Archive for April, 2013

ASD is  the most common acyanotic heart disease  with  left to right shunt . Highest qp/qs  are  seen  with ASDs

The shunt  begins  from left  atrium  and goes on to complete a circuit.


In this circuit all chambers  enlarge except the LA . (Inspite of the fact about 200-300 % cardiac output traverses this chamber )

Why ?

Post -test

The most popular answer in the above poll  is LA is  a transit chamber .

If it is so . . .  RA is equally  a transit chamber ,  why it enlarges significantly ?

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For STEMI management there are  6 management protocols available

  1. Thrombolysis
  2. Primary PCI
  3. Rescue PCI
  4. Facilitated PCI
  5. Pharmaco -Invasive approach
  6. CABG

*CABG is rarely used except in  severe mechanical complication.

There is some  issues in differentiating  facilitated PCI and  Pharmaco Invasive Approach.

What do we facilitate ? How we do it ?

PCI in acute STEMI is done in a thrombotic milleu. So we get sub optimal results .Hence to facilitate it we try using

either 2B-3A antagonists, Newer Heparins, or even thrombolytic agents before submitting them for PCI

Where is this facilitation done ?

Facilitated PCI is done in small hospitals where  there  is no cath lab or cath lab is available only during office hours.

Facilitation can be done in either in same hospital or on the way to big hospital

Is there a time window to start  this ?

The main aim was to was to facilitate the PCI .Hence time window was not considered vital in few studies (Wrongly though !) ideally it should be started as early as the first contact . Since facilitation can be started earlier the time window is 0-24 hours .

What happened to the concept of f-PCI ?

It died a premature death  and  last rites were  completed when the FINNESE trial was out .

But it left behind a daughter concept ie in selected patients if the facilitation is done early , especially in those patients who are going to get the subsequent PCI late ,or in high risk individuals  , the initial  pharmacological facilitation* was indeed useful.)

*If  facilitation was with   fibrinolytic agents (Not 2a/2b )  .It is very important the benefits of facilitation is mainly  attributed to the time gain in achieving partial opening of IRA  making it more complete salvage of the subsequent PCI .

This aspect later on named as PIA .

Pharmaco- invasive approach(PIA)

We know p PCI is a race against time .We also  know fibrinolytic therapy  fares well in this race  but   pPCI  beats in   effectiveness  .

So what prevents us to combine the swiftness the fibrinolysis and the robustness of pPCI ?  That is  like getting the best of both world .( It is not that easy thing accomplish after all 1+1 in medicine is rarely 2 !)

In it’s core principle it  is same as f-PCI . But facilitation is done only with fibrinolytic agent (Not 2B-3A) . Pharmaco Invasive strategy can be started in any small hospital/ In the ambulance /. It  is routinely followed by PCI whether the initial thrombolysis is successful or not . PIA should not be done before 3 hours window if  a timely pPCI is feasible.  Hence PIA has a typical time window of 3-24 hours .


f-PCI is combining  various anti-platelet and fibrinlytic strategy prior to PCI . It was found  to be useless if it is used routinely in all cases of pPCI. (Rather 2B-3A  was useful  if  only the facilitation was done within the cath lab to prevent procedure related issues) .Time window can be between 0-24h .

Pharmaco Invasive approach (PIA)   is actually a type of f-PCI where  fibrinolytic agents are used routinely which is followed by mandatory angiogram and PCI in all deserving cases.Many still  believe the facilitation in PIA is primarily accured in  shortening the   time to reperfusion  rather than altering the thrombus load and morphology  ! Time window is usually between 3-24 hours.

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Interventional   cardiology has  grown leaps and bound in the last few decades  .We are able to clip the wings of mitral valve  without surgery when it prolapses

We  can deliver a huge aortic valve and fix it with wires .

But  . . . we have no proper  preformed   guiding catheter  that can  sit into RCA ostium directly   and snugly  for a long time to enable complex RCA angioplasties !

An now try this one .


Here is  a  pending patent for  a preformed RCA catheter

preformed rca catheter

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The mechanical atrial function   during atrial fibrillation remain a mystery . In fact , the general  belief  is during  AF  the mechanical function of atria is zero. This is why AF  is promotes stasis and   LA clot formation. It may appear theoretically correct  , still   AF especially coarse  still imparts some amount of  mechanical motion .But this usually does not translate to any useful hemodynamic function .

If atrial booster pump is lost (which is said to be 25 % of  LV filling )  suddenly one expects dramatic symptoms  especially if there is associated LV dysfunction or aortic valve disease .

But in real world AF is well tolerated arrhythmia in most  .  We know by land  mark trials AF  is as good as sinus rhythm  if the rate is  is under control

This is a definite evidence the AF  may not compromise  LV filling   even if   it nullifies  the  atrial contractility .

There is one  more evidence for  retention of atrial mechanical activity in spite of AF .It is well recognised , pre-systolic accentuation is preserved  in many cases of mitral stenosis with AF.

*Crazy hemodynamics : For an attached LA clot to  dislodge ,   one needs some amount of LA contraction isn’t ?  Unfortunately  a fibrillating  atria always  tend to  have this one ! This again is a senseless  proof for some  mechanical activity of LA during AF !

