Archive for June, 2011

The link between migraine and PFO is  . . .

  1. Incidental  & man-made
  2. Almost certain
  3. Definite
  4. A wild imagination

Answer : One of the above  is correct  , but  we do not know  which one is   !

There has been many  patients with TIAs , cryptogenic strokes , who  had  documented PFO  ,complain of prolonged  head aches . This was the beginning of suspicion of PFO as a cause for migraine .Then the device industry foresaw a huge opportunity . Things began to unfold and  the concept is currently as nebulous as it can be .

Mechanism of migraine in PFO

(All are  presumptions )

  • Right to left shunting of  vasoactive amines from venous circulation (Serrotonin)   which bye- passes  the lung where they are supposed to get filtered.
  • Venous micro emboli (Antiplatelet agents reduce migraine as well as TIA ! )
  • Hypoxia transient – cerebro vascular hypersensitivity
  • Atrial naturetic  peptide spills more into systemic circulation through  PFO

Counter arguments

  • If right to left shunting is causing the migraine , why it  is not fully disappearing even after closure of  PFO (MIST data with  starflex  device ,  migraine persisted in a significant chunk !)
  • What is the incidence of migraine in the  prototype  right to left to shunt situations like TOF, Eisenmenger , pulmonary AV fistula ?  if shunting is the mechanism , logically  migraine incidence  should be very high  in this population , but it is not .
  • Migraine occurs in 10 % of population, PFO  is present in 20%  .  What are  the chances of over lap ?  It could be the simple statistics at play !

Where is the evidence  ?  The mystery called MIST study.

This study , done in UK generated more controversy , which  it was supposed to remove  . Still  this  study is considered to be a major evidence for the link between PFO and migraine . Star flex device  was promoted by NMT medical Boston .


Link to  best review article on PFO


Final message

The link between migraine and PFO can be a fact or myth depending upon our belief in current  methods of  research in  science. The issue is  debatable . Of course ,  one issue is probably  closed  forever  , even  if they  are  linked casually (or seriously )  device closure can  never be a  sensible treatment  option for migraine ! *

We  expect a  proof / disproof  in this   mysterious migraine -PFO  hypothesis very  shortly.  Of course , many  cardiologists  already  have their  own conclusions !


*Please note , PFO  device closure  for  stroke in young is a different story

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HCM is due to  hereditary mutation of myocyte sarcomere .The molecular defects are  located  in  myosin, tropomyosin, titin .Depending upon the protein  involved the hypertrophy can be regional or localised.

Non obstructive types most often involve tropomyocin mutations. Obstructive types predominate with myosin mutations.

HCM types

Non obstructive

  • Simple ASH
  • Apical HCM


  • LVOT
  • Mid ventricular

When the hypertrophy is in the LV apex there is little hemodynamic consequence

Apical HCM can still be prognostically and practically  important even though there is no  hemodynamic impact.

  • Arrhythmic risk persist(Any focal hypertrophy can be substrate for reentry due to slow conduction)
  • More  importantly  apical HCM is the commonest myocardial condition mistaken  for unstable angina  and they wrongly enter the ACS protocol and might land up in cath lab tables as well !

Always remember  high voltage qrs with deep T wave inversion (90 out of 100 times)  is due to  myocardial pathology not ischemic.


  • Reassurance (First advice is,  not to search for more information from the internet ! It may confuse them !  )
  • Just follow up with yearly echocardiogram .Follow up the siblings too.
  • Marriage counseling . (Not contraindicated )
  • Holter monitoring or  extended loop recording may be done to  detect any sub-clinical of arrhythmias.
  • Beta blockers are generally not indicated  routinely  may be given if family history of sudden death .



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  1. Left to right
  2. Right to left
  3. Can be in both directions
  4. No significant flow at all !

Answer :   Every response can be correct

The patent foramen ovale is a physiological orifice , which  becomes  pathological if persist into  adult hood .The incidence is estimated to be about 20 %  of the population (Amounts to 100 crore PFOs roaming  in our planet!). It makes  no sense  to  believe  just spotting  a  PFO  in routine echocardiography be termed  as pathological . But recently  (Adding much to  interventionist’s  delight ! ) the presence of which is being linked with migraine and stroke in young.

The size of the orifice can be from a single millimeter to one centimeter* . The direction of blood flow in PFO   is determined by the mean gradient across the orifice. It has to be  left to right  as the LA pressure is  generally   higher by few mm mercury  ,hence there is a small  tide of flow entering into RA with each left atrial filling or contractile wave .(v and a ). This  quantum is miniscule and has no hemodynamic significance in most life situations.

