Posts Tagged ‘stemi’

LV ejection fraction (EF) is the most commonly used  LV systolic functional index.Since , it is an  easily acquired parameter,  it’s popularity has zoomed among both learned and novice cardiology professionals .(Not withstanding the serious shortcomings!)

In one of the evening rounds  in my CCU , a young cardiology fellow told me about a  patient  with acute  anterior MI with ST elevation V1 to V5.

The patient  was lying supine with trunk up . HR was 110 . BP was  100 /70 There were few basal crackles .The patient was undergoing  lysis with streptokinase.

It was  suggested  to me by the  fellow  that  the patient is  going in for “Impending  cardiogenic shock since his EF is just 30%”

That prompted me to ask this question

How good is the EF  a measure  of size of MI during STEMI ?

EF during  STEMI  is highly variable parameter.The following are important con-founders in LV EF measurement during STEMI.


  • Acute ischemia induced LV dysfunction .(Ischemic stunning from  the watershed zone  significantly over estimate LV dysfunction)
  • Mitral regurgitation  if present will underestimate it
  • Effect of tachycardia and bradycardia can be significant
  • The posture of the patient and  measurement errors (A good Simpson score is rarely  possible in a sick patient )
  • Associated  hemo -dynamic drugs like NTG/Dopamine etc which alter  pre and after load   and changes the frank starling forces.

* Please recall  , LV EF is never included as a criteria to diagnose cardiogenic  shock, confirming the  flimsy  nature of this parameter during acute phase of STEMI !

Final message

The purpose of echocardiography during STEMI is to rapidly identify any mechanical complication , not to waste time in calculating EF.

EF is not a good indicator  to  quantify the extent of STEMI  or it’s prognosis. LVEF cannot be used  to risk stratify STEMI in the first  48 hours .One can expect  the true LV function  to prevail only  at discharge.

Ideally ,LV  function should be reevaluated by 2 weeks to get a fair idea of true myocardial function .By this time all  confounders will resolve.

Clinical implication

Since many of us are suffering from an academic obsession and blindly follow the scientific guidelines, a hurriedly diagnosed  “severe”  LV dysfunction post STEMI may land our  patients to  inappropriate intervention !


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LVH is   a common ECG  finding .Classically  it should produce tall  R waves and deep S waves in V1-V3 .

But it is well known deep q waves also can occur in LVH  especially in severe  forms of pathological LVH.


Why the septal R disappears in some is not clear .( due to  myocardial dis-array ? )

LVH  results in  secondary ST /T  changes either inherent or associated  conduction delay. (In-complete LBBB )

Final message

Errors  mistaking LVH for STEMI  is more common than we realise . Propagation of the  term  Q -LVH with ST elevation  will help  reduce this common error in coronary care units.


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A patient with  extensive anterior STEMI  presented 18 hours  after onset of  chest pain . He  was  other wise stable and free from angina but had persistent ST elevation (5mm in V 1 to V 5 ). He had a  total occlusion of LAD  with TIMI zero  flow . He had a  tight PDA lesion  as well . A bed side echo revealed LV EF  of 50% . The septum was hypo-kinetic but did not appear severely dysfunctional .

So , it was decided to open up the LAD. The moment  LAD was opened he developed severe acute LVF  /   flash pulmonary edema   .  Even after a 30 minutes of  heart (Fire )  fighting  he could not be resuscitated .

What is the mechanism of death here ? Expert  STEMI interventionist  from core  labs  may answer this !

An acute ischemic MR with myocardial disruption was suggested . Why it  was triggered after opening the IRA ?

Three mechanisms were discussed

  1. Re-perfusion injury
  2. Collateral  damage
  3. Physiological  de-stabilisation of  Contra -Lateral lesion (Remote lesions )

Re-perfusion Injury ?  How relevant it is in cath lab ?

Is re-perfusion injury  electrical  ,  mechanical or  both ?

