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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

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.

Up to 25 % of LV filling is done by atrial contraction. Atrial booster function is important in LV outflow lesions. This can be critical in patients who have diastolic deformities of LV. ( an audible or even palpable S4 confirms the atrial kick in these situations )  This is how we were taught for decades right. Still, it may hold good in many left-sided condtions, but in HCM it definitely seems to be not true. 

A succinct review of this topic makes a good read.

Incidence if AF in HCM is about 20% (Mostly paroxysmal 70 % , Persistent /Permanent 30 %)

Mechanism of AF IN HCM

  • Increased atrial wall strain(Proven by strain echo studies)
  • Atrial dilatation
  • Atrial pathology (Atrial myocyte  disarray,  myosin is present in atria too. )
  • Unrelated to HCM (SHT etc)

We can confirm with large observatory data, left ventricle handles AF so well. (Ref 1)The onset of AF, (at the least), is, expected to cause some new worsening dyspnea. Even that is not universal (very surprising isn’t it ?)

Does AF correlate with syncope?  again no is the answer. So it’s the LV outflow behavior that determines the hemodynamics not what is happening at the inflow. Even hard outcomes like heart failure, sudden death, net mortality was not found to be altered much by the lesser chamber fibrillation. But, the only issue relevant here is thromboembolism that has to be taken care of.

How is that AF make little hemodynamic Impact in HCM ?

It is difficult to comprehend this scenario. For this to happen the mean LA pressure should remain within the physiological range even when the atria goes to fibrillation. But it seems distinctly possible as many patients with HCM are not aware of this arrhythmia. The LA pressure-volume loop is an enigma. It is likely LA “v” wave loop can adjust to “a” wave deficiency in an exemplary manner.

Further, the hyper-contractile left ventricle can assist itself by sucking blood in very late diastole (to be precise with the onset of systole )and so it need not really depend on the atrial kick.  A similar phenomenon explains the persistence of presystolic accentuation in the murmur of mitral stenosis. The fact that rate control in AF is able to compete with rhythm control in  AFFIRM/RACE study vouch for the negligible hemodynamic impact between SR/AF.

Clinical implication

  • A well-tolerated AF doesn’t preclude the need for thromboprophylaxis. We must ensure  NOAC/Warfarin in all those with persistent AF.
  • Attempts to convert AF to sinus rhythm with all those Invasive LA mapping and Pulmonary vein is unwarranted if not contraindicated.
  • When ICD is indicated additional  Atrial leads to reduce AF is again becomes reductant. 

Final message

Many of the hemodynamic concepts we have learned over the years could be based on logical perceptions that may not manifest at the bedside. Constant flux in our understanding of cardiovascular physiology is required. 

Reference

1.Rowin EJ, Hausvater A, Link MS, Abt P, Gionfriddo W, Wang W, Rastegar H, Estes NAM, Maron MS, Maron BJ. Clinical profile and consequences of atrial fibrillation in hypertrophic cardiomyopathy.Circulation2017136:2420–2436. 

 

The branching pattern of the human cardio-vascular tree is as unique as one’s fingerprint. One such hugely variable anatomy is the SA nodal blood supply.

Certain salient features

  • Variation can be seen in origin, course, and termination.
  • Now it is estimated to arise from RCA in 70% (Moved up from 55% in old studies )
  • From LCX (25%)
  • Dual SA node supply(5%)
  • Direct from Aorta

It is heartening to find this good anatomical review on this topic.

A) From the Right Coronary Artery; (B) From the Left Circumflex Artery (proximal); (C) From the Left Circumflex Artery (distal); (D) From the Left Coronary Artery; (E) From the Aorta; (F) Dual origin from the Right Coronary Artery and the Left Circumflex Artery. Image source : Vikse J, PLoS ONE 11(2): e0148331

Implication for the surgeon

The whereabouts of this tiny, yet important artery is critical to the surgeons’ as they incise and explore the atrial roof. (A gateway, that gives access to so many cardiac surgeries) The SA nodal artery mostly goes retro caval but it can be peri-caval or even anterior to SVC.

