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.

The relationship between Aorta & PA is the key to diagnose many complex congenital heart diseases. Here is a simplified illustration for gross understanding. Please refer to other sources for complete review.


Further reading

CONGENITAL HEART DISEASE| VOLUME 118, ISSUE 9P1390-1398, What Determines Whether the Great Arteries Are Normally or Abnormally Related?   https://doi.org/10.1016/j.amjcard.2016.07.050


Caution: Some language 


It is heartening to note the apex body that is leading the fight against Covid in India, has responded well. It has either recalled or censured many of the Investigations & drugs, procedures that were used in this pandemic. (Not because they are futile, but they also resulted in a meaningless escalation of cost and possibly worsened the outcome)

So, what?

Beware, “non-scientific mutations” are common in medical research even in ordinary times. It is omnipresent now, and no surprise they end up as a premature evidence base. The consequences of this can be as adverse as the viral variants we fear. The global economic drain of this pandemic is definitely more than what it really deserves. The bulk of resources consumed by Remdesviers, Tociluzumabs, Ivermectins, etc. will easily cross few billions. Further, it is estimated 100s of millions were spent on Indiscriminate diagnostics like CT scans and, Interleukins, D dimers, and even RTPCRs that made a mountain out of a mole. Infinite doses of antibiotics are diligently prescribed for a viral disease knowing fully well it won’t work. One estimate In India says 800 crores worth of Zinc and vitamins were sold over the counter. (The same budget for 1000 bedded state of art hospital!) Heartless marketing. It was painful to watch hard-earned savings was siphoned from not so wealthy & poor for a simple hospital stay.

 It must be acknowledged the Government (both state and central) is doing an exemplary job taking care of both private and public health against all odds. However, on a global scale, It is unfortunate many Governments of low GDP countries were politically compelled to spend on flimsy interventions for a self-expiring pandemic. If only these funds are diverted properly, that would help us build permanent health Infrastructure in each of the underdeveloped districts. The only thing, that’s worthy to spend now, is towards the largescale manufacturing of a quality vaccine. Health economists from WHO shall genuinely audit the global expenditure of this pandemic that will help tackle future pandemics better.


The virus has decided to play its own game with humanity for whatever reason. The great news is that the vaccine is working. We hope the virus will show enough mercy and leave us shortly. Please follow the required covid hygiene and learn to live in a  personal lockdown mode so that countries need not shut down. Meanwhile, a strict embargo on excessive covid related information in the public domain seems as critical as the vaccine. (the demarcation between true knowledge and misinformation is as blurred as one could Imagine)


Wishing for a  smooth landing with abundant common sense (Image courtesy TIME magazine )

Happy days will be here again soon. But, never forget the harsh lessons taught by this tiny virus .“We must learn to cohabitate on this planet along with other lives peacefully. If we are adamant, God is likely to lose his patience and may not hesitate to discard us permanently “



3D printing technology is growing at a rapid pace. Both cardiologists and cardiac surgeons are expected to benefit a lot.It helps us in understanding deformed anatomy in complex congenital heart disease as well as planning for synthetic cardiac implants. 

Currently, the technology is limited only by the chemical material used to print the heart and its components. The American chemical society is working at it to create more realistic heart models. Once we master this,  biological printing with synthetic tissue equivalents is the ultimate aim. 

Major Indications

  • Planning cardiac reconstructive surgeries in congenital heart disease. 
  • Aortic grafts in Marfan syndrome and other endovascular grafts.
  • Valve prototyping

What could be possible in the future?

A dream possibility is that, 3D printing of a patient’s own coronary artery that is diseased with an exact replica that may either act as a surgical graft or deliverable percutaneously.

It is 3D cloning of a coronary artery with a live blood flow experimental setting.(Image clipped from above video)

Final message

It is a merger of biology, chemistry, tissue engineering, and computing. Already it is used in specific conditions.(How about ordering a designer RVOT in severe TOF ?) We are approaching fascinating times in cardiology. Of course, everything would come at a price. We can reap the benefits of this path-breaking progress in science, if and only if, technology is regulated well, Indications are liberally coated with common sense.


