Archive for February, 2010

Cardiology  is  among the top medical  specialty  in the current era. It deserves this  special status as it is probably  the  a specialty  which  is based on maximum  scientific evidence and  involves ,   the  most advanced diagnostic and treatment  modalities.

As on today ,  a cardiologist  can deliver a stent  anywhere along the coronary tree and even  implant  a valve percutaneously . A surgeon can put multiple grafts in a beating heart  with a patient totally awake !

A  person can live with an  artificial heart for months and a cadaver  heart can give  fresh lease of   life to a terminal heart failure patient .

Why such a glorious filed of cardiology  should often   evoke a pessimistic reaction  in the minds of  public and media ?

This is because  for a   simple reason , in the name of technology , we tend to  indulge in scientific excesses.

This article in Circulation is not a  surprise then . . . Click on the link, Thanks to AHA this  comes free of cost !

For pdf article click on  the image

Note : Non adherence , inappropriate therapy,  Class 2b  indications ,  are  simply semantics in stage  play !

Actually these terminologies are synonymous with

  • Guideline violations,
  • Unscientific ,
  • Empirical.
  • Unethical or  even quackery

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We generally  believe  drugs  and devices are prescribed  by  physicians with strong scientific basis .Unfortunately  it is  not  true  in many instances.  A drug which is approved for one disease is assumed to be useful in a similar disease  (But not tested in  clinical trials ) and it becomes  an unapproved  indication .This is often termed as off label use (A decent terminology for unscientific usage !) .But ,there are pros and cons to this type of physician behavior .


The best example  is  the role of sildanafil in pulmonary arterial  hypertension(PAH)  . A drug which was introduced for erectile dysfunction , was found to very useful in regressing pulmonary arteriolar pressure  (Mistaking pulmonary arteriole for penile vasculature  !?) .  A new therapeutic concept was born  for a  hither to difficult problem of PAH. This  successful  discovery  was  attributed   to off label  usage  of a drug .


But this is a rare  success story of off label therapy.  In real world , we  tend  to  overuse this in many situations and harm is anticipated.

Drug eluting  stents was used extensively in off  label situation ( Acute MI in a thrombotic milieu, very small vessels , in close proximity  to bare metal etc all these are non label or off label  use of coronary stents   which  resulted in many deaths )

Who gave the freedom and liberty for the physicians to use a drug or device off label ?

No body gave  it , we assumed ,  we have it .

When somebody uses a drug for an unapproved indication is it not unscientific  and guideline violation ?

It is a violation , but we can afford to do it because every body does so !

Is there any scientific  body to sanction and desanction off label  usage ?

Unfortunately  not !

So what  is the solution ?

Self regulation  . . . Can it  be  a  fool-proof method  ?

or  Is it foolish  to expect it so  in this   era of commerce  ?

Related video in youtube hosted by me.


Related article

Guideline violation in cardiology practice

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Common sense would  indicate  medical care is  meant for the sick and ill  . Relieving  the mankind  from all those  suffering  with a healing hand has made the  medical profession noble and sacred .Medical science   grew with this sole aim  many centuries ago  .Some  times  we succeeded   and many times we failed  and the journey is  continuing .

In those days ,scientists were dedicated , inventions were genuine and were driven by a need to conquer a diseases .Some where along the line, (May be in the last 2-3 decades?)   our quest for money power exceeded commonsense  . Commerce entered   every  walk of life and  medical science became the biggest causality.

The purpose of noble   profession was forgotten . Simultaneously   public awareness and quality if life vastly improved in many of the developed countries . So the traditional illnesses  either disappeared  or reduced   to a great extent . Then came the life style diseases.The cost of treating  an illness spiraled too much especially   in the scientifically advanced countries . What was perceived  as great health care system  became  the  most ridiculed  health system in the planet  ?

Why ?  The simplest answer to this q  is

In the name of science  and  modernity , medical treatment  was glorified beyond the level it deserves ,  and hence  the  cost of treatment is  kept at artificially  & foolishly high  (This often involves  diagnostic   exploration of human body with modern gadgets without any meaningful   purpose )  .

ie , In  a  nutshell  of modern medicine is   often a medical mirage than a miracle . We know ,  the chances of success  as we  try  to chase it. If we think the  world is   waking  on this issue .