How is this possible ?

Is it a  purely volume dependent filling   ? ( Or )  is it  the  Intrinsic LA starling forces that do not depend electrical atrial activation .

This is definitely an  issue to ponder over . A good LV contraction makes the atria empty more completely . This would  somehow  mean , LV relaxation  is facilitating atrial function . During  AF the LV  handles effectively  the additional burden  imposed by the loss of   25  %  booster pump of atria ( Accelerated LV relaxation ? )  A  constantly  changing  RR interval makes LV diastolic function a more complex event .

Final message

Atrial fibrillation is  a well tolerated  arrhythmia in vast  majority of patients  . This  implies either of the two things.

  1. The so called  physiological atrial  booster pump is redundant  or dispensable in otherwise healthy heart
  2. The booster pump is indeed important  . . . but it is less  affected by AF as long as the rate is under control !

It is to be  strongly emphasized , Heart rate and  LV function  will ultimately determine  , how one is going to tolerate the AF  !

It is  a small gesture  from LV  to LA  at it’s hour of crisis  . . . in return  for  it’s lifetime assistance  as a booster pump ! 


How  rate control  prevails over rhythm control in spite  zero atrial contractility in the  former  ?

Comments welcome !


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TAPVC Total anomalous pulmonary venous connection left vertical vein

An animated version

tapvc total anomalous pulmonary venous conncetion vertical vein

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stent graft vs coronary stent principles aortic stent graft 002

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In HCM every myocyte is  genetically made  defective . Myofibrils are in disarray every where . Still , can we identify some vulnerable zones that acts as arrhythmic  focus ? If that is possible , we  have a opportunity to abate that focus .

In HOCM  , which is the most stressed area ? LVOT ?  Septum, ? When we say stress , it can mean either mechanical or electrical .


Does electrical instability involve the same zone as mechanical stress ?

How often VT originate from LVOT in HCM ?  For this we have good clinical model _, the patients who underwent alcohol septal ablation.

What happens to the incidence of VT  post septal  ablation  ?

“It is reported  post septal ablation the incidence of SCD  becomes  equal to general population” (Read the paper below )

If that is true , it is obvious the  arrhythmic  focus is also ablated along with LVOT myocardium .

Outcome of HOCM after alcohol septal ablation

Though many studies claim  so !  It  fails to convince us  .  HOCM is a diffuse disease of  myocardium.  Even a cluster of myocyte disarray  with fibrosis   can be a future focus  irrespective of it’s location .

However ,  it is always possible relieving the mechanical stress of the LV can definitely reduce the likelihood of an electrical event .(Even if the arrhythmic focus is intact elsewhere !)

* We know RVOT is  developmentally arrhythmia prone zone . We also know HCM involves RVOT (After all ,  IVS  is legally shared by both ventricles !  ) . Some of  the monomorphic  VTs with LBBB morphology may originate from RVOT in HCM .

Management of recurrent VT in HOCM

  • Drugs (Amiodarone/ Calclum blockers/ Beta blockers/Disopyramide)
  • ICD- (Probably mainstay  )
  • Very rarely ablation (If localised focus is well documented )


1.A case report for successful ablation of  VT in HOCM   http://www.ncbi.nlm.nih.gov/pubmed/9255687



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Systemic hypertension (SHT )  is the commonest  clinical entity encountered in cardiology consultations . 95 % of  HT is considered primary. The remaining 5 %  form the most important class of HT (Secondary to renal parenchymal, vascular , endocrine,  etc)

How  intelligent is this traditional classification of HT  ?

The incidence of primary and secondary  HT varies depending  upon the level of investigation we do . One of my  regular patient  who gets to me for  HT .He  is 42 year old man  works in financial institution  with lots of work stress and he was marginally obese as well .  He was investigated for all known cause of secondary HT and every parameter  was found to be normal and was being treated as   primary HT.

When he was about to leave my clinic he  bowled  this google !

Doctor , why do  you call  mine as  primary HT   ?  . . . When you yourself  say  my stress and weight is responsible for  high blood pressure ?

Primary vs secondary HT

Valid question is it not !  . .  . I told him   “somehow”  ,   we have not  been taught   in medical schools  , to consider stress  of life  as a factor  responsible for  developing secondary  HT !

Final message

Strange  definitions in medicine continue .  Not every one with high stress  levels develop HT  .There  are  some unknown factors operating  .Till we know that we  will keep calling them as primary HT .

( Who  knows the  man  who raised this question  may   show up  with adrenal hyperplasia  or a renal parenchymal dysfunction 5  years down the lane !)

We live by perceived  knowledge  on a moment to moment basis  ! . Ignorance  tries  to lock the doors of knowledge .

But we  continue to open new doors . That is the  only  purpose of medical research !

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Q waves are  neither  sacred  nor sinister waves . It represents   either of the  following .