A review article on 3D printing in cardiology Nature review 

Giannopoulos 2016


This 90-second video clip is a “perfect provocation”

Allan Savory  is a renowned ecologist from Africa. He is a global leader in environment and eco protection. He is making this famous comment, during one of his interviews from the deep forests of Zimbabwe, after years of ground-level work in the field of desertification and climate change. I can understand his feelings, as we also encounter similar situations at ground zero of the health care delivery system. (I wonder if there is anything called peer-reviewed bedside caring)

We realize wide gaps between academia, patient care, and research are the norm, not an exception. One reason for this is, even well-learned medical professionals find it difficult to comprehend, that the practice of medicine is essentially an art, administered with love, care, service-mindedness. A cost-effective infrastructure with an immense amount of teamwork is critical ( Of course, guided by a fair amount of knowledge, expertise based on good scientific principles)  

Final message 

As Savory says, let us hope, the future looks bright, that welcomes young researchers from the fringes of the scientific community. Let them be conferred with all courage and resources to course-correct medical science from its frequent aberrant and awkward turns.


The concept of Fractional flow reserve ( FFR) has dominated the coronary interventional field for over a decade. It gave us a (false) sense of security and pride that we have been advocating physiology-based appropriate stenting.

The much-expected FlOWER-MI trial was presented in ACC & NEJM a week ago. (May 16th  Issue 2021)

FFR, though physiologically an attractive concept, has many well-known confounders right from the technical factors, lesion-related errors in physics, mirage of true hyperemia induction with Adenosine, finally & most importantly microvascular dynamism. The value of FFR in the ACS setting was always a suspect. So, no surprises with the FLOWER trial conclusion. It has concluded FFR guided interventions in the non-IRA vessels following STEMI had no use in terms of the hard endpoint. Lesson: We can’t really expect true coronary physiology rules to be alive when severe pathology has set in)

Wait, there can be quixotic ways to Interpret this study be as well.

FLOWER trial reveals the number of stents used with FFR guidance was 50% less (mean 1.01 vs 1.5 stents). Though there was no difference in deaths, the incidence of nonfatal myocardial infarction was more in FFR group 18 (3.1%)  than the non-FFR group (1.7% ). Similarly, unplanned hospitalization leading to urgent revascularization was more in FFR  (2.6%)  than non-FFR (1.9%). Though all were not stat significant, FFR has helped reduce the number of stents in non-culprit lesions. Still,  recurrent non-fatal MI and urgent revascularisation were high in the FFR group. So, is it possible FFR related procedural hazards are real? Who can (& how) quantify that? or Is it Inappropriate non-stenting due to FFR misguidance responsible for this trend?

There is one more risk with the potential demise of FFR as a concept. Extreme scientists, might ditch physiology to the backyard and go for free for all stenting again. (Back to shadow physiology & oculocardiac reflex) 

Final message

There is an extrapolated lesson to be learned from DEFER*/ FLOWER trial combo. FFR or no FFR, never touch the non-IRA lesions in stable STEMI* however tempting it may be. (*This rule applies even in some unstable STEMIs (Please recall Culprit shock trial ) 

*DEFER 15 year follow up EHJ 2015 ( Note : DEFER contain significant non ACS population)

Next to the atmospheric pressure, the most curious pressure to understand is stored within the human circulatory system. Yes, it is the “blood pressure” fondly referred to as BP by both physicians and patients. (When worried men & women visit us and say, that they are suffering from BP, please make it a point to clarify, BP is a sign of existence of life, rather than a dreaded pathology ) 

Why should blood have pressure?

BP is lateral pressure exerted by flowing blood on the vessel wall (or is it the propelling pressure head ? It is to be noted, cuff pressure doesn’t measure this !) BP is generated by the heart in systole and sustained by the vascular system in both systole and diastole. BP is measured as mmHg. It can also be expressed as PSI(Pounds /sq Inch)  or Pascals or ATMs. If you allow me to spoil with some physics. Pressure is force per unit area ie Newton/m². So, pressure is essentially a force. Force is mass times the acceleration. Mass is weight independent of gravity, while the acceleration of blood is essentially the force of gravity added to the velocity of blood flow. If you think gravitational waves and planetary positions might influence the mass of blood (and hence the BP)  you may not be insane. (Environmental & astrological influence of BP and cardiovascular events need not a be mythology) (Oomman A,  J Indian Med Assoc. 2003 )     (Robert D Brook Cardiac clinic 2017)

How is it regulated?

