Why didn’t you do it … for this patient?

 “I thought, he was not the right patient for the procedure. I believe, what I did was the correct decision. Why all this fuzz? after all, the patient is doing so well without that procedure,.. are you worried about that? 

“No, I need an explanation, we have a fully functional cath lab in our center. The patient came in the right window period. Still, you haven’t offered the best mode of treatment”.

“I can reiterate it again sir. Just because a lab is available 24/7, it doesn’t make all patients eligible for a  PCI. I think I didn’t commit a professional misdemeanor when I decided in favor of fibrinolysis. In fact, I would be guilty had I rushed him to the cath lab, just to satisfy the misplaced scientific position we have decided to adopt. If you think, I am culpable for successfully treating a patient without taking the patient to the cath lab, you may proceed with the penal action.

Before that, I would request you to please read the current edition of this book we all revere. (Which continues to mentor physicians all over the globe for the past 50 years)


The current edition of Harrison 2022 is just out. I thought, there is something great learning point in Cardiology chapter, specifically about the reperfusion strategies in STEMI

My hearty thanks to the editors of the chapter for the crystal clear expression about this much-debated procedure* and specifically choosing the word “PCI appears* to be more effective ” (even) if it is done in experienced persons in dedicated centers. The choice of the word used by the authors is Intentional and must be applauded. This message must be propagated to all our fellow physicians. What a way to convey an important truth pertaining to the management of the most common cardiac emergency, while many in the elite specialty are so dogmatic in their assertion without verifying the reality.

*  The verdict is still under the jury even after 3 decades, since the PAMI days of the early 1990s. Thank you, Harrison. What a gentle, but a righteous way to express an opinion about a procedure that is apparently enjoying a larger-than-life image based on a handful of studies and a flawed meta-analysis.

Final message 

Primary PCI is just an alternate form of treatment to fibrinolysis in STEMI. Both are equipoise in the majority of patients. Extreme care and diligence are required to harvest the small benefit the PCI seems to provide.  There are lots of ” if and buts” that decide the success of this procedure. Get trained, and do it selectively for those who really need it.


You may call yourself a super-specialist. But, please realize, If you have any doubt about key management strategies, never feel shy to take a cue from Internal medicine books. The greatness of these warrior books is that, it comes devoid of all those scientific clutters backed by premature evidence. 


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.



HF is the inability (or reduced ability) to supply oxygen and other nutrients to fulfill the body’s demands. In the process, the heart either fights or flights, and results in symptoms due to hemodynamic alterations, or adversities of neuro-hormonal activation.

Now, what is Anemia? Anemia is a condition with reduced or dysfunctional RBCs. that directly interferes with oxygen delivery to tissues. It is not at all a coincidence, the core functions of the heart and blood are strikingly similar and intertwined. While the heart is the powerhouse of the circulatory system, without good-quality blood, the greatness of this vital organ becomes redundant.

A mechanically compromised heart should not be burdened with one more compromise, ie with a defective cargo.

Fortunately, RBC and Hemoglobin have an adequate reserve, and real metabolic issues happen only after a 30 %  reduction in hemoglobin. During this time the heart works more to compensate by maintaining high output. When HB falls less than 6 to 7 grams the heart itself suffers from hypoxia and goes for intrinsic failure. So, when anemia coexists with cardiomyopathy imagine the tissue’s plight.

Anemia in Heart failure 

While there are many links between anemia and heart failure few things are worth emphasizing. It can be discussed in 4 categories.

  1. Primary anemia that results in heart failure is a separate topic and comes under high-output HF.
  2. Anemia as a part of the same disease process as heart failure. (Anemia of chronic illness) 
  3. Nutritional anemia associated with common forms of heart failure (Ischemic and non-ischemic DCM) 
  4. Anemia of CKD and coexisting heart failure 

*Category 2 is often missed, while category 3 is often ignored

Prevalence of anemia in HF.. Up to 30%. (Iron deficiency anemia is the most common)

Diagnosis: Criteria Ferritin less than100 or 100-299 μg/L with transferrin saturation <20%). 

