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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. 

Reference

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.   

Postamble

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 .

http://www.heartlungcirc.org/article/S1443-9506%2810%2900076-4/abstract

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.

Reference

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/226907

William Heberden first introduced the term angina to the medical community in 1772. His descriptions became immortal. Still, no one would ever know what was the angina-related artery, Heberden was alluding to.

Now, some jobless cardiologist is asking this question after 200 years. How is angina from the LAD system differ from the RCA  system? or let me put it another way, How does angina of anterior circulation (LAD) differ from posterior circulation (RCA/LCX)? Though there is distinct hemodynamic profiling of RCAvs LAD ACS, surprisingly, cardiology literature does not answer the chest pain aspect of it. One rare study, done  4 decades ago throws some light

Here is a curious little study, with a simple & crisp conclusion.

chest pain and IRA localisation angina LAD angian RCA

It concludes, that LAD angina rarely radiates to JAW or epigastrium. While RCA angina relay radiates to the left shoulder.

So, why does this happen?

What I could guess is the ubiquitous vagal fibers that travel in the posterior aspect of the heart, and carries pain signal directly up to the jaw whenever these areas become ischemia. LAD is less likely to irritate the vagus. Of course, there can be a definite overlap.

OMG, give me some time to keep in touch with  basic science 

Now, fellows of cardiology, please take a  pause from your regular aggressive cardiac cath lab workouts and get a break at least once in a while. How does the ischemia of myocardial tissue generate pain? Why it is severe in some, trivial in others, and even dead silent in some, 

The chest pain genesis is initiated by sensory electrical neural action potential, that captures the epicardial neural plexus first, switching over from somatic to the visceral pathway and trespassing the para ganglionic plexus and traveling further to the spinal cord. Where it may collide with other incoming sensory signals ascends in specific myelinated and non-myelinated neural cables, reaching the brainstem, interacting with local nuclei, and finally reflecting on subcortical and cortical pain matching centers.  We haven’t yet located the exact center for anginal pain. (Perithalmic and amygdala could be closer to real centers) 

So, it is a really complex sensory world yet to be understood fully. Mind you, I haven’t touched upon the neurophysics of referred pain, linked or clandestine angina.

  • What is the effect of cardiac denervation, autonomic neuropathy, or on the perception of chest pain(Does a quadriplegic feel angina ? or post-transplant heart immune to angina ? (Gallego Page JC,Rev Esp Cardiol. 2001) 
  • Is it biochemical or neural, can substance P in blood cause pain hitting the amygdala? 
  • Will hypoglycemia and anemia cause angina due to lack of glucose and oxygen?
  • Finally, how is Infarct pain is different from ischemic pain (Ischemic)

Where do get the answer to these questions?

This paper from Dr. Robert Formean(Ref 2) university of Oklahoma is just the best source I think, to explore and understand the topic. (Reading time 60 minutes: Let me tell you, it is worth more than a time spent on an insignificant angioplasty of painless PDA lesions)

Final message 

So, what have you learned from this post? Does this question about angina matter at all? Surely not. in this space-age cardiac care where we are right inside the coronary even before we listen to the patient’s complaint properly. We are always at liberty to do what we want( or love) to do. But, the urge to understand the foundations of clinical science is the last remaining hope, that will keep the specialty of cardiology enchanting. 

Reference
 
 
A comprehensive reference for the genesis and signal processing  of chest pain 
 
 

This graph is a rare treasure in CAD therapeutics (fished out from a huge, often conflicting chronic CAD literature) that elegantly shows us the complexities involved in the revascularization of ischemic hearts with risks and benefits criss-cross each other. Our job is to identify, that critical point in a given patient’s CAD timeline for optimal management. To make things difficult, this point is a moving target and makes this delicate clinical exercise truly complicated.

It conveys a simple message in strong terms. It says the inflection point is around 10-15%. When the total ischemic areas are beyond this the benefits increase and when it is less there is sure shot harm.

Now comes the tough part. How best we can identify and quantify the true area of ischemia?

There is no such thing called coronary mathematics. Even if we try to make out one, vascular biology will giggle at us. Still, we have no other option but to go for sophisticated imaging modalities. Stress Echo, Nuclear Imaging, Scar imaging, MRI, PET, quantify total ischemic burden, plot it with corresponding coronary anatomical zones for a potential correction.

What this curve does not convey is the complex interplay between Ischemia vs symptoms. Ischemic myocytes have so many invisible tricks to adopt themselves. Should I go after the burden of Ischemia (Often Imaginary) or the burden of symptoms? Despite the lack of benefit in most trials on CTO in hard endpoints, it is yet to rectify the thinking patterns of many elite evidence-based cardiologists.