We are in for a surprise ! Even as  every one  is asking for outcome analysis in modern health care

more and more countries just imitate the failed ( Scientific and moral failure ) western models of health care .

When major illness are reducing in a society what will the health care providers do ?

Feel happy ?  Yes that’s what   a  sane   mind  would   do .  In a capital  rich ,   health conscious ,   knowledge  driven  society the opposite happens .

When  the patient  input  into a top hospital  reduces , the MBAs   in  them plan strategies  to bring  increase the bed occupancy rate and  maintain  patient  parity.

If sufficient  patients  are not there in a community what shall we do ?

Create  more  patients

Creating  new patients is a too dangerous game ,  what shall we do ?

In the  name  of preventive screening   let  us  label   normal  persons as patients .

How to do it ?

The following examples  are personal observation made in  huge city of educated elite  in a developing country . Excuse me if it offends a few  . . .

Define, redefine all criteria that define the disease (There are

  • Make, 130/85mmhg of blood pressure as pre hypertension and make them visit our HT clinic every month.
  • In the  name of risk stratification do CRP, Micro HDL , Apo a   etc and  catch them  for primary risk reduction for a non existing illness
  • Let us  label  all the   age related  bone loss as  deadly osteoporosis and do bone graft.
  • Let us  call  the occasional post dinner stiff stomach as non ulcer dyspepsia   and  insert a  endoscope  into the patient tummy .
  • Do a 64slice CT  in a master health check and convert many  of the healthy  normals into carriers   soft  coronary plaques.
  • Do a ultra sound scan  in every one who takes alcohol and  give our brains a temptation to label  the normal  fatty streaks  as infiltrative  fat disorder .
  • Do routine pelvic scan and detect  sub clinical fibroid uterus as potentially  malignant and  post them for hysterectomy on the next operation day.
  • Convert all healthy women as a  potential cervical cancer  and administer  herpes vaccine and help  the vaccine company share  move up in wall street !
  • Finally , screen  all  our  playful   kids for   learning disability and   label them as slow attention deficit disorder  and  make their  life permanently   miserable .

The list is endless  . . .

Final message

We  are in a  era ,  where  even   a  simple  illness  ( common cold ? )  can be converted into a billion dollar industry . ( Are you aware of H1N1 fiasco ,  The role of   WHO  and  mystery labeling of pandemic !)

While the above  misadventure  with scientific excesses   goes  on merrily  , lest we forget , millions of children  and adults  suffer in misery for want of  live saving  investigations and drugs  in any country .

When a person with a head injury dies due a  missed   subdural  hematoma for want of CT scan in one hospital  ,  ” in the adjacent hospital”  a wealthy and healthy man  ( who got admitted for master health check up ) undergoes  a series of scans  all over the body   even as he is  watching   the  satellite TV in  the comfort of a  five star suite   !

God will never  forgive  the  noble professionals   if they are part of this  negative health care  forces

Finally  ending with a very positive note !

The new   initiative by  Obama   , ” Health care  for  the uninsured ” is to be welcomed as great move  and will do a world of good .

But , our  only  request  to WHO ( or related   bodies )  is to create a forum or authority  to  impeach all fancy diseases from the medical   literature  !

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The same channels , that  create the  deadly prolonged  QT interval  by  delaying the  repolarisation  in the heart  is  responsible in the for the deafness  as it interfere with inner ear

Mechanotransduction of sound into neural signals .

For proper auditory function  , the cochlear hair cells   needs  a continuous flow of endolymph which  maintain a voltage gradient for  nerve  signal  transmission  .The lymph secretion is  is regulated by potassium channels  KCNQ1 and KCNE1 . Mutations of this gene impairs  the K + content of the endolymph. It results in  a compromised  endocochlear potential (Difference between peri lymph and endolymph potenial )  .This result in irreversible deafness .

Link to   a good   illustration from Medical physiology

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Cannon Sound

A loud first heart sound (S 1)   which is  heard intermittently in patients with complete heart block (CHB)  is  often referred to as  cannon sound .