Physics uttered at the bedside is sure to appear as nonsense for practicing physicians. Forget It. BP is not only a continuous variable, the neural, hormonal, cardiac control mechanisms are also in a dynamic flux. What we need to bother is, how to sustain a mean BP of around 90 mmHg within the human circulation, with robust autoregulation. (For the fellows in cardiology, it is a dangerously simplified teaching & belief  that cardiac stroke volume determines systolic BP and PVR determines diastolic BP) In fact, It is the systolic pressure that confers the energy required for diastolic BP. Regulation of BP is all about large vessel stiffness,  neuro-humoral tone of small vessels, water and sodium metabolism. This makes the kidney a central organ for long-term control of BP. It must also be emphasized BP is regulated in a regional and organ-specific manner. (Ex -The cuff brachial artery pressure may tell little about what is happening at the glomerular perfusion pressure )

Who are the guardians of BP?

Though general Physicians , Neurologists, Nephrologists even Endocrinologsts  have more geograhcial rights  cardiologists have largely taken siege over the entity of SHT because the heart happens to be a glamorous victim organ. We are witnessing an almost intoxicating number of cardiovascular trials on hypertension, right from Framingham’s days of 1970s to just released BP LLTC in 2021, trying to bring down cardiovascular risk. Based on the accrued evidence, the guardians of human  BP in various global institutions bring out strategies to reduce the risk of vascular injury. Have we succeeded in this  Intravascular number game.? I think we are. At what cost?

Two repeatedly asked two trivial questions 

  1. What is normal BP  &  When to start treatment?
  2. How much lower is best for our body?

Probably, we have got an answer for the first question from this Impactful publication. 


I think this study is trying to tell us, there is no normality for blood pressure in terms of risk reduction in cardiovascular disease. (Please recall, one JNC -Joint national committee  was dissolved after  including a controversial term pre-hypertension in healthy public  few years back) What will be the implication for this study? Its core conclusion is about 5 mmHg BP reduction across any subset of adult population will reduce CVD risk considerably. I am sure this study is so intense and powerful it will take at least a decade for its conclusion to fade away. So, can we make these funny conclusions? Hereafter we need not measure BP before starting treatment. Just administer drugs to any live adult who has blood & pressure. (J or U curve need a big debate later)

Mind you, sustained  5mmhg reduction* can be brought by any of the following habits. A salt moderated fruit-rich diet, reasonable physical activity, good sleep, a stroll in the park, yoga, a deep breath, having a pet, watching a movie in a quiet evening, having a loving  family, and so on so forth (Of course, 5mg Amlodipine, 40 mg of Telmisartan, or a  paradise device can do the same, with an add on pride)

*There is a big catch in this landmark paper. Read the title again. The important take-home point is that this 5mmhg lowering should strictly come by pharmacological means, not by any other means. (Correct me if I am not correct)

Final message 

We got the final answer from this marvelously done meta-analysis for the toughest question in cardiology. Hereafter  It’s going to be a celebration time for mankind, who struggle in a hypertensive world.


True, sustained high BP is a major risk factor for stroke, heart failure, and CVD. However, it is also true BP can’t* do much damage to the coronary artery without the help from its naughty cousins DM & dyslipidemia. All three parameters must be optimized in unison. May I propose a rough rule? It may be called DFL index for the collective CVD target.  Diastolic BP, fasting blood sugar and LDL all should converge around a unitless number of 70 to 80. 

*HT is a powerful risk factor for stroke and HFpEF. 



No doubt, the heart is a biological wonder with its non-stop pump function. Still, it cannot function as a continuous rotary pump like the electrical motors do. It has no other option but to contract in a pulsatile manner. However, the mean pressure in circulation is fairly constant, flow is kept continuous, and fairly laminar. This is made possible by the built-in elastic pressure in the aorta and the poorly understood but vitally important parameter vascular tone. Aging widens the pulse pressure due to dissipation of vascular tone. Atrial fibrillation adds new bizarre dynamism to this pulsatility and challenges the aortic wall’s competence and compliance further. This is the basic mechanism behind the classical description of an irregularly irregular pulse in AF. The pulse can be  so unpredictable, it was originally referred to as acute confusional status of heart (Delirium cordis)

What is the effect of AF on systolic, diastolic, and mean blood pressure?

In AF systolic BP varies considerably from beat to beat. Diastolic BP does show some changes but less obvious. So far mean pressure fluctuations in AF have not been given much significance.  

Clinical significance of AF on the brain: Thinking beyond stroke 

From a stroke perspective rate and rhythm control did not show much difference. The prime reason for AFFIRM  trial not showing benefit with rhythm control was embolic stroke was much more common from sources other than left atrium proper and hence the usage of oral anticoagulants was more important than rhythm control in overall stroke control. 

