Significant MR is a contraindication for PTMC. However,  If MR jet is central , and mild (some times little more than mild as well ) PTMC can be safely done. The MR may not worsen .It may even disappear.

Note: Eccentric MR jets are indirect evidence for sub valvular disease. Its very likely to get worsened and may require a mitral valve replacement .

Here is patient with severe mitral stenosis, the MR is in all probability safe.

Angle of eccentricity 

One must realise , the eccentricity of a jet is not very objective .What may appear as central jet in long axis may be wall hugging in 4 chamber view. This is very important to recognise. Further , even central jets can reveal a invisible eccentricity detected only on 3D MR jet reconstruction.

One simple way to ascertain central jet is to  check whether the MR jet align in the same angle as diastolic color jets of MS into LV inflow . (Looking carefully ,the diastolic color jets also provide us info about sub-valvular disease )

More anatomical distortion in this patient 

Incidentally , this patient also had another anatomical adversary  ie ,the bulge of IAS into right atrium. This can happen two ways .Septal aneurysm or a normal septum bulging to RA due to raised mean LA pressure.



Miral stenosis with Atrial fibrillation showing the changing mitral inflow jet .



The radius of curvature of IAS bulge Indicates its more of septal weakness that contributes than the raised pressure. There is a small risk in these patients the IAS flap may give way during the procedure and a small ASD may be created .(Hemodynamically may not be significant though)


How does the MR disappear after balloon dilatation ?

If you ask this question , it means your are a thinking cardiology fellow , good.

Guess your answer. Its all about physics of  MVOs behavior  in systole and diastole . The mitral valve tissue attachment and adhesion causes not only a  diastolic narrowing but also a fixed systolic regurgitant orifice.Once you relive it the leaflets begins to co-opt normally without a systolic leaky orifice.

Final message

Though there are clear contraindications ,suitability of mitral valve for PTMC is more of a personal experience and confidence. A MR jet of grade 1  may be acceptable. A huge LA, Distorted IAS anatomy, a clot confined to LA appendage are relative contraindication only. The puncture site on IAS , minimal manipulation guide wire within LA, a gentle over the wire technique to cross mitral valve or some of the tips for success.

Never hesitate however to refer complex cases of mitral stenosis to the surgeons. Of course , you can’t insist them to do a valve preserving OMV .It is unfortunate(They have good point of argument as well)  most of the surgeons have have made Mitral valve replacement as a default modality

Post ample :

When we were cardiology fellows , we used to have a mitral valve scoring system for suitability for PTMC. Its called Wilkin’s score. Its a purely an anatomical score. (I guess still its expected in Board exams) What we need is comprehensive anatomical and physiological assessment of mitral valve. With due respects to  published literature this scoring system lacks  two  vital parameters we look before PTMC , namely the extent of commissural calcium  and degree of MR.


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)


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.



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)

Let me see how many find sense in this Nonsense !

Cath labs are propably the best place to practice preventive cardiology . . .

Practice of medicine is primarily guided by Infinite Information , plenty of Intuition, little bit of Intelligence and unquantifiable amount of Ignorance.The science of coronary reperfusion is standing example for variable mix of the above.The term no reflow is a jargan used liberally in cath labs right from first year fellow to super consultant without knowing what exactly they mean by it.

What really is No-reflow then ?

The academic definition :According to Kloner no-reflow is defined as suboptimal myocardial reperfusion through a part of coronary circulation without angiographic evidence of mechanical vessel obstruction.( Kloner RA, Ganote CE, Jennings RB. “The “no-reflow” phenomenon after temporary coronary occlusion in the dog.” Journal of Clinical Investigation, 1974; 54: 1496–1508.)

With due credits to his seminal paper, I always wonder what exactly Dr Kloner meant when he labelled it as No-reflow!

No is ok , Flow is ok , What does the adjective “re” mean to you ?

Re stands for repeat ? recurrent ? Yes , it may mean any one of it. It may mean nothing in many patients as their post PCI flow is same or found to be no better than pre PCI flow with no significant forward flow at all ! In this situation No-reflow is same as No-flow (Never flown ) in physiological terms irrespective of epicardial patency.

