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

Coronary  atherosclerosis is the number one killer of mankind. Many would consider it as an  essential  process of aging .Modern  life styles and habits make this appear  very early in life . There is currently an endemic (or even  a pandemic ) of   CAD due to premature  atherosclerosis. We need to recognise CAD is not a  primary heart disease  .It is an irony, heart is an  innocent bystander  to the  biological derangement  of coronary  vascular system  when  it is infested with atherosclerotic plaques .

So , when we  are confronted  with  serious atherosclerotic lesions in a coronary artery   what shall we do ?

We have three options

  1. Take on the enemy in a direct confrontation (Like war on terror ) : This is  some times called as Interventional cardiology .Caution is required as the battle  is within the human coronary artery ,  cross fires and collateral  damage  are unavoidable.

2 .Next  method  is to  find the basic cause  of  terrorism , identify  the perpetuates, facilitators    and try to correct the   root cause of it (CAD ) .This approach  also refered to as medical management  in cardiology community*  . It  aims  at regression of plaque  by statins, and life style modification and preventive cardiology. This modality is most ridiculed and  insulted by the main stream cardiologists.

*Comparable to  bilateral peace talks for a political solution to terror

3. And third option is a  real  surprise !   This  neither  confronts   the lesion   nor does it  address the initiating factors . It   just ignores  the lesion and by pass it with a LIMA /SVG  fly over ,  as if  nothing has happened in this vital high way leaving the culprit scot-free  .This option is  executed by surgeons as  CABG surgery . . . and  for mysterious reasons  this is a  well accepted one .

CABG :Here the atherosclerotic  burden is untouched by surgery . The graft can get diseased  sooner or later , native vessel disease  shall  progress some times encroaching  the ostia of distal graft site . Incidence of acute coronary syndrome following CABG is not greatly reduced for the simple reason we are not doing anything primarily to the inflamed plaques .These issues  are left ,  to be  taken care by the  medical  management .

* This article  does not want to defame these great development in cardiology(PCI/CABG) . They have a  specific role to play. CABG AND PCI remain the only option for critical  lesions with limiting angina .But please remember without  proper  medical management  ( ie Targeting  the perpetuates of  crime )  both  PCI and CABG will be a big sham !

Final  message

Avoiding   the  lesion  or  attacking the lesion  is a  primitive  method to tackle CAD  . Passifying   the lesions  in a slow and gentle manner,   preventing  further progression  or regression  of lesions is the only  “sane” method for combating CAD   . PCI and by pass surgeries  can be termed  as  21st century’s   medical  adventure sports  which  has  limited role ,  in the overall control  of CAD  for the human kind .

And  now  answer this question . . .

Cardiologists attack the lesion and  surgeon avoids the lesion ?  Who is the winner in our fight against CAD  ?

Both of them are  clear losers .The winners are  all those  humble physicians and parmedical workers (or even the responsible lay public ) who  help recognise  the early forms  of  CAD  and  counsel properly to prevent it .

This is  what  Dean Ornish   in 1991  documented in  Lancet  which was never considered scientific   for the simple reason it has no commercial value !




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 . . .

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.

If thrombus is the chief culprit in any vascular emergency  there can be  no second thoughts as it needs immediate  arrest without warrant! (STEMI,Acute pulmonary embolism , DVT, Acute limb ischemia etc) Since pharmacological lysis of thrombus is easy and  be done immediately  it will continue to play a major role still , in many clinical situations that critically compromise organ function .

However , large  thrombus burden  (or in which medical therapy fails to do a good job )  we must  intervene mechanically  to change the course of event.Though vascular surgery is a definitive option its always better we try out catheter based thrombectomy.

Many hardwares are being developed in the recent times. Aspiration catheters, baskets etc * .This  one from vascular capture (Minnesota USA)  appear promising as its a universal capture device that can be  used anywhere coronary , pulmonary or even in deep veins .

Clinical case examples using megavac : Video

*Few  examples of Thrombectomy devices.

