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Pardon ,this video is nothing to do with cardiology. It is from the archives of the United nations library .This can teach some important lessons in art of communication , sharing to all folks, especially medical students. It was recorded in 1959 in Newyork, UN head quarters.Four 17 year old school girls & boys were invited for a debate on a complex topic. Does God exist ? How do you pray ? and what is the purpose of different religions ?

I keep wondering , how these youngsters accumulated so much wisdom and express it in such a polite manner too. Mind you, this was recorded , when learning happened with out any digital aids.The word Internet was unheard off. No ego, no bluntness, no diatirbes that has become a norm in many debates now. I got a punching lesson from this clip, be gentle when taking extreme views in any topic.

I wish, every medical debate in class rooms should happen this way.The key to succesful debate is, to accumulate knowedge, willingness to question the convention, and respecting the oppositie point of view.

The highest point of talk show, (for me) was, when the Brazilian girl(due respects, she should be nearing 80 years now) tell us casually some things are not meant to be understood in life .I tell the same when some patients ask too many questions about their illness which may not have an answer.

Wishing every one of you an Enlightening New year. As we begin a new journey around the sun, yet another time, let us re-dedicate ourself, to use science, for the welfare of our planet & people.

Thank you , for visiting this site and make all its worth.

Just one memory of 2022, lingers ! Retired and left Madras medical college,Chennai after 3 decades, which grew me up as a Cardiologist.

 

 

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.

Postamble

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. 

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

This is an ECG of a 25-year-old, recorded in master health check-up. 

It was reported as ERS pattern of concern. When he went for an expert opinion, he was suggested to understand, there is a small risk of SCD. That’s it, the panic has set in already, which got amplified in the following conversation..

How small is the risk,?  he wanted to know.

Yours’ is possibly an intermediate risk.

Intermediate means what?  Do I have any genetic or EP studies to predict the risk accurately?

Sorry, we have some gene mapping but all primitive. We aren’t sure. But keep calm, nothing will happen.

Do I need to screen my parents ?

No, but if you are anxious you may take an ECG for them 

If they also show the same pattern, it becomes more significant, is it not doctor?

Hmm yes, maybe.

This is a brief story of this young man, whose life was made miserable by the apparently widening knowledge base of cardiologists

ERS: A brief opinionated review

The term early repolarisation in ECG is used for more than half a century. It’s about the behavior of the Ito channel, at the left shoulder of the action potential, when phase 0 hands over the baton to 1, at the onset of repolarisation. The problem is the rapidity with which K+ exit from the cell, which is heavily influenced by genetic control. Not only that, the ratio of epi vs endocardial density of these Ito channels determines, the timing, magnitude, and shape, of the J point.

 It would be mind-boggling to know the prevalence of such ERS patterns in the general population. One estimate suggests it could be anywhere between 3 to 13  % depending upon the criteria used. Let us assume the mean as 5 %. Then, it would be 30 crores of human beings in our habitat show this ECG pattern. If applied, in my city Chennai alone 5 lakh people could carry this tag.

While it is true, some forms of ERS and J wave syndrome can be markers of serious ventricular arrhythmias, either spontaneous or at times of Ischemia. Currently, It has become a fad, in cardiology academic circles*, to propagate the idea that ERS is no longer a benign condition. This is not acceptable at any degree of cognition. This happened mainly after few studies in powerful journals created some alarmist views. (*Maybe there is a bit of truth there. I still have doubts about whether we interpreted the Michel Haïssaguerre  study properly)

Final message

ERS is a widely prevalent normal ECG variation with a minuscule risk. High-risk subsets need to be screened only if the J waves encroach and spill dangerously into the ST segment as well. Of course, this pattern is of serious concern if there is a family history of young SCDs has occurred.

The purpose of scientific knowledge in medicine is to reduce suffering. I wish, at no point in time, it can increase anxiety. We need to introspect, whether to report such ECG entities at all. In the name of patient empowerment,  let us not create Iatrogenic, knowledge-induced panic. Labeling a person with a fearful entity and then keep reassuring and asking him to forget, is not a fun exercise. Meanwhile, indiscriminate reporting of such mass ECG phenomena can potentially turn out to be a cunning commercial game.

For advanced readers: Important queries for fellows

  1. Why Inferior lead ERS is more risk prone than lateral?
  2. What happens to ERS pattern during exercise?
  3. What is the genetic and structural overlap between ERS and Brugada? 
  4. If ERS develops unstable angina will the ST elevate or normalize or depress?
  5. How will be the RVOT and RV wall motion in ERS?