Final message

However, It will be an unpardonable act of omission if we miss or fail to offer the benefit of opening a critical LAD disease that has troublesome symptoms.

“Publish or perish “

This sound bite is regularly uttered by all academic leads in any university or medical school. I don’t know, why this bothers me. Looking back, many of our mentors & professors never had any great publications. Still, they were extraordinary teachers and wonderful clinicians with great wisdom. They created generations of high-quality doctors who are present all over the globe now. Is scientific publication that important in a doctor’s life? After pondering for quite some time, got a hazy answer to that query in one of my sleepless early morning academic dreams.

Hippocrates was one of the applicants for the post of professor of medicine at Harvard medical school.His application was rejected for a dismally low H index. The reluctant father of medicine tried to impress the authorities, by telling them that his experience was vast and used to teach medicine 2000 years ago, well before their country USA was discovered. The father of medicine almost begged to reconsider their decision.The miffed Harvard academic office ridiculed the old man and insisted nothing will work, except a minimum H index of  50 or atleast 10 papers as first author in a peer reviewed high Impact  factor journal. A dejected Hippocrates returned to Kos islands and asked his new generation fellows, what is this H index and Impact  factor stuff ? His students were worried about their guru’s ignorance. They some how convinced the greatest ever medical teacher to urgently subscribe for a platinum membership of a premium medical authourship services located in the Boston suburb and fixed a 30 day deadline for his first manuscript.

(What is this H index ?)  Why is it so popular?)    Ref : J. E. Hirsch  An index to quantify an individual’s scientific research output

Off to Kos Islands 

Now, let us travel back in time,2000 years ago to this picturesque nation, Kos islands in the Aegean sea,. This is where Hippocrates taught lessons under his favorite tree. No teaching apps, No 4k audiovisuals, The humble noise from within his lips became great wisdom thoughts. All that students had were set of ears to hear him. Hippocrates became the celebrated father of medicine for two reasons. He was the first to dispute the then-prevailing thoughts about human health and disease. He first proposed for every illness there is a hidden reason ie the beginning scientific basis. He insisted and negated the idea that diseases are bestowed upon by evil forces and spirits. The second one is more important. He realized knowledge, skill, and power are a deadly mix for the healing industry if they lack responsibility. He foresaw non-academic factors that will try to challenge the integrity of medical professionals and the health care delivery systems. It is astonishing to note how he could predict this 2000 years ago and wrote the behavior code for medical professionals which has become immortal.

How to grade the quality of medical professionals?

Scientific publication is just one of the indices of quality assessment for medical professionals. Grading them based on a few manufactured rating systems is beginning to look like an academic comical. There are many more visible and invisible, quantifiable and non-quantifiable quality assessment parameters that deserve attention.

Research  & Innovations are indeed the pivotal pillars that take us to newer frontiers of medicine. But, It is explicitly clear now, the prime purpose of research is definitely not aimed at the growth of science. It is more of a survival tool, intertwined with commerce, status symbol, pride, peer pressure, self-esteem, rivalry, or just a filler for CV. 

Final message 

Blanket statements like Publish or perish at any cost could be a dangerous doctrine to adopt in medical education which is essentially about healing and caring (& whenever possible, curing). In one sense, medical teaching is little to do with research. Many of the great professors in our country never published a single paper. Unfortunately, research and teaching have been made to look inseparable. Beware, history has repeatedly taught us medical professionals need not be hyper-intelligent. They need to be just wise, men /women of integrity, enriched with sincerity, righteousness. Proper consumption of knowledge is much more important than the creation of it. Let us hope the future will be at least as perfect as the past. 

Postamble

My  H index stands at 15, I must confess I am confused a lot. Should I bother for more, or be just be happy to reach the H index of our mentor and father of medicine, which is numero Zero, and propagate his work. 

Reference 

Grzegorz Kreiner The Slavery of the h-index—Measuring the Unmeasurable..Front. Hum. Neurosci., 02 November 2016

2.Academic excellence does not always require publication  Ernest L Boyer argued in his 1990 book, Scholarship Reconsidered: Priorities for the professoriate,(BoyerScholarshipReconsidered)

3.Too much academic research is being published https://www.universityworldnews.com/post.php?story=20180905095203579 

 

 

A path-breaking research is coming up from Jhon Paulson school of engineering, Harvard.

It is all about a tiny lab-made bio-hybrid fish that is mechanically engineered with cardiac stem cells. It can generate enough mechanical force that can transform into a biological organ (or assistance)to the heart. Early lab experiments are exciting. We will soon see a stem cell-enriched bio-fish that will dance to the tunes of the cardiac cycle.

