Archive for the ‘cardiology innovation’ Category

As we practice this Noble  (&  Delicate )  profession ,we often tend to Ignore the  warnings  even from our learnt colleagues , Why ?

Wisdom ego quotes brainy best dr s venkatesan top inspirational




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Many decades ago Potts  shunt  (Central Aortic -PA shunt)was used to increase pulmonary blood flow for severe RVOT obstruction mostly for TOF  and tricuspid atresia .With the advent of  ICR and  Fontan role for central aorti shunts waned.

Now, read this

Chronic ,refractory pulmonary hypertension of any cause has dismal  outcome.In  patients with severe PAH  many patients  reach supra-systemic pressures . RV   a volume handling chamber faces a uphill task of overcoming huge RV after load. As cardiac physicians , we  struggle  to  perfuse the lungs in such situations.

The only option  seems to be  lung transplantation !

How to perfuse the lungs if the RV is failing ?

Is there any other alternative ?

Why not,use LV contractility  to perfuse lungs .

Great Idea isn’t ? After all , how can we allow left ventricle known for it’s  robust bumping function  sit idle and relax  when it’s counterpart is struggling with heavy load ?

How to use LV for increasing pulmonary blood flow ?

Create a central Aortic -Pulmonary shunt.

That’s resurgence of Potts shunt.

Dr Julie Blanc from France suggested this approach in in NEJM as a letter  (Potts Shunt in Patients with Pulmonary Hypertension N Engl J Med 2004; 350:623) .  It  was a great Idea.

Since then lots of patients  have a benefited from this vintage surgery.

potts shunt in severe pulmonary hypertension

Final message

A surgery blamed for early onset of pulmonary vascular damage due to potential Eisenmenger reaction is back .Indication for refractory Eisenmenger syndrome to perfuse lungs  at very high pressure Nothing is obsolete in medical science .Nothing is ironical as well !

Another Innovation : Now Transcatheter Potts Surgery

potts shunt for eisenmenger and severe pulmonary arterial  pht pah

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Few Innovations are real breakthroughs in cardiology . Here is an imminent technology waiting to explode in the  permanent pacing . Expected to hit market next year (2014 in Europe ) FDA approves clinical studies .


Click over for the animation video  of the procedure .

  • The wireless pacemaker has many advantages. (It’s devoid of all those pocket and wire related issues.)
  • The ability to change batteries is  a  going to be a  new paradigm shift in the filed of electro physiology. .
  • Down side would be,  right now it can be only VVI pacing . All that hype about    physiological pacing  will go to the background !

Future directions in Permanent pacing.

The only threat for this technology is the  concept of biological pacemaker Converting ordinary myocytes into  pacing cells by genetic engineering.This is expected to happen within few decades.

biological pacemaker

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I stumbled upon this  web   site . I think this  can be  glorified as the  standing  example  for     “Democracy  of science”

INTECH open science  open mind


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Heart disease was  once considered as   rich man’s disease  . . .  It’s no longer  true .  We in India ,  are witnessing an epidemic of CAD . The reasons are  varied  . Apart from  conventional factors ,   social   factors  like changing demographic pattern  ,  life style , ethnic  risk  like  south  Asian metabolic profile are responsible .

While  Rheumatic heart disease (RHD ) continues to be a huge burden , CAD  is  the number one  cause for cardiovascular morbidity and mortality .

CAD affect the poor and rich with equal vengeance . The later is better equipped financially to tackle it . Of course ,  it has resulted in maximum inappropriate interventions. The poor (or borderline poor ) have  no  other  option  but  to knock the doors of Government  hospitals. It is heartening to note, various state  Governments   are  gradually involving insurance schemes.

Still , many struggle to find the required  finance for  a major cardiac intervention. It roughly costs 100,000 rupees  for PTCA  .While  PCI is required in all symptomatic ,  critical coronary occlusions , still . . .  majority of the  CAD in general population  do not require it . There are 675 cath labs in India performing 180000 angioplasties every year  on an average of   15000  PCI per month ( 500 /day )  This is grossly inadequate . We  have huge potential

What is the hurdle ?

  • Expertise ?
  • Hard ware ?
  • Awareness ?

No  . . . it is all about  financial resources

Recently I stumbled upon an  advertisement on Times of India

cardiology ad ptca

Disclaimer: This article does not in any way defame any hospital that offers the scheme.It just want to debate the concept.

Hospitals  want  to  market the procedure . Convert angiograms  to angioplasties . That’s   corporate boardroom mantra  . And one fine day ,  bankers and medical doctor sat together and brought a brilliant idea.

Why not do the procedure  on credit and  push the patient  life long  into a financial debt !

Wonderful idea  . . . many thought .Thus came the financing scheme for  cardiac procedures.

Final message

Financing a poor patient  with good intention is welcome. But, there is big caveat .In a vast country   with high  illiteracy , inappropriate  procedures   may be thrusted upon  on   the  poor  souls.

