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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.

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.

Caution: Please don’t expect much scientific content in this post. I Hope, you can spare a minute to answer this hypothetical question.

What will be the shape of the curve,  If you plot BMI in the X-axis and LDL/ total cholesterol in Y-axis from a thousand normal adult populations?

  1. It will be linear for sure.
  2. Maybe a little curvilinear.
  3. Its likely J shaped with age 
  4. I think it is U shaped
  5. No, it is Inverted U
  6. Sorry, I don’t know.
  7. No one knows.
Answer: Though linear relation is the one we expect, all sorts of shapes are reported in various correlation studies, making the response 7 likely to be correct.

Why BMI refuse to go along linearly with LDL (Cholesterol)?

Only an ultra-fraction of total body fat is represented as cholesterol within the vascular system. It’s worthwhile to note, total body fat store is about 8-10 kg,  the amount of cholesterol in circulating blood is hardly 10 grams. It is presumed another 30 grams is present in cells. Body synthesise 1 gram /day.I don’t know whether I can make this statement. It may appear total body fat and cholesterol are almost unrelated things in spite of the dynamism of Intermediary metabolism exogenous and endogenous cholesterol levels are modulated to keep the intravascular cholesterol within an amazingly narrow range

How justified are we to expect a good correlation between BMI and Cholesterol? 

Apart from the presumed logic, there are other dynamic factors that dictate how any person deals with excess lipids/cholesterol. 

  • Genetics profile(Hereditary dyslipidemia)
  • Dietary habits 
  • Various hormone sensitivity to cells.
  • Physical activity 
  • Age /Gender 
  • Ethnicity

Most excess fat gets deposited within adipocytes. So it is scientifically impossible to guess the serum cholesterol level by just looking at overweight people. 

Final message

Even after 50 years of vigorous research, we are clearly ignorant about this fundamental question in lipidology and clinical cardiology. This is directly reflected in myriad dietary guidelines that flooding in the academic and public domain. Let us be transparent to our patients about our knowledge or lack of it. At the minimum, we should stop confusing all those healthy, active people with borderline obesity.

Further, we need to come out of our villainous portrait of fat in general. Let us respect the fat as an essential building block of every cell and hence the whole body. We still need to pursue a long journey to identify &  target only the high-risk population who have atherogenic dyslipidemia that impacts the cardiovascular outcome.

Counterpoint

There is indeed a correlation between body weight and serum lipid. Don’t be dogmatic with limited research and knowledge and confuse the academics. Go through the literature right from Framingham /MRFIT/Monica to Interheart study. There is scattered evidence to show BMI do have a reasonable correlation with blood lipids. 

Yes, scattered is the right word, it can mean anything.

Reference

This well-conducted study suggests, within the normal BMI range there could be a correlation with LDL. I don’t know how useful is this data in clinical practice. 


Coming next 

There is one more question, which has not clearly answered. What is the relationship between seum cholesterol and Intra plaque cholesterol?

For lighter reading , Ruben Meerman is able to kindle the hidden science.

When you lose weight , Where does the fat go ?

We can consider Jugular veins of the neck as a naturally present right heart catheter. It faithfully reflects the live pressure and waveform data  from right atrium and ventricle .

Can JVP tell us anything about left heart pressures? Is there any relationship between JVP and PCWP or LVEDP ?

If you tell JVP reflects LV filling pressure in any graduate medical exams, you will be admonished. However in DM or post-doctoral exam, if you say there is no link between the two, you are likely to be chided.(It is unfortunate the answers vary depending upon the level of training , which I feel is not academically correct )

Though the JVP-PCWP link, apparently appears Illogical, it does  have a scientific basis. It is true, there is a huge (& multiple) anatomical barriers between the left heart and Jugular vein in the form of pulmonary arterial & venous circuits, the right ventricle and right atrium.Still ,the hemodynamic principles demand, whenever left heart filling pressure increases, the right heart pressure should increase correspondingly to drive the blood from RV across the pulmonary circuit.This raise should be in the mean pressure. (or diastolic pressure,) it’s rarely related to systolic pressures as RV systole normally generate more than twice or thrice the LVEDP.