  1. Electrical activity that goes away from the recording electrode.
  2. Or whenever there is a  electrical insulation or hurdle that interrupts the flow  of current  towards the electrode ( and if it is sustained )  it  can result in q waves (Minor interruption produces  a notch or  slurs . Please note a major slur becomes a q wave equivalent  )

Here is young women of 42 years with  a diagnosis of  old  anterior MI for   over 5 years ( Getting a dedicated care from a cardiologist!  The prescription included Imdur/Betaloc/ Statin/Clopidogrel and Aspirin )

This was the ECG . It was very convincing for  old ASMI.

epicardial fat and poor r wave in v 1 v 2 v3 q  waves

It  happened ,  I did an echo for her .

epicardial fat and q waves in ecg pesudo infarct non infarct 2  q

She lacked wall motion defects even after a meticulous search .  Instead   she had a   good layer of epicardial fat measuring 9 mm .That was more localised in  anterior wall extending little to LV apex.Her EF 65 % .

*She was a  fairly obese (not gross )  individual with a BMI of 34 .The fat pad thickness was not that huge  , I thought , still it was producing the q waves . I  have seen much thicker fat pads with good R waves in ECG . I  wonder ,  is it the type of fat that adds up to electrical insulation ?

This patient was sent back to me  again  for ruling out ASMI .  Echo was  done  two weeks  later . No evidence for  ASMI  could be detected.

epicardial fat and q waves in ecg pesudo infarct non infarct fat 2  q

What is the normal thickness of epicardial fat pad ?

It is less than few mm . Exact normality is not known .(Empirically < 5mm ) it is very rare for fat deposition  in infero posterior aspect , except in morbid obesity.

What is the function of epicardial fat ?

  • Long considered inert . Now , found to be a metabolically  active lipid pool.
  • We also know  heart  consumes more fatty acid than an other organs for moment to moment energy consumption .
  • Inflammatory mediator in atherosclerosis ?
  • It may also act as a mechanical cushion effect along with pericardium
  • Rarely fat infiltration can compress the heart and may result in restrictive  AV filling defects in doppler  .(May explain the unexpanded dyspnea  in many obese patients )
epicardial fat a dynamic depot athreosclerosis

Role of epicardial fat depot in the genesis of atherosclerosis

Subcutaneous vs  Epicardial fat.

We know thick chest wall can also interfere with ECG. Epicardial fat is more likely to record  q waves than  sub cutaneous fat ,  as the insulation is more closer to heart in epicardial fat . In thick chest wall current leaks from heart and  well scattered  hence  poor R wave is more common in such situations rather than q waves !

Following things can generate  q waves (Other than Infarct  )

  1. Fibrosis-Myocardial /Interstitial
  2. LVH
  3. Thickened pericardium
  4. Thick chest wall/ Epicardial fat
  5. Air/Fluid in pericardial space

Final message

In obese men and women  anterior Q wave can be  misleading .Such  medical errors can be so convincing .

After thought

If epicardial fat can  extinguish   R waves  and  replace it with  q waves  , these  innocuous  looking fat pads has every reason to  influence the ST segment shifts during  an episode  of ACS  as well !  .  Isn’t ?  . If so  . . . how reliable is  our ECG criterias  to diagnose  acute coronary syndromes  in grossly obese men and women ?

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News : It seems the pharma companies are worried   about  the new MCI  (Medical council of India ) guidelines  that restrict  sponsorship  for conferences and freebies to individual  doctors  . They think it is a  big set back  as it  may interfere with doctor’s  education and knowledge  !

ethics and pharma compnaies

They have proposed new amendments and  has asked  the health ministry to advice the MCI accordingly .(ie To help them bring back  the corrupt and bad practices  that  influence  doctors prescribing behavior  !)

It is true , for the  growth of medical science , we  require some sort of  a business model and  tax holidays for the companies for true  &  land  mark discoveries  . Currently the MCI allows to sponsor  medical  events or a conference  for an institution or organization .  But  what these companies want is  official permission to provide  incentives to individual doctors and influence them  ! .  More shockingly  they said  doctors knowledge will  suffer without these industrial support . It is an outright insult to all doctors who get educated  for over  decades* . In fact the heads of pharma companies require  few lessons from the medical fraternity  ,  how many drugs with  dubious scientific value  is playing havoc in  health of  the society !

Of course ,we can not blame the pharma companies  for  all . It is a collective evil.

Counter point

*This  is a  second  slap on the face of  medical profession  !  I am  sorry to say this ,  many of us ( Including  the blogger  ! )  are some way responsible for this state of affairs  . Shockingly ,  few of  our  colleagues are  proud  to  have illicit relationship with drug companies !  Younger generation   no longer consider  this as an offense  , since they are born and brought up with  capitation fee as their principal fodder. Commercial forces  has taken over  medical  profession . Many of the  colleges are owned by business barons and alcohol vendors  in India . It is a well known  fact , MBBS seats are now  sold for 50lakhs (like  3 bed room flats )  . Agents transact black money in secret basements of   medical colleges  once considered  as  temple  of  the  noble profession .

So what is  in-store  for the future ? . . .  Self regulation is best  regulation   . . .   Mahatma told us ! . It  may be  the most idealistic     solution   . . . but  currently   it appears   self  regulation is  as bad  as no regulation !

Link to the article


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