1.They can be mechanical rotational devices like Amplatz Thrombectomy Device (ATD) Microvena,  Straub Rotarex (Straub Medical, Wangs, Switzerland) and the Tretorotola Device ( Arrow International, USA) employ a high-velocity rotating helix or nitinol cage that macerates the  thrombus.Disadvantage is endothelial contact with moving mechanical parts.

2.The Angiojet device (Angiojet; Possis, Minneapolis, USA) uses a rheolytic mechanism with possible   less endothelial injury as there is no true contact with endothelium.

3.Ultrasound mediated lyis ( EKOS Endowave (EKOS Corporation, USA) and Omniwave (Omnisonics Medical Technologies,  USA)  fragment with high frequency ultrasonic waves.

Effect of PCI on Long-Term Survival in Patients with Stable Ischemic Heart Disease are just out in NEJM.

The results are as expected !

“Let us get more Courage , to say no when we want to say no !”



These are the common ECG terminologies with which clinical cardiology is being practiced over the years .In this era of instant interventions the exact meaning for these terms  may not matter much for many of us.Still , Ischemia could denote a more benign connotation , while injury suggests an emergency (like an accident) .Of course , this is a dangerous way of defining them. Still, there may not be an entity called  “chronic injury”. while chronic ischemia is all too common.

Logistically , both could  mean the same (except the perception) and related to the intensity of the index reduction in blood supply to the varying thickness of myocardium.While injury is diagnosed by ST segment elevation , ischemia is diagnosed by ST depression  or T inversion.

No, its wrong , come again please ,

Shall we say . . . most injures are ST elevating  while most ischemia are ST depressing , but  still injuries can be ST depressing  as well.  We know Ischemia can be sub-endocardial , transmural or  rarely sub-epicardial ,while injury can either be sub-endocardial or subepicardial (Rarely transmural ?)

Can you refine it ?

Only  subepicardial ischemia(Injury)  elevates  ST  segment while sub endocardial ischemia depress it.The leads facing the affected subendocardial and epicardial surface will determine whether its going to be ST elevation or depression .

Go further,

Does the opposing sub-endocardial and sub-epicardial forces negate or  cancel out  ? If so what is the status  of reciprocal ST depression in STEMI if remote ischemia occurs in sub-endocardial  or  sub-epicardial zones ?  Can there be reciprocal ST elevation for primary ST depressive forces ?

If ischemia and Injury are to be defined only with reference to ST segment , which area of myocardium is linked to  critical T wave ischemia (Both Tall T and dynamic Wellens type T )

Still more , If Injury is  represented by ST elevation,  then what represents  infarct ?

ST elevation in acute MI-STEMI is actually due to  transmural* injury while infarct is represented by Q waves in strict sense.In that case not all acute STEMIs are not true Infarcts.Thats why many STEMI can get totally aborted with zero LV dysfunction and negligible enzyme release.  (Should we call these as Non Infarct STEMIs ?)

*Though STEMI results in  transmural ischemia , it is the sub-epicardial zone of injury that elevates the ST segment. This  implies any degree of subepicardial injury is suffice to elevate ST segment (eg pericarditis) and transmurality of ischemia is not mandatory.

What is reversible vs irreversible Injury ?

If irreversible injury is equivalent to infarct , reversible injury is same as ischemia ? (Whats the histopathological  correlates , Cell swelling, mitochondrial / nuclear death .(We know , enzyme release are  linked to cell death even in  chronic stable angina )

Where is the epicardium  for the IVS ?

Most ACS involve interventricular septum .In this case does septum has  any defined sub-epicardium or endocardium? How does septal STEMI forces behave with reference to partial or full thickness septal  infarct ?

Final message

Acute Ischemia and injury can mean “one and the same thing” or  “totally different” entities  depending upon  the totality of obstruction within the coronaries and  sparing of  sub epicardial zones of  myocardium. In my view , any acute ischemia can be labeled as injury.Bifurcating ACS into STEMI and NSTEMI has largely removed the embarrassment of these entities .

Be grounded

Forget the basic science , electro-physiological concepts can wait.Lets live in a realistic world. Get to know the underlying lesion . What can be done for it ? Go ahead , wheel your patient to cath lab . Alert the staff .Be pragmatic ,make sure your patient has sufficient insurance coverage to open up  all his blocks ! That’s it !


