Archive for December, 2011

A strong willed  person rarely develop syncope.  We know  weak hearted (Or is it weak brained ?)   men and women may  faint  when  the emotions swing unexpectedly  .The  commonest cause of syncope is  neuro-cardiogenic  syncope (NCS) . (Formerly  called as  vaso-vagal syncope  VVS ). Few facts need to be  emphasized  here . There are  many  critical  circuits  and components to  common syncope.

  1. Trigger
  2. Afferent
  3. Center
  4. Efferent
  5. Fall /Near fall
  6. Prompt recovery after the fall.

Trigger can be emotional or mechanical (Prolonged standing ,  dehydration , etc )  . It occurs generally  in an emotionally  charged  environment with a high  basal sympathetic tone .

Afferent for  NCS   is  mostly sympathetic but it can be  para- sympathetic also (Sensitive GI tract ,  Micturition etc )

* Many times a  trigger and afferent pathway can overlap with each other.It is still unclear what exactly constitutes the afferent , since  triggers can be either sympathetic or para- sympathetic .  ( Pain, GI stimuli, vascular puncture etc) .  Further , afferent  can be be same as the trigger and reach the brain  stem directly  or touch  the heart en route .  ( Cardiac axis  in classical NCS)

The  center is  in the medulla  . Both vagal and sympathetic centers  are involved with potential  spill over on either side.

Final efferent  pathway is the strong  vagal surge resulting in bradycardia and peripheral vasodilatation , cerebral hypo-perfusion  and the person usually falls .( Near fall or aborted NCS  is also a common theme )

                                        If stress increases the blood pressure , absence  of stress  will have to  lower the blood pressure . If anxiety cause hypertension  ,  depression is expected to   cause hypo-tension.

These  inferences  may  appear  correct by logic . As  is always in medicine ,  such   logic works only partially ! ( We are told  the  Sadhus of Himalayas rarely record  blood pressure  beyond 100mmhg systolic  !)

There are strong reasons to believe common syncope (NCS)  is primarily related to the state  of mind and  the neural regulation. Dizziness ,  giddiness  near syncope  are closely related  to  psycho-somatic disorders. Strong willed men and women rarely develop   syncope.Their vascular   tone is well in control even in critical times .This fact has been  well observed  in  the setting of   traumatic  and hemorrhagic   shock  in critical care units  ,  where  some  hold their blood pressure well  even in   adverse circumstances  and few sink without any fight .

Is psychogenic , situational , pain syncope  same as NCS ?

Technically it may not be same. But all of  them  share at least 50 % 0f the  circuits of  NCS.  .However  there is no consensus  to call  psychogenic and   pain syncope  as  types of  NCS.

One critical aspect of  the debate is ,  we do not know whether the  cardiac axis is involved in these  syncope or not. It is preferable to call these types of syncope  as neural syncope (NS)

While in the classical NCS  heart has a  central role in generating hyper active sympathetic afferent from  myocardial stretch receptors. In psychogenic and pain syncope cardiac stretch receptors  are not much stimulated instead ,  the  spillover occur  directly from sympathetic to parasympathetic  nucleus in medulla.

In pain induced syncope parasympathetic limb  gets vigorously stimulated in isolation  to cause a severe  vaso-dilatation  . But once the syncope sets in we often observe bradycardia  and cardiac  limb may get activated as well.

* Presence or absence of cardiac limb in NCS and NS is critical with reference to efficacy of  beta blockers in NCS. The current guideline of NCS  management(  ESC 2010) is strongly biased against beta blocker (Class 3 -level A)  which we feel is  incorrect . Bulk of the patients with NCS respond well to long term beta blockers  .

Please realise , beta blocker  is the only drug which  can break the  NCS  circuit at multiple levels .(Sympathetic trigger, sympathetic afferent, cardiac stretch !

So what is the message ?

It doesn’t require great brains  to realise  vascular  and neural system are  intimately linked  . We know today,  NCS  is primarily a neural phenomenon  hence the  mental status has a  dominant  control over the vascular system especially at times of stress .

