Posts Tagged ‘acc aha’

For medical science  to  defy   logic , is a not a great  new discovery . “Diabetes is a major  risk factor for heart disease   but controlling diabetes may not  remove this risk factor” Similarly  severe mulitvessel CAD  occurs without  any symptoms and compromise on LV function . It is a natural human  instinct  to open of  any thing  that is obstructing   on  their  path . The same logic applies in   physicians when we encounter blocks in the vascular highways  .

For a moment compare  it with an express way .

We realise many  roads have a  reserve capacity . Even if the road is  half  blocked , traffic  congestion  rarely happens  as the  original road’s width is  sufficiently  large for the projected traffic . Some other roads have emergency  service lanes (Collaterals) that can take care the flow of traffic.

Another  question to ask is , Where does the road  lead to ? and why  we are  traveling ?

If it leads to a “dead  sea”  or a “bottom less cliff’  there is no purpose  to travel further . Similarly , when you find a destructed kidney with little nephron mass( or dead myocardium  ) there is absolutely no purpose  in opening the block . (Some  may  believe  the act  of  opening  block , by itself   is a success /  sorry- story !)

This is what happened in the lase decade . Interventional    radiologists , vascularologists , cardiologists started  opening  renal artery obstructions , at their whims and fancies, in  many elderly and middle-aged population .To their surprise (This surprise is due to ignorance )  they found no worthwhile benefit  either in the BP reduction or worsening renal function .

Now comes the evidence  in  2009  as   ASTRAL  trial from UK . ( As usual   the evidence came   late after ,  few lakhs  of kidneys   been injured !*

* Renal interventions are notorious for many complications , which is often not reported . Read this article to know  it better.


Final message

Common sense can  work great wonders than the much hyped RCTs . (Except ASTRAL  of course !) In this era of scarcity of  such  sense we can expect another study soon , to nullify ASTRAL  and give us further license  to pursuit the  good old  human instinct  ! Already silent noises  are made in interventional  corridors questioning the  outcome of ASTRAL.

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This article is in response to the prevalent belief  about  primary PCI for STEMI   endorsed by world cardiology forums. (Caution: A highly personalized version)

Time window in STEMI

  • Is the window half-opened  or half closed ?
  • Is it open at all ?
  • Or ,does it open only for primary PCI  ,and tend to close down  bluntly for thrombolysis

Modern medicine   grew faster than our thoughts .We have witnessed the audacity of advising  arm-chair treatment  for MI  till later half of   last century . Now we are talking about  air dropping of patients   over the  cath lab  roofs  for primary PCI.

Still ,we have not conquered the STEMI. While ,  we have learnt to “defy  deathin many patients  with cardiogenic shock , we continue to lose patients(“Invite death “)  in  some innocuous forms  of ACS due to procedural  complications  and inappropriate ( rather ignorant !) case selection.

Note : The ignorance  is not in   individual physician mind ,   it is prevalent in the whole cardiology knowledge pool.

The  crux of the issue for modern medicine is ,  how to reduce risk  in patients who are at  high risk and how not to convert a low risk patient into a high risk patient by the frightening medical gadgets.

In other  words ,  arm chair treatment for STEMI was  not (Still it is not !) a dustbin management . It has a potential to save  70 lives  out of 100. What many would  consider it as  ,  nothing but  the natural history of MI .

Medical management of STEMI is ridiculous !

That’s what a section of  cardiologists try to project by distorting the already flawed evidence base in cardiology. Some think it is equal  to no treatment. Here we fail to realise, even doing none has potential to save 70 lifes out of 100 in STEMI who reach the hospital.

Out of the  remaining , 10 lives   are saved by aspirin heparin (ISIS 2) and the concept of coronary  care . Another  7  lives are saved by thrombolysis (GUSTO,GISSI) . PCI  is shown to save saves one more life (PAMI).The remaining 6-7 % will die in CCU  irrespective of what we do .

Of course , now medical management has vastly improved since those days  .  A  thrombolysed ,  heparinsed ,  aspirinised ,  stanised  with adequately antagonized   adrenergic ,  angiotensin system   and   a proper coronary care ( That takes care electrical  short-circuiting  of heart)   will score  over interventional approach in vast majority of STEMI patients.

Now comes the real challenge . . .

When those 70 patients who are likely to survive  , “even a arm-chair treatment“, and the 20 other patients  who will  do a wonderful recovery with CCU care ,  enter  the cath lab  some times in wee hours of morning  . . .what happens  ?

