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Rheumatic heart disease is rampant in India.  Advanced forms of mitral stenosis are  still common.

Critical mitral stenosis with LA clot formation is often seen.

But here is a  women in late twenties  presenting for the first time with syncope .

And what  you see inside is  not a fiction  . . .

Left atrial clot occupying the whole cavity ! Where is the blood bound for left ventricle ?

4 chamber view

Luckily the clot is   so  big and MVO is less than 1 sq cm. It is highly unlikely the LA clot can negotiate the orifice.

Small fragments can dislodge .This patient developed syncope whenever she bends and lie down at a particular position.

What needs to be done in this patient  ?

Can it be lysed ? No ,Emergency surgery is required with concomitant mitral valvotomy or mitral valve replacement.

Is there a temporary aortic filter available to prevent systemic emboli from heart  ?

Distal protection devices are  available only temporarily in the coronaries and  carotids during interventional procedures.There is no aortic protection devices  for LA,LV clots in high risk patients .  When IVC filters  are used  block a potential pulmonary   clot why not aortic filters  for preventing systemic emboli  ?

Why we have not thought about  this  . . . is  surprising . May be intensive anti coagulation is as effective .

Some say medicine is a funny science . . .  it is true  at times. It will remain so , as long as we convert  a fact into a myth and a myth into a fact at our convenience . It  is  often   fueled  by the  whims and fancies of modern research  ! This phenomenon is happening in a regular  fashion  for  many decades now.

The number one killer disease of heart  is  the atherosclerosis  . Atherosclerosis means hardening  of arteries. The advent of coronary  calcium score with CT scans ,  it became a craze among many physicians . (It was   replaced later  by 64 /128 slice MDCT with unprecedented  commercial over tones !)

How can we  conquer the atherosclerosis ?   when the enigma of calcium in coronary artery is yet  to be solved.

The next few decades will be crucial   as  we are  trying to find answer to the following question .

Is  coronary calcium  good ,  bad or neutral   in CAD  ?

This article in American journal article begins the new year 2011  with good news for people , who show some calcium in their plaques.

What makes a plaque vulnerable ?

Plaque contents , it’s distribution and consistency make it vulnerable. Soft spots  formed by   lipids   may  result in  plaque cracks and fissure.   Semi solid  , mixed  ,  gel like soft  plaques   are dangerously prone for  rupture . Oxidation of LDL,  LDL  liquefaction and tissue metalloprotinase , thickness of fibrin caps , all promote softening.  If none of above  mechanism is operative in a given patient , the   plaque becomes  stiff and hard.

Calcification is the ultimate in hardening . Calcified plaque  is resistant to mechanical deformation.If  stiff  plaques   are less vulnerable , hard plaques ( ie calcified  plaques ) must be least  vulnerable . Calcification   can be called an end result of coronary atherosclerosis.

So , calcified  coronary artery  can be referred to as  a failed  mission of  atherosclerosis .It is  equivalent to  death  of atherosclerosis and denotes the end process of this dreaded disease process.

Calcification tames atherosclerosis  in it’s own den

What is the implication of a stiff hard, sharp calcified plaque lining  (or even projecting ) in the coronary lumen ?

As this study has shown , calcium in the walls of coronary artery is innocuous  . Of course , calcium should not be dense and obstruct the blood flow . This will  require  intervention. Many  consider , calcium as  a foreign body in the coronary artery . But the prevalent understanding is ,  presence of non obstructive calcium  is often  a  non issue or in fact a welcome issue in some.

After all , millions of  human beings  happily roam around  with the hardest possible substance  lining their  coronary artery called  stents.

Caution about calcium

This article does not portray calcium as a healing molecule in  CAD . In  the realistic senseit is  too complex to make such a generalization.  The  message is  , calcified lesions are less likely to result in acute coronary  events than soft , non calcified lesions.