Reference

Here is a good review of this topic by

1.Dr. KK Sethi et al.Indian Heart Journal. 2014

2. Hanboly NH. Haissaguerre syndrome: The gray area still exists. Nig J Cardiol 2017;14:59-64.

 

The main reason for all those jitters, we cardiologists, get every time we puncture the IAS is not due to a lack of expertise and experience perse. There are two more reasons. First and foremost, it is still largely a blind* procedure. (Even in this era, where drones with HD vision shoot one-meter targets from a 1000 KM range )  *TEE and ICE are there, but they rarely give enough confidence. 

The second reason is more important and is rectifiable. It is the perception error in our anatomical cognition, that is fed to us from first-year medical school. We are made to believe (at least to people like me ) The right atrium is aligned like a perfect box on the right side, sharing a wall called IAS, and the left atrium is obediently placed left of the right atrium. Please realize the heart is such a complex twisted single tubular organ, the venous end, in a stunning backward loop brings the LA  most superior and posterior to the right atrium overriding the left-right relationship.) 

The right atrial terrain and IAS with multiple bumps and holes. Note the true IAS constitutes only 20% . This is where our punctures need to be.

Development of IAS 

IAS development and the number of layers it sandwiches, the tortuous tracts of PFOs, the fossas, and its variable limbus is a big topic. Further, It is worth recalling, the true IAS hardly forms 20 % of the area of the interatrial contact surface.

(the differential regression of sinus venous,  along with infolding of the roof and along with curious septum spurium , the ubiquitous septum secundum make the texture, area & shape of IAS, a fascinating creation, though troublesome for the cardiologists ! ) Whoever named that part of vanishing  IAS  as spurious, (I think it is Henrry Grey ) has much fore-vision.

 

Forget about all this. Tell me how to cross this difficult terrain 

Coming to the real world of interventions,  we need to do targeted punctures in different spots of IAS in various interventions.(Mitra clips, LAA device, PTMC, PV abaltions, Mitral paravalvular leaks , TMVR etc) This has made this task even more tricky. Experts are always there to help us out. Like swimming, it can never be learned in books.

This 19-minute clip from. Seoul, South Korea is an excellent resource. Thanks to  Dr. Sang Weon Park 

 

Along with sound anatomical knowledge, improved hardware, and imaging like deflectable sheaths, TEEs, and ICE (intracardiac echo ), let us hope, it will soon become an easier task for everyone.

Final message

 Understanding “attitudinal cardiac anatomy” with fluoroscopic overlay is the key. Again, it needs to be stressed, “Right is not right, and left is not left” when it comes to true atrial geo position. LA is equally posterior, superior, and of course to the left of RA. Some of my colleagues are blessed with a special 3-dimensional skillset  (Inherited ?) I failed miserably to understand this, till very late. I am sure, Dr. Park’s video will help all our youngsters to cross the difficult gateway to the left side of the heart. 

Reference 

One more good read

B. O’Brien et al. / International Journal of Cardiology 233 (2017) 12–22

 

Fibrillation is a continuous, chaotic muscular activity. In AF, atrial muscle is expected to lose all coordinated contractions with fibrillatory waves replacing P waves. Have you ever spotted a suspicious  P wave in a strip of otherwise explicit AF?  If not, this write-up is not for you.

An evolving rare theme in Atrial fibrillation 

Have a look at this ECG 

Here is an ECG, that was reported as AF, multiple APDs, or Possible AF, Pre AF. I suggested the term AF in transition. While few agreed, many said it is a straightforward SR with APDs, making it appear irregular RR. 

But, the fact of the matter is, ECGs are insensitive to pick all fibrillatory wavelets. It can selectively pick a few coarse F waves and make them appear as P. I think, in this era, we should not diagnose AF by proxy, ie absent P waves. Rather, we need to look actively for fibrillatory wavelets. (Imagine all sinus arrests will qualify for f fine AF with a slow ventricular rate  is it not ?)