The confusion between classical  NCS and psychogenic  / situational  syncope can be largely avoided  , if  only  we call these entities  as simply neurogenic / neural syncope (NS ) ( Omitting the word cardiac is helpful ,   as cardiac axis is not vital  here  ? Non existent  )

Clarity is still  elusive  in defining the  trigger  and afferent limb for the NCS  , fortunately  the final common  efferent pathway that makes the patient fall is indisputably   vagal  !   .  Medullary  vagal nucleus  though fires independently  , also gets  powerful central  parasympathetic flow  from  cortical areas  . Paradoxically ,   controlling sympathetic outflow (Anxiety ) is often an easier  way to reduce parasympathetic flow. This is referred  to as competitive , accentuated  antagonism.

One can prevent recurrent  syncope  by vigorous  mind  control at times of  extreme stress. This is  confirmed  indirectly , by the fact  reassurance is the key to successful  management  in vast majority of  patients with NCS .We learnt this  simple fact  after trying exotic methods like DDDR pacing  and so on .

Final message

Power of  the mind can never be under estimated even in cardio- vascular hemodynamics .  When  pathologically high,   it can spike the blood pressure and break  few vessels in brain , while  if it  is inappropriately  low ,  may induce a syncope or result in persistent  hypo-tension .

Let us learn to use  our  mind over  body  properly .Yogis do it style  and live for 100 years !





Iam surprised why this post has been looked so negative by the readees. Almost all  rated it  as very poor.

Iam still pondering over it. Realised to lable patients as weak minded could be one of the reasons.

I think what I wanted to convey was there is link between mind and vascular system.

Please let me what is seen as offensive, let me learn and correct in future.







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Most  cardiologists  are familiar with  “Circulation” . We know  it  is a top  cardiology  journal with highest impact factor.  Few of us are  aware  of  a journal called  “Circulation  research” ( I wonder  why it is named  like that ,  as if  the regular   circulation journal  does  not carry research stuff  !)

It is one of the  path breaking   journals that regularly  churn out state  of  the art , often  mind  boggling research stuff.  Once in while we should get a feel of  basic science  research  as it  happens.

How else we are going to know an  atrial cell is to be bio engineered  shortly to behave like a  SA node  in patients with sinus node dysfunction. (Biological pacing )

This team from academic  medical  centre Amsterdam   should be credited   for  publishing   this gem of  an  article   from  a  study  involving the  measly mice !

It  deals elaborately  about the embryonic basis of AV nodal  disorders  . Specifically it  explains  the genesis of  WPW syndrome and how AV rings get muscularised  .

(It  is  due to   error in  bio-genetic forces ,which  affect the    incorporation  of AV nodal tissue  in the  fibrous  skeleton .This   results  in ectopic  junctional  tissues appear   any where along  the AV ring . This is the basis of  accessory AV pathway and   clinical  re-excitation.)

Final message

Once in a while  we should develop the habit of reading  tough  journals  like circulation research . After all ,   if a cardiologist  is not reading   these stuff who else  . . . will  ?



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A middle aged man who owns a petty shop in a small  town of south India   came to us for stable angina .His RCA looked like this.

Normally if one coronary artery is obstructed the other comes to the rescue .It seems , this RCA do not trust it’s sibling LAD . See how it  self supports  its own  territory .(The most fascinating and mysterious aspect of coronary circulation is the collateral circulation. LAD  has big brother attitude  . . . it hesitates to help others while   RCA is more philanthropic , we know  it sends prompt  collateral to  LAD  whenever it is  distressed !)

However , there is one advantage of  such   self-sustenance of RCA  (Intra coronary/homo-collaterals ) . If  the  RCA  has to live  at the mercy of LAD  it  runs a risk of   neglect  at times of  distant LAD ischemia as well  !


Single vessel disease , total occlusion , long segment lesion , still  the  PDA  is protected and the vital postero- basal area of heart perfused well ! What to do ?

Scientific  cardiologists  would like to meddle this  RCA with  multi-pronged guide-wires and other weapons  . Non -scientific cardiologists would  send him  home with medicines  . This patient preferred the later ! In the process  he  saved a  lakh ,  which  I  believe was meant for his daughter’s  education . He profusely thanked me for not hijacking his hard earned money for  frivolous  reasons . I said he should thank  his collaterals  and not me , for getting his money back  !