What is the optimal Hb %?  Should be 13 grams

Iron deficiency is much more than anemia 

It is worthwhile to go back to the basics, anemia is just one aspect of iron deficiency. Humans live their life, essentially inside the breathing chambers of mitochondria in each of the 12 trillion cells.  Without an adequate iron supply, the citric acid cycle will come to a creeping halt. It is now recognized, altered mitochondrial function is one of the key peripheral defects in HF. (Ref 1) Iron deficiency could be an Incidental marker for a more important tissue deficit elsewhere. 

What do the trials say about the role of routine Iron supplements in HF?

As usual, trials blink with data on either side of the truth. Small studies suggested benefits. But large studies with Iron supplements and Erhytopoitn analogs failed to show benefits. IRON-OUT, RED -HF (Ref 2,3) . But in a popular study from the Lancet , showed ferric carboxymaltose improved the outcome. (Ponikowski P,l. Lancet. 2020 Dec 12;396(10266):1895-1904).

Final message

We, as modern-day cardiologists are always pre-occupied with measures to improve LV ejection fraction at any cost (Since we fell into a false knowledge trap of defining HF solely on the basis of  EF% ) To make HF patients walk 30 meters extra in a 6-minute walk test we have complex and costly procedures like CRT, Mitra clips, and IAS flow regulators,  etc.

However, experience tells us there are many parameters other than EF that can improve functional capacity and quality of life. Breathing exercise is the best example. Let’s add one more to this list. A simple correction of anemia with iron can make your cardiac failure patient walk many blocks more. Trials are not consistently confirming this though. Don’t bother them,  just have a try. If prescribing tablet iron without evidence bothers you with scientific guilt, ask your patient to take a diet with rich iron content and see the difference.

For advanced readers

Anemia and  Aortic afterload: The apparent advantage

There is one curious concept. Anemia makes the blood thin. Reason lowered viscosity. As a consequence afterload falls. , hypoxia-induced peripheral vasodilatation and enhanced nitric oxide activity also contribute to this.  Vasodilatation also involves the recruitment of microvessels and, in the case of chronic anemia, stimulation of angiogenesis. So, anemia apparently has a double edge, and one of them seems to be beneficial.

We must also beware, the risk of iron overload is genuine in some of these patients with HF. This makes us wonder, in ancient times venesection was used for so many undisclosed illnesses, which might include heart disease as well.


1. Melenovsky  V, Petrak  J, Mracek  T,  et al.  Myocardial iron content and mitochondrial function in human heart failure.  Eur J Heart Fail. 2017;19(4):522-530

2. Lewis GD, Malhotra R, Hernandez AF, et al. Effect of Oral Iron Repletion on Exercise Capacity in Patients With Heart Failure With Reduced Ejection Fraction and Iron DeficiencyThe IRON OUT HF Randomized Clinical TrialJAMA. 2017;317(19):1958–1966. doi:10.1001/jama.2017.5427

3. Swedberg K, Young JB, Anand IS, Cheng S, Desai AS, Diaz R, Maggioni AP, McMurray JJ, O’Connor C, Pfeffer MA, Solomon SD, Sun Y, Tendera M, van Veldhuisen DJ; RED-HF Committees; RED-HF Investigators. Treatment of anemia with darbepoetin alfa in systolic heart failure. N Engl J Med. 2013 Mar 28;368(13):1210-9. doi: 10.1056/NEJMoa1214865. Epub 2013 Mar 10. PMID: 23473338.




The definition & intended purpose of patient empowerment

WHO defines empowerment as “a process through which people gain greater control over decisions and actions affecting their health” and should be seen as both an individual and a community process.1

Four components have been reported as being fundamental to the process of patient empowerment: 1) understanding by the patient of his/her role; 2) acquisition by patients of sufficient knowledge to be able to engage with their healthcare provider; 3) patient skills; and 4) the presence of a facilitating environment.2

Based on these four components, empowerment can be defined as A process in which patients understand their role* and are given the knowledge and skills by their healthcare provider to perform a task in an environment that recognizes community and cultural differences and encourages patient participation.




We have enough evidence to question the superiority of the presumably best practice in cardiac pacing namely dual chamber pacing. Apparently, the DDD failed to show gross benefits in both  AV block as well as sinus node dysfunction. (UKPACE, MODE-Selection Trial) in studies done nearly two decades ago.

It is 2022. Here is one more study in the Indian heart journal, coming up from JIPMER Pondycherry,on this concept. It is an intelligently designed cross-over study. The same patients were switched between DDD and VVI modes. This study reaffirmed the lack of appreciable hemodynamic and clinical benefits with DDD mode yet again. 