The semantics of AF nomenclature is long. Intermittent AF, and paroxysmal AF, are well-known entities. It is now clear, AF can occur for a few seconds and vanish too. It seems we need to play some more linguistics with the most common cardiac arrhythmia. (Non-sustained AF,  evanescent AF, etc )

Some thoughts on this hide &  seek P waves 

  • Apart from the conventional list of absent P waves, one more example is repetitive APD can stun the atrial muscle for a few moments or minutes.
  • Then, we always have the issue( eluded to earlier) of sinus node paralysis, with irregular junctional escape mimicking AF.
  • Amiodarone can reduce fibrillatory rate, and (AF cycle length ?) Coarse F waves slow and stabilize it to mimic an organized P wave
  • P on Ta waves (Like R on T ) can trigger a nonsustained AF for a few moments in a functional manner without real pathology in atria.

 

A funny memory  brings back an EP truth 

During our student days, my Professor used to trap us with this question, Which atria would fibrillate in mitral stenosis?  Many of us blinked, and few had no hesitation to say, it is the LA that fibrillates. Now, after 50 years we realize, how fascinating the secrets AF has unfolded. Some organized activities are often in the right atrium, even as LA begins the process of AF. It is possible it may take variable time for the left atrial chaos to spill over to RA*. During these electrical uncertain times, some of the right atrial P wave activity refuses to die down.  Even more dramatic one Atrium alone can permanently fibrillate and others completely insulated by blocking the signal in the Interatrial pathways. (Ref 1 ) Ndrepepa’s paper in the JCE 2000)

Final message.

True scientists rarely bother about questioning a dictum. The concept of non-uniform AF was first thought of by (Schrmp et al Ref 2) 100 years ago in 1920, and Zipes(Ref 3) hypothesized this in 1973. now, in the Year 2000, Ndrepepa confirmed it with EP studies. The spotting of occasional  P waves is not forbidden in AF if the contralateral atria decide to block the incoming AF signals and keep generating their own P waves 

Young EP guys, now that you are equipped with the sophisticated intracardiac GPS,  please pursue this provocation in AF. One more piece of evidence we observed in the echo lab. Try to look at Tricuspid doppler A velocity waves in full-blown AF patients. You can see the surprise for yourself. This is very good research work to do. This is one of the ideas I gave to my fellows at MMC. Now, it is free for all to pursue whoever wants to do this. The clinical implication* will follow.

* A lingering query, how common is RAA clot in mitral stenosis with AF and the possible threat of pulmonary embolism?

Reference

1,Ndrepepa G, Zrenner B, Schreieck J, Karch MR, Schneider MA, Schömig A, Schmitt C. Left atrial fibrillation with regular right atrial activation and a single left-to-right electrical interatrial connection: multisite mapping of dissimilar atrial rhythms. J Cardiovasc Electrophysiol. 2000 May;11(5):587-92

2.Zipes DP. DeJoseph RL: Dissimilar atrial rhythms in man and dog. AmJCardioi I973;32:6l8-628.

3.Schrumpf P: De 1’interference de deux rythmes sinusaux. Preuve  du dualisme du nodule de Keilh. Arch Mai Qwur 1920;l3:168-173

Postamble

The snapshot from Ref 1 . The term Isolated AF confined to one atrium could be a rare event, but, no one can deny we have plenty to learn from them

 

LA dimension and volume have become vital parameters in recent times, especially, with the entity of HFpEF is becoming so common. LA not only acts as a live barometer, reflecting all that happens in LV, but it is also a chronic marker of LV diastolic function. (Funnily referred to as HBA1c of diastolic dysfunction) 

What is normal LA dimension & volume ? 

  • Normal left atrial diameter < 4.1 cm in men or < 3.9 cm in women
  • Normal left atrial volume indexed for body surface area (BSA) is 34 ml/m2 for both women and men 

Which part of the cardiac cycle do we measure? 

Ever since Wiggers introduced the overwhelming concept of LV systole and diastole, most of us ignored the fact that atria do have a separate contraction relaxation cycle, independent of what happens in the ventricle. Of course, atria and ventricles act as a single chamber in diastole. In reality, atria lack true boundaries when it acts as a conduit. The LA dimension varies considerably during the atrial cardiac cycle. Look at the  LA pressure-volume loop, which can frighten anyone, with its horizontally lying figure of 8 pattern. During every cardiac cycle, the volume reaches atleast two troughs and one peak.

Don’t get frightened with this graph, spend some time, and you will get it right, Begin at  “3” o clock position with the onset of diastole with a downsloping green loop, that continues as the red line of atrial contraction to end up in systole. The entire black loop, that happens during ventricular systole depicts the true reservoir function. with MV closed. ,

 

As of now, we have a consensus, LA volume is measured typically in LV end-systolic frame. ( Rather, we measure it at maximum LA volume ) However, we have 4 different LA  volumetric components to assess, as this article excellently depicts. (Hoit BD. Left atrial size and function: role in prognosis. J Am Coll Cardiol. 2014 Feb 18;63(6):493-505.)