It is well known ,  calcium can be problematic for the interventional  cardiologists  .It makes life tough for them in deploying  stents. Calcium rich lesions exerts  radial force in a diagonally opposite direction and interferes with stent approximation.

It is also believed localised , sharp calcium crystals may tear a plaque  and cause   plaque dissections. This  happens if the calcium is lying in an eccentric fashion overhanging the shoulder region of the plaque   abutting a soft spot.

Final message

It is now clear ,  why calcium  score in CT scans  failed miserably to predict  high risk subsets of CAD. In spite of repeated studies  the researchers failed  to show a positive correlation .  The studies are flawed  as they  were trying to look for a positive correlation  which is non existent . In fact , the above study seems to suggest calcium  score may indeed  predict low risk individuals!

Calculating the pulmonary vascular  resistance (PVR)  has been a  big head ache for all those involved in pediatric and (for many )in adult cardiology as well  . The complex formulas , the delicate  oximeter samples, the catheters, a sick child , an arrhythmia prone right ventricle , restless staff  nurses , and  finally the mathematics  !  all make it a dreaded exercise .

Echo is a great physiological tool  . . . It is now been used  over 50 years . It is our earnest belief ,   Doppler can measure the flow and pressure any where within the heart   however dynamic  the chambers may be !

Then ,why can’t  we have a simple formula  by  this  non invasive method  to calculate PVR  ?

Yes ,  Dr Abbas et all  from the desert hospital  of Arizona  raised  this question and  reported a new equation to calculate PVR.

Their  hypothesis is as simple as this . . .

  • Pressure     =    Resistance X Flow
  • Resistance = Pressure /Flow

Pulmonary vascular resistance = PA Pressure/PA FLOW

Substitute PA pressure with TR jet

Substitute PA flow by   RVOT VTI (  Velocity time integral )

And  we  get

PVR = TR Jet velocity/ RVOT VTI x  10

This  is the simplest way to arrive at PVR at the bedside .

An example

Is it validated ?

Yes .

Then,why it is not being followed widely ?

It is  a  too  simple  method to  use   !  That  is  the biggest excuse ! We are tuned  to  think  ,  a  complex parameter can not be measured in a  simple manner  .  Any thing simple must be  wrong !

But the reality is  . . .

Cath calculations are   much more  complex with so many variables   which  can  get terribly wrong .

The irony  about this  hypothetical  science of PVR is ,  we do not know  which is  gold the standard ?   In fact , none can be  a standard .  So ,  to label PVR  derived by echo ,  as an   inferior modality  can not be accepted  .It is all the more funny ,  as  we are  trying to  define a new  formula    with  the help of   flawed and battered   parameter  namely  the cath derived PVR .

Final message

Abbas’s  formula  is  indeed a  realistic way of arriving at PVR by echocardiogram. If only we measure it routinely  /serially in as many patients as we can , a new data base  will  be created .Which can later be  proven as a fact.It is suggested every cath lab should try to validate this formula.

Link to full text article : Courtesy of JACC

Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol 2003;41:1021-7.

Doctors are obsessed  with science .  Science is man-made , often , the quality of which is far from perfect (Apart from scientific inaccuracies , personal and commercial conflicts creep in )  .Hence  ,  patients   may not get  the true benefits of genuine science  today . This has a huge moral and economic implications .

The entire life time savings  of  our population , is threatened to be consumed by the vagaries of modern medicine. A recent WHO  report  reveals  , the  major cause for  poverty  is attributable to  the frivolous and  greedy   modern health care delivery system. Many times,  bulk of the nation’s wealth is  being  spent on  prolonging the final   few  months  of     lives(Often unproductive ! )  of their fellow citizens.

The irony is ,  many of these expenditures have questionable benefits.