* Some call( Wrongly ) 1cm PFO  as small ASD.

When can Right to left to flow occur ?

When the right atrial pressure increase more than LA pressure it is obvious  blood can enter LA . It is well-known this occurs  in any pathological situations like RVOT obstruction severe PHT , tricuspid valve obstructions etc.

Physiological  Right to Left flow :

Forced expiration (Valsalva) can cause transient  right to left flow. This  may happen in many real life situations like straining, heavy isometric exercise, blowers, muscians  etc.

Which is clinically  significant ?

Left to right or right to left  ?

Left to right shunting is rarely an issue as there is no systemic  desaturation.

Right to left  shunting  can be  important for two reasons

  1. Arterial desaturation( transient )
  2. Shifting of venous debris into arterial side  can result  in potential paradoxical embolism .(This can be air, clot fat , amniotic fluid etc)  This is the reason stroke in young is closely linked to presence of PFO.

PFOs during positive pressure ventilation

PEEP is a classical example where a right atrial positive pressure ,  shunts the blood in pulsatile manner into left atrium .

Platyponea  hypoxia  syndrome .

This is  postural right to left shunting  across PFO .It  is a less recognised (but a common entity) where -in ,  when the patient  lies down there is a  right to left PFO shunt and transient hypoxia .This is often corrected as the patient sits up. The reason being  the valve of PFO , the   door like flap  which guards  the orifice  ,  is aligned   in such a fashion , it  opens up in a  lying posture(Aided by gravity ?)  , shuts down in  sitting posture .It should be noted  The PFO valve is not a constant feature  . The size  of this valve , the stiffness , the hinge points , ability to  float  are highly variable .Hence the clinical variation in PFO syndrome.

The IAS septal aneurysm is an  important variation where the valve of PFO balloons out into left atrium  may become a nidus for thrombus or a focus for atrial arrhythmias .

Stroke in young  and PFO  :This  topic  deserves a separate article



Excellent PFO images from Yale university library  ( http://www.yale.edu/imaging/chd/e_pfo/index.html)





Excellent PFO images from Yale university library

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A 50-year-old man was referred to us with suspected  angina. Here is his ECG.

Epicardial fat : One more cause for Low voltage QRS

He was an obese man weighing 105 Kgs. He was put on a tread mill  .It  was convincingly  negative .
The echo cardiogram revealed a prominent epicardial pad of  fat measuring 6mm throughout the anterior surface.He had  normal valves and normal myocardial function.It was concluded the low voltage and poor R waves , and T wave inversion was due to the thick epicardial fat.

ECG -Fat correlation

The lack of R wave progression  is attributable  to the insulation effect of fat .Chest wall fat rarely dampen the electricity .Epicardial fat does it more.T wave inversion may not be  due to dampening effect of fat  .We think epicardial fat when adherent to true pericardial surface of the heart it alters  the epicardial  action potential  .It is possible  electrical  neutralisation by the fatty infiltration of epicardium  reverses the direction  of repolarisation  towards the epicardium .

Other ECG manifestation of thick  epicardial  fat

  • Poor R wave progression
  • Anterior Q waves
  • T wave inversion in ;leads v1 to v4 or V5

Final message
Epicardial fat deposits can have clinically  important influence on the surface ECG recording .
Simple chest wall obesity causes only diminutive  R wave . If fat encircles epicardium it has high chances of  producing repolarisation   abnormalities  in the form of T wave inversion or flattish   ST segment.

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Human body is a bundle of mystery.   In an  average  life span of human beings,   millions of   afflictions come and go . Most are benign . Our body has a  full-fledged defense ministry    armed with sufficient weaponry in the form of , immune cells, thousands of regulating enzymes, hormones ,  cell service molecules  etc  .It can tackle most of  the ailments our body encounters  with out a doctors help (Jungle animals rarely die of disease!)  .

Of course , the body  needs  external help  when it’s  intrinsic resources fail . There are few   serious disorders that has to be intervened .However ,a big  fraction of them  will   die  in spite of whatever we do .

Is it not  fascinating to know more than  100s  of chemicals  act day in, and  day out ,  to  prevent our  blood  from clotting and keep it flowing .  If only the natural lytic mechanism fails  for an hour , and  create a  vascular  chaos   we will realise  importance of it !