This image shows (a,b,c) the course in relation to SVC, Developmentally as the venous pole go posteriorly to fix the SA artery behind it.Image source : Vikse J, PLoS ONE 11(2): e0148331

For the Interventional cardiologist

A rare but distinct mechanical compression of SA node artery is reported with large ASD closure device. The plane of compression is usually occurring in the superior aspect of IAS when the SA node artery cross over the RA to reach the SA node. Should be suspected whenever unusual bradycardia occurs during the manipulation of the device or just after deployment. Always mind the delicate gap  between the antero superior rim and disc where SA nodal artery is likely to trespass.

AV node Ischemia with ASD device

With precise imaging modalities, new secrets are emerging. Additional AV node arteries from proximal RCA is documented.This is a surprising learning point for us. This artery is referred to as the right superior descending artery, which provides an alternative blood supply to the AV node from the proximal right coronary artery. The transient compromise of this hitherto unknown AV nodal twigs by the ASD device cause AV blocks. With this new info, we also got an answer to one more lingering question, why would disproportionate bradycardias are observed in inferior MI even when distal RCA is flowing well. We can’t blame high vagal tone always.

SA node compression by ASD device amplatzer

A CT angiogram showing how the ASD device encroaches the SA node artery. Image Source:Tsunehisa Yamamoto JACC 2016 (Linkedbelow)

The original article has an excellent video clipping of how an ASD device hugs the SA node at the superior edge of ASD.

Final message

Human anatomy is not the subject meant to be read in the first-year medical school cadavers, & forget thereafter. Surprisingly. the field of anatomy is also evolving with new mysteries exposed by modern imaging.SA nodal arterial blood supply is one such interesting aspect of cardiac anatomy. Young fellows in cardiology shall pursue further anatomical dark spaces in the heart (One such topic is how cardiac lymphatics compete with the venous system in draining cardiac interstitium)

Reference

Vikse J, Henry BM, Roy J, RamakrishnanPK, Hsieh WC, Walocha JA, et al. (2016) AnatomicalVariations in the Sinoatrial Nodal Artery: A Meta-Analysis and Clinical Considerations. PLoS ONE 11(2): e0148331

It’s gratifying a unique and committed group exclusively doing research in Anatomy. It Department of Anatomy, Jagiellonian University Medical College, Krakow Poland.

http://www.eba.cm.uj.edu.pl/

Corona has triggered the scare of the century, even among the scientifically savvy brave men & women. The scale of the panic was unprecedented. However, one positive outcome of this pandemic was, this 20 nm RNA particle forced many of us, to ponder over the true purpose of life. It demanded a course correction in those who found one. Now, after 9 months Corona, in its second wave seems to be somewhat kind to humanity. The case fatality rate is dropping to nearly one-tenth of its peak in the first wave. 

 

 

 

 

Where is the evidence coming from?

Apart from our own personal experience from 1500 bedded corona hospital, this paper reports data from 53 countries.

 

Note, the red covid mortality curves are not matching the black positive waves (Both Europe and Asia)

Link to the original article https://doi.org/10.1111/tbed.13819

The possible reasons for the low case fatality rate.(Personal observation)

  1. Viral apologetic  behavior*
  2. Second wave affecting more healthy younger who fight it better.
  3. Less panic in the health care delivery system
  4. Though there is no specific therapy, at least some basic treatment strategies are in place.(Timely steroids & mindful oxygen did the trick)
  5. Initial aggression out of Ignorance (ie ventilator deaths) has largely ceased.
  6.  RT-PCR(which helped In diagnosing /isolating ), CT scans,(helped in grading) the Remdesvirs(gave peace of mind ) the Tocilizumab(did nothing great ) has at best played a minuscule role at a huge cost.

Among all these factors, which do you think is the most important contributor to a declining fatality?

The single important factor could be, “The virus has decided unilaterally to forgive the frightened human beings, and become less virile“.(At least in those people who sincerely respected the viral might by wearing masks and other paraphernalia) Sorry, for uttering this forbidden stuff in science, still it could well be the truth. 