The intention is not to confuse the readers.Only to make us realise ,the gap in  basic science is “huge and wide” which I hope is  filled up by the generation next !

There is something to understand in the movement of dissection flaps with reference to incoming coronary blood flow.Why some dissections dangerously escalate and totally occlude within moments while some others seal spontaneously ? Though uncommon ,  retrograde dissections has some unique hemo–anatomical property .

dissection flaps antegrade vs retrograde




benign dissection no flow limiting self sealing

This year’s Noble prize for economics was conferred  for Dr Angus Deaton  from Princeton,  for an unique revelation, that measurement errors in economic indices such as estimation of poverty and nutrition levels in society  is real and huge .

The crux of argument (My version )  could be , data collection errors , planning with that contaminated data , sets in a chain reaction , that sustain a flawed intellect in young researchers , which  ultimately leads to human beings becoming  victim to their own  data . While Deaton addressed this in economic issues,  one can guess how critical these errors could be , when  one deals with a  continuously variable  biological parameters .

Every day , medical professionals are confronted with  diverging data measured with dubious methods. Measuring health as quantifiable semi mathematical parameter itself is intrinsically flawed , unfortunately this is the only way we can do it as of now.

If  logical extrapolation is the accepted norm and poverty is the most prolific disease  of humanity  (coded in ICD by WHO) its obvious Deaton’s work will have tremendous impact on medical science than any  other field .

As a cardiologist ,I struggle to understand for the past 30 years  , why we need to work towards a goals of  reducing few mmhg of blood pressure  (or few mg of LDL ) in elderly population knowing fully well the evidence for which is  soft with questionable end points. It  appears some times comical , when healthy people who are not taking these medicines in poor countries  are labelled as medically deprived ! by certain non Governmental agencies.

Final message

With existence of people like Deaton , there seems to be light at the end of tunnel , (Hope we don’t create new tunnels) It is heartening , we are witnessing major innovations in the assessment of health outcome,efficiency and impact in recent rimes.. Let us hope some common sense would be infused over the complicated number science !


Here is an awesome piece of writing  by Reetika Khera an associate of Angus Deaton at  Princeton .(Reproduced with the courtesy of Of “The  Hindu ”  -From the open page,   on the significance  of  Nobel Economics this year 2015)

Angus Deaton, the winner of this year’s Nobel in economics, has contributed immensely to the understanding of poverty, prices, nutrition and well-being in India. His work has been guided by the belief that economic progress must lead to better lives for everyone.

Much of the work by Angus Deaton, the winner of this year’s Nobel Memorial Prize in Economic Sciences, has been focussed on measurement issues. He has questioned the quality of data collected in large surveys and suggested ways of improving the surveys. He has also thought very hard about how these data could or could not be used, how to reduce measurement errors, and what inferences one can, or cannot, draw from data that might suffer from measurement errors.

Boring as that may sound, it has ensured that economists pay attention to detail, and do the hard work that empirical analysis demands. Good data is fundamental to good economics.

One example of this is from India. His contribution to the understanding of price indices and relatedly, poverty estimation, has been very important. He has highlighted the problems with the computation of price indices in India and how these affect poverty estimation. His proposal to use prices implicit in the data collected by the National Sample Survey Office was implemented by the Suresh Tendulkar committee some years ago.

His book on these issues, The Analysis of Household Surveys, published in 1997, remains the best to learn about data issues. Along with poverty estimation, he has applied his deep understanding of several disciplines (ranging from biology to philosophy) to work on mortality, health, nutrition and well-being. In his latest book, The Great Escape: Health, Wealth and the Origins of Wellbeing Inequality, he generously acknowledges Amartya Sen’s influence on this aspect of work.

India-focussed work on poverty

Much of this body of work on nutrition in India (and elsewhere) has come since the 2000s. A large part of it is India-focussed, much of it co-authored with Jean Drèze. In 1999-2000, there was a lot of interest in the poverty estimates as these were the first post-liberalisation estimates. Supporters of liberalisation were keen to show that poverty had declined, and that its rate of decline had accelerated since liberalisation. Those against it were unwilling to accept this.