What is the mechanism of loud S1 in CHB ?

We know , the intensity of S 1 is  mainly determined by the  relative position of mitral leaflet (To be precise, the  anterior mitral leaflet(AML) )   at the onset of systole.  We also know the  PR interval  has an intricate relationship to  mitral leaflet  position .

The shorter it is ,  wider the leaflet separation  and a longer PR interval makes a mitral leaflet assume a almost closed position   by the time the ventricle contracts.this happens because  a long drawn PR interval fills the ventricle more completely and LVEDV  reaches the maximal levels and LV blood column lifts up the mitral leaflets , and hence the LV  contraction  which follows does not close it with a  bang. In a short PR interval the opposite happens and hence a loud S1 .

In CHB we have variety of PR intervals ranging between  very short to long   ( falling just before the qrs complex) It is not difficult to understand this , as P waves are totally dissociated with the QRS complex  in CHB.In fact p waves have a liberty to fall any where in the ECG tracing , some call this as marching through the qrs complex !.

Hence typically the S1 is variable in intensity , varying between loud to soft.  When  P wave falls just behind a QRS complex , it generates a very  loud S 1  that is called cannon sound .This happens intermittently.

Cannon wave

This is entirely different phenomenon except that it shares the word cannon . Cannon a wave is  a visual finding on the jugular venous pulse.(JVP) .It is a systolic event . It is also seen in CHB as like a cannon sound

This is a giant a wave  in  JVP  when the right atrium contracts against a closed tricuspid valve. In physiological situations atrium contracts with an open AV valves , so that ventricle gets  filled . So atrial contraction  does not does not cause any reflux of blood back into vena cava.

But, when the atrium  contracts and  finds , the AV valve closed  there is no other option   for the incoming blood  to reflux  back into  the neck veins. This is seen as giant a waves called as cannon ” a “waves

With reference to ECG  location ,  this cannon”  a” wave occurs   whenever p wave falls within the ventricular systole ie  the QT interval .The cannon waves also occur intermittently like the  cannon sounds.

What is the  peculiar relationship between cannon a wave and   sound ?

In fact , it is  a non- relationship.  Though  , both the sound and wave   can occur in a given  patient with CHB ,   they can not occur simultaneously .This is because ,  for cannon sounds   to occur  the  P  wave has to fall before  QRS  and for cannon waves to occur the  p   waves must fall after QRS  ie with QT interval .

Clinical significance  of  cannon wave

Complete heart block is the most common situation for cannon waves to occur.

Ironically ,the VVI pacemaker which is used  to treat CHB does not prevent the cannon waves , and atrial contractions continue to occur at random , causing various degrees of intermittent venous reflux into the veins .This may produce, worrisome venous palpitation in some (Usually settles down after few weeks !)

Some attribute , the so called pacemaker syndrome ie giddiness, dizziness to this abnormal venous waves triggering the carotid baroreceptors (Venous -artery spillover )

Will DDD pacemakers  eliminate venous cannon waves ?

We hoped so , it does in fact . But,  it really happens only if the A sense V pace mode . A pace V pace mode with programmed PR interval is not a realiable way to produce AV synchrony. It is  common ,  many of the DDD pacemakers fall back to VVI mode either intentionally or by mode switching  for various reasons.


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There are many  cardiology journals we read , trust , and celebrate  . . .

Many of us are not aware of   few other excellent journals

This is one is different

It is  from  Scandinavia &  deserves a special status.

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Internet is  a  wonderful gift for  for mankind   but  only  occasionally we find great resources .

Hats off to Dr .Pybus from Australia for his efforts

A must read for  all cardiologists rather  everyone involved with echocardiography

Click on the Image to reach the site


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Thrombolytic therapy was a  mini revolution  when it was introduced two decades ago .It has since evolved  , not only in the  molecular structure  but also in it’s usage pattern.

The first generation streptokinase is continued to be used even today  . While the latest generation thrombolytic agent TNKTPA(Tenekteplase) is threatening  to push the  old warrior out of  CCU.

