Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !


When false truths are synthesized to conceal a true myth . . . where will the poor myth complain ?Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !

  • Primary PCI  is a greatest innovation  in modern day cardiology .Without this modality  most  STEMI patients will buy Instant  tickets to grave yard !
  • A cardiologist who intends to  thrombolyse  a STEMI is considered as a low quality cardiologist .
  • Streptokinase should have  no place in the crash carts of modern coronary care units.
  • There is nothing called “Time window” for rescue angioplasty.
  • VVI pacemaker  will convert an electrical problem of heart block into a mechanical one by depressing LV function .
  • Digoxin is an obsolete  drug even in well established cardiac failure with dilated heart.
  • Beta blockers not only fail to control  blood pressure smoothly , it often converts  a hypertensive individual into a unhealthy one  by it’s prohibitive side effects !


Here is a  video recipe  !

Please click here to  see more videos from my you tube site

” This is post is 5 years old , Newer developments should be given considerations”


STEMI is the “Numero Uno” of  cardiovascular emergency .The  treatment has evolved over decades,  right from   the primitive  arm chair approach to the  air dropping of  patients  over the cath  lab  roofs  for primary PCI ! We realise by now ,both are extreme forms of treatment and  may  have unique  hazards. What we forget is the , the natural history of STEMI is too  much dependent on the degree of initial damage to the myocardium , and it is very difficult to alter this,  however good is the therapeutic strategy .  We are yet to find an answer regarding the mechanism of primary VF and modes of preventing it. We also have no answer for  ,  why  some  develop myocardial damage  very fast and  the  cardiogenic shock occur in an  accelerated fashion. (Fate ?)

Many would consider  ” non availability of   infrastructure and expertise ”  is the major issue  for  primary PCI . But the real problem is much more than that .When an  illusion of knowledge is  created by constant bombardment of data  , it is natural for human beings to believe whatever is told or printed in books and journals. We cardiologists are made to believe thrombolysis is a far . . .  far  inferior treatment than primary PCI in STEMI .  It is not so in any stretch of imagination !

The fact that,there is no entity called ” Failed primary PCI ” in cardiology literature  , would  suggest how biased we are against thrombolysis. Every cardiology  resident will  recognise  thrombolysis fails  at least 40% of time .Yes , it is  a  fact  , but the irony is , this   is  often  used   to convey a surrogate  meaning , that  is , primary PCI is  near 100% successful !

How  do you assess success of primary PCI ?

Unlike elective PCI where the criteria is too liberal, we can not afford to adopt the same in an emergency PCI. Here the aim of the procedure is entirely different (Salvaging dying myocardium vs pain relief  ).

It’s still a  mystery ,  while  thrombolysis is vigorously assessed  for it’s  effectiveness   primary  PCI is rarely  subjected to the same scrutiny  . A check angiogram  after the procedure ,  is all that is done . . . and every one  leaves the cath lab happily. The  effect of primary PCI on ST segment ECG resolution must be documented immediately after PCI. While ,  It is mandatory to take ECG after 60 -90 mts after thrombolysis , this sort of protocol is rarely  followed after PCI.

If the ST segment  fails to retract  > 50% immediately  following PCI  the procedure  should be  deemed to have failed . Further , unlike thrombolysis  in primary PCI , the ST segment has to regress within 10  mts , as IRA patency occur instantly .If we apply this criteria , the success rate of primary PCI would be far less than what we believe*

* Not withstanding the official lesion , hardware, related failure. If we encounter a severe triple vessel disease , with a bifurcation lesion and thrombus it’s  a tough exercise as we are racing against time .

Primary PCI  Camouflaging  in semantics

  • A successful but  delayed   primary PCI  is actually a failed PCI
  • A  complicated  primary PCI  often  reach the equivalence  of   failed PCI
  • No  reflow is almost synonymous with failed primary PCI as successful correction of no reflow occur in minority.
  • Not all TIMI 3 flow is converted into myocardial flow.
  • Renal dysfunction following excess dye has a  high  morbidity
  • If patient  develops significant  LV dysfunction following primary PCI it is a failed PCI.
  • Finally if the cost of primary PCI exceeds the insurance limit it is  economically a  failed primary PCI as the patient  has to spend double or triple  the amount of sum insured .This stress has resulted in many recurrent coronary events .