We have also contributed a little on this issue. It was found cardiac failure in VVI pacing was not a real big issue in the long-term follow-up. We presented and published in world congrees of cardiology Dubai 2012, and Circulation journal. 

How is that? A dual chamber pacer with AV synchrony fails to show a hemodynamic benefit?

The answer is simple..VV desynchrony is a common denominator for both VVI and DDD pacers. Providing AV synchrony without VV synchrony doesn’t make real sense in the long term to overcome the altered physiology, Still, DDD pacing continues to enjoy a popular mandate by hiding behind a vague outcome measure called quality of life.

What is the physiological pacing then?

Just because, DDD and  VVI pacers are equipoise,  can we presume the new pacing kid LBBB pacing would be physiological? We wish so, but unless and until we replicate the entire conducting system right from SA, and the AV node which includes many miles length of delicate Purkinje cables, every pacing system we use is currently pathological. (If that sounds too harsh, let’s make it non-physiological)

Having said that, VVI pacing is one of the most remarkable Inventions in medical science since the last century, that plays God’s own function and gives a new lease of life to all those patients with critical AV blocks and trouble some SNDs.

Final message

It may be difficult to digest for true scientists. Restoring the atrial booster pump is not bringing in the desired benefits. It is clear that VVI pacing will never become obsolete. This fact was established long before. We must argue and wonder, why we need to keep proving a scientific truth again and again?  There could be a good justification too. Real-time cardiologist behavioral patterns clearly tell us, as a genre, they often struggle to get detached from futile modalities even after good published evidence (PCI for CTO, Revascularisation for Ischemic DCM, are a few more examples)



“Never take your eyes off the monitor and the pressure curve” It is one of the basic instructions given to the fellows & technicians as they start engaging the coronary artery and Intubating the coronary ostium in their early cath lab postings. There are two commonly heard noise bites in the cath lab for the beginner. 1. Damping 2.Ventricularization.


It is the deformation of the normal arterial pressure curve, with a blunting of both systolic and diastolic pressure that drops compared to aortic pressure. Extreme damping can mimic a straight line with few wavy undulations. It means the forward flow is impeded as the catheter might be blocking the coronary flow at least partially, if not completely. Immediate pull back and adjustment of catheter is required to prevent adverse events that includes cardiac arrest. (Of course, catheter kinks, blocks, and air in a circuit are to be ruled out first)

Mechanism of damping

  1. The catheter tip is too large for the ostium.(Technical)
  2. A left main or RCA ostial lesion*(Most significant clinically)
  3. The coronary artery wall is thin and goes for spasm
  4. Catheter diameter is too small and glides into the coronary artery (The catheter tip hitches against the lateral wall of the coronary artery often over a plaque, a silently staged perfect setting for a dissection )

Unique features in RCA damping

In RCA, damping could simply mean it has engaged conus branch. Damping is more common in RCA and it tends to get sucked in deeper for two reasons. We know , the RCA catheter is not preformed, the tip seeks the ostium, looking for a negative pulling pressure from within the RCA. Further, unlike the LCA, the flow in RCA is continuous in both systole and diastole. Another possible factor is the inspiratory swings of RV transmural pressure is more than LV.

Transient bradycardia due to compromise of SA /AV nodal flow is common. It is well known that RVOT is a thin and VPD-prone zone , compared toLVOT. Hence it is more vulnerable to ischemia and triggers a VT/VF if damping is prolonged in RCA.


This is tracing during the engaging of a left main ostial stenosis. The diastolic pressure drops on the third complex, and the pulse pressure becomes large . Note the small “a ” wave slur as well near the diastolic nadir. The aortic pressure curve is restored once tip adjustment is done. Image courtesy Thoraci key.https://thoracickey.com/coronary-angiography-3/

It simply means the pressure curve starts looking like a ventricular pressure curve. The issue is not that simple. It is still a mystery, how could the coronary artery pick up ventricular pressure. In fact, it doesn’t. It was initially thought to be either deformed aortic pressure or a wedged coronary artery pressure .or a combination of the two.