(Of course the  American Physician & Pharma  community  never  gave the due respect to  streptokinase  !)

The two common indications  for thrombolytic therapy  are

  • Acute pulmonary embolism

Uncommon indications

  • Stroke( Can be common in few institutions)
  • Prosthetic valve thrombosis
  • Rarely DVT

From the beginning , there has been a controversy  about the thrombolytic  dosage and  the speed with which it is to be administered .Let us recall , streptokinase was initially  used  in  various regimes ( 5-30lakh units between a 10 -3hr infusion )  Later ,we arrived at a consensus at  15L units  in 1 hr infusion . TPA also experienced the same . Which  settled  for front loaded regimen(35 + 65mg)  . The confusion reappeared when we developed bolus thrombolytic agents( TNKTPA) .

In STEMI thrombus formation  is  often a one time process  while thrombolysis is a continuous process. In pulmonary embolism both  thrombus formation  and lysis  is often continuous process  .

The success of thrombolysis depends on the sustained  drug concentration ,  the pressure at which the drug interacts  the thrombus.

Many times it is prudent to administer  intensive heparin after thrombolysis  to prevent recurrent thrombosis. Further ,  most of the pulmonary embolisms  will require long term anticoagulants.

How to maximize the success of thrombolytic agents ?

  • Local catheter based thrombolysis can be tried  within the coronary ostium (Largely unpopular)
  • Within the pulmonary artery for pulmonary embolism (Still considered an useful option )

It  makes sense , to administer these thrombolytic agents over a prolonged period of time so that the lytic process gets wider recruitment of the natural lytic mechanisms.

When a drug is infused continuously , the drug  reach the thrombus in  a pulsatile manner , which facilitates thrombus dessication  (Like drip irrigation ) . A long acting drug even with a high concentration may not be  very effective , since  the  drug is required to produce a mechanical effect  here . (Unlike say a long acting antibiotics !)

TPA in Pulmonary embolism

The inadequacies  of  2 hour infusion of TPA is  glaring in acute pulmonary embolism .We believe   a 48-72 hour streptokinase infusion   has a definte edge   over a short and brief TPA infusion.

Issues need answer

It is yet , not understood why we can’ t infuse TPA as  a   long term infusion like streptokinase .

Advantage  of bolus TNK TPA  in  pre-hospital phase of STEMI

The argument in favor of bolus dose  thrombolytic agent  is  the ease of administration .

The other the major advantage claimed  is ,  a 10 second  TNK TPA   in STEMI  can  substantially  reduce the time window   and facilitate  early completion of thrombolysis .

Counter point

But , the  later concept is hard to prove  . . .

In fact , there  are  no controlled studies  available for assessing the   efficacy of TNK-TPA   vs  Streptokinase   with reference to various time windows. We presume so many things. An  incomplete   early thrombolysis  may not be better than a  more  successful  but  slightly delayed TIMI3 flow .

As scientists,  when  we try  to answer these  question we  ask for data .  Are we getting it any way ?  Are the existing data reflect  fact ?     We  wonder,  will we may never get   an  hourly  angiographic  data base  about the IRA  patency  in  TPA bolus  vs streptokinase infusion .

It is most unfortunate,   with  many of the critical questions   still to be answered ,  the cardiology community believes ,  they  have  reached the  summit  of  knowledge  about thrombolytic therapy . Current perception is , the research on  existing  thrombolytic drugs  is  deemed to have been complete .

In this hyped  era of interventional coronary  care  ,   it is a remote possibility   to have any  further comparative studies on thrombolytic agents .

The greatest threat faced by  us  today  is the destiny  of  modern medicine is   often  decided in  few corporate board rooms  and   hence   research questions  rarely  emanate from bed side !

In this scenario, where we are not likely to generate   genuine  clinical  data ,  the only way to move   forward is   to go  by  our experience – ” Genuine  experience to be precise . . .”

Final message

Ease of administration should never be the criteria in choosing a thrombolytic agent . It   can severely    compromise the quality of thrombolysis  ! especially in pulmonary embolism and to a certain extent in STEMI.  Success   rarely  comes  with ease  . . .