  • A simple car is prone for fewer errors but it still serves it’s purpose .A hybrid car which switches between hydrogen, petrol and electricity  is obviously vested with numerous unexpected issues.
  • An ordinary  cell phone is easy to operate,  while an Andorid 2.2 phone  is loaded with great  applications  ,  but the  original purpose of a phone  ,  namely communicating with others is often   compromised.
  • Modern medicine  is a monster machine  with  thousands of  visible and invisible switches . The funny thing is most of us do not even know jobs assigned to these switches .Worst of  all , these controls  can self ignite  or put off  on its own . One can imagine . . .  the potential errors  from this monster controlled by a  minuscule master of medicine .

Does your patient aware of all those uncertainties ! Why is it so difficult for us to communicate  the above facts to our patients ? Mankind can benefit ,    if we put across the  following  doctrine to our public domain.

A medical  non  intervention can be as safe  as  an  intervention ,  but one has to accept the occasional complications  arising out of a  non intervention . In this context  it should be  realised  ,  we never hesitate to  accept the   consequence of  a  modern  intervention.

Why and how our  mind is readily accepting even deaths  during an  inappropriate procedure , while we struggle to accept  even a temporary set back  for not doing a needy intervention.

What is the solution ? We need to uncomplicate  medicine . . . simplify them .When doctors intervene with common sense as a weapon  to tackle the  scientific excesses patient is bound to  benefit.

Don’t ask don’t tell  dogma   should be replaced by ‘”Tell  without asking” .Be transparent about the limitation  of science.

Documenting and adhering to protocols is satisfying for upholders of science , but one should realize being unscientific also   can help our patients many times.

When your hospital protocol says check for hypoxia in every patient  with dyspnea ,  mind you it may land your patient to a totally   unwarranted  ventilator assistance for a very transient hypoxia reported your fellow over phone.

Here is an article that reveals ,   how a  few oral words of   advice could help  both financially and academically in critical care.

http://chestjournal.chestpubs.org/content/138/6/1475.abstract

 

Final message

William Osler said   ” Lesser is better” in medical  communication  . It may not apply today.

Did Osler  was  referring to  falsehoods in medicine ? , Then ,  probably he  is 100 %  is right . . . for the current times !

STEMI is an cardiovascular emergency . We alert  instantly the services  of  911/108/1066 . What we fail to realise is , the  physician’s thought process  should also  be equally fast  . Before dispatching  a STEMI patient by ‘air mail” to the nearest cath lab ,   spend few thought full moments ! We have  a simple and   equally effective option  ,(If not superior )  of revascularisation  , right in your clinic or hospital ! Use it liberally , it is not a inferior treatment !

This article  is from the prestigious  journal  “Annals of emergency medicine” .It confirms a longstanding doubt regarding the efficacy of  air lifting of STEMI patients.

A shocking observation . . . is . . .  many of those patients who are air lifted  for primary PCI   receive none of revascularisation  modalities !  Learn  how  many  of our patients have a futile helicopter ride in the golden hour of STEMI  !

Final message

Even airdropping of STEMI patients to cath lab for primary PCI is not  enough in this unique   race against time  . So , in the management of STEMI ,  we need lots of non -medical  sense* !  .Please judge    “the delay”   due to transfer carefully   and  always consider administering  the thrombolytic agent  when a patient  with STEMI  arrives   within 30 minutes.

A definite primary thromolysis (Within 30 minutes ) is  often  better than a PPCI  (Potential primary  PCI), which  may  or may not materialize in time  !)

*Please  realise  even  inclement weather  and traffic jams can have a impact on coronary patency !

See  comment about this article in Heart wire

What next ?   On site  mobile cathlab ?

Cleveland clinic is a leading centre for cardiac care .Major technological breakthrough occurs from this institute than any other place. Thousands of articles come out every year. Some articles , get global attention and make  a huge impact. These are usually related to a new hi- tech modality like CRT devices or percutaneous aortic valve deployment etc ,etc.

                                                Some articles , which are very important  may not get the due  attention . Journal editorial boards often  have a scorecard called impact factor .That is ,   how  a  journal  is  impacting the practice habits of  medical professionals . Ideally we need to have to grade individual   articles with impact factor .Many articles may not have any significant  impact  however good the impact factor of the journal.

