Dr.Richard Asher,  a British physician from Sussex addressed a group of young passing out medical students way back in 1948 in London. The lecture was titled seven sins of medicine! We should thank the Lancet for having published this brief speech the subsequent year in its journal making it immortal medical teaching!

Seven sins of medicine lancet 1949

Seven sins of medicine

Though he was listing these sins among medical students, it is very relevant to every health professional.

1. Obscurity
Asher endorses the use of clear communication and plain language whether writing or speaking. Obscurity may be used to cloak one’s own ignorance, or due to an inability to communicate with those outside of the medical profession. “If you don’t know, don’t admit it. Instead, try to confuse your listeners.” is not uncommon. Regardless of the intention, whether to misdirect from incompetence or to foster a feeling of superiority, the patient and those surrounding them are often left confused and uncertainiy.
2. Cruelty
 This sin is perhaps one of the most commonly committed by doctors and medical students. Whether it be the physical thoughtlessness of a half-dozen students palpating a painful tumor mass, or loudly taking (or presenting) a patient’s history in a crowded room, one of the first things that is unlearnt by a medical professional is to treat the patient as they themselves would like to be treated.
3. Bad Manners
 Often overlooked, rudeness or poor taste in humour is condoned within the hospital setting. At the end of the day, many doctors and students are simply rude to patients that do not suit them. Whether it is a snapping at an uncooperative patient or making a cruel joke about them after leaving the room, the impact of these “coping mechanisms” (as they are considered to be by many) must be taken into account.
4. Over-Specialisation
 In a growing trend by the medical establishment, over-specialization and under-generalization is a growing problem in the wider medical community. Ignoring aspects of one’s education in favor of more interesting aspects is a behavior that is pathological and outright negligent in a student. Failure to diagnose or to treat a patient because “their signs and differential fall outside of my field, let’s turf them to another service” ought to be a seriously considered Supervisory & Training issue.
5. Love of the Rare
 (aka “If you hear hoof-beats, think horses. Not zebras”) The desire for rare and interesting diseases causes many medical students and young doctors to seek the bizarre rather than seeing a mundane diagnosis.
6. Common Stupidity
As well as the standard definition for this sin, the specific example of “using empirical procedures rather than tailoring for the patient” or the young doctor “flying on autopilot” must be mentioned. Ordering another test that is redundant, and for which the results may already be interpreted from the history, before starting treatment is such a situation. For example: requesting a hemoglobin count before beginning transfusion, despite the fact that the patient appears obviously anaemic.
7. Sloth
 Laziness. Also includes ordering excessive numbers of tests, rather than simply taking the time to take an adequate history

Final message

 It is astonishing, to note  Dr.Asher made this observation in the very early days in the evolution of modern medicine,(No critical care units, no HMOs, No industry nexus with research, & commodification of medicine  )  I wonder what Dr. Asher would have to write if he is alive in 2021.

Wish, every medical professional shall find their Asher score. Looking back on my career, I must confess my score would be 3 ( may be 3.5 !) out of 7.  Now, desperately trying to get rid of them. Mind you, the 4th (Overspecailisation)  and 6 th (common stupidity) is inherently built into the system. I think, very tough to avoid them.

Who is a doctor?  Where are they made?

I haven’t clearly understood the true meaning of customary Dr tag, my name carries for more than 3 decades, till I saw this. Wish, this video is played to all young medical students on their graduation day.

             I am realizing with guilt, it requires a Holywood movie buff to remind us the true meaning of the famous WHO – definition of Health, done in the most holistic fashion in the year 1948. 

Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity.

So, technically, whoever serves to improve these three components and alleviate human suffering becomes a doctor. 

Happy to share this on July 1st, the official Doctor’s day in India in memory of the Bharat Ratna Dr.B.C.Roy of Bengal. 


The clip is from the movie Patch Adams, Directed by Tom Shadyac.  A Hollywood celebrity movie maker, Virginian professor of communication turned philanthropist, now retired to a minimalist life. He is also known for his famous documentary I am that talks about the problems faced by the world. Though his works are much appreciated, I  must say, they are underrated. Deserves more than an Oscar for communicating his thoughts on the medical profession perfectly and for social equality.








I think it is an Invalid question. Whether you like it or not , medical science and philosophy are always bonded together and its relationship is eternal. It doesn’t make sense to separate them. I think we have misunderstood the meaning of philosophy. While science is presumed truths, philosophy is trying to believe in unknown truths. Philosophical truths are built-into every decision a medical professional takes.

If the expected natural history of any disease is science, unexpected deviations are philosophy. (RT PCR testing for diagnosing  Corona is science, why 90% of them are not infective and don’t transform disease is philosophy) When something is not seen or quantifiable like human immunity, it is a perfect example of concealed science or manifest philosophy.

Taking about what we think we know is science, Talking about what we really don’t know is philosophy. The term Idiopathic syndrome finds a  proud of the place in every specialty in medicine, Isn’t? 