Why is it important to recognise failed primary PCI ?

For failed thrombolysis we have a strategy . Unfortunately , even in this modern era  we have  no useful  strategy for failed primary PCI . Handing over a patient to a surgeon in a such a situation is considered by many as a great rescue strategy but in real world it does no good in most of the patient.

Doing an emergency CABG in a sinking patient with a battered coronary artery is no easy job /Many times it only rescues the cardiologists from the embarrassing situation of facing the relatives who ask for explanation.

So , what can be done at best , in failed primary PCI ?

  • CABG can be an option but still questionable !
  • Most times  there is  no other option except to fall back on the medical management.
  • Intensive anticoagulation and one need to consider even a rescue thrombolytic treatment !
  • Some times we can only prey !  Failed primary PCI for a patient in cardiogenic shock with IABP support is near death sentence !

Final message

  • Remember ,  success of primary PCI   is  not in  wheeling out a  patient  alive out of cath lab   , with a TIMI 3 flow  in the IRA ,  but in  garnering significant   myocardial salvage   which  should have an impact on   intermediate and long term  outcome .
  • Do not ever think primary PCI is a sacred treatment modality in STEMI  and the job of the cardiologists ends there. It is vested with  lots of important complications – defined, undefined , recognised,  unrecognised, reported, and unreported ,  concealed ,denied, poorly understood, etc etc.
  • There are  equally  effective, less dangerous treatment modality available .
  • Decision  to do primary PCI  must not be based   only on the  “affordability and  availability”  of  cath lab and expertise !
  • In  clinical cardiology practice,  no  procedure  is  great   & nothing is inferior either  !  Every thing has to be used judiciously , appropriately  and  intelligently (Intelligence is synonymous with common sense many times!)

Coming soon

Surgeon’s real time experience of operating  on a failed primary PCI. To our surprise , only a handful of surgeons  have this experience

It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

Syncope is a classical feature of LVOT obstruction especially with valvular aortic stenosis.The mechanism of exertional syncope in Aortic stenosis is traditionally attributable to the fixed obstruction .This fixed obstruction is not able to cope up with increased cardiac output as demanded by the exercising muscles . But exercise  induced reflex as well as local vaso-dilatation mechanism is intact . The consequence is predictable. A critical fall in SVR amidst a obstructed LVOT precipitating a syncope.

However , If the above mechanism is the sole reason for syncope in Aortic stenosis , we have a problem to explain why syncope is  rare even in critical mitral stenosis which is also fixed LV inflow obstruction ?

Is there some thing unique in LVOT obstruction that causes syncope ?

No, it is nothing to do with LVOT .To generate a true pathological syncope, reduction in cardiac output per-se may not be enough . It appears there should be an inappropriate systemic vasodilatation as well to precipitate a syncope.This can happen only if the parasympathetic system gets activated by some means . The trigger is located in the mechano- receptors of left ventricle . Hypertophied left ventricle with high Intra cavitory pressure (Often above 200mmhg) generated due to LVOT obstruction activates the syncope circuit.The same rule may apply for RVOT as well .One could get syncope with critical valvular PS or severe pulmonary hypertension when RV mechanical receptors get a triggered.

What happens in mitral stenosis ?

In mitral stenosis , LV is under- filled ,  wall thickness is normal .There is little likely-hood of LV mechno-receptors to get stimulated as the LV wall stress is normal. This is the reason syncope is less common in mitral stenosis. However , this is not  absolute rule , syncope can still occur in severely narrowed orifice of mitral valve due to low flow state alone or a ball valve thrombus and paroxysms of arrhythmia .

Femoral artery puncture is still the default technique for cardiac catheterization even as the radial access has gained huge popularity in recent years.Though patient  comfort and access site complications are clearly low in radial approach, complex procedures still demand femoral access. The true draw-back of  the obsessive  adaptation of radial access could be the  gradual loss of expertise in the fine art of femoral artery puncture.