What are the chances  of   a patient  who would otherwise be saved by an arm-chair treatment be  killed by vagaries of  cath lab  violence  ?(With due apologies ,statistics reveal  for every competent cath-lab   there are at least  10  incompetent  ones  world over !)

In the parlance of criminology , a hard core criminal may escape from  legal or illegal shoot out  but an innocent should  not die in cross fire , similarly ,  a cardiogenic shock patient with recurrent  VF  is  afford to lose his  life , but it is  a major medical crime to  lose a simple branch vessel  STEMI (PDA,OM,RCA )  to die in the cath lab,  whom in all probability  would have survived  the arm chair treatment.

Why this pessimistic view against primary PCI  ?

Yes, because  it  has potential to save  many lives  !

Time and again ,  we have  witnessed  lose of   many lifes  in many  popular hospitals in  India ,  where a   low risk MI  was  immediately  converted  to a high risk MI  after an primary  PCI with number of complications .

I strongly believe I have saved 100s of patients  with  low risk MIs by not  doing  for primary  PCI in the last  two decades.

*The argument that PCI confers better LV function and longterm  beneficial effect is also not very convincing for low risk MIs .This will be addressed separately

The demise of comparative efficacy research.

Primary PCI is superior to thrombolysis  : It is agreed , it may be  fact in academic sense .

Experience has taught us , academics rarely succeeds in the bed side.

“superiority studies can never be equated  with comparable efficacy”

Only the  questions remain . . .

  • Where  is comparative efficacy  studies in STEMI ?(Read NEJM article )
  • Why we have not developed a risk based model  when formulating guidelines for   primary PCI ?
  • Is primary PCI for a PDA /D1/OM infarct worth same as PCI for left main ?
  • Is high volume center guarantee  best outcomes ?

Who is preventing comparative efficacy studies ?

Primary PCI : Still  struggling !

This study from the archives  of internal medicine tells   us , we are still scratching  the tips  of  iceberg (Iceberg  ? or Is it something else ?)  of  primary  PCI

Even a  pessimistic approach can be  more scientific  than a optimistic  !

When WHO can be influenzed and make a pseudo emergency pandemic  and pharma companies  make a quick 10 billion bucks  ,  Realise how easy  it is  for the   smaller ,  mainstream cardiology literature  to be  hijacked and contaminated .

Final message

Why we reverently follow the time window for thrombolysis,  while  we rarely apply it for PCI ?   This is  triumph of glamor over truth . The open artery hypothesis remains   in a  hypothetical state with no solid proof  for over 2o years since it was proposed.

Apply your mind in every  patient , do a conscious decision  to either thrombolyse  ,  PCI or none . All the three are  equally powerful approaches in tackling a STEMI , depending upon the time they present .Remember , the third modality of therapy comes free of cost !

Never think ,   just because  some one  has  an access to a sophisticated cath lab 24/7   , has a iberty to overlook the  concept of time window  !

Remember  you can’t  resuscitate   dead myocytes , however advanced your enthusiasm and   interventions are !

Realise , common sense is the most uncommon sense in this hyped up human infested planet.

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Drug eluting stents are liberally used  worldover .

It is very unfortunate ,while the jury is still confused about the role of DES  “even”  in chronic coronary syndrome ,

There has been widespread use of DES in  the   potentially hazardous    thrombotic milieu  of STEMI  . It is well known  the DES ( polymer and drug)   has a dangerous liaison  with the thrombus.

Even as the evidence base was about to accumulate against the DES in STEMI , there was  an undue haste in the use of  this stent in STEMI .

Now in 2010 the results are out the DEDICATION trial

  • The culprit is out
  • The truth exposed
  • DES kills more life than bare metal stents   during primary PCI

Read this article  ,just released in Atlanta 2010


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Cardiopulmonary resuscitation (CPR)  is  the major discovery of last century  that has saved many lives over the years. In spite of  this , there has been lot of debate over the exact methodology adopted  .The much published techniques  of Basic cardaic  life support (BCLS)  which is in vogue for over 2 decades has failed to deliver the  results  as  one would have expected.

The main reason identified was ,  the protocol seemed too complex and people hesitated to do the  mouth to mouth breathing in a stranger. Many were not confident about doing  proper chest compression and  inter spaced with breathing support.( The ratios  of chest compression : ventilation 30:2 /15: 2 tend to be too cumbersome in an emergency !)

Many of the  potential  resuscitators  preferred to  become silent spectators !

The world bodies ACC/AHA/ILCOR has been watching this evolving pattern and behaviour . Mean while when we looked into the data of survivors of cardiac  resuscitation  , we  realised even an  improper  and inadequate CPR had some positive  effect on survival . How was this possible ?