Here is an article,  which excellently depicts the principles of management of ACS.  It was published in 2003 JACC,  by Steven Nissen  from Cleveland,  Ohio .It deserves more attention . Every cardiologist , involved in ACS management should read this, especially the interventionist.

Link to article placed her with courtesey of JACC

Acute coronary syndrome  is primarily a disease of blood vessel , which perfuses  the heart.  It can even be a disorder of blood, often called vulnerable blood which predispose  for intra- coronary thrombus .

Mind you  , heart is an innocent bystander ! to the onslaught of  coronary atherosclerosis !

Hence , we  often use two terminologies .

CAD : Pure vascular (Coronary )  disease without  any structural and functional impairment of heart  ( No Angina, No myocardial damage ) Most of the asymptomatic plaques  , non flow limiting  lesions, incidentally detected by the modern coronary imaging gadgets  fall in this category.

When does  CAD becomes CAHD ?

CAHD : Coronary artery heart disease .Here not only the coronary artery is diseased , but it has it’s mission fulfilled   ie target organ either damaged structurally (STEMI, NSTEMI ) or functionally (EST positive , Chronic stable angina CSA )

Does the heart does any wrong to suffer from Acute coronary  syndrome  ?

No, it is simply not .The fault lies in one or more  of the following   .Generally at-least two these factors are enough to impede blood flow )  . They  combine to produce an ACS.

  • Blood defect
  • Vessel wall defect
  • Slowing of flow (Stasis)

This is called as Virchow’s triad   suggested over 100 years ago . Still valid in the era of per cutaneous  aortic valve implantation.

* The concept of de-linking  disorders of  coronary  vascular disease  from myocardial disease  is vital  in understanding the implications of current modalities of treatment. 

Even though we PCIs target the culprit ie blood vessel , it need to  realised , we  always fall short of real target . . .namely the heart . In coronary interventions  the catheters and wires roam around superficially over the heart  and they never even touch the heart .This is the reason PCIs are struggling to prove it’s  worthiness over medical therapy in many CAHD patients , which can reach deep  into the vessel, heart  and even every individual cells of heart.

Many (or . . . is it most ?)  Interventional  cardiologists have a bad  reputation for ” failing to look  look beyond the lesion” .  It is estimated  a vast  number  of cathlabs  and CABG theaters worldwide  are engaged in futile  attempt to restore coronary artery patency after a target organ damage is done .This is akin to building flyovers  to dead and closed highways .

Salvaging a coronary  artery and reliving a coronary obstruction is an entirely unrelated and futile  exercise to  a patient who has a problem  primarily in  musculature .

The much debated concept of  documenting  myocardial viability  , before revascularisation  died a premature death as the concept  by itself , was not viable commercially . (Viability studies   , tend to tie down the hands of device industry further , some  interventional   cardiologists began to see this concept  as an  interference to their freedom to adventure  )

Of-course , now  we have  other parameters  phenomenon  like  FFR estimation by Doppler , epicardial  -myocardial dissociation, slow  flow , no re-flow are  gaining importance.

Final message

ACS is primarily a disease of blood vessel but it’s impact is huge on heart. We need to look beyond the lesion .Restoring  a blood vessel  patency  to an ailing organ (Heart ) is not synonymous with total  cardiac intervention  and protection . There is lot more to cardiac physiology other than it’s blood flow. Heart muscle is a too complex organ to be controlled by few balloons and wires  which beat around the bush.

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A classical restrictive cardiomyopathy . Both atria balloon out as they face stiff resistance from the ventricles

Restrictive cardiomyopathy(RCM) is a common form of myocardial disease which was difficult to recognise  in the past.It was also commonly confused with constrictive pericarditis. Today , one can easily recognise this entity.A simple clue is bi- atrial enlargement  with relatively normal ventricle size.The above case is a classical form of RCM.