Now, an important study trying to look at this hitherto ignored aspect( Andrea Saglietto,  EP Europace, 2021). It raises concern about the impact of AF on long-term cerebral function. Should we restart the debate in favor of rhythm control? No doubt, the pulmonary venous electrophysiologists will be too glad to welcome this concept.

Now, we have new evidence based on near-infrared spectroscopy AF does cause unpredictable beat-to-beat changes in cerebral microcirculation that leads to neurocognitive dysfunction. It is possible there can be a breach in cerebral autoregulation limits in a significant number of post-long RR  beats. We may soon look forward to a new entity of “dementia cordis“as a sequel to chronic AF.  



1.Andrea Saglietto, Stefania Scarsoglio, Daniela Canova, et al Increased beat-to-beat variability of cerebral microcirculatory perfusion during atrial fibrillation: a near-infrared spectroscopy study, EP Europace, 2021;, euab070, 



Here is an uncommon story of a patient with palpitation,SVT , Troponin +ve, and suspected ACS.

Palpitation in ER ⇒ {Tachycardia +Troponin positive ≠ ACS}

Mechanism of troponin elevation following any SVT

  • At high heart rates (>200) myocardium is subjected to non-Ischemic mechanical strain & squeeze. Minute amounts of Troponin is let out like a myocardial juice into the circulation (Like atrial natriuretic peptide release which causes polyuria during AVNRT)
  • Tropinin releases have been shown to correlate with both heart rate and duration of ST depression (Subendocardial strain /AVRT left lateral pathways)
  • Short diastole induced low coronary perfusion pressure and a true transient (but insignificant) Ischemia
  • Finally, SVT (especially in the elderly) is a natural “exercise stress test” equivalent, ST depression with Troponin positivity is a true marker of significant epicardial CAD


False alarm of ACS is the most important issue. (Except one study which showed a different conclusion Chow GV, Prognostic significance of cardiac troponin I level in hospitalized patients presenting with supraventricular tachycardia. Medicine (Baltimore) 2010;89:141–148. doi: 10.1097/MD.0b013e3181dddb3b. [PubMed]

Note: If AVNRT occurs with aberrancy, or AVRT presents as antidromic tachycardia with a wide qrs tachycardia the confounding effect is perfect as it can no way be differentiated from true Ischemic VT or atrial fibrillation.

Final message

It is no ER room secret that a single spot Troponin value has lost its credibility considerably in segregating ACS from non-ACS conditions. It is falsely elevated in a long list of cardiac and noncardiac conditions. It is a worthy point of learning, among the cardiac conditions, the commonest cause for false elevation is during any tachycardia. This should be kept in mind. Because a patient with chest pain who present with benign palpitation due to prior SVT (Arrival ECG could be normal) a false raise can trigger a chain of inappropriate reaction that may land the spot even in the cath lab.


In spite of these limitations, non-diagnostic ECGs, we expect Troponin and CPK to guide us in chest pain screening. We now have added one more marker, high sensitivity Troponin Assays. Let us believe, it doesn’t add to more confusion. I think the main purpose of these biomarkers in the future, would be to arrest the habit of using cath lab as triaging place for chest pain instead of ER room. (A brief review from ACC https://www.acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians)


1.Troponin elevation in supraventricular tachycardia: primary dependence on heart rate. Ben Yedder N, Roux JF, Paredes FA Can J Cardiol. 2011 Jan-Feb; 27(1):105-9. [PubMed] [Ref list]

2.Kanjwal K, Imran N, Grubb B, Kanjwal Y. Troponin elevation in patients with various tachycardias and normal epicardial coronaries. Indian Pacing Electrophysiol J. 2008;8(3):172-174. Published 2008 Aug 1.
3.Carlberg DJ, Tsuchitani S, Barlotta KS, Brady WJ. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: outcome after ED care. Am J Emerg Med. 2011;29:545–548. doi: 10.1016/j.ajem.2010.01.041. [PubMed] [CrossRef] []

This question might squeeze the collective coronary knowledge of any cardiologist. (At least, it does for me !)

What is an intermediate coronary lesion? (ICL) 

Traditionally it is an “angio-ocular reflex” measurement of coronary arterial diameter stenosis that lies between 40 to 70% (Mind you, 70 diameter stenosis is 90% area. So, we must be clear what we really mean in any revascularisation debate).