What could be the limitations of the traditional end-systolic measurement?

No single measurement will give an overall LA function assessment. But still, Somehow, we have measured the maximum LA  volume as a reference of true diastolic function. This happens in LV end-systolic point where atria reach the maximum size. But, here is a catch, we assess the left atrial function before its main physiological function of emptying takes place.

How about assessing  LA efficiency after it completes its job, ie end diastole? 

In LV function end-systolic dimension has pride of place as it is devoid of influence from loading condition. If applying the same logic, the “end atrial” systolic dimension(Which is the same as LV end-diastolic point/or post A ) should be perfect. It can also help measure the residual LA volume after its systole.

A potential advantage of LV end-diastolic dimension (The Heart & Soul study )

Maybe, this is less affected in the presence of MR systolic jet will spuriously elevate LA volume. In AF also this parameter is less likely to be influenced by LA preload.

Final message

Suddenly, we are debating a fundamental Issue, ie timing of LA measurement. While the end-systolic size/volume is the current standard, the LA dimension in the end diastole also provides useful info. There are at least 4 different LA volumes, at different parts of the LA cycle that need to be studied for a proper understanding of diastology (Unlike LV which has only two).

Now, we may need to ponder, if there is a mean LA volume, measured with the 3D volumetric analysis or MRI, that could be representative of the global LA function. 

Reference

Thadani SR, Shaw RE, Fang Q, Whooley MA, Schiller NB. Left Atrial End-Diastolic Volume Index as a Predictor of Cardiovascular Outcomes: The Heart and Soul Study. Circ Cardiovasc Imaging. 2020 Apr;13(4):e009746. doi: 10.1161/CIRCIMAGING.119.009746. Epub 2020 Apr 20. PMID: 32306763; PMCID: PMC8846436.

 

Myocardial infarction, a gross pathological entity renamed now as STEMI for clinical purposes, continues to be the most famous medical emergency that triggers a series of calls, right from 911 to the ER, that eventually ends up in CCU or a 24/7 cath lab. The heart, can’t wait for all these external responses when it is challenged with a vascular accident. The moment ATO occurs, two things happen. The endogenous fibrinolytic led by native tissue PA (Tpa) tries to get rid of the thrombotic plug by all its means. It succeeds in 15%. We call it spontaneous lysis or aborted MI. Many lives are lost in the remaining before they reach the hospital..

Meanwhile, the immune high-command deputes scores of neutrophils to the ground zero Fig 1) to supervise what is happening and try to heal the injury. It is worth, understanding, that activated WBCs, sort of convert myocardial infarction from a vascular event to inflammatory pathology, as the hour progress.

 

Fig 1  Infarcted myocardium Invaded by neutrophils

 

 

What do these neutrophils do?  

It will be our ignorance, if we think, they simply crowd around the myocytes helplessly, that is hit by ischemia. They are sent with a specific purpose to protect and heal the myocardium. Very often it fails in its mission is a different story. These fighting neutrophils send a subtle signal  of their presence with a mild increase in temperature during ACS  ( Patel  Prognostic usefulness of white blood cell count and temperature in acute myocardial infarction  Am J Cardiol. 2005 Mar 1;95(5):614-8. )

Is neutrophil invasion good or bad for the myocardium?

These are pro-inflammatory cells. meant to promote healing and mitigate Injury. Interleukins and Leukotrienes do have a healing power as well. But, what happens, in reality, is, still a mystery. As of now, it is tempting to think, it does more damage than good. Its role changes over time. 

 Acute reperfusion Injury in Primary PCI 

Neutrophils are quiet obedient cells generally, but once activated, their behavior can’t be predicted. It may start attacking the host cells, We know reperfusion injury is real and poorly understood. Delayed reperfusion, is well known to cause myocyte softening and lysis. What we know for sure is, primary PCI, induced accelerated flushing of these angry neutrophils is definitely related to no flow, microvascular plugging, and cardiogenic shock.  (The fact that no-reflow and reperfusion injury is less of a problem in fibrinolysis  demands introspection)

Diagnostic & prognostic value of neutrophilia 

Neutrophilia is such a nonspecific response, faces ridicule for its clinical utility. But, In reality, it can be a worthy parameter, to time the age of the infarct (or even confirm* the ACS ) in otherwise equivocal clinical presentation.(Ref 2) More importantly, it provides prognostic information. One more potential use is Neutrophil count to guide the timing of surgery post-MI (as in VSR) A neutrophil count could help avoid the active phase of inflammation.