In late stages of RCM ,both LV, RV begins to dilate and can mimic a dilated cardiomyopathy. Doppler filling pattern  , and tissue Doppler motion of mitral annulus are recently validated methods to identify RCM. Still ,  2D features  are  very useful .This implies , the anatomical changes in the chamber size  are as important as physiological AV filling profiles. It is generally believed , physiological impairment precedes anatomical defects.( But not proven concept yet ! )

Note: The ventricles are not dilated and retain good systolic function

In the above patient  , etiology could not be confirmed and was labeled as idiopathic RCM  as tests for amyloid and eosinophilic infiltrations were negative.

M -Mode of the same patient confirms good systolic function

One would  call  for doppler mitral filling profile here ,  to confirm restrictive physiology ( A short DT , Short IVRT  . A reversal in  pulmonary veins , E/E’ ratio etc etc ) But all these are redundant here.

How is RCM different from non dilated cardiomyopathy ?

A new entity is being recognised in the cardiac  muscle disease.This is often referred to as NDCM (Non dilated cardiomyopathy)  .Global  systolic LV dysfunction  with normal  LV dimension.This a similar to the terminology MDCM (Minimally dilated  cardiomyopathy  where LV dimension increases  not more than  15 % of basal size ) .

This is seen in CKD and diabetic individuals.Atria may be enlarged .Diastolic dysfunction may co exist.  It is no surprise,  this entity closely mimics RCM. But in RCM LV systolic function  is not greatly compromised till late stages , while NDCM it begins with systolic dysfunction. This is the only difference .There can be overlaps .

Many strongly believe ,  both  RCM  and NDCM are one and the same entities ,  that present in different time frames in their natural history.

Final message

Diagnosing RCM is no longer difficult in established cases* . The message from  this article is , 2 D echo can  strongly suggest  the possibility of RCM (or even clinch it)  .  Never ever  diagnose RCM with normal 2 D echo. Doppler filling profiles are useful  additional tools . We  can not diagnose RCM with doppler features alone , but we can  be fairly certain about RCM when we encounter  typical bi-atrial enlargement and a normal LV by  2 D echo.

Caution : Patients  with longstanding atrial fibrillation of any cause , can dilate their atria and could mimic RCM .They can be some compromise in LV function due to chronic tachycardia .

* Recognizing RCM ,  very early in the course is still a problem . Here the  newer modalities like Phase  MRI, tissue doppler, speckle tracking, and velocity vector imaging may be useful.

Dilated cardiomyopathy (DCM )  is the commonest  cardiac muscle disease .Diagnosis is simple and straight forward. All that we  require is,   documentation of LV dilatation and contractile dysfunction.The nomenclature of cardiomyopathy has remained a difficult exercise .This   is primarily  due to   iatrogenic  & intellectual confusion  among  cardiologists . They mixed up etiological and morphological entities together ,   later on  they  wanted to de-link  etiology from morphology  ,  ultimately they realised  when illness strikes the heart ,   it   can not differentiate the  morphology, etiology and pathology as we would want to   . So , whenever possible we have to label  cardiomyopathy with all components (Dilated cardiomyopathy due to alcohol with some restrictive features.)

This article  tries to evoke  some thoughts    about  why  LV dilatation  is central to the understanding of cardiomyopathy.

DCM is the prototype where LV dilates with global hypokinesia.The upper limit of   LV diameter is generally considered to be 56mm in diastole.  (Range 35 -56mm) .This cut off  point is too empirical  for the simple reason, the  left ventricle can dilate   up to  50 %  from it’s basal diameter and still technically  be within normal limits.( A 3.5 cm LV ( end diastolic diameter ) can dilate to 5.6 cm ,i e  a 50 % dilatation , still LV  has not reached the upper limit of normal  )

Even as we do not have a clear  answer to the above issue , we  recognise  left ventricle muscle can hypertrophy, progressively  dilate , transiently dilate, fail to  dilate ,  regressively  dilate  or  hypotrophy .These changes can be dynamic and heavily influenced by hemodynamic and local pathologic factors like fibrois, interstitial proliferation etc. Meanwhile , the pharmacological ,   surgical /catheter injuries we  inflict    , modifies  the muscle behavior in a positive or negative manner.