If corona is losing its sting & steam what would be the realistic role of the vaccine? What is the likelihood of vaccine getting false credit*?If we are allowed to be optimistic, Corona in all likelihood is waiting to say goodbye after a feeble third or fourth wave. All these are speculative, still, one thing looks positive. Unlike the much-quoted fact about the Spanish flu of 1920, which resulted in more damage in the second wave, which is unlikely to happen with corona.

Disclaimer

* This article never intends to undermine the importance of preventive measures and vaccines for this worst pandemic in recent human history.

Counterpoint 

The decline in case fatality is may not be uniform as fresh data from Europe suggest. It’s hyperbole to expect corona’s second wave to bring good news. It is largely left to the people’s behavior to contain the pandemic than to get a pardon from the virus. 

 

 

 

 

 

How many times you have treated cardiac arrhythmia in both emergency & non-emergency situations?

Infinite times.

How many times did you really bother to know the mechanism of a given arrhythmia before ordering medication or shocking?

Hmm,.. let me think. (Except for AVNRT/ AVRT, and few VTs, very rarely I have worried about the mechanism  !)

Why is it so? because treatment takes priority and we are able to tame the arrhythmia even without knowing the real mechanism.

The following slide is a gross summary of the cardiac arrhythmia mechanism

Understanding cardiac arrhythmia is vitally important for a few reasons in a few settings.

  • In acute settings, we need to know automatic tachycardias will not respond to shocks. Reentry tachycardias will respond more promptly. (Of course, we may not know it till we shock ) Calcium blockers like verapamil might block triggered activity in MAT. Overdrive pacing is the answer for many automatic tachycardias and some refractory reentrant tachycardias (ATP protocols in ICD has taught us this ) 
  • In the chronic setting when you contemplate mapping, locating, and ablating arrhythmias, mechanisms are important. The task here is locating slow conduction paths and decoding the diastolic circuit around the scar  (If you plan ICD, knowledge about mechanism  becomes redundant again)

  • Finally, knowing the mechanism of arrhythmia is a fascination by itself to help understand the great subject called cardiac electrophysiology, where 100s of ion channels work nonstop drawing the action potential on a moment to moment basis sustaining our life.

A challenge

Can you localize a VT and find the mechanism in a patient who is Ischemic /hypoxic and acidotic? You can never do it. Please note, most polymorphic VTs can’t be localized. The mechanism is either automaticity, trigger activity, or even micro-reentry. You need to shock and look for the causes.(Link to How does the treatment of monomorphic VT differ from Polymorphic VT? )

Final message

Should we need to know about the mechanism of arrhythmia we treat?  Definitely yes, if you have that passion to know the truth, or else just order Amiodarone or shock and check out of CCU. (Of course, we have a very good option of calling EP consult the next day.)

 A review article on mechannism of cardiac arrhymias

Rev Esp Cardiol. 2012;65(2):174–185

 Aorta probably is the most critical structure in the entire circulatory system. (apart from the heart of course !) It is a 1.5 to 2.5 mm thick tube, with a diameter of 2.5 cm/length of 30 -35 cm from the aortic valve to the iliac bifurcation.(Eric Borsero 2011) It handles about 7500 liters of blood every day. Understanding the Aortic pathology has vastly improved at the molecular level with deep gene sequencing that defines fibrillin phenotypes.  Meanwhile, CT ,  4D MRI and 3D prototyping have landed us in a new era where we can feel the exact models of a patient’s virtual aAorta for monitoring and treatment purposes.

 

While acute Aortic syndromes is the one that bothers us most, even chronic aortic enlargements are equally risky as at any time it can become acute. Though the risk of aneurysm and rupture is related to the histology and molecular disruption at the level of aortic media, we can only rely easily on is its dimension. Traditionally we bother about the diameter since it is the aortic radius that Influences the stress through to Laplace law.(Wall stress equals twice the radius /Thickness of wall)

Click over the Image for ESC Aortic disease guidelines

The annulus is the narrowest part, it gains about 50% width (10mm) at the level of the sinus of Valsalva to reach about a maximum of 35 mm and again narrows at ST to a junction (almost to the same diameter of the annulus) It continues further as ascending, arch and descending aortas with gradual tapering. 

