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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.

Somehow the concept of  Evidence based medicine (EBM )never excited me in spite of great strides it has made. Probably the main reason for this is, EBMs origin, quality, and credibility is currently severely compromised. (Though It appears to ooze science 24/7 and make us believe in it too !) Herewith, sharing some of the forbidden thoughts(with lots of pun)  for a (un)successful practice of EBM. This is definitely not meant for young and novice medical professionals. Strictly for the ones who can segregate sense from non (S)

Evidence-based Doubting 

 

Reference

 

Yes, Its “evidence-based fun”. Forget all those anti-platelet trial dramas … showing in the cardiovascular theatres near you . There is only one genuine drug , that’s the good old humble Aspirin . Mind you ,none of other  actors can ever be imagined for primary prevention.

By the way , there is absolutely no controversy for the role of Aspirin in secondary prevention after established CAD.(We know , how Aspirin has taken up a critically  Integral role in saving the life of the stents  as well as  patients,  post PCI)

Oh , what a disgrace for this drug when it comes out of the glamorous cath lab zones. Its use is often frowned upon for preventing simple CAD. (All due to a single factor, fear of bleeding ? No , its exaggerated in most studies)

Overlap between Primary and Secondary prevention 

In primary prevention of CAD , what do we attempt to prevent? How do you differentiate established CAD from  “Established coronary atherosclerosis  but Non-established CAD ?”

The fundamental flaw in this perceived controversy is in our inability to define what is significant CAD in the asymptomatic population.Do we need a clinical event to say, established CAD?

For the attention of  evidence-based script writers , a long query  . . .

“How much evidence we have to conclude , that a  patient with manifest clinical CAD carry more risk for a  recurrence  than an asymptomatic  high-risk pateint  who is likely to develop the first clinical event (with a bang that could be a major ACS ) due to underlying silent Atherosclerosis.?  

Reference 

Click  here to for more  unscientific review on primary prevention of CVD.

 

 

 

 

*When I tried to condense three decades of my learning into the medical profession in three lines, I scribbled this. Sorry folks, if It doesn’t sound scientific for some of you! 

By the way, What is successful medical practice? Success for the Doctor, patient or both?  The answer to this question is never simple. 

 

 

 

Pericardial effusion can be detected in many normal pregnancies. The Incidence is up to 40%.The normal fluid within the pericardial sac is around 25ml. A thin sheet of echocardiographic fluid collection in diastole up to 5mm is considered mild.

A trace  or minimal effusion may be a better terminology that describes most physiological pericardial fluid compartment. They have no physiological significance.Mechanism is due to overall increase in size of vascular compartment and especially the right heart volume overload.

Pericardial fluid drains through systemic pericardial veins and lymphatic channels also drain into venous system through thoracic duct . In pregancy these drainage pumps work overtime at its peak capacity. It’s natural it might get fatigued and show some residual fluid collection which should never exceed mild.

We also know thyroid hormones is one of the housekeeping hormones within the pericardial space.Physiological hypothyroid state is possible.Effusion in true pathological Hypothyroidism causes secondary dyslipidemia. Here, some unknown lipid sub-particles clog the lymphatic and cause pericardial effusion which is actually a part of widespread systemic edema. (Myxedema)

https://www.ncbi.nlm.nih.gov/m/pubmed/12756478/

Reference Hurst’s The Heart Valentine Fuster  Mcgraw Hill, 14th edition Page 2347

Poverty is a cruelest disease of mankind , the infective vector is not any deadly HINI or retro virus , but mostly the fellow humans themselves ! This is why WHO has included poverty in the ICD code (Z59.5 ) as a disease .

I used to wonder , as a member of Noble profession , should we fight against this disease or be happy to spend my entire life time cleaning the coronary arteries of affluent human-beings and earn few bucks !

Can growth of money eliminate poverty ? 

We may think so  . . .  but it doesn’t most times .Of course ,  affluence bring more jobs to the poor , logically it should alleviate poverty. But , we  know the reality. Its not that easy concept to understand . However we have robust evidence for the opposite ie affluence can aggregate poverty .