*I recall my surgical professor’s emphasis on leukocytosis to confirm acute appendicitis during the first clinical year. 

Final message 

There is no academic by-law, that forbids full-blown interventional cardiologists from having an affair with basic science. Unless the core science is irreversibly bonded to the bedside, we can never reap the true benefits of translational research. Hematological aspects in STEMI is one such underrated discipline. Also, we must encourage every postgraduate student in pathology/biochemistry/physiology to visit the CCUs or sit in the cath lab gallery more frequently. Watching the cardiology stalwarts plowing through the blocked coronary arteries, racing against time, is sure to kindle young minds, for a potential molecular breakthrough in cell survival and healing following myocardial hypoxia.

Reference

1.Ma Y. Role of Neutrophils in Cardiac Injury and Repair Following Myocardial Infarction. Cells. 2021 Jul 2;10(7):1676. doi: 10.3390/cells10071676. 

2. Thomson SP, Gibbons RJ, Smars PA, Suman VJ, Pierre RV, Santrach PJ, Jiang NS. Incremental value of the leukocyte differential and the rapid creatine kinase-MB isoenzyme for the early diagnosis of myocardial infarction. Annals of internal medicine. 1995;122:335–341. [PubMed] [Google Scholar]

3.. Cannon CP, McCabe CH, Wilcox RG, Bentley JH, Braunwald E. Association of white blood cell count with increased mortality in acute myocardial infarction and unstable angina pectoris. OPUS-TIMI 16 Investigators. Am J Cardiol. 2001;87:636–639. A610. [PubMed] [Google Scholar]

4. Bhatt DL, Chew DP, Lincoff AM, Simoons ML, Harrington RA, Ommen SR, Jia G, Topol EJ. Effect of revascularization on mortality associated with an elevated white blood cell count in acute coronary syndromes. Am J Cardiol. 2003;92:136–140. [PubMed] [Google Scholar]

 

Welcome back to the big molecular science of PCSK and its antagonist Evolocumab, a monoclonal antibody designed to target and prevent the LDL receptor catabolism inside the lysosomes. Evolocumab was approved by FDA for aggressive lowering of LDL, following a  customary study published in NEJM 2017, that released this double-edged anti-lipid molecule into the human domain with all fanfare.

It aimed to reduce the LDL as low as possible in selected patients with familial LDLemia & and those who don’t tolerate statins.  Now, a study was silently released in BMJ open, at the fag end of 2002, which is causing ripples in the pharma world in the new year.

In fact, this paper can’t be called a study. It looks more like an FIR. It questions the missing death counts, which were not included in the landmark trial, that led to its approval.  It took time for the news to sink into the world lipid community. 

Final message

I am surprised at the reactions to the reanalysis of FOURIER data. Any reasonably experienced cardiologist will agree, getting regulatory approval with manipulated data and analysis is more of a norm and not an exception (Ref 1). In a trillion-dollar pharma industry, do you think hiding deaths is a big crime? Is there a solution to this menace?  Yes, let us hope so, with movements like this one (Doshi P et all, Restoring invisible and abandoned trials: A call for people to publish the findings 

 

Counterpoint (Q&A)

Q  

Damn this post. Don’t blame a phenomenally successful scientific breakthrough that intercepts the immune destruction of LDL receptors. Instead of being cynical, try to come up with a scientific analysis of the FOURIER study. Please read this rebuttal from the TIMI group, https://www.tctmd.com/news/study-alleges-mortality-miscount-fourier-trial-timi-group-disagrees

 A 

I agree, let us not blame Evolocumab. It is an innocent and intelligent molecule. Culprits are elsewhere. It is a reserve drug in a highly selected population with refractory LDLemia.The lesson from the FOURIER  to all the clinical trialists is, when credibility is lost every thing is lost, even truths can become a casualty. We have to live with that. 