 What will be your answer when your patient wants an assurance that a stent, you had just implanted will not get occluded in the next 6 months or so.“I don’t know, I cant assure you about that”  will be your most likely answer. (Though, we do it in style, hiding behind  the scientific hyperbole decorated with numbers,  also referred to as statistics) Please realize, this is the expression of medical philosophy in the finest form.

Final message 

My Impression is, philosophical truths should be liberally used in a regular fashion right from the first-year medical school to advanced specialty teaching. This seems essential as science in the current times suffers from too much sanctity. This has spilled over to the doctor population as well, and make them appear invincible. 

If only we realize science often trails behind the philosophical truths at least by a few decades, our patients will not be injured inappropriately and prematurely. Mixing science with philosophy in the right composition ( a perfect academic cocktail ) will bring out the best from the noble profession.   


Can anyone guess, why scientists are given a doctorate in Philosophy degree  (PhD ) ?

A young man aged around 40 years, had a STEMI was promptly thrombolysed in a small hospital located about 40 KM away in the suburbs of my city Chennai. They did an awesome job of saving the patient life and salvaging the myocardium.

Now begins the story . . . one of the non-medical person who is the owner of the hospital has an unfortunate working  business relationship with a frighteningly big nearby hospital  which had signed a memorandum of irresponsible understanding . It demanded any  patient who arrives in the small hospital with MI should be transferred at earliest opportunity to them.

So, an ambulance was arranged  and the patient (with a fairly well reperfused heart ) was shifted  in an emergency fashion . It reached desired destination after nicely chugging along the choked chaotic Chennai evening traffic for 45 minutes.

The guy was taken directly to cath lab through the side doors to perform a second salvage  procedure on a successfully opened IRA. Young cardiology consultants  in designer cath suite welcomed the smiling ACS patient to their posh new lab .Did few rapid radial shots, mumbled among themselves for few minutes,  decided to stent  a minimal LAD lesion for a patient who was in  zero distress with well-preserved LV function.

*The relatives of the patients were curious when they were asked sign a fresh set of consent which elaborately  mentioned about possible life risk during the procedure.

The patient’s wife  was clearly  amused and she pointed out to the superior cardiologists about  the earlier briefing by the Inferior freelance cardiologist who treated him in the previous hospital. She recalled , “I was told in confident terms  that  Initial thrombolysis  has been spectacularly  successful and bulk of the treatment is over and risk of complication has dramatically reduced”.

Then why is this distressing risk taking story again ,  she asked ?

The doctors hurriedly explained ,”this procedure is different. We are sorry to say we have no other option but to add  further risk to you” ! but , its all for your good !

Why should I ?  If the initial lysis is very successful  why do you want to meddle with it again ?

No Madam , you are ill-informed , you can’t talk like that .This is what modern  science  is all about. Leave the professional decision to us. We need to check immediately  whether the lysis is really successful .We can’t rely on the ECG.Further, true success lies in stenting the lesion as we fear the ill-fated site may close again.We are  taught to practice protocols based on standard scientific guidelines. This hospital has highest rating in-terms of quality care. That’s why we got updated ISO 2000  NABH accreditation

The women who is a soft ware engineer was smartly and  scientifically silenced in 5 minutes flat !

Post-amble :

What happened  to the patient then ? (When you fear something it happens is in’t the  Murphy’s law ?)

The apparently asymptotic and comfortable patient had uneventful PCI. A  long drug eluting  stent  was  implanted in recanalized  lesion in LAD with around 30 % narrowing that ended with an innocuous looking diagonal pinch. The procedure was uneventful , however next day he developed some fresh ECG changes and chest pain . The worried team took him for another angio found  stent was patent But , ultimately after a stressful 3 days of stay , some thing went wrong he ended up with new LV dysfunction.He got discharged fine with a caution  that , his stent needs to intensively monitored for the next 1 year since technically he had recurrent ACS !

Lessons we don’t learn from such cases.

When two procedures are done to accomplish the same aim (Reperfusion) , but with  differing success rates, expertise, time ,and unpredictable hazards , the benefits from them may not add together. There is clear knowledge deficit here. Scientific data can never provide fair answers to  these questions  as all real life cofounders can never be recreated in study population.

While we expect 1+1 to become  two in pharmaco-Invasvie strategy  ,one should realise it may end up with  either zero or even  – 2 .

1 -1 = 0

-1 + (-1)=  -2 ?

Learning cardiology from lay persons 

The patient’s shrewd wife threw this question ,

After two modes of re-perfusion done sequentially in my  husband’s  heart ,  at a total cost of Rs4.5Lakhs Why he  is  still left with significant LV dysfunction (Which was  around 40% EF.)

The query raised by the lady appeared much more crucial and logical than the ones discussed in many top-notch live interventional workshops we attend every few months!

As usual , I started mulling over the issue. There is something wrong with the way , we  understand  the pharmaco invasive approach-PIA .You go with it only if  initial pharmacological  approach has failed.