Many believe , the choice  between  streptokinase   & TPA    goes much beyond it’s academic reasons.  TNK TPA (Tenektepalse) has come in a big way to replace streptokinase  even   in developing countries.  Ofcourse it is backed by a huge study  ! (ASSENT) .

The cost effectiveness and worthiness  of TPA over streptokinase  was  never proved comprehensively.

Note of caution :

The observation made above is   based on personal  opinion  in  about   20 patients  . Readers are  argued to do their own  analysis on this issue and come to a conclusion .

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Coronary artery anomalies are relatively common . It can be either in it’s origin, course ,  or termination etc.

There are two major sub groups.

  1. Anomalies associated with other congenital heart diseases (Both cyanotic and acyanotic)
  2. Isolated coronary artery anomalies .

The second category  which we encounter in cath labs frequently  does not have major implications . RCA and LCA arising  away from it’s respective sinuses ,Separate origin for LCX, or conus, RCA from left sinus or a high take off of RCA are the common anomalies.

While  coronary anomalies are commonly associated  in complex congenital heart disease (TOF, DORV, TGV, etc )

Isolated  complex anomalies of coronary arteries are extremely  rare

This happens , when one coronary artery arises from pulmonary artery instead of aorta and   it becomes a fascinating disease !


When the LCA originates from PA it becomes a  rare cause  of  left to right shunt .it is referred to anomalous origin of LCA from PA (ALCAPA) .

The ALCAPA is many times common than the “ARCAPA”

We report a case of ARCAPA (Anomalous orgin of RCA from PA )

The unique features of ARCAPA  could be

  • Isolated ARCAPA is very rare.
  • Only a handful of  patients reported in literature
  • These children present with more of right heart failure as RV function is compromised .
  • A continuous murmur in 2nd LSCS without cyanosis gives a clue
  • Angina is rare unlike ALCAPA
  • Mitral regurgitation is uncommon as LV function is relatively intact.
  • The q waves in V5 V6 we see in ALCAPA is conspicuous by it’s absence
  • ARCAPA is often ssociated with bicuspid aortivc valve, VSD etc
  • Left to right shunting can be significant .
  • 64 slice MDCT is a great investigation in this entity
  • Surgical ostial transfer is preferred so as to restore twin coronary circulation

Image and video of the ARCAPA will be uploaded shortly


1 http://asianannals.ctsnetjournals.org

2 http://ats.ctsnetjournals.org

3 http://ats.ctsnetjournals.org

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It is said every clinical diagnosis needs to be substantiated with  documented objective  evidence .

Probably,  the commonest cardiac emergency , that can be  diagnosed purely by history is UA.

Yes , unstable angina is a symptom not a  disease entity !

By definition UA is

  • Any  new onset angina  of severe grade
  • Progressive crescendo angina
  • Angina with radiation to new site
  • Angina not controlled by nitroglycerine
  • Any angina after a PCI /CABG

If you read the definition again, you will realise ECG or enzymes never come into the  diagnostic picture .UA can be diagnosed even before one has a look at  the ECG ! So, it is too obvious one can diagnose UA irrespective of whatever is recorded in the ECG. Normal ECG is one such possibility.

When a patient is having severe  compromise  in the  blood supply to his / her heart  , how  on earth ,  it  is possible to have a normal ECG ?

It only tells us,  ECG is not a fool proof method to exclude ongoing ischemia . When we know , ECG can miss even a STEMI  it is not a big deal it misses a UA.

Apart from  the electrical blind spots of conventional 12 lead ECG, following are the other  explanations offered for a normal ECG in UA.We know UA occurs with ST depression(Classical ) , T inversion,  rarely ST eelvation

So UA can occur with

  • Pseudonormalised t waves
  • Pseudo normalised ST depression
  • Cancellation effect of two  opposing  subendocadrial ST segment vectors ( As in multiple active plaques PDA   and LAD lesion )
  • Even Ischemic cascade

Final message

Even though  UA  CAN  occur with normal ECG  , we are uncomfortable to   diagnose  UA without   documenting ECG changes . We should realise this fact , as missing a diagnosis of UA , just beause the ECG is normal  could have very costly consequence !

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