There have been  innumerable instances of  individual and institutional reports   about  many lives that  have been saved  simply  by compressing the chest  after cardiac arrest or  at least  kept the person alive  and breathing to  be taken  for advanced cardiac life support.

cpr hands only ilcor lancet

This simple experience has since become strong evidence when Lancet got it published in 2007 . Subsequently the ILCOR/ACC have also adopted a new advice namely compression only CPR

Read complete ILCOR  recommendations http://circ.ahajournals.org/content/vol112/24_suppl/

Excerpts from the above article reproduced

cpr chest only

Compression-Only CPR

The outcome of chest compressions without ventilations is significantly better than the outcome of no CPR for adult cardiac arrest.In surveys healthcare providers well as lay rescuers  were reluctant to perform mouth-to-mouth ventilation for unknown victims of cardiac arrest.

In observational studies of adults with cardiac arrest treated by lay rescuers, survival rates were better with chest compressions only than with no CPR but were best with compressions and ventilation . Some animal studies  and extrapolation from clinical evidence suggest that rescue breathing is not essential during the first 5 minutes of adult CPR .

If the airway is open, occasional gasps and passive chest recoil may provide some air exchange. In addition, a low minute ventilation may be all that is necessary to maintain a normal ventilation-perfusion ratio during CPR

Laypersons should be encouraged to do compression-only CPR if they are unable or unwilling to provide rescue breaths .

Final message

In this world of hi tech life support devices like LV  assist systems, implantable defibrillators robotic surgery  ,  it is  heartening  to note a pair of human hands can save a human life  or  at least sustain a life till the advanced emergency service reach the patient.

The fact that hands can act as a artificial heart lung machine at least  for few minutes  could be the greatest invention for the mankind by the mankind.

cpr hands only cpr lancet ilcor

* Note of caution

Under ideal conditions both chest compression  ,  proper airway , and assisted breathing is always better than simple chest compression .This blog wants to convey the point chest compression  alone could  also be  a effective CPR measure .



Newyork times  reports chest compression  only  CPR

cpr hans only newyork times

Click below to read the article .


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Myocardial infarction (STEMI)  occurs in two distinct arterial  territories .The anterior LAD circulation and postero- inferior RCA/LCX circulation.The incidence is equally shared.

There has been some  learned and unlearned perceptions about Inferior MI.

Inferior MI is less dangerous than anterior MI.  True or false ?

Answer: Essentially true in most situations.


Inferior wall of the heart (strictly speaking there is no walls for heart , only surfaces , which blends with adjacent areas)  inferior wall  is formed by diaphragmatic surface and posterior surface.Inferior MI can occur by either RCA or LCX obstruction.The outcome of inferior MI is determined by mainly by  the extent  of   LV myocardial   damage it inflicts.To  quantitate this  we need to know , how much of LV is supplied by RCA , or LCX or combination of both ? This depend on the coronary dominance .It is estimated , the bulk of the LV is supplied ( up to 75%  ) by LCA. This becomes further high in left dominant circulations . In fact , it is believed LV can never get involved in non dominant RCA occlusions. This has brought in a new terminology  called “Small inferior MI”.Inferior STEMI due to PDA  occlusion or in a co -dominant circulation is not yet studied

Apart from the above  anatomical considerations the following clinical observations  have  been made regarding inferior MI.

  • When thrombolysis was introduced , many studies  suggested the the ST elevation in inferior  leads toched the isolectric levels  in most situations even without thrombolysis.Technically, this implies spontaneous , successful thrombolysis are more common in RCA. Among the thrombolysed ,persistent ST elvation is a rare phenomenon.
  • The well known difference in the conduction defect between anterior and inferior MI  is an important contibutor for better outcome in the later.(AV blocks in inferior MI , are often transient, non progressive, supra hisian location rarely require permanent pacemakers)
  • During acute phase cardiogenic shock occurs in a minority (That too , only if RV shock is included )
  • Even in the follow up the ejection fraction in inferior MI is  almost always above  40%. In many EF is not affected at all.
  • Progressive adverse remodelling of LV is rare

When can Inferior MI be dangerous ?

Anatomical factors

Inspite of the  above  factors  inferior MI can not be taken lightly . Especially when it  extend into posterior, lateral , (Rarely anterior) segments.

While  posterior extension  is often  tolerated , lateral extension is very poorly tolerated .This is probably explained as  the extension involves the vital free wall of LV and the laplace forces could precipitate LVF. Free wall rupture is also common in this situation.