Of Course ,there is one more modality possible ie Pharmaco -Angio strategy where in, you look at the coronary anatomy and take a call ! This sounds good , the only issue is taking a right call ! My experience suggests wrong calls are the rule and  exceptions are rare. Then a whole new issue erupts about all those non IRA lesions

Final message

So,  til we have gain complete self-control over our evolved ignorance and evolving knowledge , it is better to follow this proposed  funny new ACS algorithm called “Pharmaco -non invasive” approach (PNIA)  in asymptomatic ACS patients  who have had apparently successful lysis.

*Please note, Incidentally  PNIA actually  refers to simple good old traditional stand alone thrombolysis.

Counter point

No one can deny Interventional cardiology carries a risk of untoward effects.Don’t blow this out of proportion. Do you know, how many lives have been saved by routine Pharmaco -Invasive approach ?

I am not sure , my experience may be limited.Let me ask the readers. Is routine PIA is warranted in all asymptomatic , successfully lysed STEMIs ?

100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component’s  contribution in the genesis of  STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thrombotic STEMI with  just a residual endothelial  erosion and hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion  seems to be biased and misunderstood scientific fact .

What happens once 100 % occlusion take place ?

Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of  tissue plasminogen system. In this aftermath  few succumb . ( Re-perfusion arrhythmia  generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus ,  and the elasticity of fibrin mesh , location of  platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3  flow !)

thrombus propgation
What happens to the natural history of thrombus in STEMI ?
Thrombus formed over the culprit lesion can follow any of the following course

  •  Can remain static
  •  Get lysed by natural or pharmacological means
  •  Progress distally (By fragmentation or by moving en-mass )
  •  Grow proximal and and involve more serious proximal side branch obstruction
  • Organise and become a CTO

Factors determining thrombus migration

The interaction between the hemodynamic  forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by  platelet vs RBC / fibrin core,  totally of obstruction,  reperfusing forces , re-exposure of raw areas and  the distal vessel integrity all matters.

While, logic would tell us,  thrombus more often migrates  distally  assisted by the direction of blood flow, an  opposite concept also seeks attention , ie since the blood flow is sluggish  in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.

(In fact, its presumed  in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to  queue up proximaly and  clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)

What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?

If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still  we don’t  know why thrombus aspiration in STEMI is not consistently useful. We also know little about  the length of the thrombotic  segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like  “cutting a slice of  butter” in some , while in few we struggle and  end up with severe no-reflow inspite of great efforts .Why ?

What is the Impact of distal collateral flow in flushing fresh thrombus ?

The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it’s soft and fail to get organised early that would help cross the lesion easily.

medical education critics cardiology evdnce based medicine growth ethics

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. !

Here is a  video recipe  !

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

Prosthetic valve implantation has revolutionized the management of  valvular heart disease . The original concept valve  was a ball in a cage valve  , still considered as a  fascinating discovery.  It was conceived by the young Dr Starr and made by Engineer Edwards  .This was followed   by long hours of arguments,  debates and  experiments that ran into many months . The  silent corridors of  Oregon hospital Portland USA remain the only witness  to their hard work and motivation.  At last,  it happened , the first human valve was implanted in the year 1960. Since then . . . for nearly  50 years these valves  have done a seminal  job for the mankind.

With the advent of  disc valve and bi-leaflet valve in the  later decades of 20th century , we had to say a reluctant good-bye to this valve.

There is a  lingering question among many of the current generation cardiologists and surgeons why this valve became extinct ?

Starr and Edwards with their child !

We in India , are witnessing these old warrior inside the heart functioning for more than 30 years.From my institute of Madras medical college  which probably has inserted more Starr Edwards valve than any other  during the 1970s and 80s by Prof . Sadasivan , Solomon victor , and Vasudevan and others .

It is still a mystery why this valve lost its popularity and ultimately died a premature death.The modern hemodynamic  men  working from a theoretical labs thought  this valve was  hemodynamically  inferior. These Inferior valves worked  like a  power horse  inside the hearts  the poor Indian laborers  for over 30 years.

A Starr Edwards valve rocking inside the heart in mitral position

The cage which gives  a radial support* mimic  sub valvular apparatus, which none of the other valves can provide.

* Mitral  apparatus has 5 major  components. Annulus, leaflets, chordae, pap muscle, LV free wall.None of the artificial valves has all these components.  Though , we would love to have all of them technically it is simply not possible.  The metal cage of Starr Edwards  valve partially satisfies this  , as  it acts as a virtual sub valvular apparatus.Even though the cage has no contact with LV free wall, the mechano hydrolic  transduction of  LV forces to the annulus  is possible .

Further , the good hemodyanmics of this valve indicate , the cage ensures co axial blood  flow  across the mitral inflow throughout diastole. .Unlike the bi-leaflet valve ,  where the direction of  blood flow is determined by the quantum of leaflet excursion  in every beat . In bileaflet valves  each leaflet has independent determinants of valve  motion . In Starr Edwards valve the ball is the leaflet . In contrast to bi-leaflet valve , the contact area  of the  ball and the blood in Starr Edwards  is a smooth affair  and  ball makes sure  the LV forces are equally transmitted to it’s surface .