It’s true femoral artery puncture can be troublesome at times by palpatory method .How to get into a difficult femoral artery with a poor pulse either due to anatomical reasons, extreme obesity or a compromised hemodynamic status ?

There are times, blind puncture based on anatomical guess could work. Alternate ways do exist. One can access the femoral artery by ultrasound guiding  with or without  smart needle system . More practical is the empirical  puncture based on surface anatomy  over the head of femur in fluoroscopic screen.The later method is not really crude as some would  think !. It was suggested by Grossman and popularized by none other than father of Interventional radiology Dr Dotter in 1970s .(Radiology Apr;127(1):266-7.Fluoroscopic guidance in femoral artery puncture.)
By fluroscopy , in AP view the head of femur can be divided into 5 zones.(Huggins) Zone 1 and 5 or superior and inferior to head of femur.The zones 2,3,4 are divided into upper, mid and lower third.
Where does common femoral artery bifurcate ?
The bifurcation of the CFA occurred in zones 2, 3, 4 and 5, which was 1%, 9%, 43% and 47% of the time, respectively, and thus occurred within the lower third of the femoral head or below the lower border of the femoral head in 90% of patients.

femoral artery puncture by fluroscopy

Image source Cardiovascular Intervention and Therapeutics January 2014, Volume 29, 18-23 Madjid Chinikar

femoral artery puncture by fluroscopy 2

Image source Cardiovascular Intervention and Therapeutics January 2014, Volume 29, 18-23 Madjid Chinikar

How to approach ?
A 18 G needle could be ideal
Puncture the skin at zone 5 inferior border of head of femur. Enter the artery at mid point in the Zone 3.
The chances of hitting the femoral artery is near 95 %


1.Fluoroscopic localization of the femoral head as a landmark for common femoral artery cannulation. Garrett PD1, Eckart RE, Bauch TD, Catheter Cardiovasc Interv. 2005

2.Fluoroscopy vs. traditional guided femoral arterial access and the use of closure devices: a randomized controlled trial. Abu-Fadel MS1, Sparling JM, Zacharias SJ, Catheter Cardiovasc Interv. 2009 Oct 1;74(4):533-9
3. Fluoroscopy guided vascular access: asking the right question, but getting the wrong answer? Turi ZG. Catheter Cardiovasc Interv. 2009 Oct 1;74(4):540-2

4.Imaging or trusting on surface anatomy? A comparison between fluoroscopic guidance and anatomic landmarks for femoral artery access in diagnostic cardiac catheterization. A randomized control trial. Madjid Chinikar, Azam Ahmadi, Abtin Heidarzadeh, Cardiovascular Intervention and Therapeutics January 2014, Volume 29, 18-23

5.A Prospective Randomized Clinical Trial of the Use of Fluoroscopy in Obtaining Femoral Arterial Access Chadwick E. Huggins, MD, Michael J. Gillespie, MD, *Walter A. Tan, J INVASIVE CARDIOL 2009;21:105–109

6..Puncture of the popliteal artery using a Doppler-equipped (SMART) needle in transpopliteal interventions.Kluge A1, Rauber K, Breithecker A, Rau WS, Bachmann G.Eur Radiol. 2003 Aug;13(8):1972-8. Epub 2002 Nov 22

Heart transplantation  as a treatment modality was conceptualized  by Christian Barnard in 1967 . Still considered as an  “Act of God” this  surgery is regularly performed worldwide by dedicated  transplant team consisting of cardiac surgeon , physician , Anesthetist , pathologist and others .Unlike other organs , heart transplant cannot have a “live donor” .Though  started  half a century ago, the real  pace has  picked up only in last 2 decades .Currently it is  “globally accepted  standard” intervention in terminal cardiac failure (Including pediatric heart conditions)

How are the survival rates ?