(See the video below) 

Final message

Will it become real? or a just a grandeur thought?

We have just done Xeno heart transplantation and the mechanistic possibility of a fully functional total artificial heart is always there. Now, let us look forward to this bio-hybrid organism*  that will break the ultimate barrier in the biomechanical support for failing hearts.

Reference

*Biohybrid organisms, are devices containing biological components.

KEEL YONG LEE ,SUNG-JIN PARK , DAVID G. MATTHEWS et al  An autonomously swimming biohybrid fish designed with human cardiac biophysics SCIENCE • 10 Feb 2022 • Vol 375Issue 6581 • pp. 639-647 

 

 

Spanish flu battered our planet in 1918. How did we overcome that? (Did we really do anything ?) About fifty million lives were lost. At that time, we didn’t even know, cells had a fully functional nucleus, forget about the DNA & RNAs. Spanish flu was tackled only with our primitive understanding of microbes, cells, and immunity. Masks and common sense were the weapons.

Now, one century later the next pandemic is In. It is an advanced medical world out there.100 Noble prizes have been won for medicine since then. We do the whole-genome map of not only human cellular DNA but also for the viral particles.

A recent paper on this topic. 

How effective is modern science in controlling the current pandemic ? 

We did wonders saving thousand of life with the help of critical care units. Some precious (elite)lives were saved by ECMO, Even lung transplants saved a few lives. We mastered the art of creating RNA interrupting biologicals. Even as we reap the benefits of stunning discoveries of science, we have equally misbehaved with it and largely undid whatever we should have achieved. We lost more lives due to a lack of simple measures. excess of futile measures, manic dependence on diagnostics.

Where did we collectively lose our sense and decide to chase multiple variants with a full genome mapping on a global scale? Who decided to call the viral variants attractive names and give larger-than-life images to amplify the panic? Even after getting a final vaccine solution, why the World is denied sharing the benefits in an equitable manner. 

There is no meaningful evidence that extensive  RTPCR,  antigen, or antibody testing has impacted this pandemic in a significant way. Testing is meant before the onset of community spread or if there is a specific treatment for the disease. How do we explain countries with maximum testing, maximum vaccine coverage, maximum booster dose had a maximum recurrence and damage?

Final message 

Science is sacred & Godly if only, its creator’s Intentions are pure. The risk-benefit ratio of modern science, (Rather, the way we understand and assimilate it ) in tackling this pandemic is threatening to tilt in an adverse fashion. Definitely, WHO must realize this. Let us go back and read the foundational lessons of clinical epidemiology and pandemic handling. I felt awkward to write this post but truths are rarely sweet.

This article  by Dr. Anand Krishnan, Professor of  community medicine, AIIMS New Delhi, has some enlightening content

https://timesofindia.indiatimes.com/india/whys-pandemic-policymaking-still-short-of-science/articleshow/88650912.cms

“We have a 24/7 cath lab with an open door policy. Our cardiologist arrives at 15 minutes’ notice. Door to balloon time is less than 60-90 minutes”, 

“Great, so, you can always offer a successful treatment for STEMI”

“No, that we can never guarantee.” 

 “Oh, It Is not the answer, I  expected”

“I agree, it sounds disappointing, but. truths are less pleasing. What I am trying to say is, there are a number of factors other than the availability of a grand cath lab and agile and effortless hands, that try to reperfuse the myocardium in distress.  I agree, we do save lives occasionally in a dramatic fashion. Recently we resuscitated an almost dead man with CPR and ECMO-guided PCI. But, most times it turns out to be just a customary ritual that takes us to the legal and therapeutic  endpoint* of STEMI management”

*Both salvage & non-salvage

“I didn’t get you, Can you explain further?

See this curve and try to understand it yourself. (I would say, this is the ultimate curve to understand in the entire field of coronary care)

Can you guess what will be the outcome for C to B, or B to A ?  In the real world, a substantial number of interventions take place at an Invisible point E beyond A  Source: Gersh BJ, Stone GW, White HD, Holmes DR Jr. Pharmacological facilitation of primary percutaneous coronary intervention for acute myocardial infarction: is the slope of the curve the shape of the future? JAMA. 2005;293:979–86

Slippery slopes and edgy Interventions

At what point the patient lands up in the curve & at what point the interventional cardiologist intervenes (or does not intervene) matters the most. 