In this back ground ,  we have found a new entity called NDCM .

Apart from  DCM, a newer form of  cardiomyopathy  is being recognized  .This is often referred to as NDCM (Non dilated cardiomyopathy)  .Global  systolic LV dysfunction  with normal  LV dimension.This a similar to the terminology MDCM (Minimally/Mildly  dilated  cardiomyopathy  where LV dimension  do not  increase  beyond   15 %  upper limit of normal  ) .

This is seen in CKD and diabetic individuals.Atria may be enlarged .Diastolic dysfunction may co exist.  It is no surprise,  this entity closely mimics RCM. But in RCM LV systolic function  is not greatly compromised till the  late stages , while NDCM it begins with systolic dysfunction. This is the only difference .There can be overlaps .

MDCM was reported in 1990  . Keren gave a excellent insight about the condition  ,  It is unfortunate it failed to take off as a popular  clinical entity .  Cardiologists are argued to use this term liberally in their clinical practice .

Final message

Cardiology is not  that  simple as one would like to ! The two components of cardiomyopathy ie   LV dilatation and LV dysfunction can be temporally dissociated  one may precede the other. To  complicate the matter further, one of them may not manifest at all !

Few ,  still consider many of the RCMs and NDCM are one and the same entities that present in different time frames in their natural history.

So the simplified  concept  to decode the cardiomyopathy conundrum  could be

  • When both  dilatation and dysfunction occur it is classical DCM
  • When dysfunction  alone occur without dilatation it is NDCM
  • When both dysfunction  and dilatation are less it is RCM*(Relaxyl dysfunction must)
  • When dilatation is mild and dysfunction is severe it  is MDCM

Medical profession is the noblest of all !  . Doctors are akin to God in  many ways  ! They  have the potential  to remove the  sufferings of  mankind  . These are the often made  quotes about doctors   for  many centuries. Today’s medical professionals are ,  a  strained   lot  to fulfil their role expected of them .They have to maintain the social identity and earn enough to sustain their image in society. The onslaught of commercial and pseudo-scientific concepts have ruined the profession considerably.

Those were the days when the family physician  concept was flourishing , where in  a doctor was taking care of entire family. This  concept has  taken a different avatar now .

Now a doctor feels , once the patient is seen by him becomes his/her  patient rather a property! This perception has grown in a malignant manner , many doctors do not refer to a specialist even in deserving cases  fearing patient poaching .

This  possessiveness  of doctors about their patients leads to many  of the  unethical behavior .

My case . . .my patient . . .   my fees , . . .this sort of approach though appeared  good in the past ,  is rapidly becoming a liability for the patients  .Lack of organised health  care   by private and Government sector also amplifies the issue .It is pathetic to note         ,  at least Govt hospitals have some accountability ,  majority of private health systems  do not have  mortality or morbidity auditing . 

The my patient, my property  doctrine is playing havoc in medical health delivery system  .The following are the situations where a patient genuinely suffer due to this abnormal thinking pattern of many of the medical professionals today.

  • When general practitioners want to have control of their patients even after referring them to big tertiary care centres.
  • This is being encouraged  by the corporate desk of big hospitals as they probably send financial benefits to the referring doctors. Hence doctors are worried their property may get lost during  transit or inside the  big hospital. There are instances , I  have witnessed , where severe mitral stenosis are manged medically by some established physicians fearing that their property will be lost .
  • Patients with severe angina are not offered angiogram and remain on medical treatment fearing loss of monthly consultation fees.
  • When the care takers energy and thought process are consumed in many non academic activates one can expect how the illness can be taken care off.
  • When investigations are ordered the primary referring doctor feels he is being denied of  kick backs from costly investigations which is enjoyed bu the specialists .so these general practices what to finish of all required investigations in their desired lab and sent to the specialist.
  • This has led to  curious  situations  where a  ENT surgeon calls for  a  64  slice CT scan and obstetrician asking  for MRI brain (  because the patient is theirs  ! )  

The sequale is two fold . 