Even as we debate appropriateness of medical care  in this  21st century   here is startling scenario ,

When a child  presents  with physiological hypertrophy of lymphoid tissue  , as their body begin to  learn and record the micro biological mysteries  of our environment  , it is  often “cross labeled ” as  tonsillitis  or appendicitis and  end up in surgical tables.

This article just released  in  European heart journal , tells us ,  how the rampant use of appendectomy and tonsillectomy in the early child hood  may make them susceptible for CAD in later age group.

The role of medical professionals is identify the trivia ! and prevent unnecessary interventions.

Unfortunately  or (Should I say dangerously)   many of  the   professionals  understood it  in a diagonally  opposite manner . Identify the trivia ,  instill fear in our patients  and intervene ,   in the process injure  our great biological system.This is also applicable to many cardiac  interventions.

Final message

Heavens sake ,  youngsters  , please  remember  , medical  profession is all about removing suffering from patients  . Do not fish out “non -existing” illness from your patients  body !   Let me remind you ,  professional approach means  , whatever you do it should be in the  interest of our patients . The moment  you deviate ,  you cease to be professional .

Also realise  ,  good   intentions can never be an excuse for  inappropriateness !



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It is  a well proven concept   beta adrenergic blockers have a useful role in controlling   the  frequency, and intensity  of  vaso- vagal syncope .

One may wonder how an anti adrenergic drug help to counter hyper vagotonia syndrome !

This is because  during  vaso -vagal  syncope ,  the  inital trigger is  sympathetic . A   sudden hyper adrenergic  surge occurs   that stimulate the vagus, ( Which  overshoots the   initial  quantum of adrenergic signal)   and  cause a systemic vasodilatation ,  hypotension and bradycardia.

How does adrenergic surge stimulate the  vagus?

By two ways

  • Brain stem spill over effect in medulla (Vasomotor to tractus solitarius)
  • Cardiac  stretch caused  by hyperadrenergic activity . This stretch initiates a  vagal reflex  especially from  the base of the heart (Similar to Bazold Zarish reflex ). This  mechanism is  thought to be more important than brain stem spill over  , that’s why  it is referred to as  neuro-cardiogenic syncope .

How does beta blocker help?

  1.  It   sedates  the  adrenergic centre which  modulates the trigger  .It  also blocks the  sympathetic  afferent limb of the syncope circuit.
  2.  Anxiety  and panic reactions are close associate’s of vaso- vagal syncope. They are  not only  considered as  prodrome for syncope  but also act as  important triggers.This is effectively tackled by beta blockers .
  3. Finally , beta blockers  soothes the mycardial  stretch  receptors by reducing the  ventricular shear stress (Reduced contractility and wall stress )  hence neuro-cardiogenic  axis is  pacified.

It is important to remember beta blcokers can only  prevent/  reduce  episodes  of  vaso vagal syncope. It  may aggravate  the situation   if administered  shortly  after the event , as bradycardia and hypotension  is dominant  in the recovery phases.

*During an episode of vaso vagal syncope atropine group  of drugs is most useful .

Which beta blocker ?

Propronolol is the prototype  as it has non selectivity and good penetrance  of  blood brain  barrier ,  which is  the most appropriate site for suppressing hyper adrenergic drive.

Cardio selective beta blockers  do have a role as cardiac stretch  receptors is  one of the two target sites .

Final message

Ironically ,   in the long term management of  vaso-vagal syncope , anti adrenergic drugs  have a major role  rather than atropine like drugs .

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There was a time  , even  cardiac catheterisation was contraindicated if the aortic valve  is  significantly calcified. LV angiogram was judiciously  avoided in all such patients . Why ? A significant increase in disabling strokes were witnessed .Those were the time  a sense of  fear (common sense ?)   prevailed . Every one was following this dictum with sanctity .

Now in 2010 .TAVI has  arrived with great fanfare . We not only cross the calcific valve , we literally play  a violent contact sport   in the aortic root  for over two hours with all sorts of pushes  and passes  on  a  fragile valve.And  we are happy to  claim that  stroke rate is comparable to aortic valve surgery and TAVI is not-inferior to AVR in high risk surgeries .

How is this possible ? As the times  changed ?  Is it true , our stroke  fears are just imaginations  or have we lost our  faculty of  reasoning and  sense ? (Will it be logical to  fund a research  if someone claims a  surgical  technique  to replace  aortic valve in  a beating heart without aortic cross clamping !)