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VPDs are the most common arrhythmia  that  confront  us  in  cardiology clinics .While  it can be a totally  benign   manifestation in some  ,  it may signify a sinister condition in others. ECG  is the easiest  and surest way to identify VPD.However  a shrewd echocardiographer can detect the VPDs while imaging the heart.It is often missed if one do not concentrate on the mitral valve motion.

Note :The VPD convert the typical M pattern into a inverted U pattern in mitral valve.

One of the important hemodynamic side-effect of VPD is intermittent mitral regurgitation.

Effect of VPD on mitral valve opening .

By  conventional thinking   VPDs  are expected   to impact  more on the  mitral  valve closure than it’s  opening .In reality it has indirect influence on mitral valve  opening as well. The retrograde  conduction(VA conduction) of the VPD determine the timing of atrial contraction and hence the   mitral valve opening. If the VPD gets blocked retrogradely  within AV node , the normal sinus impulse will activate the atria in an antegrade fashion .Note ,  he atrial activity  occur randomly when multiple VPDs occur.This makes the cardiac cycle too complex to assess especially the diastole. (In fact true  physiological diastole  may  not occur here !)

If  the mitral valve opening  is interfered by a   VPD  (Early diastole is  the  favorite time  for VPDs to  appear  !  )   .When it occurs the AML is    suddenly pushed  upon superiorly  by the premature ventricular activity and hence resets the  mechanical diastole. Please note electrical resetting of atrium is different from mechanical resetting.

It is also possible atria and ventricle contract simultaneously .This is the time , a cannon wave  may occur inside LA .VPDs can result in pulmonary venous canons and may even elevate pulmonary venous pressure   if  this  occurs repetitively .

Another possibility  is ,  VPDs  may not initiate a ventricular  contraction at all .It may be  simply  be an electrical event. That’s why  we changed the name of extra systole  and premature contraction into just   premature depolarisations.

Why is it important to know about M Mode motion of VPDs

Cardiologists  continue to  engage wide qrs  tachycardias   in the  wrong side  of their   brain for many  decades .The ECG debate about wide qrs tachycardia  is expected to  continue  for generations . !  Few smart cardiologists would  rapidly put  the echo probe  over the mitral valve and able to  differentiate  instantly a VT form SVT   with fair  degree of accuracy.

Detection  of regular M shaped mitral AML  will exclude a VT with a high degree of precision .(AV dissociation by echo )*

Even  presence of trivial  MR*  (More often diastolic )   which occur  irregularly  will  definitely indicate it is VT . SVT  hemodynamically   can not result in this  MR is gives us evidence for AV dissociation

* No reference for these observed indices in our lab. (Class 1 Level C expert opinion(  No one calls me as expert though ! )

What is the mechanism  of VPD induced  mitral regurgitation ?

It is well-known VPDs can cause   mitral regurgitation .Not every VPD cause MR.

  • The timing is important .
  • It can be  either systolic or diastolic MR .
  • If VPD occur in early diastole (After the T wave , the MR jet  will collide with  diastolic mitral flow. )
  • Paradoxical septal motion induced by VPDs can alter the pap muscle alignment transiently and result in MR
  • We dot not know how a LV apical VPD  differ from RVOT  VPD in the genesis of MR.
  • Logic would suggest RVOT  VPDs are unlikely to result in MR as there is  a time lag for the impulse to reach the LV base

What is  the effect of  VPD and Aortic valve opening ?

While  every VPD promptly  hits the mitral valve ,  aortic valve may or may not open with VPDs .Again timing and focus of VPD could be  important.This is the reason during  multiple  VPDs  only few open the aortic valve , that  explains  pulse deficit. (The so called missed beat )

Final message

Anterior mitral leaflet (AML) is the most mobile structure  of  the heart . Hence ,  it is not surprising to note  sudden unexpected ventricular contraction will  have maximum impact on this valve .

When VPDs occur in clusters or at random it has a complex effect on the mitral valve motion. This is responsible for  palpitation , minimal mitral regurgitation and rarely trouble some pulmonary venous cannons and raise in pulmonary venous pressure .