In this particular patient even though there was a total LAD occlusion , the segments supplied   by  the LAD  was partially functional and  it was contributing to LV  pump function.  The moment  a trickle of   flow was established  , some thing happened and the whatever  little mechanical function  his LV  had  was also interrupted  . The LV came to standstill and the patient died .

If re-perfusion Injury is  simply an   electrical  event   like VF ,  it can be resuscitated . If it is mechanical  outcome is bad ! This is not a new concept  . It is  part of the  once famous  concept called myocardial stunning . There are  lots of reasons   for stunning  to be a  clinically relevant phenomenon .Unfortunately   if any cardiologist talks about it in 2012 ,  he is at risk of  labeled  as old fashioned !

Collateral damage.

One more mechanism which we feel that  might have contributed to death here  is   the  “collateral damage” .(This is not cross fire !)

We know collaterals can be recruited within 12 hours in many STEMI patients . In some  it can even salvage  significant mass of  myocardium . The acute collaterals to LAD may be interrupted  during primary PCI . Once you poke the lesion the coronary  vascular  bed which had dilated  (as a response to total occlusion ) may react with inappropriate vasoconstriction . This raises the local hydrostatic pressure (Myocardial edema)  and further impede  the   incoming  micro collateral flow . This a very  critical time  for the myocardium  where antegrade and retrograde flow are kept in a fine balance .

Interference with remote lesion Hemodynamics .

Another possibility  is  the  opening the  LAD lesion some how  impact on remote lesional  flow as well (PDA  in this patient  )

Please remember ,

Even a transient hypo- tension can have  devastating effect in  the  hemo -dynamics   of  non IRA  territory  especially if it harbors a critical lesion !

Final message

Coming to the title question  , Is no – flow better than  slow- flow in late presenters of STEMI ?

Common sense dictates whenever  an artery is obstructed  just get rid of it.  When  it  comes to the heart it must be done in an urgent basis That is the essence of primary angioplasty  . . .  agreed . But in this  patient  I believe ,  the  common sense  was proved wrong !

Truths are always hidden.  The  science of  myocardial re-perfusion is a perfect example . We need to learn a lot still !

This I  call as  Para cardiology : Heart  facts without  evidence !

Counter point

One may argue this   is an  exceptional case  in STEMI  intervention. Don’t  hype   exceptions  and undermine the importance of a great concept ! Exceptions  and rules  are directly related to our  experience  we have accrued.  Exceptions are the great  knowledge substrates  and help  crack  medical  mysteries !

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In the management of STEMI , many  of us  believe  , contraindication  exists only for thrombolysis . In fact  , there is  a big list  of contra’s for primary PCI as well  . Few  books mention about it and  few discuss about it  . It comes under many broad categories .Time , technical, patient  and  concept  related

  • Late presentation > 12 hours (This is the most important  contraindication  . 12 h is the time taken for  death of  myocytes . Myocardium will not  bother by which modality it is going to be rescued ! It simply  won’t give any  grace time  and never feel privileged to be rescued by PCI !)  The supposedly time independent beneficial effects of PCI  was  never proved convincingly !
  • Uncomplicated , fully evolved, spontaneously re-perfused   ( successful  )  STEMI  (At-least  10 % of STEMI population  ) . This is  common in RCA STEMI .
  • Primary PCI  should not be done in  low volume centers with poor expertise  ( less than  2 -3 per month ?)
  • Lack of sufficient hardware .
  • Co-Morbid conditions
  • Very elderly ( Controversial … some may call it as an  absolute  indication ! Such is the status of EBM in 21st century !)
  • Any recent bleeding conditions carry equal risk as that of thrombolysis

The list of relative contradictions  that are  widely reported in literature  for thromolysis may apply in PCI as well .The risk of bleeding is many fold higher when  multiple anti-platelet agent /Heparin are used .The usage of 2b -3a is also rampant in many centers .  A recent hemorrhagic  stroke is  an absolute contraindication  for PCI as well.(If only you do a PCI without anti-platelet  agents).With number of complex anti-thrombotic drugs knocking the d0ors of cath lab , the problem is set to grow further.