Data shows  even if  distal protection devices are  used the stroke rates  can reach to  objectionable levels .It remained  a mystery ,  at least to me how no body was  questioning this ? I was happy to find this editorial in NEJM which  just stopped  short  of   banishing  this modality in its current form.


What price it asks ?  and leaves the readers to guess  the answer ? NEJM wants to be too decent and polite , but in science politeness is generally not required  ,  as long as  your  observations are  correct !

For all those enthusiastic  interventional cardiologists  here is  a positive message .

Nothing comes easy in science.Great  inventions do have problems  initially .  Without  major hurdles  there can be no progress ! It is  because of   you  modern cardiology is making giant strides . Remember  the early days of angioplasty , early days of pacemaker  .  But  please realise  the most important issue  is ,  whatever  we   innovate or discover it  should be shown   superior to the  best  existing modality in all aspects(Technique,  procedural  complications, long term  outcome ,costs, side effects etc  ) .It is awful  to note   new drugs or devices  are  rarely compared with  the best treatment that is currently available .

A  new  treatment that simply  complements  or proves  non-inferiority  can never be considered an invention. How can we   portray radio frequency  renal denervation (  a complex  lab procedure ) for controlling blood pressure   as a great innovation for man kind  while we  have   so many drugs and  modalities  available  at a fraction of the cost  with  little  consequence .



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Human coronary artery branching pattern is unique in every  individual . Left circumflex shows many variations.

The important ones are  a separate origin , variation in the angle of bifurcation, the number of OMs  .Further, the length of  mainstem  LCX  and its course in the AV groove are quiet unpredictable.The diameter of LCX vs are generally equal  (or LAD >LCX).

The division of  left main is such that circumflex  generally gets a lesser share  of blood flow . If  LCX is dominant this  ratio  may be little balanced. But if the LCX  is huge LAD definitely suffers !When left circumflex equals the size of left main  the pattern is distinctly  unusual.

This patient   we encountered recently had 4mm sized LCX   and  presented with a tight LAD lesion .

This man's LCX probably will never sufffer from atherosclerosis !

Other observations about large bored LCX

  • Narrow ostiums are prone for  atherosclerosis .A large mouthed  LCX rarely involves  in left main  bifurcation lesions.
  • Disproportionate size of LCX when compared to LAD  can  have hemodynamic implication of provoking LAD disease  .

The implication of  differential  sharing of left main blood flow is not fully understood .It needs further insights.

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Coronary  atherosclerosis is the number one killer of mankind. Many would consider it as an  essential  process of aging .Modern  life styles and habits make this appear  very early in life . There is currently an endemic (or even  a pandemic ) of   CAD due to premature  atherosclerosis. We need to recognise CAD is not a  primary heart disease  .It is an irony, heart is an  innocent bystander  to the  biological derangement  of coronary  vascular system  when  it is infested with atherosclerotic plaques .

So , when we  are confronted  with  serious atherosclerotic lesions in a coronary artery   what shall we do ?

We have three options

  1. Take on the enemy in a direct confrontation (Like war on terror ) : This is  some times called as Interventional cardiology .Caution is required as the battle  is within the human coronary artery ,  cross fires and collateral  damage  are unavoidable.

2 .Next  method  is to  find the basic cause  of  terrorism , identify  the perpetuates, facilitators    and try to correct the   root cause of it (CAD ) .This approach  also refered to as medical management  in cardiology community*  . It  aims  at regression of plaque  by statins, and life style modification and preventive cardiology. This modality is most ridiculed and  insulted by the main stream cardiologists.

*Comparable to  bilateral peace talks for a political solution to terror

3. And third option is a  real  surprise !   This  neither  confronts   the lesion   nor does it  address the initiating factors . It   just ignores  the lesion and by pass it with a LIMA /SVG  fly over ,  as if  nothing has happened in this vital high way leaving the culprit scot-free  .This option is  executed by surgeons as  CABG surgery . . . and  for mysterious reasons  this is a  well accepted one .

CABG :Here the atherosclerotic  burden is untouched by surgery . The graft can get diseased  sooner or later , native vessel disease  shall  progress some times encroaching  the ostia of distal graft site . Incidence of acute coronary syndrome following CABG is not greatly reduced for the simple reason we are not doing anything primarily to the inflamed plaques .These issues  are left ,  to be  taken care by the  medical  management .