The gaps between benefit and harm can change in a few strokes of time. The reperfusion tamasha can get more curious if we realize both the slope of the curve & its absolute position are dynamic. It can shift to the right or left with reference to the patient’s Initial medications, MVo2 confounders, the quantum of collateral circulation, myocardial hypoxia threshold,  previous ischemic episodes, conditioning, etc. So, basically, we are reacting to events and trying to rush up things. Don’t worry about all this. Cardiologists have every expertise and equipment to tackle untoward events.

STEMI is not always myocardium under fire

Finally, and most importantly STEMI, though a cardiac emergency. all should not be equated with the house(myocardium) on fire analogy. It can also be a spontaneously aborting, settling, or evolving, self-extinguished controlled fire, and the myocardium may take it easy. All that it requires is some deep ischemic slumber. Don’t try to poke it with all our violent hardware at one go in the name of salvaging. What is required is proper CCU care to take care of potential arrhythmia, angina, or failure. One may create more damage if trying to dowse non-existing flames furiously, which expresses in the form of reperfusion Injury and no-reflow to the myocardium. (Which might have reperfused at leisure without experiencing the injury.)

It is worth pondering over this question.

Why does even an apparently well-timed primary PCI of IRA leave behind a significant LV dysfunction or even a  scar? This is a clear case of “successful PCI failed reperfusion syndrome”. It is better cardiology community defines successful primary PCI with reference to predischarge  LV function, not on the IRA patency and mystery endpoint called TIMI 3 flow.

Final message

Cath lab doors that are open 24/7,  with experienced cardiologists may matter little if we are double-blinded against multiple scientific and non-scientific factors that are visible as well as invisible. 

Counterpoint

How good is late PCI? Are you not aware benefits of the open artery hypothesis?

You need to learn a lot man, before posting such posts.

“It needs both. obviously”.

“Which is difficult? Innovation or regulation?

The answer is easy, am I right?

“If we are not able to regulate science …what is the purpose of magnificent Inventions & Innovations?”

“Who will take the responsibility for all motivated false research and resultant adversaries? 

Final message

Is shutting down (or grossly down-regulating ) research an option?

Foolish option…but

  • Who Initiated, funded, and masterminded the gain in function experiment with the innocent RNA viruses which were happily enjoying their nucleic acid life, along with the friendly bats in the wild forests, far away from human infestation?
  • Who ordered to hijack them to (in)human labs and hurt the sleeping viruses with sharp molecular knives to earn its violent wrath?

The New England Journal of Medicine (NEJM) the premier journal in medicine originated two centuries ago, in 1811, when  John Collins Warren, a Boston physician, along with James Jackson, submitted a formal prospectus to establish the New England Journal of Medicine and Surgery and Collateral Branches of Science as a medical and philosophical journal. 

Subsequently, the Massachusetts Medical Society (MMS) purchased the Journal for US$1 and, in 1928, renamed it to The New England Journal of Medicine.

NEJM’s New Journey

It is 2022, after 200 years of providing explosive knowledge in medical science, MMS  starts a new journal, fresh and bold. It is called NEJM Evidence. Can you guess, what is the need for such a journal now? I think the most battered word in science in current times is probably “ evidence”.  It has a unique character of appearing most sacred as well as scandalous at the same time.

NEJM has remained the torchbearer of almost all advances in the medical field seen in the last two centuries.  It is heartening to note the newborn is named as NEJM evidence. It has come at a critical juncture. I am sure, everyone will acknowledge that we are at difficult crossroads. Overwhelmed with unregulated scientific discoveries and publications, struggling to deal with self-inflicted knowledge pandemic. In the process, we have lost “not only” the ability to ignore trivial health issues “but also” failed to provide simple, cost-effective care to the real patients who desperately need it.

Let us hope, (& wish,) NEJM’s new prodigy will guide medical science towards a successful, meaningful, and ethically fulfilling journey for mankind. Meanwhile, let us pray for every medical scientist to be blessed with the required strength and courage to steer in the right direction, weeding off both academic and non-academic contaminants.

 

 

What is in store for the future of cardiology as of 2022?

Here is one of the rare lectures (A grand rounds by Houston Methodist)  by legendary cardiologist Dr. Euegne Braunwald who shares his wisdom, vision, and research and finally his advice for the generation next cardiologist.

 

For those, who are short of time to listen to the father of modern-day cardiology, let me share a preview. The talk is divided into 6 subsets.