Posterior extension , predominantly involves the surface of RV which is less important hemodynamically. Of course incidence of MR  due to it’s effect on posterior mitral leaflet can be trouble some.

inferior MI ECG

High risk clinical catagories.

Out of hospital STEMI  are at  equal  risk irrespective of the territories involved  .This is because,  primary VF does not differentiate , whether  ischemia comes from RCA or LAD .

  1. In elderly , dibetics and co existing medical condtions  the the established  benign   character  of  inferior MI disappear, as  any  muscle loss  in LV has equally adverse outcome.
  2. Even though  inferior MIs are immune  to cardiogenic shock  , a equally worrisome  prolonged hypotension due to high vagal tone, bradycardia, plus or minus RVMI can create trouble. Fortunately , they respond better to  treatment. Except a few with extensive transmural RVMI outcome is good.
  3. Presence of  mechanical complications of  ventricular septal rupture , ischemic MR can bring  the mortality on par with large anterior MI.

How different is the clinical outcome of infero-posterior  MI with reference  to the  site of  coronary arterial  obstruction   ?

The sequence of  outcome  From  best to worse  : Non dominant RCA* → Dominant RCA but distal to RV branch → LCX dominant with large OMs

* It is believed   an  acute proximal  obstruction of a  non dominant RCA may not be mechanically significant, but can be electrically significant as it retains the risk of primary VF and SA nodal ischemia. The ECG changes  can be very minimal or  some times simple bradycardia is the only clue. One should be able to recognise this entity (Non dominant  RCA STEMI)  as the outcome is  excellent and these patients  would never require procedure like primary  PCI

** A inferior MI due to a dominant LCX and a large OMs have comparable outcome as that of extensive anterior MI. The ECG will reveal ST elevation in both inferior and lateral leads.

***In patients with prior CAD  and collateral dependent  multivessel disease  the  inferior anterior sub classification does not make much sense as  entire coronary circulation can be mutually interdependent.

Final message

Inferior STEMI  generally lacks the vigor  to cause extensive damage to myocardium in most situations .Further they respond better to treatment. Risk stratification of STEMI based on the location of MI has not been popular among mainstream cardiologists. This issue needs some introspection as  the costly and complex treatment modalities like primary PCI  is unwarranted in most of the low risk inferior MIs.

Related posts in my blog:

1.Why thrombolysis is more effective in RCA?

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NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

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Left main coronary artery disease (LMCAD) often evokes  a panic reaction  among cardiologists .Not every LMD deserve that re. To  label  it as  significant, we have a criteria ,  that is 50% diameter stenosis.  So what you do , for a tapering  or narrowed left main with 40% stenosis. Isolated insignificant left main is rare *, but real incidence is not known.  LMCAD  is  most often due to  , atherosclerosis of left main coronary artery without limiting the flow.

What are the options ?

  • Leave it alone, with intensive medical management assisted by high dose statin(80mg)
  • Elective PCI with stenting , even though the lesion is not significant.

*If associated LAD  or LCX is there decision making is easier .

How  significant is a coronary stenosis ?

The significance of a coronary lesion with reference to “lumen diameter obstruction” is basically flawed. The significance of a coronary stenosis, by tradition is  based on it’s hemodynamic impact ,right from the  CASS days in early seventies.Unfortunately our mind set has not changed even after realising    non obstructive – sub critical lesion is more prone for acute coronary syndrome.  Is it not ironical to call a  40% lesion a non significant one !

So, the  significance of coronary stenosis is two fold.

  1. Hemodynamic  significance
  2. Clinical and  pathologic significance

The former predisposes to often chronic stable angina, later likely to result in ACS.

How will you approach a apparently insignificant left main disease ?

A 40 % lesion in left main is hemodynamically not significant , but pathologically very significant.It needs intensive treatment. Plaque passification with medical approach is first choice.If the lesion morphology is eccentric,  has irregular margins or involves  LAD  or LCX ostium doing a PCI or even a CABG is to be considered in spite of the lesion is  hemodynamically insignificant .

Why , PCI is   considered  “not appropriate”  for   less tighter lesions , even though these lesions  have great clinical significance ?

The answer is simple, The risks  and the  potential cost are more than the benefit !

And further ,  stents are  not innocuous devices  either  , they  always carry a risk of sudden occlusion as like  a sub critical lesion  !

Answer to the title question

True incidence is not known . Our experince (Class 1 c evidence) would suggest Left main disease constitutes up to 10 % of CAD.Among this one third would be hemodynamically insignificant

Suggested reading

Handbook of Left Main Stem Disease

edited by Seung-Jung Park



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