It s now accepted it’s due to total occlusion of the coronary artery the ventricle muscle sucks the catheter and pulls the diastolic pressure markedly down even lower than LVEDP. The systolic pressure also falls but not much of it is noticed.The fact that ventriculaization happens less commonly with RCA gave us a clue to its mechanism. (Most of the RCA travels over RV and since RV muscle mass wields less negative suction force )

How to differentiate true LV location from ventricularization?

If the catheter enters the LV cavity, the systolic pressure will match that of aortic systolic pressure and diastole will reach the LVEDP. In ventricularization there can be a slight drop of the systolic pressure, but the diastolic is the one goes far down. Further, the ascending limb is shallower, the descending limb is steeper in coronary ventricularization. Apart from this if we carefully look “a” waves will be visible in ventricularisation in the late diastolic phase.(Could it be the modified Incisura ?)

Relationship between damping and ventricularization ?

Discussing damping and ventricularization together is more of an academic tradition. Please realize, both may not be two exclusive entities. In fact, they can occur at the same time, or sequentially or interchangeably if the catheter tip swings back to partial to total occlusion and vice versa. if complete wedging occurs it becomes ventriculariszation.

Which is more dangerous damping or ventricularization?

How can you ask such a question? Both can be harbingers of serious hemodynamic issues if ignored and accidentally injected, The dreaded one is the dissection. Apart from mechanical injury, Injecting dye during damping or ventricularization causes dye stasis, and may trigger VT or VF if it is prolonged. There is a biochemical component too. As the contrast swirls around for a few seconds it can cause transient hypocalcemia by chelating this cation.

I don’t have a clear answer to the above query. In my understanding, forceful injections during ventricularization could be more riskier as injection happens over a total occlusion in a wedged position and dye has direct access to the microcirculatory bed. It is true, expert cardiologists do shoot in damped positions occasionally to see the anatomy quickly. They may be your mentors, still don’t learn this trick, till you become a true expert (Famously referred to as hit and run technique)

How to overcome these pressure curve malformations?

Most times, it is a simple technical artifact issue. Deep Intubation with an oversized catheter could be the commonest cause in the otherwise normal coronary artery. Proper catheter sizing, angle of alignment, and adjustment is the key. If it is a spasm nitroglycerine might help. Using catheters with side-hole perfusion catheters is an option in difficult anatomies. Mind you, side holed guide is a two-edged weapon, it can mask true hemodynamic adversaries by falsely showing a good aortic pressure tracing.

(One of the good cath lab habits is to have a look around the patient face at least once in a while when performing complex procedures. We have many times recognized serious hemodynamic issues only after the patient starts behaving bizarrely due to hypotension. Pressure curves can fool you, but patience will never.)

Final message

Recognizing abnormal waveforms during engagement is a crucial step for the beginner (Experts can’t ignore though) Please remember LMCA stenosis should be the default alarm for any damped pressure curve as you engage the LCA. If you take things casually consequences can be lethal for the patient as well as the consultant in charge.(Fellows can’t take it lighter though). It is an undisclosed fact, that many of the serious complications in the cath lab happen not out of ignorance or lack of expertise, but because of ignoring some basic principles and lack of cath lab discipline.


1.Baim DS, ed. Grossman’s Cardiac Catheterization, Angiography, and Intervention. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2006. 2. Judkins MP. Selective coronary arteriography, a percutaneous transfemoral technique. Radiology 1967;89:815.

2.T Pacold I, Hwang MH, Piao ZE, . The mechanism and significance of ventricularization of intracoronary pressure during coronary angiography.Am Heart J. 1989 Dec;118(6):1160-

3.A good review from Journal of Invasive cardiology .

Though all of us are aware, the incidence of heart failure is increasing exponentially and is the leading cause of global disease mortality, what we fail to understand is, we still lack a good definition cardiac failure. 

Defining HF based on EF% is convenient but adds more complexity, and is less scientific too. Still, as of now, we have adopted this. I think, one of the important factors that apparently increased the incidence of HF is the creation of an entity called HFpEF. (Formerly diastolic heart failure)

Thanks to ESC, we have a consensus document, which has defined HFpEF based on functional, morphological, and biochemical features. This is a more refined model from the original Mayo clinic H2FpEF score.

Both are given below.