Risk of rupture

Are you aware aorta keeps growing with age?

Unlike many other organs, growth of which gets arrested by adulthood, aorta appears to grow well into middle and elderly age.The aorta grows by 6cm in total length between age 20 to 80 (Ref 1)   The average growth of the ascending aorta is .18mm /year

This fact was reported 70 years ago Dotters famous study Circulation 1950  https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.2.6.915

I used to wonder in many elderly why chest x-ray shows wide superior mediastinum still echocardiogram didn’t show any dilatation.This we call it as aortic unfolding. The term unfolding of aorta may represent the elongation of both ascending and descending aorta. The mechanism is due to multiple factors, like lax ligamentous of aortic attachment, dilatation, and longitudinal elongation.

Unfolding of the aorta . (How to measure unfolding Lee JW, (2014) Aortic Unfolding Determined Using Non-Contrast Cardiac Computed Tomography: Correlations with Age and Coronary Artery Calcium Score. PLoS ONE 9(4): e95887. )

How Important is the length of the aorta?

Risk of Aortic aneurysm is usually attributable to the diameter (Accepted normal 2.1cm/m2) . However, in IRAD registry, 50 % of aortic dissection happened in aortas less than 5 cm. So there is something more than the diameter that confers the risk of an aortic event. Is it the length and elongation?  After years of observation, we now realize it is indeed true. It is a surprise we didn’t realize  elongation of aorta also confers the same aortic wall weakness like that of Increased diameter (Longitudinal deformation/Stretch )

How to measure the length of Aorta?

It is best measured by CT scan or MRI. There is a new parameter called  Wu Index, which is based on both length and width of the aorta , which predicts the risk of aortic event. 

 

 

Jinlin Wu, Mohammad  Zafar, Yupeng Li,  J Am Coll Cardiol. 2019 Oct, 74 (15) 1883-1894.

Final message 

Aneurysm of the aorta is traditionally defined based on the degree of dilatation. It’s time, Aortic length should also be included in defining aortic aneurysm. We need to monitor it periodically as well in the population at risk. 

Reference 

1.Adriaans BP, Heuts S, Gerretsen S, et al. Aortic elongation part I: the normal aortic aging process. Heart 2018;104:1772–7.

 
The comprehensive reference 


Today is one of the most auspicious days in Indian traditional festive time. Saraswathi pooja, a celebration of the Goddess of knowledge and education. I would like to share one of the all-time great quotes on learning from Thiruvalluvar a sage poet who lived in the southern Indian state of (mine), Tamil Nadu in 4th -5th century BC  2500 years ago.

 This Thirukural number 391 in the chapter of education goes on like this. (In the Tamil Language)

In English

Karka, Kasadara, Karpavai , Katrapin,

Nirka , Atharkku Thaga !

It says

Karka : Learn

Kasadara: Here comes the punch. Kasadara means pure.  He says simple learning is not at all-sufficient. One has to learn from good sources, learn deep that should be devoid of errors, contaminations, and falsehoods.

Karpavai  : Thus you learn all lessons in life meticulously.

Katrapin:  So, after this hard and enlightened learning, what we should do?  He answers next.

Nirka Atharkku Thaga: This means , don’t just stop with learning, follow it with action in a righteous way. Unless we do that he warns to conclude ( in another poem in the same chapter) there is no purpose of learning itself and we are again at risk of becoming illiterates.

So, what does this Thirukural teach the Nobel professionals who follow cutting edge medical research?

I think I need not elaborate . . . Acquiring knowledge and true learning has become two different processes.

It’s just a sample of one kural (Quote) among 1330 poetic quotes written in 133 chapters by this great philosopher of Tamil Nadu who shared the same timeline with Aristotle and Socrates of ancient Greece 5000 miles west of India. For those ,If you are interested in his monumental work on literature which can be referred to as the manual for effective living  (I wish to call it as “Standard operating protocol”  for human life)  please follow the link.

