Archive for the ‘STEMI-Primary PCI’ Category

Last week  there was a heated debate in our CCU regarding thrombolysis for  a patient with severe rest angina  and ST elevation in AVR  and ST depression in V2-V5  as it implies  Left main disease  Few argued left main disease is an exception where one can thrombolyse even with unstable angina !

One of my fellows argued ACC guidelines vouched for lysis in UA involving left main .( I do not agree )

A logical attempt to differentiate Left main NSTEMI//UA and STEMI

(In the strict sense Left main NSTEMI is misnomer as AVR shows ST elevation  isn’t ? )

left main disease

Final message

Such  patients with suspected LMD   are to be rushed to cath lab .  . . agreed . If it is not feasible , manage it as high risk unstable angina and do not thrombolyse .Let it be left main disease . Indications for lysis are clear. ST  elevation in AVR alone can not be taken as an Indication for lysis.For thromolysis to be effective there should be high thrombus burden with total occlusion . ST elevation in single lead (AVR ) is not a good  marker for left-main thrombus !

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Time is muscle. This quote  became  sort of ” cardiology sermon”  in the last  few decades .Cardiologist think  they stand  on a 100 meters sprint track once a patient with STEMI arrives .This is indeed true ,  if we  agree  time is  muscle and  our urge is to reduce the door to balloon time .Please  remember ,  this rush matters  much ,  only if the patient comes through very early  when the muscle is really getting damaged . (No issues  . . . even if the fire engine comes in  slow motion if the  house is burnt fully !)

Time is muscle agreed  . . .  but  muscles are  kept alive by  factors other than time  !  So muscles can  defy time if God  is willing !

Time is one of the important components of management of STEMI.  Other things matter too !  Age , baseline co-morbidity ,  underlying extent of CAD, collateral support of IRA territory , and finally  individual variation in hypoxic damage in myocyte is (Rarely  been studied in detail.)

Door  to balloon time for a patient  who lands up within  1 hour window need  to be  much  different from a patient who comes at 10 th hour .The issue is important  because  we use a procedure which requires delicate decision-making ,(IRA-Non IRA issues etc)  the results can be  sub optimal ,  and even be hazardous in low risk STEMI . So , door to balloon time  may be a less  important  component of  time window in a patient who comes after 6 hours .This is the reason  overall outcomes are not changing in a large cohort  of rapidly performed PCI.

The presumed  absolute  relationship  between  “Time  and  muscle”  concept is  always been a suspect . This  is proven by a flawless study from  NEJM .

nejm stemi most important article


This study should infuse more sense to  us ,  time and again, we are  hijacked and sedated by high dose of  pseudo scientific concoction .In fact ,  indiscriminate rapid PCI may not be in  the good interest of  all  patients with STEMI ,  if it is not properly done  .Without realising this fact many developing countries are indulging in extravagance of  costly STEMI programs wasting  the exchequer.

This landmark NEJM  paper convincingly underscores a fact  that  achieving  rapid door to balloon time  is not  going to be the game changer in  conquering  the Global   STEMI  championship  . We have to take the coronary care into the streets  or to their homes as well .This is where the pre-hospital thrombolysis will  emerge in a big way in the future .

A slow and steady thrombolysis beats a fast and furious primary PCI on any given day in all uncomplicated STEMI .This we have proven for over three decades in  one of the India’s largest coronary care unit .( Where is the data man ?  Genuine experience is data . Why  we require , the act of publication to convert an experience into evidence . Often times ,  I  would feel , data is the most unscientific word in medicine . Many Truths  lack evidence , false hoods come with plenty !  For all those  scientific  homo sapiens  , please recall  70 % of ACC/AHA class 1 recommendations are backed by level C evidence ie simple opinion from  perceived experts! )

Final message

A fast and furious primary PCI may not be  the answer in all STEMI population

Thrombolysis  can be  done  with near  zero time delay , it does not require special expertise where an ambulance driver can reperfuse   a myocardium without much fuss and glamor ! He does not have to  split his hair to identify which is the IRA in a complex multivessel STEMI as well ! The streptokinase and TPA will home in  to the target site  smoothly and swiftly .