Literally, the term no re-flow tell us, there has been a dramatic procedure related*( or preexisting ) destabilization in distal blood flow. It can be any downgrading of basal TIMI flow. ( Example : TIMI 3 becoming Zero , or TIMI 1 becoming 3 then back to 1 or Zero.) The terms slow flow, low flow, stuttering or trickle of flow all fall under the common  category No reflow. In a crude manner one may conclude no reflow to be  masquereding term  for failed PCI.

*Mind you , No reflow can also occur with pharmacological lysis as well.(Less common)But personal experincee suggest it has a less benign course.

Mechanism of No- reflow

Many mechanisms has been proposed and disposed by experts. However , all suggested mechanisms end up in the final common theme ie micro vascular obstruction.

Can no-reflow precipitate a fresh ACS ?

Could be yes . How ? The distal thrombus migration clogs the active collateral channels at its entry point.This is probably the most unrecognised concept which is difficult to prove though.The problem is , we may not realise this as it could be silent or may just present as LV dysfunction , Infarct extension, or Ischemic cardiac failure.

Why is treatment of no reflow is so dismal ?

I think, by now you can guess the answer and get it right too !

Is no flow better than No-reflow?

It may seem a foolish question one could come across in coronary hemodynamics. The prevailing coronary doctrine, as we understand is , all ATOs need to be opened in STEMI in an emergent fashion. (Other wise patients or their myocardium can’t be salvaged )But, we also realise ATO do get converted to CTOs in a safe manner following a STEMI in a significant number. It’s the ultimate myocardial mystery when we realise even the ATO fails to damage the myocardium significantly in some patients.

Presence of acute collateralisation to IRA from non IRA is observed instantaneously and spreads rapidly towards myocardium in distress.It is observed in atleast 40% of all patients.(Ref 2,3).

The anatomical and physiological codecs of acute collaterals in ACS is secretly located close in the God’s domain.But, Interfering with it, is definitely in human domain.

Should we need to worry about the impact of PCI on these acute collaterals ?

It is estimated up to 5 grams of thrombus could spilled over to the distal coronary bed. Mind you thrombus formation is not a one time process.Can you guess where these thrombus lodge in ? We don’t know what is thrombus clearing capacity of LAD/LCX/RCA vascular bed. But. we have observed naturally formed thrombus is less likely to disseminate and migrate than the catheter and wire induced.My presumption is , coronaries show their dissent and disapproval in the only way they know, ie non stop generation of thrombus (Not withstanding our DAPT/2b 3a /Bivaluridins etc)

Acute collateral shutdown : A new concept

We are not sure if there is a collision between two streams of reperfusion that happens after a STEMI. One spontaneous from the collateral and other from antegrade(Either spontaneous or man made)

Is it benefitial, detrimental or neutral ? We don’t know the answer for sure. My understanding is some of subset of critical STEMI are heavily dependent on this life line however miniscule it may be.

It doesn’t require a double blinded study to prove what would happen when a hurried cardiologist attempt hurried PCI who often has to a change his target to thrombus instead of myocardium .

When aggression is shown on the thrombus, it’s more likely you end up in no reflow . One possible new mechanism(Proposed by the author) of No reflow is distal dissemination of thrombus debri that plugs the lateral entry points of collaterals.

This is the time , no reflow shows its violent face. Invariably hemodynamic deteriation occurs and the entire reperfusion team would seem to count their luck than expertise.

Can we perceive, predict and prevent this ?

We should , we need to , but how ? Since we know the true success rate of no reflow is miniscule, serious introspection to be done. Funnily (but realistically) one can take a famous cue from the most underrated medical specialty Social and preventive medicine .

Yes it’s “Prevention is better than cure” and mind you, if there is no cure, how important prevention becomes.Strangley , preventive cardiology is meant for lesser professionals , who and talk about diet, excercise and lifestyle.

No , it’s not . Preventive medicine needs a new defintion , rather new understanding .Its’ all about preventing an expected or unexpected adverse event anywhere.

How many of us really believe there is no effective cure for No-reflow and it is directly related to aggressive thrombus clearance strategies .

Should we argue new age Interventionists to practice preventive cardiology right inside the cath lab and do away with non-academic temptations.(Surprise , this is exactly mega trials on thrombus aspiration told us (Class 3 Indication for routine thrombus meddling)

Final message

Stable and comfortable, late ATOs need not be opened like defusing a time bomb. We will never know which side of the bomb the cardiologist is sitting.