Final message

Never underestimate the  potential  peri -procedural bleeding risk during PCI  .It can easily  exceed that of a thrombolytic agent  in susceptible individuals !

Primary PCI is a great innovation and is a gift  of modern science to human race . But , when  selecting the patients  ,  many of us  continue to interpret  this issue  wrongly. We seem to think , in a given patient  , if  thrombolysis is contraindicated  ,  he or she will automatically become eligible for  primary  PCI It is a dangerous assumption and  is rarely true  . There are umpteen number of situations were both are contraindicated . I  argue the  intervention community to publish specific guidelines with absolute and relative contraindication  for primary  PCI as well .

After thought

If  a patient is not eligible for both thrombolysis  as well as PCI what to do ?  Is it not a crime to watch a patient with STEMI simply losing his myocytes ?

It may seem so  , when we look at  superficially   but  be reminded even simple heparin therapy has saved many lives in such a situations .

Link to related You tube video


That  elusive  uncommon  sense

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A 55  year old man came with a BP of  1o0/70 with vague symptoms of back  pain to our ER.

Troponin T  was positive

Can we thrombolyse ?

There is a minimal ST elevation in inferior leads  but not amounting to  the required criteria 1 mm

Technically No , Academically yes , scientifically No , logically  yes

*I wont thromolyse but i will take him to cath lab maybe the modern answer

 What we did ?

We did neither !

Just observed in CCU with heparin infusion , Aspirin and clopidogrel .

Note: The ECG becomes almost normal .The initial suggestion of inferior MI is stands questionable

Serial ECGs  were taken .

And now . . . after 24 hours a new complete heart block appear with classical evolved pattern of inferior MI.The most interesting feature is patient has been comfortable all along even as his posterior aspect of heart is experiencing terrible electrical earth quakes.

Is troponin Guided thrombolyis  an accepted  concept  ?

Yes ,  only in few situations like , posterior MI ,   LBBB  , pacemaker rhythm, re infarction .(Note , true posterior MI do not elevate the ST segment but depress it ) .

One may be surprised why we shouldn’t lyse a patient  whenever  troponin is elevated in acute coronary syndrome  (After all it denotes myocardial necrosis and infarct !)  The point here  is ,  troponin can raise in all forms of MI (NSTEMI, even in some cases of chronic stable angina )  Read in this link Why thrombolysis is contrindicated in UA/NSTEMI

The benefits of thrombolysis  is not proven in small and micro infarcts.  ECG  ST  eelvation   remain the  sole criteria for thromolysis for STEMI because  of  high degree of  correlation with total coronary occlusion .

In this era of rapid interventions the treatment concepts has blurred as we tend to do PCI and stenting  most cases of ACS including UA/Unstable angina

OK , what happened to this patient ?

Temporary pacer  was kept stand by with a sheath and catheter in situ.

Next day  morning  AV block disappeared .Patient was comfortable .

To our surprise , in the same  evening his ECG showed a complete heart block with AV dissociation . Still the heart rate was good . The demand temporary pacemaker didn’t take over .

On the third day , every conduction disturbance disappeared and  patient was sent to the wards. He is being discharged in a  stable condition with std drugs .there was  a minimal wall motion defect in infero-posterior segments with an ejection fraction of 50 % . He is  scheduled for coronary angiogram  2 weeks later.

What is the pathology ?

Pathologicallyit could be a small focal area of Infarct  incidenataly invloving the AV node .(This is alss refered to as vital area Infarct”  )It is hard to differentiate whether AV block is due to revrible ischemia or necrosis  , simple tissue edema ,  high vagal tone . or combination of above .If the block recovers it can be concluded necrosis is not the dominant theme.