If indeed ,  time is the major factor in STEMI , we have many other ways to tame  the time . If muscle is more important than time ,  pPCI is  rarely  the answer !

Some India specific  thoughts

Is it not a shame  , we talk about primary PCI  for all  our patients  who do not even get timely Aspirin* after a STEMI! .It is something akin to what we witness every day ,  as our country folks  wield touch screen  Androids  . . . conversing  in open air toilets !

* While the importance of  Aspirin is undermined , It is different story altogether , these patients  get sorbitarate promptly whenever they get chest pain  (mis-placed and  dangerous priority ! )  prescribed by the  roaring  GPs ,  who suffer from discontinuous medical education ,  propelled  by the deeply penetrated 1000 crore oral Nitrate market .

And STEMI workshops are conducted by self-proclaimed experts  every few months in posh  7 star hotels all over India .

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This  is the story of a 55 year old  women ,  who was received  in our CCU  with a  dramatic STEMI (ECG looked like an action potential ) ,  LV  S 3  and  hypotension.    It was impending cardiogenic shock.Since we do not have full fledged primary PCI  program  , thrombolysis was planned. She had  cardiac arrest   immediately after  starting streptokinase infusion . She  was  promptly shocked  and  revived .  The ECG changes rapidly  reversed(ECG -3) . Every other  hemodynamic parameter got stabilised as well . To our surprise   ( few hours later ) this patient  was  so comfortable , sat up on her bed ,  demanded a discharge . (Which was refused of course !)  One week  later coronary angiogram was done, a near complete recannalisation of RCA was documented.

ECG 1 on arrival
Inferior MI 2  

ECG -2 Developed cardiac arrest  10 minutes  after  starting the Streptokinase Infusion

primary VF 2

ECG -3 .Taken few minutes following   the VF

inferior MI evolved 2


Acute myocardial infarction (STEMI)  kills more than a million life every year . Majority of death  happens within an hour of onset of symptoms. Ventricular fibrillation  is the arrhythmia of death. Why this occurs  only in  few , while  many are  immune to it ?

God keeps  this secret  close to his chest ,  how and why  he selects   candidates for this arrhythmia !

Scientists are still  far away  in finding the truth . But , one thing  is obvious .The  moment   coronary artery is totally occluded  , the heart begins a fight  and try  to  get rid of this obstruction . In the process ,  it  goes into convulsion (VF)  with a foolish belief  , it  can shrug of the thrombotic insult . Death often   ensues if  not intervened . (Very rarely  VF can be a non sustained one  and patient survives cardiac arrest !)

VF  as  a electrical  response  to  reperfusion injury .

Often times ,  we witness patients  to  go  for  VF  very early following thrombolysis . The  thrombus in situ is an irritant , it  triggers the inherent fibrinolytic system (Natural TPA included) If it is successful  it opens the occlusion ( atleast partially )  and salvages the myocardium .If the fate is against  the patient , very early reperfusion of IRA triggers  VF  .  If this occurs at home   survival  is  low .If  the VF occur at hospital the probability of survival is near 100 % .

               The  intensity of  natural lytic mechanism  is the major determinant  of   early reperfusion . Ironically  the same  factor   determines  occurrence of the deadly  VF .

I would believe  , the STEMI patients  who die early (even before reaching  the hospital ) are (un) blessed with a  fighting  heart  ! Ironically , the lazy hearts  reach the hospital  alive ! (slow &  steady win the race !) .  Of course , reperfusion  injury is not the only mechanism of VF . Other common suspect is  left main STEMI .

Link to related video “Ignorance based  cardiology ”


Final message

While , VF  is  referred  to as arrhythmia  of death , it may  in-fact , represent  a common form  of  reperfusion arrhythmia in  the setting of  STEMI !  .  . .  Hence , it can  Initiate  a new lease of life in  many   lucky ones !  I hope the title of this article  makes sense  !