It appears,antiplatelet agents are waging a turf war on the CAD battlefield. It is no secret either, the fight often goes beyond academic reasons. Though NSTEMI connotes a true cardiac emergency, it consists of a highly heterogeneous population. A patient with UA can be treated even at home (Low-grade angina with little ECG changes, when it’s due to Increase demand situation). While, in the other extreme of NSTEMI, a patient with a GRACE score >200, in Ischemic  LVF, might need an emergency multivessel angioplasty along with Mitra clip ±  ECMO support. 

Antiplatelet agents along with heparin will remain the cornerstone* in the management of NSTEMI/NSTEACS, irrespective of our fine catheter skills within index lesion. They are administered right from the pre-hospital phase/ In ER, CCU/ or on way to the cath lab(upstream)/or within the cath lab/or after CAG /PCI.  It is the right balance between the prevention of stent-related coronary thrombus vs systemic bleed we are worried about. Definitely, DAPT is warranted. (See the chart below) Prasugrel has been reinvented as the most powerful P2/Y12 blocking antiplatelet agent. It squarely beats its other colleague drugs like Aspirin, Clopidogrel, and Ticagrelor in terms of potency as well as its risk of a bleed. This is the current antiplatelet protocol in NSTEMI in a patient planned for PCI after visualizing the coronary anatomy. Note, Aspirin plus Prasugrel combination occupies the top slot among various options. The principle of DAPT strategy is all about Initial escalation to match the heightened risk of thrombosis/ cardiac events and later de-escalate once the risk period is over (Which can vary between 1 month to 12 months or even 2 years)* The popular concept of attributing NSTEMI to platelet clot and STEMI to fibrin clot is no longer valid. The contribution of the individual component(white vs red)  in a given load of coronary thrombus was never quantified accurately. That’s why antiplatelet agents alone are grossly inadequate in NSTEMI. This will be vouched by this NSTEMI algorithm, which begins with red clot busters heparin. 

So, how to handle sharp-edged drug-like Prasugrel?

A powerful drug-like Prasugrel is at high risk of being misused. It has taught us some harsh lessons in stroke. So, we have to be wiser to extract the maximum out of this drug in the presence of a high thrombotic milieu (or at risk of developing it after a PCI.)

Since ECG and clinical features are not sufficient to predict the coronary thrombus. It is suggested to have a look at coronary anatomy and decide only if a PCI is contemplated.Some of the situations where Prasugrel is likely to be Indicated  

  • Any PCI with a stent in the culprit artery.
  • High  thrombus load
  • Prolonged procedure time

     

    When to Avoid Prasugrel?

    Just looking at coronary anatomy is not sufficient.  Estimating the risk of bleeding is required. Attempting to use various scoring systems during a cardiac emergency is a self-inflicted mathematical burden. In my opinion, none of these scoring systems(CRUSADE , ACUITY,  ARC-HBR) truly discriminate patients in a useful way. Mindfulness with an eye on co-morbid conditions is required.This has to be matched with coronary lesion /PCI complexity. Realistically, the confidence in our technical adequacy of stent deployment shall decide the need for aggressive post PCI  DAPT or anticoagulation

Final message

Just because we know the coronary anatomy, don’t expect prasugrel to be kind enough to lower the risk of stroke. The risk is the same whether we know anatomy or not. It is the funny evidence base we have created that makes us believe it so. Routine DAPT for all patients with ACS is not warranted without assessing the bleeding risk. Meanwhile, there can be an important subset of patients who can really benefit from prasugrel even within coronary care units who are unplanned for PCI. (Which the current guidelines seem to forbid without any valid reason)

Postamble

We know, stents love to befriend thrombus instantly, that demands aggressive antiplatelet/anticoagulants) which beget bleeding. So, should we stent all lesions in a given patient with NSTEMI ? is a very valid question (rarely asked though) needs to be answered by the custodians of patients’ heart. When dealing with a complex PCI case scenario, simple mindfulness with an eye on comorbid conditions and downgrading ourselves to a good general physician mindset is welcome.

Reference

1.The DUBIUS trial downstream vs upstream use of antiplatelet agents in NSTEACS- No difference

https://www.acc.org/latest-in-cardiology/clinical-trials/2020/08/31/21/44/dubius

 

 

 2.