Reference

Marcia Angell,the former NEJM editor’s  book

 

Management of recurrent ventricular tachycardia has developed a lot in recent times. Anti-arrhythmic drugs(AADs) were a cornerstone for most recurrent and refractory VTs till recently. Surgeries including CABG,  repair of the aneurysm, and subendocardial resection has helped to control many post-MI ischemic VTs. Soon they became obsolete. Realistically, PCIs had little impact on post-MI VT for some unknown reasons. However, with the advent of ICDs and RF, ablation, a new dimension is added to this field. 

ICDs, though an attractive device, don’t prevent a VT but vow to nullify the consequence of VT. This is problematic. ICDs in spite of their ability to prevent SCD effectively, it has little say in preventing non-sudden deaths of in any form of cardiomyopathy. (In fact, there is some evidence ICDs might increase myocardial damage with inappropriate shocks )

Hence, RF ablation can be called as true curative therapy by extinguishing hot spots of VT genesis. Still, we need to understand ablation is technically creating new dead myocardium (in alreadly  damaged myocardium) and hence, can’t avoid a consequence. More importantly, ablation as a modality is technically more demanding. We have accumulated huge experience with the help of electro-anatomic imaging and cutting-edge hardware in the last few decades. Still, we find it difficult to zero in the target area of RF ablation, with all available techniques of mapping (Activation, substrate, entrainment, and pace mapping) The reason is,  VT circuits can be really complex ones. Not only different loops but also it can travel deep into the myocardium (Intramural or epicardial) making a single approach endocardial often futile. Success rates vary between 60 -70% (Some may claim 90 +)

This post wants the young fellows to take on this fundamental issue and learn in-depth about the arrhythmia circuit.(Get Inspired by Dr. Samuvel Asirwatham of Mayo clinic work )

What is the best site to ablate ventricular tachycardia?

  1. Exit point 
  2. Central isthmus
  3. Entrance 
  4. Inner loop
  5. Outer loop
  • Though logic would tell us we can intercept an arrhythmia by ablating anywhere in the circuit. But the issue here is we need to permanently ablate it. not just interrupting. 
  • The best site to ablate is the exit point or entry point. Maybe isthmus. I am not really sure. But, one thing is clear, the outer and inner loops are not important. Further, live tissues are the culprits and not the scars and infarcted zones. 
  • One more possible answer is to try to ablate all (or maximum) points in the circuits.

How to identify entry points and exit points?

Not a simple answer .EPs apply their life experience to do that, assisted by technology. Not everyone who has a Carto -GPS can do that.

One simple answer for the fellows is, in entrainment mapping,  critical sites can be somewhat arbitrarily labeled as exit, central isthmus, or entrance on the basis of the Stimulus-QRS interval relationship to the TCL. Exit sites will show an S-QRS interval < 30% TCL (QRS onset shortly after pacing), central isthmuses will show an S-QRS interval of 30% to 50% TCL (some delay in QRS onset after pacing), and entrance sites will show an S-QRS interval of 50% to 70% TCL 

Ruairidh Martin et all Circulation: Arrhythmia and Electrophysiology. 2018;11:e006569

Final message 

Key to the successful ablation of VT is the accuracy in choosing the target site. Locating the target is meaningless if we can’t reach that site. Reaching the site is again futile unless we are able to deliver adequate burning or icing with sufficient contact.

Meanwhile, AADs can never be ignored in spite of the apparent side effects, for the simple reason they reach the VT circuits without any fuss. The Pharma industry has almost lost its interest in AAD research and the hyper-talented EP guys are squarely responsible for this unintended consequence.

Future directions

RF energy modification and newer catheter designs will help. While cryoablation shows a promising advantage over RF, it is still to prove its sustained efficiency. Meanwhile, other ablation modes are being tried. Transvascular ethanol ablation and stereotactic radio ablation have both shown promise for arrhythmias that fail other ablation strategies.

Some more questions

  • What is the difference between arrhythmia focus of origin and entry point? 
  • Once the VT is set in, what is the relevance of its origin? 

Reference

One of the very good reviews on the topic.

1.Gustavo S. Guandalini, Jackson J. Liang, Francis E. Marchlinski, Ventricular Tachycardia Ablation: Past, Present, and Future Perspectives,
JACC: Clinical Electrophysiology, Volume 5, Issue 12, 2019, 1363-1383,
2;,W.G. Stevenson, H. Khan, P. Sager, et al.  Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction Circulation, 88 (1993), pp. 1647-1670










3.M.E. Josephson, L.N. Horowitz, H.L. Waxman, et al.Sustained ventricular tachycardia: role of the 12-lead electrocardiogram in localizing site of origin Circulation, 64 (1981), pp. 257-272

The term Ischemic heart disease (IHD) was once very popular, but many abandoned it as it became an academic cliche.  CAD & CAHD are the other terms that are equally popular and prevalent. Stable IHD was in vogue till recently, which was again replaced by “chronic coronary syndrome’ now. Honestly, I feel the original term IHD to be restored however outdated it may look. it encompasses the entire spectrum of clinical cardiac disorders.