The specialist often gets annoyed  and  feel insulted  to read an investigation  ordered by a  different physician(  rather irrelevant  physician !) done  in a non friendly lab  without incentives.

  1. Either he looks at it reluctantly
  2.  Or orders  fresh investigations

 (Some physicians show   extreme  arrogance ,   as  they call for fresh investigation even if the patient is having    good quality ,    investigations  with  images done recently  !)

Finally , the most dangerous thing

A  patient once admitted  under a  doctor, the  prescriptions and procedures are  often  controlled by the admitting doctor .We  have seen a pathetic situation of plastic surgeon admitting a rheumatic heart disease and trying to manage  with the help of  telephoning consultations with a cardiologist .

There is a  chaotic  discipline  in ordering Investigations and treatment modalities  in our country .Any one can order any thing they want .In this scenerio,  abberrant patient  behavir leads to further  complications as patients  themself  decide what investigations they want.

What is the solution* ?

The concept of family physician is still a best option . It has to be continued. There need to be a proper referral services into well equipped, staffed ,  audited institution in every district and counties either controlled by Government or well-regulated. private bodies . The financial remuneration for the doctors should be constant and fixed irrespective of the form   treatment they provide.

In other words the entire health care delivery  should  be centralised and institutionalised .The need for specialist to be assessed properly and care should be rationed .

                                                           Consider this  anarchic situation –  An   asymptomatic, incidentally  detected  30 %  PDA  lesion in a rich bed ridden ,  old man   is  stented by a  3rd generation drug electing stent in a corporate hospital,  while   many  young  Indians with a productive life  with  critical  left main .proximal LAD   is allowed die in peace .

                                            Where are our medical economists and  health care planners hiding ?  ! And we are talking about billion dollar medical  tourism industry .

A general practitioner  should receive same amount as consultation as a neurosurgeon or cardiologist .If we  divide  the doctor into different grades according to the knowledge  and place of work ,  the lesser doctors  will find someway to equalize their earning with their superior colleagues.

After all , all doctors take the same oath . . .   A  doctor who treats a febrile convulsion in a remote village by administering  a timely diazepam  injection can not be considered unequal    to  a Cleveland neurosurgeon   who clips a AV malformation in the circle  of  Willis to terminate  recurrent convulsion in a similar child .

* One would  tend to  think , these solutions are highly theoretical  not implementable in today’s world.  But trying to bring order to a dysfunctional  medical  care delivery system is not a crime any way !

Final message

Most doctors continue to be noble and dedicated.  But the faith in them is rapidly eroding .This is becoming  a dangerous trend . They can not to be  blamed  in isolation.   It is the dynamics of  social and economic scenario  that  are  driving  the medical profession in a journey towards a  commercial extravaganza , where humane care is  as obsolete as a Mediterranean dinosaur !

Now young doctors are  readily manufactured  in the countryside   (Not my merit  , but  bought as commodities akin to real  estate) . A three bed room flat and a MBBS  seat roughly  costs equal in India !

There is  no wonder then  , doctors will treat their degrees  and patients  as  precious   property . Nothing wrong to consider  them as their property ,  but let them handle the property with at most concern , faith and trust !

Disclaimer *This  article does not intend to  defame any doctor or medical profession . It aims to  encourage a wider debate on the issue  . This is  about  many physicians which we come across everyday   in  our  towns and cities  .This article may be irrelevant in  many  other  countries and  to those physicians working in a completely institutionalised  health care delivery system  including  Govt .hospitals where the collective care (or is it collective no care ?)  is the norm .