  • Now, many centers  are able to reach the  bench mark Stanford- statistical rates with a consistent  five  year survival rate crossing   75% .
  • The median survival rates is 10.5 years
  • One of the estimate indicate , If they cross first year, median survival reach 13.5 years
  • There has been many living survivors who have  crossed 30  years.

Looking at these numbers  , there is dramatic impact  in terms of global disease burden and the life gained.Statistically  speaking  successful treatment by heart transplant is equivalent to overwhelming  many  cancers in a human body !

Can these  results reproducible in all centers ?

These excellent outcome is  the reward to highly dedicated teams with  pioneering work culture . One should be cautious to start new transplant center without proper facility and expertise.Unregulated heart transplant  centers is vested with risk of pulling down the excellent  statistics of this unique form of human organ exchange.

Newer developments

Patient  selection criteria and  strategies to prevent rejection is being streamlined .The major  issue is availability of donor heart and how to optimize organ procurement and increase transport survival time .Transmedics has deviced a state of the art organ transport system . The other exciting thing expected to happen is potential (Ironical though !) heart donors from  even cardiac  /circulatory deaths . (Dhital KK, Iyer A, Connellan M Lancet. Adult heart transplantation with distant procurement and ex-vivo preservation of donor hearts after circulatory death: a case series.2015 Jun 27;385(9987)

What about artificial hearts ?

As of  now biological heart has definite edge over  artificial heart.Meanwhile rapid development of LV  assist  device and near total artificial  hearts may  end up with destination therapy rather than bridge to transplant. The “INTERMACS ” data are very promising and let us wait for the day artificial heart  can  score over the biological  ones.


1. The Registry of the International Society for Heart and Lung Transplantation: Twenty-eighth Adult Heart Transplant Report–2011.Stehlik J1, Edwards LB, Kucheryavaya  J Heart Lung Transplant. 2011 Oct;30(10):1078-94.

heart transplantation
longest survival after heart transplanation
longest survivor of heart transplant

Prosthetic valve obstruction is becoming a common clinical issue .It can be either acute, sub-acute or chronic . The pathology is usually thrombus formation , scar tissue growth (Pannus) or rarely a mechanical defect. Echocardiographic differentiation of thrombus from  pannus can be difficult .Generally , pannus is smaller , linear (less round) ,encroach from the periphery to central , mean gradients are consistently lower  than thrombus mediated obstruction. Clinically  pannus related obstruction present less acutely and occur in-spite of good compliance of anticoagulant medication and a well maintained  INR .

Trans thoracic (TTE)  , Trans-esophagel (TEE ) echocardiography , and real time 3D TEE are useful imaging modalities .The value of cine fluroscopy should be never underestimated and it is probably still the the best way assess the struck metallic leaflet.

Though the pathogenesis of pannus and thrombus are considered different there  is no reason they can’t  occur in a given patient at the same time.We know at least  one patient who had been referred to surgeon for mitral valve obstruction due to failed thrombolysis  had showed heavy load of thrombus  attached over a well formed pannus originating in medial sewing ring.

FInal message

However intelligent one may be , human brain often  tends to get skewed when confronted with a sudden query like  “What is your diagnosis , This or that  ?  Pannus or thrombus ? .Most will  go with  any one of it ! However, cardiac physicians must be aware  both pannus and thrombus can occur overlaid simultaneously in a given patient .The exact incidence  of such “combined thrombo-pannus”  is not known  but bound to be higher as we look for it. In fact , many of the residual gradients after lysis is attributable to undiagnosed pannus.  There is also a  suggestion scarred  , injured  ,  rough surface of the pannus could be the initial trigger for thrombus formation .


1.Differentiating thrombus from pannus formation in obstructed mechanical prosthetic valves: an evaluation of clinical, transthoracic and transesophageal echocardiographic parameters  John Barbetseas,  Sherif F Nagueh,  Christos Pitsavos, ;J Am Coll Cardiol. 1998;32(5):1410-1417. 

We know right from our pathology days in medical school , Atherosclerosis , the killer human vascular disease has a predilection for branch points. It’s no surprise around 30-40% of coronary stenosis has some degree of involvement of branch points .