Final message

STEMI presenting  primarily as heart block is less common .  When such a presentation occurs extra caution is required.

Many  of these patients  may not show a classical ST elevation  and hence do not permit us to thrombolyse   as per criteria.

It is  the  individual physician’s discretion to do so ( or not to do  ! ) . No body is going to fault. After  all  5 % of thrombolyis world over is for  benign early  repolarisation syndromes.

The above description is  an example of complicated inferior MI  . . .  still managed effectively by conventional methods.

Further reading

Why inferior MI is considered Inferior ?


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A patient with  chest pain   is being rushed   into the ER  of  a medium sized cardiac facility in an urban county of India .The fellow briefs the senior consultant cardiologist about the arrival of  this  extensive anterior  STEMI  over phone.  The  consultant  enquires  about the “symptom to door time” and  was little concerned  when the fellow said ” it is only  2 hours sir”  .The fellow was amused with the consultant’s  reaction.

The consultant arrived in 15 minutes  and  began  the all important  discussion with the  patient  and his spouse  .(Meanwhile tablet clopidogrel and Aspirin was  loaded  per orally . Note : Heparin is not given yet )

Cardiologist : It is a  massive heart attack . One of your coronary artery  got  blocked suddenly , I have to remove the block at the earliest . There are  two ways of doing it .  One is fibrinolysis which lyses the clot .It can open up  your vessel  , though incompletely but would prevent myocardial damage  at the earliest .

The other one is PCI ,  which if performed rapidly  will completely  open up the vessel in question , what  we call TIMI 3 flow ,  But it has to be done within one hour.

Patient : Which is better doctor for me ?

Cardiologist : My cath lab  logistics  does not allow me to do a  PCI within the stipulated  time ,   still  I wish  to perform   a primary angioplasty  as i am not a believer  in thrombolysis !

So , even though you are  eligible for both modes of re- perfusion, in the strict sense doing a  PCI  which will  ultimately be  delayed  beyond the recommended time window  is technically contraindicated “

(Please  be notified : Currently , if the delay is during the procedure due to some technical issues after starting the procedure  or if the delay is at  the patient   level in arranging the required finance or insurance clearance it can be condoned without any ethical issues )

Patients spouse : Doctor please save my  husband . You  start  the fibrinolysis  every minute is risky isn’t doctor , and do the PCI once its ready doctor .

No . . . Fibrinolysis  does not combine well with PCI  in fact it will worsen the situation .   Thats what FINNESSE  study says . We can do only one of them . . . not both .

The patient and spouse (Terribly confused  by now )

Cardiologist:  By the way , what is  your insurance limit  sir ?

Patients spouse : Its 4 lakhs

Cardiologist : OK , that should be suffice  90 out of 100 times . Any way keep another lakh ready in case I need IABP.

Patient : My pain is worsening doctor at least relieve  my pain till this debate  is over !

(A patient’s relative  browses his  i phone  and argues  the  cardiologist   to administer streptokinase at the earliest . Suddenly  the patient family lobbies for fibrinolytic mode  empowered by the i phone guy )

One of them shouts “Please doctor you do something either take him inside cath lab or  start a fibrinolyitc therapy ”

How did the cardiologist  fight his way through ? ( He gulps a cup of coffee and  starts a fresh discussion)

Cardiologist : 
I am sorry , you have come too early  for PCI .  Guidelines do not allow me to choose PCI in the first hour  as our  anticipated delay for PCI is more than 3 hours . I wish you arrived after  the 3 hour window .

“Of course you are on time for thrombolysis”  which  unfortunately I am against !

Now, I am going to wait ( You may think it is a waste of time i call it as patient preparation time )  .This waiting period incidentally  allows us to cross  three  hour  time  window ,  then the issue of not lysing  does n’t creep in at all . A PCI done after 3 hours is not a race against time , while a PCI done early is like  a power play in cricket .