The incidence of new onset No-reflow can be higher than what we presume.Further it can trigger a fresh ACS by whipping up the injured and resting myocardium.(Mostly attributed to late reperfusion Injury and the acute collateral shutdown.)

Postample and Counterpoint

As an interventional cardiologist, No-reflow is one among the expected complications , which are part of the profession.Never bother about these unscientific utterrings . That’s the job of critics. You go ahead and fight with the coronary artety in every case of ACS. Only weak minded unprofessionals would love to sit on a case of ACS and play a waiting game in CCU. True professionals shall look for multiple criminal targets beyond thrombus, myocardium, IRA , non IRA, doesn’t matter . Do it with confidence.Hope for the best, don’t bother too much about the endpoint.

Mind you, that’s what , we are trained and paid for and possibly respected too in this most glamorous subspecialty of Medicine.

Coming next

*Is Catheter, Guidewire Induced thrombus radically different from natural denovo thrombus ?

*How common is angiographically blind No reflow.(TIMI 3 with good and bad blush included)

*What are the residual defects and long term myocardial sequale ? (Inspite of successful tackling of No reflow )


1.Claire Bouleti et all The no-reflow phenomenon: State of the art Le no-reflow : état de l’artArchives of Cardiovascular Disease (2015) 108, 661—674
2.L YJ,Masuyama T,Mishima M, et al Effect of pre-reperfusion residual flow on recovery from myocardial stunning: a myocardial contrast echocardiography study. J Am Soc Echocardiogr 2000;13:1825. doi:10.1016/S0894-7317(00)90038-5

3.Ha M, Sakata Y, Nakatani D on behalf of the OACIS Investigators, Sakata Y, Nakatani D on behalf of the OACIS Investigators, et al

Impact of coronary collaterals on in-hospital and 5-year mortality after ST-elevation myocardial infarction in the contemporary percutaneous coronary intervention era: a prospective observational study

Human body is intertwined collection of lives of Individual organs.We believe death occurs when brain dies , respiration stops and circulation ceases . Curiously ,when life ends , these organs  don’t die as a single unit . These three events can happen in any of the six possible permutations.Each organ takes different times to die after loss of life.It is like a crashed computer , where the mother board /RAM memory may be transferred to another and be functional . Out of these three , heart function appears to be supreme as it can function without the need of brain (Science of brain-death) and keep the body alive with intact circulation. Though the concept  called heart dead organ donors is catching up as well. (John Gill et all Use and Outcomes of Kidneys from Donation after Circulatory Death Donors in the United States    

The science of organ transplant has rapidly  evolved .We can transfer an organ from one who is dying or dead to another person who is also dying due to failure of a different organ. Though most organs can be transported and transplanted , we need to maintain life in a dead donor organ . A new and curious specialty  in medicine is emerging which could be named a  Critical Care of Dead or Critical Cadaveric Care Units !) till harvesting happens. Paradoxically ,after the harvest , the organ gains independent  life that has to be sustained.This is where the science of organ transport is waiting in to explode!

How to transport a dead man’s heart ?

There are two Ischemic times in organ donation.

  • Warm Ischemic time
  • Cold Ischemic time

Warm ischemic time refers to the amount of time that an organ remains at body temperature after its blood supply has been stopped or reduced. Cold ischemic time refers to the amount of time that an organ is chilled or cold and not receiving a blood supply. These times quiet vary with respect to different organs.

So far, we have been carrying organs in cold boxes with custodial solutions. (HTK*)


This makes the transport time a big limitation of success of the procedure. *HTK -histidine, tryptophan ,a-ketoglutarate, solution 

Whats new in organ transplant science ?

Trans medics is an exclusive company , that has pioneered  in this unique science of organ transport .They have developed separate organ care system for heart ,lungs and liver.

donor heart

It is the first portable heart perfusion system , which increase the time between the harvest to transplant . It avoids cold ischemic time ,replaced by warm perfusion with metabolic activity monitored till  it is transplanted.Ideal far long distance transplant .Soon one can expect trans-continental transplant as well !

This technology could make the difference between warm and cold Ischemic times blurred and in future one may expect to prolong the warm ischemic  period and there is near zero cold Ischemic time.