A change in the methodology for data collection between 1993-94 and 1999-2000 made a straightforward comparison between the two point estimates impossible. Deaton’s work (with Drèze) on comparable estimates disappointed both camps. They found that while the official claim that poverty had declined in the post-liberalisation period was true, the claim that there had been an acceleration in the rate of decline was not.

In 2009, Deaton and Drèze published a paper in the Economic and Political Weekly (EPW) on the nutrition situation in India which once again provoked economists on both sides of the ideological spectrum. On the one hand it led to a debate, in the same journal, with Utsa Patnaik — widely considered to be on the Left — who felt that the decline in calorie consumption was a symptom of rising poverty. They, however, pointed out that calorie intake was declining even at given levels of real per-capita expenditure, especially among the better-off households, and discussed other possible reasons for this pattern.

On the other hand, in 2013, Arvind Panagariya challenged a long-held understanding among economists and nutritionists about anthropometric outcomes. The argument was not so much about whether height is a good indicator of nutrition, human development and well-being. Panagariya’s thesis was that Indians are short, not because they are undernourished but because they are “genetically programmed to be so”. Deaton and his co-authors pointed out in their response, again in the EPW, that “all of his arguments about the role of genetics is residual: if we cannot think of anything else [we assume that] it must be genetics.”

These two debates are illustrative of Deaton’s careful analysis and unwavering honesty, his ability to separate his social commitments from what his meticulous data work suggests. Indeed, at a press conference at Princeton University just after the prize was announced, he said that sometimes his work leads him to “very uncomfortable” places.

Questioning the dominant trend

Another important part of his contribution has been to question dominant fashions in development economics. When “instrumental variables” were a popular tool to establish causality, he wrote “students no longer look for a thesis topic, but for an instrument”.

More recently, a new technique “randomised control trials” (RCTs) has taken development economics by storm. For some, RCTs are seen as the only form of evidence, disregarding not only other forms of quantitative evidence but also other forms of qualitative evidence. Deaton has been among the few voices to question our over-reliance on RCT experiments while that acknowledging it as a valid body of evidence.

“I argue that experiments have no special ability to produce more credible knowledge than other methods, and that actual experiments are frequently subject to practical problems that undermine any claims to statistical or epistemic superiority,” he said.

The “randomistas”, a term used by The Economist, have been influential in several states in India. The Government of Tamil Nadu has signed a Memorandum of Understanding (MoU) “to institutionalise an evidence-based approach to policymaking”. Some experiments have led to greater hardship for the poor — for example, delays in wage payments to National Rural Employment Guarantee Scheme (NREGS) workers — without any accountability for these adverse outcomes.

For Deaton, the problem is not with RCTs per se — some of his current work is on how to use RCTs — but rather with the view that it is the only form of evidence that matters or that it should be the only driver of policy decisions. He has his differences with arguments like that advocated by Abhijit Banerjee when he said that “the World Bank should cease to fund any activity, including presumably macro policy advice, that has not been previously subject to evaluation by an appropriate RCT.”

Advocate for a greater state role

Apart from claims of statistical or epistemic superiority, Deaton has questioned the divorce between policymaking and public discussion. His contribution has not only been as a rigorous economist, but equally as a public intellectual. He is a firm supporter of government action for social policy. Without being blind to the problems of governments in poorer countries, he forcefully argues for their greater accountability.

“The absence of state capacity — that is, of the services and protections that people in rich countries take for granted — is one of the major causes of poverty and deprivation around the world. Without effective states working with active and involved citizens, there is little chance for the growth that is needed to abolish global poverty,” he argued.

On the consequences of inequality, while some inequality can be a good thing, Deaton has argued that too much could potentially have negative consequences for us all.

He noted that:

“The very wealthy have little need for state-provided education or health care… They have even less reason to support health insurance for everyone, or to worry about the low quality of public schools that plagues much of the country…To worry about these consequences of extreme inequality has nothing to do with being envious of the rich and everything to do with the fear that rapidly growing top incomes are a threat to the well-being of everyone else.”