I do not know whether this delay which is happening  right now –  Intentional /Unintentional,  Scientific / unscientific reasons  would  damage your heart or not !

Since you have an extensive MI , I earnestly believe  with all my wisdom and knowledge, you will do well with primary PCI  even if  i do it  little late .  Please allow me to violate the standard criteria in the interest of your heart .

Cardiologist : I wonder , if you had arrived little late we wouldn’t be discussing this terrible conversation at all .Your myocardium  will also feel thrilled for getting a better mode of re-perfusion. You put me in an awkward situation by coming early !

Patient : But  . . . doctor every one  tells me ,  one should reach the hospital  after a heart attack  at the earliest  is it not ?   Please believe me doctor ,  I  made  extraordinary  efforts to  arrive early to your hospital , but you have put me on hold doctor !

Cardiologist :I agree  . . . but you won’t understand the modern jargons  in  interventional  cardiology ,  some times (Or is  it many times !) we will be doing the diagonally opposite to what  is   preached  in text books  .  Both intentional and unintentional delays are common  in the emergency cardiac  care . Do not bother about it   . . . science will take care of it !

Patient : You mean  . . . you are going to waste the golden hour in STEMI by simply arranging for cath lab staffs and machinery .

Cardiologist : You got the point right ! Just sit back enjoy the  flight !

Patient : Your wish is my wish doctor . Please handle with care doc !

* Please note this is an imaginary conversation ( Most often happens in silent mode !) in many of the cath labs which do not have 24 hour service. In a country  with  100 crore population like India ,  less than a dozen cathlabs  work round the clock . Guess  how often such a  situation would come in day to  day cardiology practice.

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During   primary PCI , the weakest link  for a  cardiologist  is  , he is never sure whether  the  metal jacket  has covered the entire  disease segment with optimal apposition .  (Geographical miss is another issue !)

This is because  , even though the inflation pressure is  uniform  within the balloon ,  the required  apposition pressure is not the same .This is obvious as the lesion surface has a varying consistency and uneven surfaces . It is a  huge guess to quantitate the relative  contribution of thrombus and plaque  within  the 100 % occlusion  that has resulted in the STEMI. Hence  some areas may get over apposed and others lesser apposed. Further , the stent -vessel wall interface  in all likely hood enclose a   layer  of clot .This is almost certain  during complex primary PCI. One can imagine the sequel if this thrombus layer dissolves later ! (Edentulous stent )

It is surprising , why cardiologists has  so far not  thought  of a  self expanding stent  which  can snugly appose the vessel wall in this setting  . The   radial strength   from the  stored potential energy can be used up future use. This is most important  in first few days following STEMI  , when the coronary arterial lumen can vary depending  upon the

  • Vasomotor  tone .
  • presence of thrombus
  • Plaque   ploughing /milking  effect
  • Vascular remodeling

Cardiologists  deploy a stent  based on the morphology  on day zero of STEMI  .This may be  totally irrelevant  , since after a  few days    the lesion may change its morphology ,  thrombus may migrate , vascular  dimension may change. In such a  situation*  , a self expanding stent can tackle these issues very effectively by constantly adjusting  and fine tuning the luminal  diameter and  the apposition pressure . It  does not give any chance  for  thrombus to form  between the vessel wall and stent .

Here is a study that gives fresh insights regarding the role of self expanding stents during STEMI .

Note the “Auto adjusting”  of stent diameter  in the first few days after  the stent deployment, depending upon the luminal needs !



* Logically  during  primary PCI for  STEMI  ,  POBA and thrombus suction  may be the best option in many as all stent related complication is instantly eliminated .But it is a battered concept ,  most of the current day cardiologists would feel guilty to come out of  the cath lab  without a stent  in  primary PCI scenario  !

Final message

Self  expanding stents during primary PCI :  Is it a  perfect solution  for optimal stent apposition  ?

It seems so  . . . but  the track record of current cardiology devices never fulfilled the initial promises !

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