The superiority of bi-leaflet valves and disc valves  (Over ball and cage ) were  never proven convincingly in a randomized fashion . The other factor which pulled down this valve’s popularity was the supposedly high profile nature of this valve. LVOT tend to get narrowed in few undersized hearts.  This  can not be an  excuse , as no consistent  efforts were made to miniaturize this valve which is  distinctly possible.

Sudden deaths from  Starr Edwards valve  .

  • Almost unheard in our population.
  • The major reason  for the long durability of this valve is due to the  lack of  any metallic moving points .
  • Absence of hinge  in this  valve  confers  a huge mechanical  advantage with  no stress points.
  • A globe / or a ball  has  the universal hemodynamic advantage. This shape makes it difficult for thrombotic focus to stick and grow.

Final message

Science is considered as sacred as our religion Patients believe in us. We believe in science. A  good  durable valve  was  dumped from this world  for no good reason. If commerce is the  the main issue ( as many still believe it to be ! )  history will never  forgive those people who were  behind the murder of this innocent device.

Cardiologists and Cardio thoracic surgeons are equally culpable  for the pre- mature exit of this valve from human domain.  Why didn’t they protest ?  We  can get some solace  ,  if  only we can impress upon  the current valve manufacturers  to  give a fresh lease of life to this valve .


This was written originally in 2009 early days of this blog. Now, re-posting it in 2021  , wonder any one has new data on this! 

We know diabetes, smoking, hyperlidemia, hypertension are major risk factors for progressive vascular disease. They damage the vascular endothelium either directly or indirectly , by aggravating the atheroscelortic process .  Diabetes apart from affecting the medium sized arteries , also affect the microvasculature.  Smoking  has a direct effect on endothelial function .It depletes vascular nitric oxide. High levels of circulating lipids injures the sub endothelial structures and invades the media by entering macrophages .So , all these 4 risk factors either operate independently or interact with each other and result in progressive vascular    disease.

While we  believe , these risk factors do not have any bias in attacking the human vascular  tree, in the real world it is observed they have their own  behavior pattern and  have unique predilection and a deadly alliance .

For example , in  chronic smokers TAO is the commonest manifestation , thrombo angitis is far too less common to occur in the coronary arteries.

Similarly  hypertension  per se  rarely results in an acute coronary syndrome while it is  the  single  important  cause for cerebro vascular  disease. Diabetes especially in women has very strong predilection for CAD , while diabetic per se is a lesser risk for stroke. Hyperlipedimia may be the one which has fairly even risk throughout the vasculature. Similarly there is  a difference in renal and   carotid arterial involvement with reference to  the conventional  risk factors .

SHT diabetes dyslipidemia coroanry risk factor

Why this apparent difference ?

We are unlikely  to get an answer to this question in the near future .  Left to the youngsters  . . . of tomorrow !

* Note of  clarification

The source for the above chart is collected from various studies and also a huge observational data from our hospital. There could be some geographical variation , a given individual may respond differently to these risk factor depending upon his genetic predisposition and susceptibility . So the above data can be applied to general population and not to a individual.

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.



AF is not only the most common cardiac arrhythmia,it is also an extensively researched entity in cardiology literature. We are trying to rein in, this arrhythmia for the past three decades with multiple strategies. Drugs, pacemakers, ICDs devices, surgical cuts, RF catheters, and the latest technique is trying to frostbite the atrial electrical circuits with ICE. ( Karl-Heinz Kuck,N Engl J Med 2016 )

It is believed that up 60% of AF originate from pulmonary veins. What does it mean?  So, when we blindly suggest PV Isolation routinely for all PAF,  there is 40% futility straightaway! Apart from the hugely variable anatomy of the pulmonary veins, there are prohibitive levels of recurrence due to  PV reconnections. Maybe, will find new technical solutions as we are now moving in 2nd or third generation cryo balloons, 4D imaging, contact force sensing, etc. But let us not forget there are other sources of focal electrical activity too  

Importance of non-PV ectopic beats initiating  AF(Ref 1,2)

  1. Superior vena cava (SVC),
  2. left atrial posterior free wall (LPFW),
  3. LA appendage
  4. crista terminalis (CT),
  5. coronary sinus ostium (CSO),
  6. Ligament of Marshall
  7. Interatrial septum (IAS) 

Ablation or no ablation, we need to reflect on two things in the management of AF.

1. AF can be triggered by totally different mechanisms like intermittent hypoxia, adverse electrolytic flux, diffuse atrial interstitial pathology or amyloid, etc. Before calling the appointment desk of the EP guy’s office please rule out all the systemic causes. This could be your last (lost) chance to save the atria from pulmonary burns.

2. This one is more important. Read carefully. It is not a divine protocol that demands us to restore sinus rhythm in all patients with AF. There is an excellent knowledge base, backed up by wonderfully done studies. (Need not mention the trial name, I think) that should effectively neutralize our compulsive &  misplaced urge to bring back sinus rhythm in all chronic AF.