This driving pressure across the lungs  is called the transpulmonary gradient. (PA mean minus LA mean) The normal being < 7mmHg. So if there is a sudden increase in LV filling pressure to 20mmhg, there has to be elevated right heart pressures.(20 +7) This will be reflected in JVP as well. So patients with acute diastolic heart failure as in HFpEF must show elevated JVP. This can be documented elegantly In patients with positive responses during diastolic stress testing.  (JACC: Cardiovascular Imaging 

There are important caveats in JVP-PCWP link

  • If the PH is long-standing and precapillary (Reactive PAH) has set in the right heart pressure will no longer reflect the PCWP.
  • If there is any organic Tricuspid valve disease (Both TR/TS) JVP can reflect PCWP.
  • Finally, any cause of RV dysfunction will immediately elevate the JVP so biventricular dysfunction makes correlation of JVP with PCWP meaningless.(Acute pulmonary embolism, and RV infarction)
  • Further confounding can occur if we contemplate RV diastolic dysfunction as seperate entity. (At what level of RV systolic dysfunction, does the RVEDP begin to raise ? I think we don’t have an answer for this . Researchers please note.)

Some more mechanisms of elevated JVP with left heart disease

  • Bernheim’s effect and ventricular interdependence can make JVP elevated spuriously without elevating PCWP.
  • Acute mitral regurgitation left atrial V waves can “tide-back” all the way to PA and the right heart to elevate the JVP
  • In ASD and Lutembachers syndrome  the RA pressure waveforms may reflect the LV filling pressure, though inconsistently.
  • Finally, and importantly in Fontan circuit JVP may exactly reflect the left heart pressure for the obvious reason, as SVC is connected to the pulmonary artery directly.

Final message

JVP will always tell what is happening to the right heart chambers only . It can, no way be taken as a direct marker of PCWP/LVEDP. However, there can be a correlation between JVP and PCWP/LVEDP in a certain subset of cardiac failure. (As in exclusive isolated left heart failure (typically HFpEF) the elevated JVP might just reflect the elevated LEDP provided there is normal RV function )

Reference

1.This study elegantly shows a correlation (or lack of it) in different subsets of heart failure. It tells us very clearly If JVP(RAP) is not correlating or disproportionate to PCWP, it implies RV dysfunction.

2. This paper suggests a really useful scheme to classify heart failure as concordant and discordant with reference to right and left heart.

It throws some interesting facts. I guess it will help us guide diuretic management and prognosticate chronic heart failure.

Covid has struck hard and this time it has consumed one of the Doyens of Neurology, from Coimbatore, India –Dr.M.B.Pranesh. Privileged to have him as my professor in Coimbatore medical college, my alma mater, watched him in close quarters during my undergraduate and MD days in the late 1980s.

Still recall, how he empathizes with the patient and their family in distress, practiced medicine in the best scientific manner at the same time with a humane and philosophical touch. I can’t forget, how the little genius standing beside the comatose patients In IMCU and tells so precisely the difference between metabolic vs structural coma without even asking for a CT or MRI scan.(We learned with awe, for the first time, how hyponatremia can cause havoc to the brain)  I have seen him so tired in many days and sleeping in the ward chair for a few minutes and comes back fresh for the rounds. He used to say sleep is a luxury in our profession. What a statement to make for our generation next.

His favorite quotes are from William Osler and ask us to read the life history Harvey Cushings. He encouraged us, to learn the history of medicine. He was so emphatic to say “Unless we know how our past physicians toiled with their astuteness and hard work, we will not understand the value of clinical medicine”

 

One of the pure souls who showed us what is the true meaning of teaching, learning, and caring. Got this small clip, wherein he continues to wish us good.

Let his legacy live forever. 

 

 

 

His bundle pacing is the new kid in EP lab. It involves exploration of few 3-dimensional cubic areas of His bundle (4-6mm³ ? ) in the crest of the IVS looking for optimal His pacing site. It aims to provide better recruitment of His Purkinje and hence more synchronous pacing. Still, the modality is in the early stages and has few key limitations. They are, requirement of very specialised leads,(Select Secure™ 3830 , Medtronic) lead instability (Susceptible to RV ejectile forces*), high threshold, and lower battery life and finally uncertainty of distal bundle disease. A need for temporary RV back up the leads in some centers will tell us how confident we are, about the concept of his bundle pacing.