Above one is the simplest expression of ICL. (* While 70% cutoff is fairly constant, the lower limit 40% is still not a settled issue. It can be 30 or even 50 %. I think we haven’t yet named the lesions 1 to 49 %. It is the spectrum that contains  Coronary erosions, ulcers, luminal irregularity, or the evasive term minimal CAD  )

Many sub-classes exist in ICL.

  1. Should ICL definition be different in proximal LAD? (A 40% PDA or OM2 lesion is not the same as 50% LAD right.Maybe we need to artery specific redefinition, left main we did it already)
  2. It can be de nova chronic (most common ) Acute  /subacute, acute recanalization (Each has a different management strategy)
  3. What about ICL with good TIMI 3 flow. Mostly safe and can be ignored?
  4. Should we bother to know the content of ICL? It could be a minor plaque or just thickened and narrowed arterial wall or even layered thrombus.
  5. Is it isolated ICL?  When ICL occurs in isolation it gets more attention is natural to ignore if ICLs are noted along with other critical lesions nearby. The risk of ignoring or risk of including ICL in the final angiogram reports is unquantified. 
  6. When two ICLs lie by next to each other (Tandem ICL) will you add the stenosis resistance in series? Does the length matter.(Can we measure net FFR ?) 
  7. Is it symptomatic vs asymptomatic? (very difficult query )In stable non-Infarct CAD Internedaite lesions do not obstruct flow, but Post ACS it is the distal microvasculature that determines the epicardial flow. so even intermediate lesion resist flow.
  8. ICLs in ecstatic segments pose a special issue. Adding to this Galovian positive remodeling mask the true plaque burden(Currently liberal use of OAC like warfarin are used in ectatic vessels with ICLs)
  9. By the way, is it true, ICLs are more prone for  ACS?  We believe it based on small studies and sort of biased teaching. Of course, there is some truth in it, but in a larger sense, it is not correct thinking. ICLs by sheer number overtake the critical lesions in terms of Incidence. So more ICLs present as ACS. But in, pure pathological terms flow-limiting lesions do carry more risk for ACS. (Of course, calcification might stabilize a few of them, and convert them to CCS) . For argument’s sake, if we agree ICLs are more prone for ACS, we should first fix these lesions than the more tighter ones.(Any guidelines forthcoming ?)
  10. Finally, the most important query Is the ICL vulnerable, or is it flow-limiting? (read below)

Imaging and physiology

CAG is just a shadow of contrast luminogram. Further, the contrast flowing across a lesion cannot be equated with the true velocity of blood flow. So, what shall we do? How do we overcome the limitations of CAG shadow? We need to go after more glamorous shadows like IVUS and OCT. They do suffer from myopia and hypermetropia respectively. Still, they are good enough to reveal important info like the content of lesions like calcium thrombus with acceptable precision, etc. The thickness of the fibrous cap (TCFA) is a current marker of vulnerability. This thickness is dynamic as do plaque liquefaction. We are looking ahead to the days of virtual histology and plaque metabolism by NIR spectroscopy. Decisions based on a single one-time snapshot from intermediate lesions would largely be meaningless. 

What about physiology? FFR, iFR,(Adenosine free)  QFR (Based on TIMI frame count) offer a more scientific assessment of flow across the lesion. Still, it is not clear. An elegantly made study is available that depicts the relation between stenosis and FFR.

Realtionship between diameter stenois snd FFR. Note even a 30% lesion has low FFR and wide variation a 70% lesion show on either side of cut off .8Does Routine Pressure Wire Assessment Influence Management Strategy at Coronary Angiography for Diagnosis of Chest Pain? The RIPCORD Study Nick Curzen circulation cardio vascular Interventions 2014.

Relationship between diameter stenosis snd FFR. Note, even a 30% lesion can have a low FFR, and a 70% lesion show the FFR to scatter on either side of the cut-off value .8 . So, what does it mean?  We have simply shifted our ocular bias to objective flow bias. Does Routine Pressure Wire Assessment Influence Management Strategy at Coronary Angiography for Diagnosis of Chest Pain? The RIPCORD Study Nick Curzen circulation cardiovascular Interventions 2014.

What is the effect of statin on ICL?

There is no specific large-scale study that looked into this. Plaque regression and stabilization are expected in most ICL with intensive statin regimens. (Seung-JungPark et al  JACC 2016) It reduces new-onset TCFA. Will it increase the cap thickness? It can be assessed by the OCT study. (Maybe it is already available will search for it ). PCSK & Inclisiran should do it if not a statin. 