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Primary PCI is presumed to be the ultimate  , undisputed reperfusion  strategy  in STEMI .  Still , time and again one study or  other strips down  this   “Numero Uno”  status of pPCI  .  If it is really supreme ,  such awkward  situation shouldn’t arise  too often . More importantly , the  major reason for  dubious real world record of  pPCI  goes beyond  the time and logistic factors (which is considered the only issue  for pPCI by most interventionist ! ) There is something more to it that is invisible ! (Is it the no reflow ?)

The nearly flawless study from Belgium ( STREAM Just released in ACC 2013/Sanfransisco ) , pre-hopsital or early fibrinolysis has proven to be superior in the prevention major end points at 30 days .

  1. Death
  2. Re-infarction
  3. CHF


The major surprise was pre-hospital  fibrinolysis  showed less  incidence of cardiogenic shock . ( pPCI

group had more of this ( 4.4 VS 5.9 %  in STREAM )

Now . . .  shall I make a provocative statement ?

while pPCI may be treatment of choice for cardiogenic shock . . . but it may  also confer a risk of cardiogenic shock in otherwise low risk MI !

Caution  and  conclusion

STREAM population applies strictly to 1 to 3 hour time window . It does not apply to either before or after that ! Simply put,we do not have  guts to compare fibrinolysis and pPCI  in patients who arrive  within one hour into a facility where 24 hour cath lab facility is available .  We call it unethical to do a study like that !  I personally feel it is really unethical  if we do not do a study in this time frame . The reasoning is  simple and very personal .In a  large  Government  hospital   where  we do not have primary PCI program  our net mortality for STEMI never exceeded 7-8 %  over a period of 10 years  , Which  is almost at par with global data on pPCI. (Our door to needle time is an unbelivebale  8-12 minutes ! that  too only streptokinase !)

Adding Further controversy

pPCI  is indeed a superior reperfusion strategy . No one can dispute that .But its superiority  is not  realised  in  every patient  who gets it.  The benefits are accrued if and only if it is  used most judiciously . In Low risk , small regional  , branch vessel STEMI ,  pPCI has never been  shown superior . It is well recognised ,  upto 15 % of STEMI is likely to spontaneously abort or experience very good spontaneous recannalisation . By rushing these  patients very early into cath lab pPCI   meddles with the natural anti fibrinolytic mechanisms . It is this population who  invite all the procedural hazards. .

Is this the reason STREAM had  more  cardiogenic shocks in pPCI limb ?

I think STREAM has  strengthened the case in favor of fibrinolysis in this  ever ending debate .

I would  seriously believe  pPCI is hanging it’s superiority over fibrinolysis with a wafer thin mortality advantage . pPCI may  not be recommended in a routine fashion to all STEMI  population even if they arrive within 6 hours and able to perform the plasty fast .  Science is   . . .  after all . . .  continuing  confrontations with our  assumptions !

Counter point

STREAM is not an exclusive study comparing fibrinolysis and PCI . It is a  study comparing   Pharmaco Invasive approach vs  pure invasive approach . 80 %  of patients in the  fibrinolytic limb ultimately received PCI and  stenting . It simply doesnot make sense to conclude fibrinolysis is superior to PCI . Most of the beneficial  effects on 30 day outcome may reflect the timely PCI  in the lytic group.


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Soft skills in pPCI 

Experience  would tell  us only about 70-80 % of STEMI are truly eligible for a  good  quality pPCI .(Multivessel CAD, Complex bifurcation lesion, difficulty in identifying IRA, No IRA-sapsms , complete spontaneous reperfusion )  The remaining 20-30 %  should , logically  be included in the failed pPCI category .This fact is largely concealed in the literature .

Beware of huge thrombus load in every patient with STEMI .The  contribution of  mechanical occlusion  vs thrombus  (in the total occlusion )  is the single most important factor in determining the intervention strategy.

Deploying a stent in a poorly  prepared (debrided of thrombus  ) lesion confers  further continuous  risk of a STEMI .Stents smartly jail  even large thrombus against the coronary vessels and they release it into the lumen in a controlled fashion  and prolong  the  acute coronary  risk phases

If thrombus aspiration  does a neat job and establishes a good   flow , if the   lumen  appear   good , think twice or even thrice before deploying a stent .It is akin to stent a  zero % lesion and we know it is foolish to do that at any stretch of imagination .(Stenting has never been proven to convert a vulnerable ulcerated lesion into stable one )

IVUS, OCT are not the answer in the above situations  as we are dealing with  emergency coronary  fire fighting !