* This article  does not want to defame these great development in cardiology(PCI/CABG) . They have a  specific role to play. CABG AND PCI remain the only option for critical  lesions with limiting angina .But please remember without  proper  medical management  ( ie Targeting  the perpetuates of  crime )  both  PCI and CABG will be a big sham !

Final  message

Avoiding   the  lesion  or  attacking the lesion  is a  primitive  method to tackle CAD  . Passifying   the lesions  in a slow and gentle manner,   preventing  further progression  or regression  of lesions is the only  “sane” method for combating CAD   . PCI and by pass surgeries  can be termed  as  21st century’s   medical  adventure sports  which  has  limited role ,  in the overall control  of CAD  for the human kind .

And  now  answer this question . . .

Cardiologists attack the lesion and  surgeon avoids the lesion ?  Who is the winner in our fight against CAD  ?

Both of them are  clear losers .The winners are  all those  humble physicians and parmedical workers (or even the responsible lay public ) who  help recognise  the early forms  of  CAD  and  counsel properly to prevent it .

This is  what  Dean Ornish   in 1991  documented in  Lancet  which was never considered scientific   for the simple reason it has no commercial value !




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It is a fashionable topic  in  cath meetings and workshops  to discuss  about thrombus loaded coronary arteries. Still  visualizing a  thrombus  in coronary angiogram is  never a  mean  task !  It needs  lots of  visual  acuity  and  imagination to recognise   intra coronary thrombus.

  • A lesion which looks fresh with multiple layers of  irregularity within the lumen is  often assumed to be thrombus.
  • An   intra luminal filling defect   is the  most often  used  “criteria  to suspect” a  thrombus

A long segment thombus with dye penetrating and coating the thrombus all around

Thrombus  vs plaque ?

Both are  radiolucent .  But a thrombus  or a plaque coated  with  dye  will make it radio opaque. The radio opacity of a thrombus is determined by extent of dye coating ,  the thickness of the dye layer, obliqueness to the x-ray beam . A thrombus plaque  interface can have two different  planes  of densities.

Theoretically dye can not encircle  a plaque  in its entire circumference as it will be attached to vessel wall (Unless  circumferential  dissection is present  )  Hence , dye can not coat a plaque fully ,  at best it can give  an appearance of eccentric filing defect  with over hanging edges .  While a  thrombus  can manifest with a  complete filling defect

Thrombus vs dissection

This is  still more complex   . Both can have a filling defect  .A  flap is a  line like  filling defect To complicate the issues further,  both thrombus and dissection occur together in the same spot .

How confidently  one can  identify a thrombus in coronary angiogram ?

During acute MI there is no difficulty in identifying it ,  as every acute  obstruction  must contain some thrombus* . Some interventionists  have special  ocular   sense   to   detect thrombus. Few others rely  on their intuition  rather than  solid evidence.

Sucking out a thrombus during primary angioplasty  has now become standard concept and is indeed  feasible  in most situations. It is obvious we have a task  on hand to identify thrombus correctly and quickly during primary PCI /UA .

Blind suction,  even though rewarding should be avoided.  Caution is required as blind  suction pulls a plaque with force !

A plaque debri  with a  thrombus, a dissected flap  all can combine together   to produce a complex  “masala”  of  coronary lesion especially after a difficult guidewire cross . This is refereed to as a battered coronary artery .These are the lesions which are prone for recurrent acute or sub acute thrombosis even if the lesion is  stented  properly.

During  primary PCI   thrombus coated dissected plaque  is just tucked  and  opposed behind the  gentle stent struts.The thin layers of thrombus between stent struts and the vessel wall is  missed  , 100 out of 100 times   by coronary angiogram . (IVUS very good in detecting this) .Because of this risk , Intensive anti -coagulation in complex PCI becomes mandatory

* Diagnosing thrombus in a chronic lesion is  much . . .much  difficult !

What are specific  modalities available  to  confirm thrombus

IVUS, Angioscopy, OCT are  hi tech tools to identify intra coronary  thrombus .(Which i feel  have little practical  value in real emergency situations)

Final message

Thrombus  may be a  key  finding  in acute coronary syndrome (Of course  the contribution of fissure, injured ,  plaques to the lesion can never be underestimated . ) Still , we have no simple , accurate method to identify it  ( Forget quantifying it) . Lots of assumption , guess work and gut feeling is at play in the cath lab .

We  expect better online , real time tools to improve out tentativeness inside the coronary artery  .


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