Archive for the ‘cardiology -congenital heart disease’ Category

Myocardial infarction is the self-inflicted ,  modern-day death sentence  especially  among the  young generation who are   addicted to the affluent life style .

We know the  cardio vascular events  are  precipitated  due to a  sudden trigger in those  people  who have a base line risk profile. The major  risk factors are ,

  • Diabetes
  • Smoking
  • Hyperlipidemia
  • Hyper tension
  • Obesity

When one or more of the above factors   progress unabated he or she is at high risk for acute coronary event .

Is that a fatal stock market rhythm !

A loaded gun  needs a trigger to fire  , similarly  in a vulnerable patient (Plaque )  any of the following can act as a  trigger to precipitate an MI.

  • Hemodynamic stress (Fall or raise of BP )
  • Any  systemic illness( fever etc)
  • Physical stress
  • Mental stress , any strong surge of  emotion (Negative or positive)*
  • Non cardiac surgery

*Anger, fear , euphoria , guilt , bereavement ,

Now there is evidence pouring in  ,   natural calamities (  perceived fear of death) can  act as trigger  for MI.

We have reports  of  excess cardiac events   following  . . .

  • Earth quakes
  • Terrorist attacks
  • Flight scares

Any events which can release  sudden pulse of adrenaline into the plaques can trigger an acute coronary event.

Now,  this study from Shangai ,  documents how the coronary events dance to the tunes of stock market movements in the financial capital of  China .


Final message

Chaos theory states no two events are isolated in this world  !   When stock market swings it can  pull down your heart too .

be cautious !

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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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ASD device closure as a modality is constantly improving  . . . but  the consensus is  , it is  yet to catch up with  of  good old surgical  outcome . The key to success is not only in the device but hugely dependent on the technique and pre-procedure evaluation  .In fact , the pre procedure TEE imaging technique  is as important as the procedure itself.

There are lots of discussion about this particular issue. TEE is mandatory we know  but now we realise it is  still better to have a  Real time 3dimensional  (RT3D ) TEE . Rim  size  and ASD  morphology estimation is  the primary aim.

There are  at least 6 named rims for ASD. For a circular  orifice  it  may not be logical to have a fixed number of  6  rims . Ideally the entire circumference must have a rim .( This happens in  central defects )In many,  the complex anatomy of IAS does not allow this. So we are compelled to fix the number of rims to six.

  1. Aortic (Superoanterior),
  2. Mitral (AV valve/ Inferoaterior)
  3. SVC  (Superoposterior),
  4. IVC  (Inferoposterior),
  5. Posterior ( Atrial free wall ).
  6. Coronary sinus rim

One can realise how important these rims are , as  they are the   foundation tissues on which the device is going to be seated for the rest of the patients life.

When do you call a rim is adequate sized ?

5mm is  considered suffice. But it varies depending upon the device and expertise.

Can we deploy an ASD device  in patients   with deficient rims?

Logically the answer is expected  is   “No” but  , many have liberalized the criteria now , after realizing   one may  not have 5mm rim in all six sites in a given patient. If you follow this criteria strictly   you can’t do more than few devices a year !

What is the resolution power of TEE can it miss a 3mm rim  ?

TEE has a good resolution it should pickup any thing equal to 2mm or more.

Which is most important rim and which is the least important rim ?

What are the potential complications that can arise if ASD device is deployed with a critically low rim ?

Having discussed  that every rim is equally vital  ,  we  need to answer this sort of questions  often .  I am waiting to get the  practical tips for the above issue from  my experienced colleagues .  I shall post it soon .

It is sometimes assumed Aortic rim may not be that important .Here is a   good discussion  for  ASD closure with deficient aortic rim from Saudi Arabia  . http://www.rmsolutions.net/rmfiles/SHA21/028002.pdf

Meanwhile let us learn . . .

How to perform the “all important” pre- procedure TEE ?