If poverty is a disease &  if  mindless  affluence is an Indirect cause for it  , then affluence also becomes a potential disease , Is in’t ? Will WHO include it in ICD listing ?

May I propose Z59.5A to be called  Uncontrolled &  manic desire for affluence ?  Since it is  made at the cost of  fellow humans , it should be clubbed along with poverty as a worrisome disease. Once its included in the ICD manual , I guess it will be unethical to ignore this disease. 

We all aim for growth in life .Nothing wrong in that .There are many facets of life that requires growth. Unfortunately , for most  homo-sapiens ,  growth is synonymous with multiplication of money . . . nothing else seems to matter ! Money when it grows unregulated ,  begins to control you and hijack your  body and mind .

One more issue to  comprehend is , rapid growth of money is possible only at the cost of something (or someone) else – Akin to cancer cachexia ,it depletes the body (Earth ) of it’s resources ( Nature abuse ,  extreme poverty , inequality ,  Third world exploitation , wars, etc ) For the  medical professionals  it is all the more important that growth shouldn’t mean money , as it has a direct and conflicting  impact on some one else’s life  !

mitosis of money 003

Just Imagine ,  if the all the car companies combine together , aim for a  dramatic growth from the current  4 %  to 25 % by 2030  and manage to  achieve it by any means ! . . . This planet will sink in the combined weight of automobile Junk !

It is obvious , uncontrolled growth in any form requires vigorous regulation and  Intervention and will eventually require a radical surgery if the growth goes unabated  !  

Counter point

It is foolish to link growing money and wealth  equivalent to cancer. Unlike cancer cells , money multiplied can be put into use for those in need .It is the principle of charity .But the reality is , human beings who are rabidly after money rarely have this mind set.In contrary the haven’ts have it in plenty. In my opinion, excess money has a dubious  capacity  to  contaminate  human values  ! (Why should some rich and elite opposes affordable health care  to poor ?)

Let us amass wealth and help others . Microsoft  is able to do it. Apple may do it later. What is the need for big companies social responsibility and philanthropy ? If the business worlds  motive and end product  promotes equality and goodness , sans exploitation , the question of charity at a later date never  arises.

Final message

If extreme poverty is a disease ,  forces that Initiates or sustains  poverty cycle can not be a bliss. In this context , the  manic affluence (& the urge for it)  should be included as a communicable disease since it seems to be most contagious as well.

In health care delivery “affluent and modern care” may also connote a sinister meaning. Poor people might think they are deprived of good care because they cant afford it. But ,truth hides deep. True sustainable caring is little to do with affordability+ , since most of the modern health care expenditure is jacked up with junk.

I know in my country people sell their life time assets for what they think as  crucial health care .(Of course universal health care insurance is just beginning to come in. Here again insurance based health care has inflated the actual costs and threatening to impose inappropriate therapies .

As a medical professional we should aim for the cheapest  and best form* of treatment to our patients . Artificially inflating the cost of therapy by worthless drugs, devices, procedures and disseminating them invariably leads to pathological  growth of science.

*If any one thinks “cheap and quality” doesn’t go together in medical care it is ignorance ! Most problems has simple and effective solution.

Post-amble 

 I object this statement -Modern health is nothing to do with affordability.

We need to go to the basics then .What is true health ? Forget about transplants, Organ Assists, Five star critical care .They seem to work in a minority , but drain the world economy. Its Impact on global health is at best minuscule. One Important analysis say 90% health care cost is wasted in prolonging the last 30 days of life of homo-sapiens.(Will get the reference for it )

Please note 

Diseases that occur to  affluent population  is entirely different topic . Can be found elsewhereDisease of affluence

 

One popular definition of Intelligence goes something like this  “It’s a global capacity  of a living organism  to deal effectively with environment and live peacefully”

When myocytes are confronted with acute ischemia , they  don’t always  jitter . It expresses many behavioral pattern.The damage inflicted is variable as  the molecular mechanism of ischemic tolerance appears to be a virtue ! This might make  much revered time window of myocyte ischemia irrelevant .Each cell has got a unique capacity to survive or die . In chronic ischemia this myocyte intelligence and intention to survive is glaringly evident. How about this phenomenon in ACS ?

myocardial intelligence myocyte memory

Art of  survival 

Why some cells die instantly , some fully recover and few go for hibernation  and others  are just stunned . While apoptosis is programmed cell death with intact cell membrane , hibernation can be termed as programmed cell survival .We don’t know how many intermediate forms of cell surviving mechanisms exists.