With respect to the overall outcome, It hardly matters whether you treat the AF by rate control or rhythm control. While there is major technological leap in our fight with AF.It is heartening to know simple measures like regular exercise can control or reverse AF by atrial fatty mass regression.

Final message

We have played with fire for quite some time within the innocent lesser chambers of the heart  (RF ablation) and burnt our reputation considerably. Now, silently we have decided to fall for a more friendly weapon ICE. But we must remember our obsession with the pulmonary vein as the only source of initiation of AF is essentially flawed. Further, all these hyper-technology-based combat of AF is indicated only in a fraction of our patients (Maybe 5-10%) 


1.Chen SA, Tai CT, Yu WC, Chen YJ,  Right atrial focal atrial fibrillation: electrophysiologic characteristics and radiofrequency catheter ablation. J Cardiovasc Electrophysiol. 1999 Mar;10(3):328-35. doi: 10.1111/j.1540-8167.1999.tb00679.x. PMID: 10210494.

2.Lin, Wei-Shiang, et al. “Catheter ablation of paroxysmal atrial fibrillation initiated by non–pulmonary vein ectopy.” Circulation 107.25 (2003): 3176-3183.


If you think this write-up is too biased, please read the CABANA trial fully before ditching this post into the dustbin.

 1908, Going back on the time machine, more than 100 years ago, world war I was all set to begin, and the great Titanic was being built in the Belfast shipyard. A parallel histroy is being created in cardiology.

This is a brief story of Dr. James Mackenzie, a general practitioner from a remote Scottish village who ended up with the title of the father of British cardiology. Dr. Harvey might have invented circulation, but it was Mackenzie who taught the science of arterial pulse and wrote a classic on the topic to the new medical world. He was able to decode the secrets of the jugular venous pulse as well and diagnosed various arrhythmias including atrial fibrillation at the bedside. He used the polygraph to record his vast observations in pulse and JVP waveforms which were popularised later by Dr. Paulwood. ECG was just beginning to enter the scene in the 1920s. This makes his work all the more significant, as his treatise on pulse and JVP were based purely on clinical acumen.

                                                  Sir James Mackenzie, 1853-1925

Apart from his stupendously successful academic life, it was through his death, that he sent out an extraordinary message to the scientific community. His deep desire to know the truths about coronary atherosclerosis was astonishing. Since he himself was suffering from angina and possibly Infarct, he became his own subject of study. He became case number 28 in his own book on cardiology. When he was on his death bed, as a last wish he Insisted his colleagues do a learning post-mortem and keep his heart in the same hospital he worked. When he died in the early morning of January 25th, 1925, as per his wish, his students Dr. Parkinson,(WPW fame) and another pioneer Dr.Thomas Lewis did an autopsy on his heart.

It is tragic to know about the final days of Dr. Mackenzie’s life and how their beloved students performed the postmortem on their teacher and later published their findings in the British Heart Journal. (BHJ link )It is one of the poignant moments ever recorded in the history of cardiology, a doctor wishing to teach cardiology lessons to the generation next with his dead heart.No surprise, he is being conferred the title of father of British cardiology.


Final message

How could an unassuming GP practicing in a remote rural place reach the pinnacle of scientific glory?

Yes, it is possible. Today’s young (super) specialists must realize, that true scientific minds don’t require exotic research labs, tools, or conflict-ridded funds from Industry for the growth of science. All we require is a passion to teach, and the curiosity to learn. The rest of the things will follow… I think that was the message in the great life of Sir James Mackenzie.


Further reading


james mackenzie heart


            No one will disagree, this is the most celebrated medical quote of modern times 

It is so unfortunate, the quote has almost become a silly cliche for every one of us including the physicians, and patients. Preventive medicine always struggles to prevail over its starry-eyed colleague, curative medicine in spite of the fact that cure is an assumption in many illnesses. Classic examples are diabetes, hypertension, and atherosclerotic disease. Many of the chronic diseases that afflict human beings have no complete cure. At best we can control them. All that we do is symptomatic and supportive treatment.

Overlaps between preventive and curative medicine

Meanwhile, we must also understand preventive medicine is not only about sanitation, nutrition, and a good lifestyle. Most facets of curative medicine are actually preventing complications of the disease. So in reality curative medicine works by preventing events. There is a big overlap.

The cure is often a mirage except in treatable medical emergencies. Still, we strongly believe every disease listed in the ICD code has a cure. It would be unbecoming of a medical professional if we don’t try for a cure. We are repeatedly sensitized that cost (& effectiveness too )should never be an issue. The Insane world of medical merchandise does this propaganda perfectly. How many of us realize PTCA and CABG are essentially poor palliative procedures in our attempt to conquer atherosclerosis and CAD? No surprise, 90% of the global cost of medical care is spent on prolonging the last one month of human lives.

Preventive medicine is less popular, primarily because it demands more effort, perseverance, and also wisdom. On the other hand, curative medicine gives a sense of accomplishment and also the glamor of modern medical modalities. Of course, one of the new chapters to be added in the current preventive medicine books is the public health dysfunction due to incongruous tertiary care.