Of course the intensive anti-platelet   protocols , will take care of  potential after effects of the intra coronary contact sport we play  !    . But . . . there is a limit for every thing. So spend as little time as possible when attempting catheter based reperfusion during STEMI.

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Dear Cardiologist , can you spare a minute  extra  in cath  lab   . . . and give many happy years for your patients !


PCI  (Fondly  called PTCA)  made  a  humble  beginning from  a Zürich hospital in 1977 . In 4 decades  it has become the staple diet  of most cardiologists ,   of course bulk of our patients benefit from that . When Gruentzig introduced the concept stent was never in the picture .Now stents have become mandatory in all most all PCI (We have gone one stop ahead (probably in  the  wrong direction !)  and given a cult status  to  drug electing stent .

Now we enjoy our work  with countless tools and techniques in our coronary automobile shop .

Suddenly  . . .   0ne primitive ,  common sense based question  is  asked !

How many seconds are required to optimally dilate and deploy the coronary stent ?

This  debate is   thrown out  live into  cath lab  . . .  by this simple and elegant study from the prestigious CCI journal.

cci journal ptca pci balooln inflation time


  • 105 patients, 150 lesions , Three different stents were used
  • Cypher Select (55%)  , Xience V (30.%), Taxus Liberté (15.%)
  • Three  balloon inflation timing
  • 5, 15, 25 seconds
  • Complex lesion (B2) formed 26 %

balloon inflation time pci ptca


This paper concludes ,  duration of stent balloon inflation has a significant impact on stent expansion. Stent deployment for >25 sec is recommended.

It again keeps the vital answer  to our guess !  Can we inflate it for 60 seconds  ?  After all 60 /120 seconds both  are greater than 25 sec is isn’t ?

Final message

This seemingly simple paper  conveys a  strong  message  .

Time is every thing , . . . we have to be fast . . . where we need to  (Time is muscle)  and we have to be slow where we  need to*  .  It has rekindled  the  basic senses  of  our  supposedly advanced brains !

I agree  . . . every minute of cardiologist’s life is precious  as  “Time is  also  Wealth”  , still few minutes of caution and   patience  in cath lab can make world of good for our patients !

* The most important determinant of cath lab complications ,   is lack of patience on the part of cardiologist .Next only comes , expertise , adequacy of hardware  etc . Surprisingly , patient factors  come in the bottom of the list in most non emergency interventions.



Further questions ?

  1. Can post dilatation be as  efficacious   as that of  stent- balloon  dilatation ?
  2. In difficult lesions  , the sum of  “Pre  / Per / Post”  balloon dilatation  gives  us net inflation  time(NIT)  Does it  add any sense to our understanding of optimal stent deployment  ?

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Guidelines are meant for simplifying  cardiologist’s life  as well as  ameliorating   patient suffering  . It should also  ensure  improving overall  outcome   with  efficient  use of human resources and  economy .

acc aha guidlines stemi 2013

These guidelines  are written from sophisticated centers  mainly for consumption  in developed countries .Though core  concepts will be same , many recommendations are neither possible nor desirable  at the exact point of delivery  in  less developed countries . Please remember these guidelines are not binding on you .Physician discretion is the ultimate principle in medicine.

So ,  let us read these guidelines apply our mind and try to  indigenise . Get maximum out of it  for the respective population .

Some  of the highlights in this 2013  guidelines
1. Therapeutic hypothermia should be started as soon as possible in comatose patients with STEMI and out-of-hospital cardiac arrest caused by ventricular fibrillation or pulseless ventricular tachycardia, including patients who undergo primary PCI.31–33
(Level of Evidence: B)

2 . Presumed or New onset  LBBB is no longer a Indication for emergency reperfusion

3 . Indication of Primary PCI has the following modification

Primary  pci Guideline in  2013 aha guidelines



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