These messages are important because public debate in the past few years in India have tended to belittle various forms of public support through terms like ‘doles’, ‘freebies’, and ‘handouts’. Repetition succeeded in creating an impression — unsubstantiated by facts — that India has gone overboard in its social spending. We have witnessed strong rhetoric on evidence-based policymaking, combined with a resolute disregard for inconvenient facts. We need to engage with Deaton’s contributions very carefully.

(Reetika Khera teaches at IIT Delhi. She did her post-doctoral research at Princeton University under Angus Deaton.)

Hot debate in STEMI

Acute total obstruction (ATO) of coronary artery is an emergency .Opening it  by pharmacological or catheter is the  standard ( logical ) protocol.However, time plays a crucial role in this coronary re-perfusion game.It can either be a sure shot of success or end up in total spoilsport. One more issue as important as time is from the overflowing scientific data  fired  by different regulators  in conflicting directions  (Also called knowledge) .

What to do with STEMI coming late ?

  • ATO with cardiogenic shock is an  absolute emergency at any time.
  • Symptomatic ATO  other than CS beyond 24 hrs still  considered  emergency for most.(Symptom should be true angina )
  • Hemodynamic instability is misunderstood term . Stabilizing it medically is not forbidden.

Asymptomatic stable ATO  beyond  24-72 hours can be  semi emergency, true emergency or as cool  as a cucumber depending upon the cardiologist’s wisdom , experience or inexperience  and the  Institutional Integrity !

*Please be reminded ,LV dysfunction is not an absolute indication for urgent intervention unless it is due to ischemic dysfunction attributable  to a critical non IRA lesion

When does a ATO become safe CTO ?

1 month , 3 months, 6 months ?

Why we are  not defining a sub-acute ATO ? or CTO in transition   ?

Is living peacefully with sub acute ATO or CTO a coronary crime ?

We don’t require a debate , whether these  questions are worth answering  or not !

Final message

Though cardiac professional  are committed  to open up occluded arteries to save  lives , reality is repeatedly teaching different stories ! The greatest danger of keeping an artery open( In disputed indications ) is the newly conferred risk of sudden closure and the attendant  unpredictable aftermath !

Or should we conclude : Living with CTO is ok , but don’t intentionally create one by denying PCI in late  post STEMI ATOs


Arguing closed artery is better than an open artery is straw man argument and inability to interpret positive things in science.  However it may still be right  when science suffers  from hostile incursions from non academic forces.

Car tyres warrant  replacement  every  20,000 km or so .Its batteries do require periodic attention. Human heart , which runs non stop from womb to tomb . . . deserves how much ? Unfortunately no one (What about your cardiologist?) can  provide  a flawless lifetime maintenance contract to this restless bio-mechanical pump ! Fortunately still, God has  created this wonder organ ,that can with stand the stress of life for nearly 10 decades . . . if we live a proper life !

However ,there are many areas in heart that are prone for mechanical stress even if it’s structurally normal .These are  the zones where the relatively fixed parts  rub against the dynamic zones .The joint between inflows ,outflows to the respective ventricle are at risk . Aortic root, along with the leaflets and annulus  formed by the fibrous skeleton is delicately close to the critical part of the conduction system namely the branching portion of AV node and His Purkinje.The process of degeneration is linked to age, valvular abnormality and genetic and  systemic metabolic profile also seem to matter in few .(Hypercalcemia and cardiac calcification ?)

Importance of the interface between Aortic valve and  AV conduction system in the current Era 

Degenerative aortic valve disease along with  the adjacent conduction system  of elderly is going to be a key cardiovascular disease in the future as the population is aging .We have made a big step forward in tackling this with innovative percutaneous aortic valve implantation  (TAVI) . However ,the artificial valve  is positioned vulnerablely  close to conduction system and incidence of complete heart block either during implantation or follow up is  high and a permanent pacemaker seems to be an integral part of this procedure for many.

aortic valve his bundle complete heart block 003

Heart seen from behind , Mitral annulus to left and tricuspid valve ring to the right .


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