We are caught in a vicious cycle of poorly administered preventive medicine and indiscriminate usage of curative medicine, with the former under siege, by the latter with its bigger design. It is almost certain, that the malignant growth of curative medicine is indirectly preventing the“preventive medicine” to reach its desired goals. 

Preventive medicine has its own issues. One ingenious way to increase the glamor quotient in preventive medicine is to increase the cost and mode of administration of (Apple watch!) No, It didn’t work. What about five-star preventive master checks? Maybe, it works on an individual patient level, but still, a suspect value on a global scale. The problem with master health checks is their skewed priorities. It aims to catch the disease very early in the asymptomatic or subclinical stage and try to administer the cure on a large scale, with an illusion of an intervention. (Recall the PSA times on the prostate, now the breasts armed with BRACAs may end up in the same story.)


Final message


No doubt “Prevention is better than cure” will be an immortal medical quote. Two things are essential. 1. The term preventive medicine is to be understood in proper context. 2. We may need to clip the redundant wings of “curative medicine” and divert the wasted resources to resurrect the much-maligned specialty of preventive medicine, for human goodness.


There are fundamental gaps between the two limbs of treatment. It sounds like a crazy regressive statement to criticize curative medicine. Both shall grow and prosper on their path.

 But … why is it not happening?


When does the high blood pressure befriends blood sugar and instigates the LDL to initiate the vascular damage? Does it sound like medical astrology? Yes, welcome to a new world of network medicine, polygenic risk score & computational genomics. Experts believe this is going to be the future of medicine.

Dr. Jospeh Loscalzo, Physician-in-Chief  Brigham and Women’s Hospital, a leader in the field gives a brief introduction.

How to understand these complex subjects? 

We need not bother much in one sense. It’s all made to look complex by big data machines and modern scientific wordplay. It is true, that the power of computing and machine thinking will help us reach hidden secrets in our bodies. However, the bottom line is, If we live a simple. peaceful, worthy, active life we can afford to forget about this sophisticated risk predicting science, which comes loaded with unlimited anxiety. Let the science grow at its own pace.

Imagine the consequence of a powerful artificial intelligence algorithm telling us in advance all the possible future biological adversaries with 100% accuracy.

Final message 

Do you believe in astrology, an ancient Indian science?   No. Never!

Do you believe in network medicine: Yes for sure!


Two good review articles on Network medicine

1.Barabási, A.-L., Gulbahce, N., & Loscalzo, J. (2011). Network medicine: a network-based approach to human disease. Nature Reviews Genetics, 12(1), 56–68. doi:10.1038/nrg2918 




The 12-lead ECG is the single most important investigation that has withstood the test of time for over 100 years. I think it will never lose its relevance in cardiology. However, the traditional sequence of the 12 lead printout could have been a little more user-friendly, especially in its ability to convey the anatomical orientation. Expecting some Innovation in the ECG reporting format. 

This illustration helps us to understand, ECG lead orientation, and coronary arterial territory, IRA localization with reference to the various surfaces of the heart. (Courtesy of visible body-modified ) Always remember the heart is an organ, made up by a complex fusion and rolling of bundles of muscles over a fibrous skeleton. It has multiple surfaces. Please avoid calling various surfaces of the heart as walls (Request the young medical students to un-tune their brain, from the inherent tendency to Imagine the heart as a well-demarcated four-chambered concrete structure built with bricks !) 


Animated version


Currently, IRA localization with ECG may seem to be a redundant exercise, as we are straightaway seeing the coronaries if taken for primary PCI or at least within 24-48 hrs mostly.

  • But, IRA localization gives us a rough idea(still useful) of what we are going to deal with during the PCI.
  • More importantly, multivessel CAD during STEMI can be very significant in the elderly, diabetic, and in women, which can sometimes confuse us about the real culprit artery. (Recanalised IRA vs other chronic lesions). Similarly, CTOs can masquerade as ATO and vice versa. Here, ECG will come in handy to identify the true culprit.

One useful tip in IRA localization of LAD 

Lesions proximal to D1 will depress the ST segment in inferior leads. In other words, if reciprocal ST depression is seen in inferior leads it is most likely a proximal LAD lesion. Paradoxically, in distal LAD lesions, ST elevation occurs in 2,3,AVF. (What may look like a global MI, is in-fact less sinister since it is a distal LAD Infarct)

* The wrap-around LAD* can also mimic distal LAD lesion with simultaneous Inferior and anterior ST elevation. *The wrapping needs to be complete and reach almost the crux (Super dominant LAD ) to cause ST elevation in 2,3, AVF.

Final message

The limitation of surface ECG in localization is real

  • Multiple IRAs or diffuse lesions, and collaterals all can confound the ECG -IRA correlation.
  • There can be overlap between large diagonal, Ramus (or even a large OM) when they all try to converge on the curvey and imaginary slope between the anterior lateral wall
  • Localization of IRA (Rather Angina-related artery (ARA) is a different exercise altogether.
  • Experienced operators will agree  there have been many occasions, where multiple diffuse lessons with delicate collaterals interwoven make IRA identification so difficult, and ultimately primary PCI is abandoned, and the patient returned back into CCU for lysis (Fortunately, Tenekteplace, and streptokinase never need to bother about IRA localisation you know !)