Mayo criteria
The problem with both these criteria is the disproportionate importance given to AF. The knowledge gap here is, AF can be initiated at any degree of increased atrial strain which can independently raise LA mean pressure without persistent elevation of LVEDP. We recognize now, left atrial obesity (fatty atrium)  is a powerful trigger of AF, still, in this situation, an Innocent LV may get blamed with a tag of HFpEF. Likewise, many HFpEF may turn out to be primary  LA dysfunction than LV failure. To make things more confusing(scientific) for diagnosing true HFpPEF, we may soon need to look into LA-EF as well. (LA-HFpEF)

Can we diagnose clinically significant HFpEF, without pulmonary hypertension?

In my understanding, the answer is No.

Looking at the two schemes (Mayo & ESC) one thing is clear. Pulmonary hypertension is the key hemodynamic expression of HFpEF. It could be either resting and persistent or exertional and transient.t is obvious the PH in HFpEF is post-capillary. (The modern term for pulmonary venous HT). Mind you, while PVH is mandatory to diagnose HFpEF, PAH (precapillary ) is also observed in most patients with significant HFpEF. This is the reason TR jet velocity is included as one of the criteria.  (To make things simple, we may need to create a new classification of HFpEF, ie resting vs exertional HFpEF.This is what the diastolic stress testing is all about.)

Final message

It is back to basics & time to dig into the fundamentals, of what exactly we mean by heart failure. Is the elevation of LV filling pressure alone sufficient? Should it happen at rest or at exertion, and whether neuroendocrine activation is necessary? Is RASS activation similar in both HFrEF and HFpEF? Try to find the answer to this. How often does HFpEF fulfill Framingham’s criteria of HF.? ( Löfström et al  ESC Heart Fail. 2019) 

Trying to understand the nuances of HFpEF, I think, we can make a statement,- HFpEF can not be diagnosed without pulmonary hypertension. It makes a lot of sense the P in the H2FpEF  scoring system denotes PH, however, It is assigned only a single point, which needs revision. In fact, there is a strong case to argue and make it an essential criterion.

Paradoxically & curiously HF with reduced ejection fraction (which is the most common form of HF) doesn’t require the presence of PAH to diagnose it. This issue may also be examined.


1.How to Diagnose Heart Failure With Preserved Ejection Fraction: The HFA–PEFF Diagnostic Algorithm: A Consensus Recommendation From the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur Heart J 2019;40:3297-3317.

2.Löfström U, Hage C, Savarese G, Donal E, Daubert JC, Lund LH, Linde C. Prognostic impact of Framingham heart failure criteria in heart failure with preserved ejection fraction. ESC Heart Fail. 2019 Aug;6(4):830-839. doi: 10.1002/ehf2.12458. Epub 2019 Jun 17. PMID: 31207140; PMCID: PMC6676283.

Does the Aortic root contract or relax during ventricular systole? Some time back, I asked this question in one of my classes for the fellows and found no takers. Not even a guess? I realized later, it was indeed a tough question. The heart is not the only dynamic organ, as we generally believe. The entire aorta which is an extension of the left ventricle has to be dynamic according to the physics of ventricular-arterial coupling and the momentum of blood flow.

What happens to the aortic dimension with systole?

Even prior to systole, there is evidence, the aorta gets ready to receive the blood from the LV. So, the Aortic root must be larger at the onset of systole. (Ref 2 ) It is been generally agreed now, that the systolic dimension is slightly more by a few mm. That is why aortic dimensions are measured in peak systole as per the American society of echocardiography.

There has been an opposite argument as well. The diastolic aortic dimension could be larger, as the aortic valve is in the closed position and the aortic root distended, & becomes a reservoir of blood that’s meant to be distributed during diastole. What determines the aortic dimension on a moment-to-moment basis?  Is it the, LV contractility, pressure, or volume, or the compliance of the aortic wall that determines the aortic dimension and pulsatility? How does a prosthetic valve alter this?

So, what exactly happens to the aortic dimension during the cardiac cycle ? 

A wonderfully done study from University Medical Center Utrecht, The Netherlands throws some important facts with their analysis of ECG-gated CT scans in 108 Aortas.(Ref 1)

It is surprising, to note the aortic root behaves independently. It either contracts or relaxes with a range of 4 mm swing on either side of the systole and diastole. Another stunning fact is, it remains static in a significant number. (One possible explanation is the true aortic annulus is less dynamic because it is bordered by the fibrous skeleton, while the rest of the aortic root only can distend or shrink )

Clinical implication of aortic pulsatility

The implication of knowing (or not knowing )the dynamism of the aorta can be huge.