The success rate of HPB pacing has not reached the desired levels.Meanwhile, the area His bundle lead explores is so thin and delicate that requires working around membranous septum. No surprise, a new adverse event is reported.  Yes, the first case of acquired VSD reported following his bundle pacing. (Ref 1)

Now, experts are moving down in the septum to capture LBBB to avoid the above-said limitations of HBP. I will not be surprised we ultimately reach the RV apex , the good old destination again, for absolute safety and stability.

*RV leads are naturally isolated and not much affected by RV contractile hemodynamics

Final message

Wish the concerns about His pacing are exaggerated , best of luck for this new mode of pacing. Medtronic is a pioneer and has a long passionate history. After all, cardiac pacing is one of their top Innovation in cardiology in the last century that made a huge impact in the management of electrical ailments of the heart.

Reference

 

 


 

Got it? One clue, you are part of these numbers! It crossed  5 million reads recently across 160 countries. Thanks. I know,It amounts to self-promotion. Such boosters are required when energy level sags. Sorry.

*The post is not meant for those who understood GLS (Global longitudinal  strain) in a proper perspective. I am writing this, after a surprising answer from many students of Echocardiography, when I asked them what is GLS?  Most answered, GLS currently is the best global LV functional index available. What a misunderstanding? The fact is, EF % will always be the best global parameter*, while GLS remains a regional function index.(*The limitation of EF% is in the methods of measuring it and not in EF itself.)

                                   We are trying hard to ditch LV EF%  by Teichholz’s / even 2D Simpson method, as they are considered a crude way to measure global LV function. Unfortunately, we are doing this without a credible alternative. GLS is being promoted as the next best. The normal GLS is around(-20 ± 2) . Nothing is perfect. Best global LV function probably can be achieved by 3D Voxel Echo/MRI)

Normal GLS with various machines

Please note, the bullseye 17 segment model though brings an illusion of a radial perspective of cardiac contraction, its purely longitudinal stain represented in short axis format.

The much popular GLS (Global longitudinal stain ) is a poor surrogate for global function. The word global is apparently misguiding and conveys a false message. When we refer to GLS, it is an adjective for longitudinal function and nothing to do with overall global LV function. (Though we have many studies to show it has good correlation with global LV function).

The longitudinal function is presumed to contribute 60 % of LV function.  This means GLS is at best 60 % accurate in determining global LV function. Mind you, the heart doesn’t work in a longitudinal plane alone. The muscle fibers of heart are arranged in three distinct fashion (LOC) subendocardial- longitudinal,  Mid-oblique, & Sub epicardial -concentric (Remember LOC ) Each fiber either lengthens or shortens.

The left ventricle not only shortens longitudinally, It also contracts radially, shrinks circumferentially, rotates clockwise at the base (5-10º) , counter rotates at apex (Up to 60º) twist,  & un-twists.  It’s worth reminding ourselves, we are ignoring all these components and happy to fall for GLS.

What can be done to improve the accuracy of true global strain?

The simplest way is, to look LV in  short-axis by 2D and confirm everything is okay with radial contractile forces and deformation. Mind you, the most accurate tool to measure stain is the good old M mode with undisputed temporal (time) resolution ad frame rate the M mode thickening best deformation parameter to measure radial stain ( at a particular plane though).

Is the measurement of true global strain possible?  (GLS+ GRS)

Probably yes. What about GLS plus GRS (Global radial strain)  GLS measured by speckle + RS (Radial thickening by 2D/aided by M Mode)  We are working on a project where the radial strain component is added to GLS. Roughly, it should pull the negative GLS  beyond + 20  (If we assume GRS is + 30 to 60 ) This should be correlated with 3D voxel Echo  /MRI .