Final message

Coming to the title question, the term ICL means nothing without the clinical background and the angiographic setting it is detected. Realize, the intermediate lesions don’t Imply intermediate risk. We can’t do  IVUS or OCT in all intermediate lesions. Even if we detect vulnerability in a 50% lesion, treatment will remain mostly intensive medical management. (There is absolutely no good evidence to show stents stabilize vulnerable plaque that does not limit flow ) 

So, the best approach to all those billions of ubiquitous ICLs scattered across the human coronary landscape is to stabilize it OMT( Open-minded medical therapy), lifestyle modification (taking style out of life), reassurance, and propagation of peace that will passively the plaques. Imaging and FFR can do wonders in an elite minority population at a considerable cost. (However, for the sake of demystifying atherosclerosis we should continue research with such modalities, sparingly though )  



It was the final case on weekend Echocardiogram review day, I asked my fellow for a brief summary of the patient. 

A 5 -minute conversation

“Yes, sir, he is a 62-year-old male retired govt officer. He has a severely stenosed aortic valve, with a peak gradient of 90 mmHg and a mean gradient that comes to almost 50 mmHg. LV  EF is 58%, GLS is 18, LVH is obvious. LA is not dilated (Didn’t measure volume though), but DT is short. Valve orifice is hovering around 1cm, mild calcium noted in LCC  I am not sure whether it’s bi or tricuspid still. The annulus is 22mm. The mitral valve is perfect, no calcium spill over to the mitral curtain and the rest of the annulus”.

“That is ok, what for he has come”?

“A GP from Tambaram has referred him after he detected a murmur over the chest”.

“Oh Ok. What are his symptoms”?

“He is denying any symptoms”.  

“Are you sure? did you ask him specifically about it during exertion”? 

“Yes, he says he can climb 3 flights of stairs. (In fact, he was sort of amused when I told him to be frank in his expression,since  he has a potentially serious obstruction in the main valve that connects his heart and body.”

“I agree, but his reaction was not inappropriate I thought, after all, he didn’t feel any symptoms right”. “So what shall we do for him?  TAVR? SAVR? or Leave him alone? Shall we put him on the treadmill? to document symptoms? Is it that risky”? 

“But , he says he can walk for a mile or two every day” 

“That’s fine. Can you really predict when his ventricle will fail and he may land up in a semi-emergency surgery?

“I think we can’t,  but why is he is so asymptomatic sir”?

“Wow, that’s more than a million-dollar question. You need to address that query to the vascular Goddess. I don’t know the answer.It is all about the ability of the heart to perfectly balance the ventricle and aorta in spite of severe obstruction. It is something like TIMI 3 flow and good FFR  in a patient with 90% occlusion.) My guess is, the LV does this by modulation of systemic pressure &  resistance in such a way , it neither feels the strain nor does it reduce the stroke volume much. By the way,  have you heard about this ? Z- Va score. I would like you to read about that. It will help you understand the hemodynamic nuances of severe AS and how the ventricle manages to serially couple the afterload of the vascular system”. 

“Make a pardon sir, I haven’t heard about it. What is Zva? 

“Never mind. It is not a new index. Was first introduced 16-years ago by Martin Briand et al from Quebec, heart Institute Canada  J Am Coll Cardiol 2005 Jul 19;46(2):291-8.  Z Va score(Valvulo-Arterial) is the collective flow impedance of the aortic valve and the entire aorta. It is more attractively defined as the cost of blood pressure in mmHg for pushing one ml of blood per body square meter area

Formula for Z va : (Systolic BP × Mean gradient)/ Stroke volume Index

Unit : mmhg /ml/m²

Normal value:  < 3.5 to 4.5 (Actually no normality, rather it must be acceptable value .It is still being defined )  if the cost is more than 5mmhg it suggests significant Aortic stenosis) A high value > 4.5 is a definite index of poor outcome. In a well-compensated heart, Zva is maintained far less than 5 and many such patients are asymptomatic as well. Zva has specific clinical value in all critical AS especially so if they are asymptomatic. It is no longer a research topic, has an important role in the bedside too. Here is an excellent resource on Z Va score from ESC.


Final message 

The timing of AVR in aortic stenosis is very critical. All symptomatic severe AS must be immediately intervened. Currently, with surgical risk falling rapidly ( & the option of TAVR looming large) even many of the asymptomatic AS need to be considered for valve intervention at the earliest before or at the onset of LV dysfunction. Zva’s score will definitely add more light to our  limited hemodynamic wisdom in aortic stenosis(Zeineb Hachicha  JACC 2019)