  1. Polygenic risk score (PRS)  Dr. Braunwald talks about how genetic risk profiling and risk factor interaction will help us identify susceptible populations. Here, he stresses also the importance of clinical risk assessment.
  2. Primordial prevention of CAD: 
  3. Anti-lipid strategies: He introduces a new concept of  Cumulative LDL score &  CHD threshold.  Dr. Braunwald argues rigorous lipid control should go beyond statins and suggest once a year Injection Inclisiran(Small interfering RNA that prevents PCSK synthesis) will reset the lipids levels by 40% and prolong life by 30 years.
  4. Anti -Inflammatory strategies: He reminds us Atherosclerosis is equally an inflammatory disease and new anti-inflammatory drugs like Canakinumab’s role could be vital.
  5. Artificial Intelligence: Will be the guiding force in the future of preventive cardiology, as well as treatment. He tells us predicting Atrial fibrillation and even LV function from the resting ECG is possible.
  6. Clonal hematopoiesis independent potential (CHIP) is a new risk factor by somatic mutations in leukocytes that accelerate atherosclerosis proven by canonical risk predicting models

    It was a great one hour to spend on a Sunday, under Covid Lockdown.  However, It was a surprise, the biggest Innovation in cardiology in the last century, PCI, and other exotic coronary and noncoronary interventions could not find a place in his one-hour lecture. I think there is a hidden message here. 

He signs off with some important advice for the generation next cardiologist.

Thanks, Methodist for bringing  this to us.

 

Here is a case report from Dr. Brugada’s group. What is your diagnosis?

Source & Courtesy Sergio Richter, Joseph Brugada et all , 100(1), 154–156. doi:10.1016/j.amjcard.2007.02.067

Whoever diagnosed AF in the above ECG need not feel bad. The rhythm is not AF, though it mimics very closely. In cardiology, especially in electrophysiology, we can get surprises on a daily basis. (Read below)

Why the ventricular rate is irregular in AF?

Atrial fibrillation (AF)  may sound like a  simple clinical arrhythmia until we ask this delicate question. The traditional and fairly accepted answer is that, AV node with all its collective decremental property filters the incoming atrial impulses (Which varies 400-600/mt) in a random fashion and allows only about 1/3rd of impulses. So, technically it is  AV block of various degrees that makes the ventricular response irregular.

Any other explanation possible?

How about AV node playing out a silent game with Atria, deciding to block everything and start its own fast escape rhythm, rather than leaking out selectively atrial impulses. Some think this is fictional, some others feel it can be real too. When this happens it can be referred to as irregular junctional tachycardia or AF with varying AV blocks. It has been tough, to prove it is only the atrial impulses penetrating through the AV node complex and exiting on the ventricular side unscathed?

Understanding AV node is not easy 

AV node morphology and function still remain a mystery.( Katritsis DG.  Arrhythm Electrophysiol Rev. 2020)The AV node shows huge variation in its size, shape, orientation with LV long axis and AV plane in short axis. The approach to slow pathways with multiple inferior nodal extensions makes a dual (or even poly ) AV pathway in any human being real. How common is dualism or multilateralism within the AV node in the general population? (More than 30-40 % ?) . Let us also mind the traffic in this busy & complex AV flyover can change on a moment-to-moment basis based on neurohormonal and autonomic tone.

Any tachycardia can become irregular if the AV node wishes so !

Though rare ,multiple physiological splits in the AV node make it possible for a single atrial impulse can generate 2 or 3, even more, ventricular impulses. (1: 2 or 3  AV conduction) Since these pathways are dynamic they can make the ventricular response irregular as well (Unlike the regularly coupled Echo beats in classical AVNRT substrate ). Hence, any supraventricular tachycardia can masquerade as AF if AV nodal pathways decide to split and share the impulses this way. It is also interesting to note there has been a documented link between AVNRT and AF (.Ref 2) . Also, adenosine-induced AF is known (James E. Ip et al Circulation: Arrhythmia and Electrophysiology. 2013;6:e34–e37)

Final message

Irregular RR interval with absent/or invisible P waves is not always AF. It can be due to the aberrant behavior of the AV node.( anatomical or functional) It is termed Pseudo Atrial fibrillation as in the above case report. Why do we need to be aware of this entity? We need to be cautious, as any overzealous efforts to ablate the pulmonary veins in such patients will go in vain.

Reference

1.Sergio Richter; Antonio Berruezo; Lluis Mont; Tim Boussy; Andrea Sarkozy; Pedro Brugada; Josep Brugada (2007). Pseudo–Atrial Fibrillation, Rare Manifestation of Multiple Anterograde Atrioventricular Nodal Pathways. , 100(1), 154–156. doi:10.1016/j.amjcard.2007.02.067 

2.Schernthaner C, Danmayr F, Strohmer B. Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias. Med Princ Pract. 2014;23(6):543-50. doi: 10.1159/000365418. Epub 2014 Sep 3. PMID: 25196716; PMCID: PMC5586929.