regimen , not the hit or miss bolus) .As a learned cardiologist we need to assess individual patients according to the type and risk of MI.Its not wise to blindly follow the guidelines ,because these guidelines , though based on evidence never answers a query in a single patient perspective !

The key “branch points”  in decision making  after lysis

  • Invasive strategy  should begin within one hour if the patient has failed  thrombolysis and has developed any mechanical issues.( Mind you, LVF requires good medical stabilization .Rushing  such patients to cath lab without application of mind can be disastrous )
  • If the Initial  lysis is excellent and the patient is asymptomatic  one need not proceed with invasive limb at all.(A significant chunk of apparently failed lysis by ECG are asymptomatic and comfortable , these are patients require delicate assessment regarding further intervention. )
  • If the MI is large and the clinical  stability is “not confirmed” one may  proceed urgently within 24 h.
  • In any case there is no role for invasive approach after 24 hours* Unless fresh ischemia  suspected to come from IRA or  non IRA.
  • Having  said that, there are many centers that do a diagnostic  angiogram alone just prior to discharge  (48-72h) for risk stratification and then take a genuine call for a possible PCI or  CABG. In my opinion it appears a sensible strategy , though a non invasive stress  test pre/post discharge can even avoid that  coronary angiogram !

One issue with Rescue PIA

Though by current definition  PIA is to be done  3-24 hours , don’t wait for the 4th hour if you have recognized a failed thrombolysis earlier than three hours.( Ofcourse , as the gap between P and I gets too narrowed it may  carry some adverse  effects witnessed in routine facilitated PCI -Refer FINESSE study ) Similarly,there need not be a blanket ban on PCI beyond 24 hours if residual ischemia is active.

Final message

PIA is a dynamic  coronary  re -perfusion strategy . Nothing is fixed in science. . The optimal gap between Pharmaco and invasive strategy  can be anywhere between  1 hour to “Infinitely deferred” depending upon individual risk perception and wisdom of the treating cardiologist.





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