Final message

Beware,The “G in GLS” is a perfect miscommunicator. * GLS  can never reflect global LV function. If EF% by M-mode was criticized, for measuring only one aspect of cardiac function ie radial, the same would apply for GLS, in that it measures only longitudinal function. Never discard M mode/2D. It still, pours unadulterated ultrasonic data from myocardial contractile units in the highest resolution. We should continue to use it. In the name of modernity, we make it look outdated.

Reference

M S Amzulescu, M De Craene, H Langet, A Pasquet, D Vancraeynest, A C Pouleur, J L Vanoverschelde, B L Gerber, Myocardial strain imaging: review of general principles, validation, and sources of discrepancies, European Heart Journal – Cardiovascular Imaging, Volume 20, Issue 6, June 2019, Pages 605–619, https://doi.org/10.1093/ehjci/jez041

*

 

Truely a great demonstration of life saving Mitra clip procedure.

Found this from

Can a bedside echocardiogram help rule out STEMI in patients with suspicious ECG?

No, it can’t  (Though, it may be tempting to use a rapid echo to look for wall motion defect to rule out ACS ) 

If your answer is No, probably you don’t need to read any further in this post.

Diagnosis of STEMI* is based on

  1. Clinical
  2. ECG
  3. Bio-Markers

*Please note, two of the most popular investigations namely Echo and Coronary angiogram are missing in the list.

A middle-aged man with  chest pain.  Can an echocardiogram help you confirm  STEMI here? Most likely not. It may still be an evolving STEMI. But, observation, serial ECGs, and Troponin is the answer. (ECG -Source http://www.emdocs.net/hyperacute-t-waves/ )

Though, echocardiography, a great noninvasive imaging tool at the point of care, it stands almost helpless in the diagnosis of the commonest cardiac emergency ie ACS. It can be called as mother of all paradox even visualizing the myocardium directly with high-quality imaging will not tell you, whether there is ongoing ACS or not. 

Relying on wall motion defects without diagnostic ECG changes to diagnose STEMI  can be misleading for the simple reason, both unstable angina and old MI can be a 100 % confounding effect. Similarly, absence of WMA doesn’t rule out an evolving STEM(Apart from the bizarre behavior of   Ischemic cascade,  In the early hours only subendocardial wall stress is noted, that is not good enough to cause visible WMA)

Role of CAG in the diagnosis of STEMI

Urgent CAG is an easy way out in confusing coronary conundrums. But, unless you know the background info even a CTO can be mistaken for ATO/ STEMI . So it is essentially new ST/T  shifts (corroborated with CAG) will be the guiding force. 

Final message 

The humble Clinical examination and ECG will prevail over all other modalities in the diagnosis of ACS. Mind you, ECG findings are built within the diagnosis of myocardial infarction ie STEMI (ST-segment) so can’t diagnose it with  Echo. Further, an indication of thrombolysis or PCI goes with ECG finding only.

Counterpoint

*Having said that, there is a key role for echocardiography in the ER to diagnose alternate cardiac emergencies like Aortic dissection, Acute pulmonary embolism or ACS mimickers like HOCM, etc. Further, echocardiography is used in a big way,  in the risk stratification or identifying complication during the ACS management.

Exceptions

In patients with atypical presentations, pacemaker rhythms, LBBB, especially elderly, comorbid, ECG can be quiet normal or non-diagnostic. Here, echo and angiogram may have some adjunct diagnostic roles.

What about newer echo Imaging modalities?

** There has been a suggestion, that regression of Global longitudinal strain(GLS) or new-onset regional loss of myocardial strain, detected by speckle tracked echo is a powerful and the earliest sign of myocardial ischemia.

A potential tool to rule out ACS by Echo -Global /Regional longitudinal strain (GLS) still trailing behind ECG.

 

GLS is proposed to be used in coronary units to rule out ACS. In spite of its Initial promise, we understand it has not been accurate enough to be included as criteria to diagnose ACS . So, as of now, it appears unlikely for echo criteria to be included in the  diagnose of STEMI.

It’s halfway way through 2020 , still miles to go.

Welcome to a non academic break.This 3 minutes video definitley helped, amidst the paronia.

 

Wish, we can retire peacefully and join this family.