A useful review on this topic

Rafl an S, Kamal A.  Localization of the occluded vessel in acute  myocardial infarction. J Cardiol Cardiovasc Med.
2020; 5: 029-033

It is likely, that the biggest Impact & influence in current medical research may not come from the IQ of our scientists, their concepts, or the sophistication of the laboratory. Then what? Can you guess? It is the man-made mathematic sub-specality called statistics. We are going to either ratify or reject any research work ( on which we toil) based on the quality of numbers we generate. Such is the critical value of this specialty. Just pause a moment, and think over. How much importance do we give to the credibility and “quality of the interpretation” of any study? We have conveniently left it to our esteemed mathematical colleagues and some other invisible forces for a proxy inference.

I don’t think we will ever find an answer for this. Whether facts are made by statistics or statistics are made by facts ?

In recent times, one technique called propensity matching and scoring is used to conduct medical research where multiple covariables and confounders play.

What does the word propensity mean?

Oxford defines this word /prəˈpɛnsət̮i(pl. propensities) (formala tendency toward a particular kind of behavior

What is propensity matching in medical research?

In simple terms, it is doing a study without a true control group. It is a statistical gimmick where in we create an Imaginary or virtual patient arm What a way to conduct a scientific study? Those days, if someone suggests a study without a true control arm, it will go straight to the dustbin. (Of course, the concept came into vogue because we can’t have controls for ethical reasons or the rarity of the condition ) We do have  many other conventional covariable analytical methods available A well-written reference  (Ellicott C. Matthay, SSM – Population Health, 2020,)

Who created this propensity score?

I thought It was a new concept.No, it was proposed by Rosenbaum et al in 1983. (Ref 1) The extreme popularity it enjoys today is unexplainable. I think it is the simplicity, joy of doing a study without a troublesome control population, and the subsequent herd behavior of medical researchers.

Read here the pros and cons

Final message

Only two questions need to be answered before crowning the “propensity score” to glory in the statistical world. 1. Who has the final authority to define, what amounts to a confounding effect?  2, What are the statistical chances of missing an important confounder in toto due to baseline ignorance? 

Most statistical methodologies are like Holywood movies, some strike gold for no reason in spite of a lot of flaws. A few examples are meta-analysis and non-inferiorly trials. Propensity matching with a synthetic control arm could be a useful methodology in very selected situations.  It is unfortunate it has become a fancy tool and doesn’t deserve the wholesome approval for doing away with the true control arm.

Statistics may be great science, but it seems to work fine, only in the absence of continuous, unpredictable biological interference with mathematics.

Lastly, can propensity score take into account of confounding effects of the non-academic mindset of many researchers in senior positions? What shall we do with many important therapeutic guidelines created apparently based on solid evidence created with poorly created virtual (propensity) matches?


Experience-based medicine, wild logical guesses, empiricism, and trial of error methods,  all these are unavoidable in medical care and research. We have to move ahead with all the uncertainties in-situ and take our patients to a positive destination. 


1.Rosenbaum, Paul R.; Rubin, Donald B. (1983). “The Central Role of the Propensity Score in Observational Studies for Causal Effects”. Biometrika70 (1): 41–55. doi:10.1093/biomet/70.1.41.

2.Wang J. To use or not to use propensity score matching? Pharm Stat. 2021 Jan;20(1):15-24. doi: 10.1002/pst.2051. Epub 2020 Aug 10. PMID: 32776719.

Propensity score in cardiology research 


Who is the guiding the guidelines, which have become omnipresent & omnipotent ?

I don’t know really. Some good people I guess. But, the doubt creeps in when they try to coerce it on us.

A brief conversation between an elite consultant and his fellow. (Caution: Grade 2 harsh language) 

Hey Doc, why is this guy’s name not found in today’s angiogram list? Any Insurance issues?

No sir, he has every requirement. Thrombolysis was very successful, ST has regressed well and it is nearly isoelectric and only T is inverted. His LV function is normal. In fact, I am not able to pick up any WMA.

Aren’t you aware, that being fine is never a contraindication for a PCI ? Which book teach you like that?

No sir, It’s already beyond 48 hrs sir. What is the purpose of knowing IRA status now? If it is open, well and good.If it is partially closed, again little to gain, right? 

Don’t expose your Ignorance. … haven’t you heard of the pharmaco-invasive strategy & open artery hypothesis. Always learn to respect science.

But sir, then why does late PCI of IRA in otherwise stable patients come under class 3 recommendation, if I understand the guidelines correctly, it is a contraindication, am I, right sir? But, this patient got stabilized by us still, why he is compelled to undergo another procedure exposing and adding further risk?  

That shows your immaturity. Doing an angiogram is never forbidden. It is the inappropriate late revascularisation of IRA that is the issue.