One of the famous questions is does the myocyte need blood or fuel for survival* ?

It is a fine balance of various cell  surviving (Anti ) mechanism.How energy is utilised with available ATP molecules is a different  science altogether .It’s  possible like brain,  heart too has  myocardial intelligence  , which does  some independent thinking aided by  fuzzy logic and problem solving algorithms  built within.

Ignorance based ACS care 

While we slog with metals inside the large coronary arteries , the response of the micro vascular territory is at the mercy of God . mRNA instructed DNA codes determine acute mitochondrial  respiratory sensitization.Finally ,the successful reversal of ischemic injury depends upon the cell repair molecule’s crisis management skills !

How else one can explain , some broken hearts recover so well from a major ischemic injury others sink with first insult !

The concepts of pre and post ischemic conditioning  are related phenomenon which can be pharmacologically  mimicked .They  are the major areas of research in myocyte  revascularisation.

Final message 

What is written above  is pure non academic fantasy . Now, read the following article by Dr Kloner which describe the molecular mechanism of  ischemia modification and its impact on clinical cardiology.

Reference 

1.Robert A. Kloner, Shereif H. Rezkalla; Preconditioning, postconditioning and their application to clinical cardiology, Cardiovascular Research, Volume 70, Issue 2, 1 May 2006, Pages 297–307,

Not every one feels the palpitation during tachycardia / Bradycardia /VPDs , Why ?

Palpitation is awareness of one’s own heart beat. It is a complex perception of sensation at cortical level (like dyspnea) . It can occur during physical and mental exertion.However , if it occurs without any physiological reasons , it becomes abnormal. It can mean an abnormality  in heart rate , rhythm or  raise in stroke volume. The first rule of palpitation is both tachycardia and bradycardia can cause it. Tachycardic palpitation is due to valve motion and bradycardic palpitation is due to both motion and increased stroke volume.

The most common mechanism proposed for palpitation is hyperactive anterior mitral leaflet

How and where  does the sensation of  palpitation felt ?

Does  it originate in  the chest wall ?  or Is it the vibrations spreading along  the flow of blood in great vessels ?  or Simply  represent  the vigorous valve motion  sensed by Intra cardiac receptors ? How it is  transmitted to spinal cord where it’s felt at cortical level  ? We are not clear yet. Paccinian corpuscles is thought to sense these vibrations and hand over as electrical signals  to spinal cord either directly from cardiac valves /walls or indirectly from chest wall.

Paccinian corpuscles are predominantly present in sensory nerve fibres located in the dermis of skin. It is also observed in nerve ending to joints, Chestwall, blood vessel and also heart .They act like pressure as well as vibratory receptors * The exact reference for Paccinian corpuscle to be present within the heart is not available to me. Readers may contribute,

Importance of age and gender and IQ

Palpitation is primarily a symptom of young age where the heart is supple and more dynamic. Women tend to perceive more for some unknown reason. Elderly people rarely complaint about palpitation .It could imply aging  with or with out autonomic dysfunction which suppresses transmission of palpitation signals to brain.Chest wall thickness also matters. My guess would be, Chest wall thickness, epicardial fat pad could absorb the vibratory  energy  and chest wall receptors fail to recognise it. One curious observation is,  palpitation is described in a succinct manner by certain patients only. Since , it essentially involves  higher cortical senses , we believe spatial intelligence of the patient  may also be important.

Why Irregularity in heart beat is well recognized?

For the given heart rate , irregular rhythms are felt  more often as palpitation than sinus tachycardia. This is the reason single ectopic beat is easily felt than  sustained tachycardia. A common sequence of  palpitation due to ectopic beat is , a suddenly  missed beat, subsequent pause and forceful post ectopic beat.