  • Age-related stiffening and onset of systolic hypertension
  • Aortic diameter, pulsatility, and shear stress are the key parameters in initiating dissection and its propagation
  • Choosing the right sized valve for AVR
  • Current interventional heart-throb TAVI involves just a passive placement of the valve in the aortic root. Imagine what will happen, if the foundations are excessively dynamic and shaky   

It is surprising, even after decades of vascular research, we lack clarity on what exactly happens to aortic root during various phases of the cardiac cycle. (Currently, paravalvular leak, & migration of TAVI remains a major worry, which has a direct relationship with pulsatility of the aortic root ) One thing is obvious,.Young cardiologists have a lot of work to do in this arena.

Final message

 Though the aorta is a direct extension of LVOT, its vaso-motion doesn’t seem to be in complete sync with the cardiac cycle. It tends to have an independent behavior, out of phase with the heart. 

As per available evidence, the aortic root dimension can either increase, decrease, or be static in response to LV contractility.


1.de Heer LM, Budde RP, Mali WP, de Vos AM, van Herwerden LA, Kluin J. Aortic root dimension changes during systole and diastole: evaluation with ECG-gated multidetector row computed tomography. Int J Cardiovasc Imaging. 2011 Dec;27(8):1195-204.

2. Pang DC, Choo SJ, Luo HH, et al. Significant increase of aortic root volume and commissural occurs prior to aortic valve opening. J Heart Valve Dis. 2000;9:9–15. [PubMed] [Google Scholar]

3. Vesely I. Aortic root dilation prior to valve opening is explained by passive hemodynamics. J Heart Valve Dis. 2000;9:16–20. [PubMed] [Google Scholar]




Welcome to Kuna island. The Kuna Indians are really unique people. living off Panama, right in the isthmus connecting North and south America, The Kunas reside in the San Blas archipelago comprising about 360 islands, of which about 60 are populated by them. They have lived on these islands for centuries, but their exact origin is not completely understood.


These innocent tribes have taught an important lesson in human blood pressure regulation, vascular biology, and salt sensitivity. We know, that high blood pressure, is a maximally researched entity in medical science in terms of etiology, vascular effects, and its control. Still, we don’t know, what are the limits of normal BP for human beings. The debate will not end until we are clear about, whether human beings evolved from monkeys or emerged as de-nova organisms. Recent studies have revealed a remarkably low level of mitochondrial gene diversity in monkeys, suggesting that there has been remarkably little genetic admixture. (Ref 2)

What we know from 3000-years-old human history is, blood pressure is directly related to the physical work done by us and the diet we eat. While salt is considered pro hypertension, physical activity is a much more important determinant in bringing it down. Normal BP in a pre-civilized world was low compared to a civilized population. They also enjoyed better vascular health. Where is the evidence? It comes from the life cycle of Kuna Indians. Here is a very unique paper published in the Hypertension journal.(Ref 1) Three cheers to the authors for confirming this long pending speculation with meticulous data collection. (See the Image)

What was special in Kuna’s diet that prevented cardiovascular events? It is been shown in the study by Hollenberg, their diet contained rich in cocoa and flavonoids that made the difference.(The salt consumption was still high though)

As Kuna’s moved out from their primitive lifestyle to first, the  Kuna Nega,(a suburb) and subsequently to a fast-paced Panama city. See the impact on their systole and diastolic stress on the heart. The loss of protective effect of the native diet is obvious.

Final message

Lifestyle is the buzzword today. It is a by-product of the new civilized world that will define human health. The human vascular tree tries to sync with a new lifestyle pushing the BP curve to the north. The true normal BP for denova-human beings may still be very much lower than what we believe. A crazy suggestion was made, that human BP should match that of non-sedentary monkeys.  I Hope, we get more evidence later for such hyperboles. As of now, we have to accept, hypertension is largely due to disorder in human civilization, development, and prosperity.

 How about embracing the styleless lives of native Kunas to take control of our vascular health.


1.Hollenberg, Norman K.; Martinez, Gregorio; . “Aging, Acculturation, Salt Intake, and Hypertension in the Kuna of Panama”  Hypertension29 (1 Pt 2): 171–176.