PCI essentially involves palliative metal bracketing of this inflammatory cum degenerative process of the vessel wall.Tackling bifurcation lesions (BFL) requires special expertise , hardware and technique as carina and two ostia (In fact three !) are exposed to complex hemo-rheological stress de-nova and more so after the metal invasion.

The complication rate as well as long- term patency are considerably more  in BFL than regular lesions. This is why a “4S strategy “ (simple single stent strategy ) is the preferred default strategy in most BFL.

There are about dozen strategies  to tame  the BFL with  stents.One such modality is dedicated BFL stent.Various designs have been proposed in both balloon and self expansion platform.

The ACCSEES is a prototype dedicated BFL stent with DES and  a self expanding system


Degenerative Aortic stenosis occur with either normal  or congenitally malformed/ bicuspid valve.This contributes to the major chunk of  aortic valve surgeries and interventions (TAVR) in elderly population  . The optimal  timing of aortic valve replacement in patients with AS is debatable inspite of  well formed guidelines.

Three factors determine it .Symptoms , severity of aortic valve narrowing  and the tactness of LV function .The last parameter is a tricky one .We used to think in the past , severe LV dysfunction is a contraindication to aortic valve surgery. Now we realise ,however severe the LV dysfunction may be , relieving the obstruction will benefit  the patient and  the LV function is  also  likely to improve.

Cardiac physicians  face a dilemma when confronted with a patient  with low gradient and severe LV dysfunction .In this situation they are advised to do doubtamine stress Echo and watch for the gradient .If the gradient  increases that would  imply true fixed stenosis . (In pseudo aortic stenosis increased contractility opens the aortic valve and gradient will fall )

While this concept appears simple .There  are few  important issues that goes unaddressed  as we have not yet fully understood the  mechanism of LV dysfunction in aortic stenosis .(Link to mechansim of LV dysfunction in Aortic stenosis.)

At what degree of aortic stenosis LV goes down fighting and fail to generate the required  gradient ?

Myocardial function  and behaviour at times of hemodynamic stress can be highly  variable and most of us believe it is determined primarily by the genetic switches of myosin and other contractile elements .This is naturally proven at times of hypertensive left ventricular failure (Only in a fraction of the hypertensive population  LV is set to fail  when BP acutely raises.)

Proposed concept

Considering the complexities in cardiac mechanics , hemodynamics (and not to forget the vast control exhibited by genetic imprints over the hemodynamic behavior of LV) , it seems highly plausible even mild degrees of Aortic stenosis can inflict significant myocardial dysfunction in certain patients . Hence the phenomenon of pseudo aortic stenosis needs further critical analysis If this is proven to be true there could be a realistic indication for aortic valve intervention even in patient with low gradient / true Mild AS with LV dysfunction.
A word of caution is required .Relying too much (Which we often do ) on gradients in the assessment of aortic stenosis has skewed our common sense. Its wiser to have a  meaningful look at the valve morphology . A normal appearing  valve in 2D can never cause significant stenosis. Pressure recovery phenomenon also is to be given due respect as it over estimates gradient .This will effectively avoid surprises and guilt on table when we find a relatively good looking valve posted for AVR /TAVI

An attempt is made to look for individual components of cell viability .See the table below. It is a generalized statement for understanding purpose only. Various imaging modalities assess the overall physiology of myocyte function (however  they test  an individual component of a cell more than the other) We may believe an unit of cell would die in “one-go” at times of ischemic injury.Reality is much complex.There is considerable variation in intracellular survival mechanisms . A cell can die in a regional fashion with residual signs of life scattered across among the different organelles. The quantum of damage to Nucleus /mitochondria may appear determine the recovery . The reverse can also happen .What is the purpose of mitochondria respiring if contractile element is totally damaged ? It becomes a “vegetative cell”. The gross discrepancy we are witnessing in myocyte cell function recovery with reference to both acute and chronic reperfusion is attributable to this gap in our knowledge.

myocyte viability demri spect thallium dobutamine contrast echo 2


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