 Agreed sir, how confident are we, that we will stop just with an angiogram after visualizing a tempting lesion in either IRA or non-IRA? (My brief experience as a fellow doesn’t tell a fair story) 

 Now, you are trespassing into prohibited non-academic zones of cardiology practice. Instead, talk about FFR, OCT, multivessel angioplasty, and ( deferred or instant ) complete revascularization. Think like a true scientist don’t get spoiled at a young age in your career with all this ethical stuff. 

Final message 

Never allow an ACS to stabilize by medical management, if he is otherwise eligible and affordable for a procedure. You are not authorized to do that. 

This write up was triggered after encountering a patient who instructed his cardiologist to remove an incidentaly found block in Right coronary artery. 

Oftentimes, It is a funny & futile world out there in modern medicine. Revealing the complete truths or accepting ignorance in critical decisions to their patients, make the Doctors feel that, their academic modesty and reputation are at stake. 

Still, many patients expect (and think) the doctors to be 100 % transparent and want to understand the nuances of disease better than the doctors themselves. The current fad of online & offline health education for patients is not an accident of technology. Though some benefits exist, I feel, It is an intentionally promoted, maliciously motivated patient empowering movement, trying to disarm the true professionals.

Dear colleagues, always realize, never allow the default ignorance to become patients’ knowledge and ask them to take decisions on behalf of you. (I know, this is diagonally opposite to current principles of the practice of medicine) Fortunately, this issue doesn’t arise in most public hospitals in our country.

This paper was written 30 years ago with great foresight.


So, act with tact. You can’t hide behind the patient’s preferences in deciding the treatment choice. It can be “as unethical as” any activity that goes against the interest of the patients under which we are taking our oath. I don’t, recall anywhere in the Hippocratic oath, that we pledge to listen to the patient’s choice of treatment. (Rather, we assure to work in their interest always)

Final message 

Let us sharpen our own skills first. We shall think about how to distill and consume the muddy knowledge emanating from the current mess of premature research spilling all over academia. Don’t try to educate too much to your patients. There is nothing called academic empathy because leaving it to our patients will ultimately end up equivalent to medical negligence.

Forget about the patient-guided treatment menu card. Think about this, if ordering a trendy new medical investigation purely on a patient’s demand is declared as medical negligence, How many doctors on this planet will be left non-negligent.(Stop. then what is a master health check-up? Who is the master ?) 

(Hope this write-up is taken from a proper perspective. No intent to create a chasm between patients and doctors relationship )


Drane JF, Coulehan JL. The concept of futility. Patients do not have a right to demand medically useless treatment. Counterpoint. Health Prog. 1993 Dec;74(10):28-32.

Postamble & Counterpoint

It all sounds good on paper. The consequence of not listening to our patients, especially if they land up with complications, will look awkward, is it not?  So, I always go by patients’ desires.

Patients tend to believe in fancy investigations and machines and not me, what to do?

No, it is wrong. You can’t justify it. Regarding your concern and impact on our reputation, nothing can be done. The medical judiciary desperately needs some reforms, understand the reality to protect us  I always tell my patients they have to accept me as a whole. (Do you enter the Aeroplane’s cabin and check the pilot’s mental and physical acumen every time you board a flight. It is trust,.. complete trust, that drives our life right !)

It is true, that medical professionals must be always under a continuous quality* control regimen.  The consequences of consulting less shrewd medical personnel, their errors in judgment, the stress of work, patients need to accept* just like a side effect of a drug or a natural history of a disease.

*, Unlike the engineering field, defining & controlling quality in medical therapeutics is a mystery exercise with multiple agendas!

CPR with BLS and ACLS is time tested method of cardiopulmonary resuscitation. The automatic external defibrillator(AED) was a real breakthrough. Still, complete recovery eveN in “in-hospital cardiac arrest”  is at best 10-15 % . (Brindley PG, CMAJ. 2002. )Here is a technology in-progress story, now I understand FDA has approved this device for emergency resuscitation in cardiac arrest.

The principle is simple. In the early minutes following cardiac arrest, it is the survival of the myocardium and brain that matters. So, occluding Aorta transiently and continuing CPR infuses more life into the brain and heart, and the possibility of revival they say is significantly increased.

Mind you, this is not for the layperson or public but can become a game-changer for the ER crew and in ambulances or even in the cath lab. Emergency insertion of ECMO is never easy and a Neurescue balloon may come in handy in the meantime.


The attraction is the simplicity of the device, just inserted through the femoral artery. Don’t know how successful we would be, in centering the collapsed femoral artery though. The balloon actually doesn’t really impede the lower limb flow.It senses and relaxes as and when necessary. 

Final message

The concept behind neurescue looks like a bedside emergency partial IABP-like (IABO-Intra aortic balloon occluder rather) but appears promising. What I understood grossly is, that potential extremity Ischemia is acceptable if it’s going to save a life! Also realize, it is not a magic device that brings back life in every cardiac arrest. It gives us more time to act so that we can do other measures to bring back circulation.