After thought

Now ,  our patients   have  one more  risk parameter to  assess   ” Number of remaining EMI( Equal monthly instalment )  and incidence of stent thrombosis”   “Accumulated  interest  and angina”   What a wonderful way to provide cardiac care !

I can recall a  patient who sold his livestock  (his sole income source ) for undergoing a open heart surgery and lost his life as well in the process  leaving the family stranded !


The only solution is  to  provide  a strictly regulated Govt sponsored  insurance scheme.  High tech procedures should be  continuously and meticulously  audited for cost effectiveness .


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In this complex world , simple innovations fail  . . . just because  they are simple !

Here is a new* PTCA  catheter which has a  two balloons  ,  the distal one dilates the lesion and the proximal one has a stent over it  . The stent is just deployed after the dilatation by the proximal balloon . The proximal balloon  not only help us prepare the lesion before stenting it also helps  in crossing difficult lesions  . Further   , it can be even used to post dilate the lesion . It can be a non compliant balloon  as well . It appears a  good  concept .

*Not really  new  I  believe  ,  Accuramed  owns the patent for  this twin balloon catheter over a decade now .(First twin balloon Gemini PTCA was used in 1988 )

gemini balloon catheter twin two ptca pci

I do not know why we haven’t adopted it yet ,  while many  dubious  innovations are making merry around the world !



The only downside could be ,   combinations of stent and balloon sizes are limited . But ,  it is not a major issue .The ability to  fine tune the stent apposition  moments  after the procedure , by h a simple pull back  is just amazing !

This catheter is  made by

Medizintechnik GmbH
Max-Planck-Str. 33 61184 Karben Germany
Tel +49-6039-9201-0 Fax +49-6039-9201-22
E-Mail info@accura.info

Final message

Two  balloons  over a  single catheter  is a  new development  .I wonder it can be  the standard of care in all PCIs . Hope somebody takes  this concept to the next level  for the benefit of our patients.

Link to the manufacture


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An awkward  argument for routine EST following primary PCI

Please remember,  primary PCI is not the end of the management of STEMI. Primary PCI is an IRA focused intervention. We need to study other lesions and their the flow pattern as well. Logically we need to do a test for adequacy of  baseline vascularity and the current revascularisation . Simple deployment of  a stent in IRA (without documentation of good flow during exertion ) is not acceptable to believers of  scientific medicine  . Resting TIMI 3 flow conveys no meaning for a patient who is going to be ambulant and active. A stress test will come in handy .

The micro-vascular integrity and resistance following an extensive STEMI is best studied by the adequacy of exercise induced  coronary hyperemia (This is physiologically equivalent to the much fancied FFR in cath lab ) . One can consider EST following a primary PCI as an non invasive substitute for the collective FFR of all three vessels including the IRA that is stented .

Does any cardiologist have guts to do a pre- discharge EST after a successful primary PCI ?

Typical responses would be

  • Why the hell I should do it ?
  • Do you know how risky it is to do a EST early after a primary PCI ?
  • If at all I have any doubt , I would prefer a non invasive PET or Thallium to study the adequacy of revascularisation.

If you think , it is too risky to exert a successfully revascularised patient early after a STEMI . . .   at the same time   argue  to do it in non revascularised patient routinely .  Do we not see a huge irony here ?

Other inference could be . . . we are still suspecting the quality of our revascularisation during PCI !

If  EST is contraindicated after a primary PCI , are we going to advice  these patients against indulging in any activity requiring moderate exertion fearing a stent occlusion ?

. . . What a way to interpret the aftermath  of a   ‘state of the art ‘ procedure called primary PCI !

In science ,  correctness is more important than politeness !

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Heart is a dynamic organ . It can alter  its force of contraction with every beat  according to the needs.Generally it responds to  length  of  previous  diastole.This is famously called frank starling law , ie the force of contraction is directly proportional to the end diastolic fiber length. So changing diastolic  duration as in atria fibrillation classically result in varying amplitude of LV contraction and pulse volume.

However , the commonest cause for  pulsus alternans  is  due to  severe left ventricular systolic dysfunction .There has  always been a suspicion about the existance of  beat to beat variation in  diastolic function as  well.  We have recently observed a  new* explanation for pulsus alternans .We know AV inflow is subjected to respiratory swings . Non  respiratory swings in mitral and tricuspid valves are rarely described. This pattern is now increasingly recognised.

These  non respiratory swings in the mitral inflow doppler pattern  is seen in  some of the  patients with hypertension and LVH.This  probably confirms the existence of  beat to beat variability of diastolic function . This phenomenon is relatively a new observation . Such pattern are common in patients who have had a recent hypertensive failure .


Here is a doppler of mitral inflow recorded from a patient with hypertension with LVH .

This is the doppler mitral inflow profile of a patient with Hypertension, LVH and class 2 dyspnea .Note the non respiratory swings in both "e" and "a" velocity

It is proposed  to  define  a new class of diastolic dysfunction that can be referred to as diastolic  mitral inflow  alternans .This phenomenon probably indicates a more severe grade of diastolic dysfunction.At the molecular level this is related to  undulating flux  in the calcium uptake from cytoplasm into SERCA .There is one more possible explanation for diastolic alternans  -Left atrial  dysfunction .