Manifestation of Ischemia heart disease 

  1. Angina
  2. Infarction
  3. Cardiac failure
  4. Arrhythmias 
  5. Silent ischemia
  6. Sudden cardiac death

 The purpose of this post is to share some thoughts on the link between Ischemia and cardiac arrhythmia. 

 

 

What is the relation between  Ischemia and cardiac arrhythmia (especially VT)

A.Strong relation

B.Weak relation 

C.No relation 

D. Recurrent ischemia protects against arrhythmia.

The fact that. acute Ischemia triggers primary VT and VF and is the leading cause of electrical death is sufficient to fix the answer without any doubt. But, the  truth is, the link between Ischemia and cardiac arrhythmia is more complex  

If we could agree ischemia is a powerful trigger of ventricular arrhythmia, will every patient with chronic stable angina be at risk of  VT after walking a certain distance?  

So, where does cardiac arrhythmia fall in the Ischemic cascade of events? the fact that chronic ischemia on exertion rarely precipitates an arrhythmia conveys a strong hidden message. 

Coming back to, STEMI where the arrhythmic risk is powerful, still, if the same acute ischemia, presents as UA/NSTEMI, with severe compromise of resting blood flow, it doesn’t trigger a VT usually. This fact should baffle us and question why even acute ischemia carries low arrhythmic risk except when it happens with STEMI.

The potential mechanisms of lack of VT in UA* (No evidence /Class C evidence) 

  • In UA, ischemia is primarily subendocardial, and the neuronal innervation which is more in the epicardial plexus fails to get stimulated. This is in contrast to what happens in STEMI. Here It is transmural ischemia and the sub-epicardial is always involved.
  • In this context, the high prevalence of VT in Prinzmeal angina where there is subepicardial injury is a point to be noted. In young NSTEMI/STEMI crossover entities like Wallens and De-winters, there is a high adrenergic drive, which triggers the VT rather than ischemia per-se.
  • Finally, even in STEMI, only a minority of 15-20 % of myocardium become arrhythmogenic and face fatal complications. What protects the rest of the 75 %? is genetics, epigenetics, or fate.? 

The practical implication of this question

  1. The VT in ischemic cardiomyopathy is related more, to the scar burden, strategically placed islands of dead and live tissues, and the overall severity of LV dysfunction. This makes the Ischemic VT, as a term,  could be a misnomer.  In fact, it is the viable ischemic tissue that is a powerful trigger.
  2. If baseline chronic ischemia is less likely to trigger any VT, revascularisation in chronic CAD (PCI/CABG) is unlikely to give relief from it as well.

Anti-arrhythmic adaptation in chronic Ischemia 

We know about ischemic preconditioning and angina relief. It may apply to arrhythmic preconditions as well. Recurrent ischemia, while we expect to elevate the arrhythmic risk, it is a curious and exciting possibility it might work as an “anti-arrhythmia vaccination” at the molecular level. 

Final message 

So, what is the true relation between ischemia and cardiac arrhythmia?  

It is not as strong as one would believe it to be( Except in the early hours of STEMI and a very small subset of NSTEMI.

Curiously, in certain lucky beings, recurrent baseline ischemia may protect against future arrhythmias.

Reference 

1.A V Ghuran, A J Camm, Ischaemic heart disease presenting as arrhythmias, British Medical Bulletin, Volume 59, Issue 1, October 2001, Pages 193–210, https://doi.org/10.1093/bmb/59.1.193

2.Janse MJ, Wit AL. Electrophysiological mechanisms of ventricular arrhythmias resulting from myocardial ischemia and infarction. Physiol Rev 1989:  69 ; 1049 –169

Few more questions worth pondering 

Why do certain VTs struggle to become sustained?

Will discuss this later (Will need to talk about the diameter of the primary Rotor, the Curvature of rotors and source-sink mismatch, etc. )

How often  Ischemia triggers AF?

I haven’t heard of Ischemic SVT, or ischemic AF much. Trying to accumulate more Info on this.