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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