A heart is perfused by transmedics system while being transported


                                              A  lung breathing in transit

A link to a video

Final message

Modern medical technology can be seen in action , in so many ways and brings both accolades and agonies in equal proportion. While, even flimsy ones tend to get due attention , Transmedics , probably deserves a  grandest reward  for uplifting the science of organ donation . I would think this is the most unique service (playing God )  . . . shipping dead man’s organ  with assured life on delivery  !


Link to Transmedics website

ocs heart transmedics heart transplantation



A middle aged women , with acute onset left sided chest pain and ECG changes was seen by a general physician. He had little hesitation in labeling the patient as  ACS( To be precious he reported the ECG as lateral wall Ischemia) and asked for an echocardiogram to rule out a heart attack  (This is how cardiology is practiced in many areas) .

This patient came to my lab  for the Echocardiogram .The echo window was poor , It showed a structurally normal heart and there was no pericardial effusion. I suspected something systemically wrong in this patient and asked for a X ray chest .

Subsequent scrutiny of this  patient revealed she had moderate left tuberculous effusion. ECG changes are attributed to this. We know pericardial disease can cause ECG changes that mimic ACS. While pericarditis can elevate the ST segment. Can pleuritis without effusion cause ECG changes.  What is the demarcation point between pleural from pericardial surface ?

What are the ECG features of pleural effusion ?

  • Low voltage qrs.
  • Poor R wave or even q waves
  • QRS axis shifts are due to true anatomical / electrical shifts
  • T wave inversion as in this patient

Mechanism of T wave inversion in plural effusion.

T wave represents ventricular repolarisation. To be frank I am not able to give an exact mechanism of such  defects in pleural effusion.

The following mechanisms are  suggested

  1. Left sided pleural effusion can closely mimic pericardial effusion .One can get low voltage QRS in lateral chest leads .
  2. Anatomically I would guess the plural fluid also hugs the heart and the inflamed pleuro-pericardial Interface (Is there fibrous continuity ?) result in some degree of epicardial interference or reversal in electrical polarity.
  3. The true effects of mediastinal shifts with large effusions  on ECG is not clear(Lead V 3 and V4 may pick V5 / V6 signals in left sided effusions )
  4. Fluid altering the electrical conduction property
  5. Associated minimal pericardial effusion and  effectively causing epi-pericarditis as a part of poly-serositis .
  6. After ruling out all plausibility one may think primary ischemic changes as well.

Teaching points and potential error

To label  a left-sided pleuritic pain with ECG changes as ACS can never be considered as a serious error.However , rushing such patients to cath lab or   lytic therapy along with heparin leads to more trouble. ER physicians should always keep in mind T wave inversion in isolation is indeed a rare cause* of ischemia. Still,  as a physician first , we need to have a check list to rule out common non cardiac conditions. Pneumothorax is one another entity that can exactly mimic a STEMI with ST segment shifts and q waves.It’s also possible left sided pleural effusions produce q waves and mimic an old MI as this case report reveals.(Constatine A Manthous Chest 1993)

I think  X-ray chest is least used modality in a coronary care unit for various reasons . Still ,the utility of which can never be undermined and should be used diligently . 

*Of course we shouldn’t  forget a sinister form of ACS  referred to as Wellen’s LAD  syndrome which may present with dynamic T inversion.


The prime job of cardiologists is to restore coronary blood flow in an emergency fashion. While we do this with reasonable success ,there is still a missing link between our Initial aim and achieved goal.

It’s all too common situation in any busy cath lab , to see two similar STEMI patients with identical time window & proximal LAD as IRA , in totally different scenarios. In the first patient we find a trickle of flow in LAD , who is relatively comfortable  with normal LV function (In whom , emergency primary PCI might appear redundant.) While the other patient , even after rapidly established TIMI 3 flow , LV wouldn’t look good at all . All our efforts to reperfuse is found wanting.  Ultimately LV goes in a downward spiral , ends up in irreversible cardiogenic shock or fatality inspite of Impellas, ECMOs and other LV assist exotica !


intra-coroanry-thrombus (2)

I can promise , you can never guess from the angiogram whether this ACS patient was very much comfortable or he is in cardiogenic shock on ventilator  unless I reveal the history. Am I right ? That is the mystery of coronary circulation and hence its so critical to serve the myocardium what it wants ? Never treat a coronary artery in isolation !