Valve morphology and impact on palpitation

Mitral stenosis patients can feel their loud first heat sound (S 1)  or varying  S1 during atrial fibrillation as palpitation; Mitral valve prolapse with redundant , hyper kinetic motion is probably most common cause of benign palpitation.

Sclerosed  and calcific  valves attenuates palpitation. Calcific mitral valve in mitral stenosis make both S 1 intensity and opening snap feeble .These patients are less likely to feel palpitation .

Individual valve pathology can generate palpitation as in Ebstein anomaly , which has a the large sail like septal leaflet that flutters to create palpitation(Apart form pre-excitation syndrome common in this condition) As a general rule ,It is possible semi lunar valves are less likely to cause palpitation than AV valves as the latter only exposed to direct contractile pressure of ventricle.

Right vs left heart origin and localised palpitation

I am not sure one can differentiate left heart from right palpitation. But.palpitation arising from right ventricular  volume overload and increased pulmonary flow like in ASD  are associated with direct local sensation over pericardium . Mitral valve motion can not be localized by  patients .However apical impulse can be felt.Neck pulsations invariably mean high flow states. Venous cannon waves due to high pressure tricuspid regurgitation can be felt with each heart beat (RV systole)

Exertional vs Non exertional palpitation 

Palpitation occurring during exertion often imply its due to excessive handling stroke volume or (Pathological regurgitant volumes) Stenotic lesions are less likely to cause palpitation during exertion it’s never an absolute rule. Exercise Induced arrhythmia always happen in any valve lesions.

Relation with LV function

A dysfunctional ventricle cannot  generate forceful contraction and hence palpitation is uncommon symptom. Cardiomyopathy presents with more of dyspnea rather than palpitation .Even,  an episode of AF do not cause palpitation in such patients .They simply feel breathless (Dyspnea ? Or is it a palpitation equivalent ?)

New age palpitation

With so many foreign bodies and accessories entering the heart  it’s not surprising for patients to feel amusing sounds and vibrations hitherto unknown in human body.

  • Prosthetic valve clicks (Sounds from mechanical valves can be  annoying .Tissue valves, TAVR are more quiet)
  • Abnormal electrical activity  from pacemakers and ICD coils.(Apart form pacemaker mediated muscle twitches)
  • Now, we have entire mechanical LV assist devices  working inside the heart with a 24/7 motors .(LVAD hum its called) Very soon heart is going to become a noisy place and patients would learn to ignore these abnormal sounds

Pleasant physiological palpitation

What brings the unpleasantness during palpitation? (applies to dyspnea as well). It is purely state of mind. While, palpitation due to extreme fear is unpleasant , palpitation due to pleasant emotional arousal (Often referred to as flying butterflies ! (Is it the wings of AML ? ) within the chest  as we hear from some of young  women & men ).Since they know the reason why they get it, cortical input welcomes it ,converts them to pleasant  beats .The Non-academic stuff  is intentionally made to understand how the limbic system and Hipocampus  areas of brain can modify the incoming signals of palpitation that comes from down under.

Thoughts to ponder 

Does post heart transplantation (De-nerved heart) patients experience palpitation ? Again, I am not sure .If palpitation is carried by cardiac nerves it should disappear. Of-course , 30 % of transplanted heart do get re-innervated. When you get a chance to meet a heart transplant patient you ask yourself and find the answer.

*Please be reminded Anginal pain almost vanishes  post transplant.In fact ,there have been instances of cardiac auto-transplant for refractory angina in the past.

Final message

Though all of us can list causes of palpitation without any difficulty , we rarely dwell into exact  the mechanism of genesis of this symptom and  its perception. As we enjoy flying in an exotic world of cardiac  interventions  . . .  the principles of  practice of medicine also expect us to take adequate efforts to understand fully the cardinal  symptoms of our patients . After all , they are the true teachers of Medicine. It is because of their pursuit for explanation for their symptom (Often vague though)  we make our professional progress.

Further  reading

John T.Shepard  The Heart as a Sensory Organ JACC Vol. 5, No.6  June 1985:83B-878

(The heart has variety of sensory nerve endings , still to be explored)