The following article which also  includes video clippings will be immensely useful for all those enthusiastic cardiologists.Thanks to JACC  for making this link free .

Three cheers to AMRITA team from India


A stylish article on the topic

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Bicuspid aortic valve is  probably the commonest congenital heart disease.

  • It can be a totally benign entity and can be incidental finding in many .
  • Only a fraction progress to pathological entities like aortic stenosis , aortic root dilatation  etc .
  • Those afflicted need periodic echocardiography
  • These valves are prone for premature degeneration
  • Intervention is rarely required

Here is a complete review on the topic from the  top rated cardiology journal circulation.


Link to the article

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A classical echo of  a common AV canal .


Note  the free floating common AV leaflet



With all chambers interconnected it is a free for all circulation . The blood  seems to get mixed at the level of common AV orifice . Even though one expects severe cyanosis in common AV canal , the intensity of which is primarily determined

Common AV canal with free for all shunting . http://www.drsvenkatesan.com


the net blood flow to lungs which is dictated by  the pulmonary vascular resistance or the RVOT obstruction. This patient had no RVOT obstruction   but had  severe  pulmonary arterial hypertension.  In spite of raised PVR ,  some amount of volume over load of lungs  occur.

How to assess the  operability ?

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In this era of  technology hype , cardiology  journals are flooded with interventional   articles. Congenital heart disease has been pushed to the back ground .  CTGV* is a   fascinating  congenital heart disease (Of course ,not so fascinating  for the patient !)

*TGV and TGA are used interchangeably  .

It is a complex disorder of ventricular looping (L Looped ventricle LTGA )

This can occur in three forms

  • Isolated CTGV
  • CTGV with VSD or PS
  • CTGV as a part of complex  cyanotic heart disease.

The irony of this disorder is , it has two errors in development that tend to  neutralise  the hemodynamic  abnormality .

 ventricular connection is abnormal (Discordant) . RA is  connected to LV and LA connected to RV . Still nothing alarming  happens  as LV is connected to  Pulmonary artery and RV is connected to Aorta .(Ventriculo arterial discordance)

In spite of this natural  hemodynamic  correction , one can not ignore this entity  ! as it is  anatomically  uncorrected  for the rest of the life.

Since morphologic RV acts as a systemic ventricle it is bound to  have difficulty in tackling the systemic pressure in later in  life .

Further , the two  complex  defects called  (also called as  ventricular inversion ) make sure that the conduction tissue and the AV valves   are distorted and  squeezed in the AV junctional arena with it’s unique double looping defect  .The his bundle inverses, the left AV valve often regurgitates .Complete heart block often ensues.


  • Isolated CTGV are best left alone .
  • When VSD /PS are associated corrections are adviced
  • It is not simple surgery , one may require a technique called double switch .(I always wonder such surgeries are ever indicated in other  wise asymptomatic population with isolated CTGV)

Here is an article from “The  Heart”  that deals with the problem of CTGV , may be  . . . in a manner no other journal  has ever done !

 Congenitally corrected transposition of the great arteries Heart 2010;96:14 1154-1161

You need some  luck  to  get a live full text link here

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Hypertrophic cardiomyopathy (HCM) manifests   with or without obstruction. Obstructive HCM ,  (ie HOCM)  is more often symptomatic .However , the risk of arrhythmias, sudden death, and some degree of diastolic dysfunction are common in both.

ECG, clinical examination are generally  not sensitive to identify obstruction in HCM  .Echocardiogram is the easiest  way to identify  the obstruction (gradients> 3o mmhg across LVOT are considered significant ).LV angiogram ,MRI, CT scans are rarely necessary today.

However , the following clinical clues will help us  to suspect significant obstruction in HCM


  • Class  2 or  3 dyspnea.
  • Exertional syncope
  • Exertional angina


  • Pulsus bisferiens (Two peaks in systole )

LV apex

  • Sustained , double apical impulse  often indicate obstruction.
  • Presence of Mitral regurgitation ( 20% can have  MR without obstruction due to intrinsic abnormalities of  mitral valve )

* It should  be realised , valsalva induced MR /LVOTO  may occur in many of the non obstructive HCM.