Occasionally one can visualise  a chaotic pattern of  diastolic filling waves  (e=a e>a a> e )  Such patterns are thought  to be markers of impending acute diastolic shutdown .

Further  analysis of  this  mitral doppler inflow pattern will be reported  later.


* Though we observed this for the first time , this is not a new phenomenon .There are few reports available in the literature.



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There are innumerable  stresses  to human beings in daily life .

Heart  experiences a few  either directly or indirectly.

  1. Physical stress
  2. Pharmacological  stress
  3. Mechanical stress
  4. Hemodynamic stress
  5. Mental stress

Squatting is rarely realised as a form of physical   stress to heart .  Rather , squatting can also  be termed as a  good exercise  ( Western toilets sans it !)

Squatting  raises the afterload at the level of aorta due to  increments  in SVR (exact mechanism not clear ,neural reflex ?)  and temporary reduction in venous return.

After load raise is synonymous with increased  ventricular wall stress  . So,  it is logical to expect wall motion defect in  vulnerable hearts* when confronted with sudden increase in afterload .(*Ischemic hearts with delicate coronary blood flow ) .Hence ,  sudden squatting , a seemingly simple  maneuver   ,  can  unmask  silent CAD .It can be aptly be named as poor man’s stress echo.

Of course , it  doesn’t   mean in any way ,  it should not be used in rich ! The  purpose of science  is  to make things simpler and cheaper . If squatting can replace  dobutamine with fair degree of accuracy  atleast in a few ,  it can help  control the escalating  costs of  cardiology triaging   due to   many futile diagnostics !


When squatting  is a stress in normal persons , paradoxically it gives relief to patients with cyanotic heart disease

Read the related articles in this  site .

How squatting relieves hypoxia in TOF ?

Squat Echocardiography in TOF

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One of the greatest medical sermon of our times  is   “Doctors must   constantly update their knowledge , Continuing medical  education is as sacred as their profession  !  If you are not updating your knowledge you cease to a doctor “

It is fashionable , but true  to state  modern medicine lacks humane  care . Modern medicine  is  challenged by a huge  technological ,  commercial  onslaught  where common sense takes  the back seat

Hence , doctors need to renew not only  their  academic competence   but also  their ethical  fitness  every  year !

Aggression  could be the other  name for  modern medical care . For every  new  invention , treatment   or guideline that  is  approved  an equal number  is shelved after few months or years  for safety reasons.

Bulk of  medical updates  for  current age physicians  is nothing , but asking   them to forget  all those wrong things that has been meticulously uploaded in their brains in the recent past  ( Recall the classical story of drug eluting stents )

If this is the  case . . . then  . . .  what for  we  are  updating ?   and  for what  we are  learning and forgetting  ?  and  . . . how frequent we need to forget ?  Of course  , there is a big chunk of   human tribe  who  can never master the art of forgetting ! Some mistakes are permanently etched in their terra byte hard disks .

Is there a place  for backdating and discontinuing  medical  education  ?

What  man- kind needs  at times of  medical  crisis  ,  is  not  the current  treatment  but the correct  treatment    .It is our duty  to  find  all those  trustworthy  drugs  & treatment modalities  that were  sent  to  the gallows by the modern medical forces   for various reasons !

If  some of  the gems in  medicine are  left behind in  past  “time domain”  ,  it is  mandatory  for us  to go  back in time and   catch it , adopt it and disseminate it !

Further ,  whenever  the  hyped   “medical updating sessions ”  turns out to be  synonymous with adding nonsense (It is  becoming all too common these days   !) we should resist   it by all means !

For many . . . Hippocrates and his medicine sounds dirty now !

If  only we back-date  our knowledge   .  .  .

Todays  youngsters  can learn a secret that liver enlargement can be diagnosed easily  with their  hands ,  without  waiting for a  CT scan report !

If only we back-date  our   knowledge  . . .

We can realise  Aminophylline can save so many  lives of cardiac  failure  , which  our newer inotropic agents are struggling to accomplish .

If only we  back- date  our knowledge  . . .

We can calmly manage  acute MI with lignocaine  even in a country side  .  Amiodarone unfairly replaced  this  efficient  anti  VT  molecule  for no academic reasons !

If only we back- dat our knowledge  . . .

We  can  advice simple non pharmacological intervention for  stage 1 HT   than prescribing the  glamorous  sartan molecules  form a  multinational  ARB shoppe.

If only we back- date our knowledge  . . .

We can  promptly recognise  cardiac failure  without  ordering  for the error prone   BNP . Back dating also  helps us to under stand  that post infarct angina is a  glaring sign  for presence of   viable myocardium  and prevent us from undertaking a  2000 $ PET  excursion !

If only we back- date our knowledge  . . .

We can  send  all our uncomplicated , asymptomatic   STEMI  patients ( in class 1 )  straight to  their  home rather than to cath lab  play grounds !

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