In CKD, LVH is a near-constant feature with echo showing thick, bright echoes from IVS. The LV mass increases, partly due to physiological hypertrophy ,also contributed by deposits of uremic middle molecules and fluid collection in the interstitium as myocardial edema.This, is recognised as T 2 weighted MRI signals. Chronic fluid stasis may progress to myocardial fibrosis. (Kidney Blood Press Res 2018;43:134–142 )  

Effect of Frusemide on myocardial edema 

We know, loop diuretics cause aggressive depletion of ECF volume and to a lesser extent Interstitial fluid. The effect of diuretic on myocardial water content is a poorly studied parameter.(Still more visible to a shrewd echocardiographer)

Effect of dialysis

While the effect of diuretics on myocardial edema is not consistent, however, we have observed definite regression of myocardial thickness, mass, and rigidity following dialysis. This transforms into a better LV systolic and diastolic function. At least in one patient, we have observed  the E velocity shrunk more than 50% the next day following dialysis pushing them to lower grades of HFpEF( A potential study topic.)

Final message 

The Improvement of the functional class of CKD patients immediately after dialysis is not only attributable to the removal of excess fluid and toxic uremic molecules, regression of myocardial edema plays an important role.

Further reading

Trinh E, Chan C, T: Intensive Home Hemodialysis Results in Regression of Left Ventricular Hypertrophy and Better Clinical Outcomes. Am J Nephrol 2016;44:300-307.

Curiously, the management of VT is simple if the patient is unstable. Just, we need to shock. Cardiologists are troubled only with a hemodynamically stable patient with VT. Some of us still think Amiodarone is a universal antidote for any VT. Though It is effective in both ischemic and non -Ischemic VT, the success rate is not uniform.

The mechanism of action of the Initial IV bolus is not a class 3 K + blocking action, instead, it is thought to be its beta-blocking action. If amiodarone fails, we may try Lignocaine,  magnesium, Flecainide. .Many times it is the cumulative dose of amiodarone that reverts the VT. In some patients, it may reduce the ventricular rate instead of reverting to sinus rhythm. This is due to the prolongation of re-entrant circuit time. The question of amiodarone worsening polymorphic VT with a deleterious effect on the QT interval is still not clear yet.

Why Amiodarone fails to revert VT in some ?(Up to 40 % ?)

One of the factors we looked at some 15 years back was the relationship between IRA patency and amiodarone efficacy. Presented in CSI meet 2004.

It was a simple conclusion. For Amiodarone to be effective IRA must be at least partially patent to enable the drug to reach the target tissue. I am not aware of any study on this issue. Request anyone to expand this study and publish it as a full paper. (Royalty-free research topic!) Please acknowledge the concept if you think it’s original.

The field of cardiology is always at the forefront of any technological breakthrough. Cardiac pacing stands tall among all Innovations. While remote monitoring and pacemaker telemetry are well-known concepts. One would have wondered why Intracardiac leads couldn’t communicate with each other wirelessly. Yes, It was just a matter of time, for that to happen. 

The leadless pacemaker Micra/Nanostim was Introduced recently but lacked the much needed physiological pacing as they were single chamber based pacing. Though mechanical sensing of atrial activity was possible with Micra TPS software patch  (A  VDD like mode) it wasn’t providing perfect AV synchrony.  (https://drsvenkatesan.com/2020/04/03/av-synchrony-in-lead-less-micra-av-pacemaker-how-does-it-sense-atria/)

 

Now, technology has made it possible for dual-chamber leadless pacer. Here atrial and ventricular channels communicate in a wireless fashion, making it a truly wireless dual-chamber pacing. Interestingly the communication between them is not Bluetooth or NFC based but a concept called low-frequency Galvanic coupled intrabody communication. (Currently Implanted  pig models.)

Final message 

We have crossed new frontiers in the management of electrical cardiac disorders. While inadvertent cross-talk between atrial and ventricular lead was an issue in the past, now we are mastering the art of appropriate talk between these leads in a wireless fashion and use it for synchronized pacing.