What happens to  clinical signs of obstruction with medical therapy(Beta blockers etc)

One would expect these signs to regress or disappear, but it rarely happens. The pulse , the  murmur show  little change .  This implies , the main mechanism of beneficial effect could be in  heart rate  reduction , and  improvement in the   diastolic properties of left ventricle.

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A related article in this blog

Un-roofed coronary sinus

Further reading :

A rare comprehensive review article on Thoracic venous anomalies

Fr0m American journal of  Roentgenology

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Tetrology of Fallot is the commonest cyanotic heart disease . In 1973 , working at Portland,  Oregon , Bonchek  and colleagues created this classic with intense clinical acumen , that defined the way   how we understood TOF   in infancy  . Such studies  have  become extinct in this fast paced cardiology academia !

With due tributes , here is a slightly modified version of Bonchek classification of  TOF in infancy .

Every cardiologist must read every line of this article  which came 37 years ago  !

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Patent foramen ovale is probably  the commonest  congenital heart defect.  (Bicuspid aortic valve will run close to it ! )

Note : PFOs  cannot be  called as a  true disease , since it is a  benign anatomical defect with little or no hemodynamic impact.

Consider  this scenario . . .

The incidence  of PFO could be as high as 20% of adult population. It means nearly 100 crore people of this planet  will suffer from this entity !

When does it become significant ?

Paradoxical embolism : In young persons with cerbro vascular accident , PFO s are more commonly observed , implicating some form form of venous to arterial embolus .

In some persons it is believed , it can shunt few CC of blood from right atrium to left atrium at times of right atrial hemodynamic stress. Like severe physical  straining  (valsalva like )

In seriously ill ventilated patients  PFOs can worsen the  hypoxia especially with  PAPP  mode .

When does it become a life saving savior ?

  • In patients with DTGV and intact IAS  even a a small PFO can sustain a life  till , emergency surgery or intervention is done .
  • In patients  with severe  pulmonary hypertension the PFO may act like a safety valve, opening at a critical moment and decompress the  right atrium and which  indirectly relieves  the RV wall stress as well .

Fancy relationships

Now , it is  considered PFO  is related to migraine by some means ! ( What means !)  The belief has strong evidence base that has lead  the aggressive  interventional cardiologists to  find a new hole to close  . This indication ,  if  approved will have a perennial supply of patients  as there are 100 crores of them .

How will you differentiate a PFO from a small ASD ?

Size alone can be a useful pointer in differentiating a ASD from PFO.

A PFO can  measure  between  2 to 10mm  ( most measuring between 4-6mm diameter)

Size matters !  The upper limit of PFO is the lower limit of ASD .

Practical experience suggest any defect  above 7mm should alert  us about the possibility of true ASD.

Other useful clues

  • PFO are always restrictive  (Use pulse doppler probe right across the PFO /ASD in subcostal view .If you pick up a gradient > 4mmhg (velocity 1 m /sec) PFO is confirmed.
  • Most ASDs do not show any significant  gradient
  • Right ventricle and right atrium should be normal in PFO  (Unless due to some other cause )
  • Doppler flow across  pulmonary valve can be very useful . If it exceeds 1.5m/sec , left to right  shunting is likely to be significant and PFO is unlikely.

Is there an entity called restrictive ostium secundum ASD ?

If so ,  how will you  differentiate it from PFO ?

Yes , we have ,especially in  cyanotic heart disease

Like TGA , Ebstien etc .

Isolated restrictive secundum ASD is extremely rare .

* There is no way to differentiate a restrictive ASD from a similar sized PFO .

What is the role of TEE in diagnosing PFO

It has a major  role in delineating the IAS anatomy .

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