What is the possible explanation ?

The first trickle (Say TIMI 1 which is usually spontaneous or lytic related ) is the one that’s going keep the muscle viable and possibly prolong the time window for the subsequent reperfusion strategies .Hence it is the timely TIMI 1 or 2 is much more critical than delayed TIMI 3 (Still rapid).

Time window woos :

Who fixed the reperfusion  time window as  6 to 12 hours ? Do you know on what basis  the acceptable delay of 30 to 60 mts related to primary PCI ? was made acceptable by  cardiology community ?  If you analyse the published data both are highly contentious and empirical. ( Suggest you scrutiny the data from DANAM2 , PRAGUE and AIR PAMI and come to your own conclusion) (*These are the 3 sacred studies done with few thousand patients  that redefined our approach  to STEMI and gave the licence to waste the golden hour ! )

I remember reading  the Robins pathology book (Bible of  pathology William Boyd as well ) in early days of medical school myocardium may die even within 1 hour with wavy necrosis, contraction bands etc. Looking back some times I  wonder how the clinicians have conveniently prolonged time window with whims and fancies of science Intact.

Concurring with the pathologists , we have learnt some harsh lessons inside the cath labs. One of them is that even ultra fast pPCI can fail to salvage  myocardium, meaning that time is not the ultimate thing in our race. (There should be other important determinants )

A brief journey back into our pathology classes : Have a look at this table 

Time window in stemi 6 hour 12 hour or 90 minutes

Please note, Irreversible Injury might happen any time after 30 minutes .Of course it can vary . But, the question is how are you going to identify these patients with  ultra short  time windows? source : Robbins Basic Pathology 9th Edition.Elsevier

Other factors that influence myocardial cell survival

Re-perfusion is not a single edged sword 

We may wish the concept of re-perfusion Injury is a myth : Unfortunately it is not ! Myocardium doesn’t relish (not always) the return of circulation in full dose. (May be it’s laying and taking the much needed rest with the initial Injury!)

Reperfused myocardium

Sudden gushes of blood leads to extravasation into the interstitium (due to damaged capillaries)  increases the Intra myocardial resistance and obstructs the microvascular flow. We have  witnessed more than a handful of patients going for cardiac arrest once IRA is opened (of course,  we might be  able to resuscitate many of  them )

Myocardial hypoxia resistance time

Please realise ,true  STEMI clock starts not with onset of symptoms but with time of total occlusion.There is more than subtle difference between the twoOnset of total occlusion to symptom time is not a well explored or understood Interval. We take it for granted that the onset of symptoms coincides with total occlusion.

But in multi vessel CAD, even a CTO can cause a STEMI through loss of distal collaterals. Further ,the presence and absence of pre-infarction angina (PIA*) , ischemic pre-conditioning (IPC*) sensitizing effect of  remote CAD , manifest vs recruitable  collaterals  all these make the fixed time windows with which we did our land mark studies of PCI / lysis academically  questionable.

* Both PIA  IPC are master confounders in the true time window calculations .We don’t know whether its due to ischemia tolerating myocytes or pain tolerating nerve fibres  responsible for this varying presentations.But the mystery is certain , when we  realise the angiographic  spectrum of ACS can range from silent ATOs to painful CTOs

Final message

Is timely reperfusion (and its favorable effect ) lies in God’s domain ? If you we  believe myocardial susceptibility , arrhymogenicity and recovery to hypoxia is genetically determined ,then the difference between fate and science Is much narrower than we think .Its appears we can change the former with the later with both positive and negative outcomes. So ,the  “f”  word may not be a forbidden at-least in the STEMI management. It resides not only  within the human genomic codecs written with double-helical nucleic acid fonts . . . but also  in the nimble and restless hands of both novice and experienced interventionists !


A study proposal 

Let me make a hypothetical statement .A significant subset of patients with STEMI have ultra short myocardial survival and we are unable to identify these hypoxia challenged hearts where primary PCI related delay could be a myocardial sin. Any one willing to prove or disprove this hypothesis ? If some body take this quixotically important study in STEMI management please give me some credit as a contributor !