(M.), LITTMAN (M.), POLZIN (D.), ROSS (L.), SNYDER (P.), STEPIEN (R.) – Guidelines for the Identification, Evaluation, and
Management of Systemic Hypertension in Dogs and Cats. J Vet Inern Med, 2007, 21: 542-558

This is the story of PCI to LAD from the customary bifurcation workshop for the budding experts, which ended up with a compulsive final OCT run-through, triggering a debate on what to do with the side branch.

What shall we do next?
  1. Just balloon dilate the distal strut
  2. Would consider a second stent. Maybe a TAP  depending upon LCX morphology
  3. At this stage, I would like to know the FFR or iFR across LCX Jail.
  4. Get rid of this OCT, Let me have look at regular CAG. I bet I can make a better decision.
  5. Leave it alone if the clinical status & profile is good

Leave it alone? Is it not an incomplete Job?

Definitely incomplete. Please realize, No job is complete in interventional cardiology. If we believe so, it exposes our Ignorance ( & some arrogance). Intentional side branch jailing is an integral part of  PCI techniques. Are we not ignoring day in and day out. 

Someone in the audience asked Why did you do OCT at all? 

The chief operator quipped “You can’t ask this silly question in a scientific workshop. We bought the OCT kit to improve the quality of PCI. We are proud of it. Really feel blessed to use it and I am sure my patients will benefit from it”. We have to agree with him. These new Imaging techniques though give us extra high-definition, but it comes with troubling revelations with their new vision. If you are pathologically honest and believe in empowering patients, it is absolutely necessary to convey the following facts in the discharge record as well. It would be something like this, “There was a 120-micron strut crossing the LCX ostium, that might continuously impede a chunk of platelets & RBCs every beat, for the rest of your life and might enhance the risk for thrombosis. (Of course, DAPT will take care of it and ask the patient not to worry)” 

OCT: One-minute review

OCT is Indeed a stunning Innovation. It can be useful in all 3 phases of PCI. 1. Assessment and preparation of lesion bed. 2. during stent deployment and optimization. ,3. Post-stenting follow up. The technology has grown so fast, now angiographic co-registration and longitudinal frame reconstruction comes inbuilt. It required 3 versions of LUMEN study and a 4 th one (LUMEN 4 ) is yet to come, expected in 2022  to prove the worthiness (or worthlessness)  of OCT. 

One attractively named DOCTORS study asked the specific question directly (Does Optical Coherence Tomography Optimize Results of Stenting)”  This is from NSTEMI patients .read yourself for the conclusion. It is not convincing to me.  Meneveau N.,  DOCTORS study (Does Optical Coherence Tomography Optimize Results of Stenting)”Circulation 2016134: 906.

Mind you, OCT is not only an expertise-dependent procedure, it also has important imaging limitations. It has low penetration max 2mm, can not differentiate lipids from calcium, shadowing behind red thrombus is an issue and most importantly it may miss the external elastic lamina (EEL) and measurement errors are real. 


If an imaging technique to assess a stent *(*Still waiting to prove its worthiness) could cost more than the device itself, realize how good our economic intellect is. Just because your lab has an OCT console, it need not transform into a technically perfect PCI. There are at least half a dozen factors other than Imaging that matters. 

Final message

OCT is a breakthrough technology that needs to be used judiciously and it definitely helps us understand the nuances of coronary stenting, especially in complex lesion subsets, and its mechanical and histological contents. However, let us not propagate a false message, that without OCT we can’t perform a perfect PCI. Give due respect to all those sharp-eyed interventional cardiologists with good techniques, who can do a better job, beating the HD vision of OCT, with their native blindness. 




Can you guess how many PCIs are done with OCT guidance globally?

It is less than 5 %. In India, it must be, I guess it is < 2% So, we are living in a terrifying world of coronary interventions, where  98 % of PCI is happening blindly, sub-optimally, and unscientifically., Data from CLI-OPCI registry adds more panic:  Centro per la Lotta Contro l’Infarto – Optimisation of Percutaneous Coronary Intervention (CLI-OPCI) registry:  It says device-oriented cardiovascular event (DOSE) is high with OCT detected sub-optimal  PCI.

So, what are we going to tell our patients who will undergo PCI (undergone) without OCT guidance in the past, present, and future?

Simply ask them to forget this OCT stuff. Just reassure them. Nothing will happen.