Careful analysis of  AML motion can give us useful clues to differentiate VT from SVT during wide  qrs tachycardia

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Though heart is  primarily  known  as a  mechanical  organ , in reality   it is a vital  electrical organ as well . The entire mesh of electrical  pathway  from SA node to  Purkinje  fiber  would easily cross  a mile or two .Maintaining and protecting  such a  delicately  woven network  needs lots of  electrical sense  .  It is not surprising to note  , VT or VF  can be induced  virtually  in  every human heart  if stimulated rapidly. Electrocution  induced  by VF is  the typical example.Cardiac surgeons  do it regularly  before  surgery .

So , inducible  VT  in the EP  lab need to be  defined in a strict manner .

  •       VT must be triggered  by a  single stimuli  (or  two )
  •       Multiple sites should not be stimulated(ideally  single site , at most two )
  •       It should be sustained.
  •       Only mono-morphic VT has  significance
  •       Induced  p0lymorphic VT  has no clinical value.
  •       Pharmacological  stimulus  such as isoprenaline   can be used but reduces specificity.

*If a VT  rapidly degenerate  into VF  it  usually  means a polymorphic VT  while   unstable irregular  polymorphic VT   could be  same as   VF )

How do you make sure  what we induce in  EP lab is same as the clinical VT ?

This is the most difficult task for electro -physiologists. In real life setting VT is  often induced by ischemia hypoxia , local  acidosis and electrolytic imbalance. However  rarely mind this issue . In EP lab we induce  it  with  artificial electrodes  . Does it make sense to compare  these two totally different  set of triggers  in real life and a virtual EP life . Ideally  to confirm ischemic  VT  one has to induce ischemia  in EP lab and look for  VT . (Adenosine  stress ? )  Further ,  only re -entrant VTs  can be induced in EP lab by programmed stimulation . Automatic VTs can not be induced by stimulation .

The chances of inducing a VT in EP lab is  directily proportional to the aggression of the electro physiologists and patience  of  the  patient ! One can afford to use  more aggressive  protocols only   if a clinical VT was  recently the   documented .

 Electrical stress testing of heart

It may be tempting  to refer    induction of VT  in EP lab  as  electrical stress testing  for the heart. But fundamentally there is a difference  between this and  the conventional EST . Unlike exercise stress  test the  inducibility of VT highly unpredictable . It has far too many variables . (The surface area of contact , number , Intensity ,  site of stimuli , scar location , irritability of viable myocardium  ,  inertness of scarred myocardium ,  and finally the cellular milieu etc  )

Thoughts to ponder over Is it not  “a fundamentally a wrong concept”  to give importance  to inducible VT  ?

Why should we  treat a clinically non relevant inducible VT ? We do not know yet whether inducible VT in other wise normal LV function  has any long-term significance . Currently it makes   no sense   to intervene in VT  if the LV function is good and the episodes  are not clinical but only inducible.

Note: If there is severe LV dysfunction (EF < 30 % ) one can implant an  ICD without   an  EP study . ( Of course   to state more dramatically   without even single documented VT  !) MADIT 2

Final message .

A VT which is inducible in EP lab has no meaning ,  if the LV function is normal , while  even a  non-existent  (potential  )VT  in the setting of severe LV dysfunction is vitally important !

Though  we  differentiate cardiac function  into mechanical and electrical for academic purposes , it is astonishing to note   how the heart is able to function  as a  single unit  . We know today , the ultimate  outcome of   VT  is  not  dictated  by  electrical status of the heart rather , the mechanical ability  to  with -stand  sudden dis-organized  ventricular  contractions ( A ventricle with good contractile function has inherent  capacity  to extinguish most episodes  of VT .(Myocytes with inbuilt biological ICDs ?)

It is a million dolor question why some VT remain as non- sustained while others rapidly degenerate into  fast VT and VF thereafter


The two contrasting studies

The MUSTT (1999) trial exposed the limitation of   clinical utility of inducible VT . Multicenter Unsustained Tachycardia Trial (MUSTT) Investigators

While   MADIT 2  (2002)which recommends an ICD in every patients with  severe LV dysfunction following MI without even a EP study .

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Murmur of Tetrology of  Fallot is generated at the level of

  1. VSD
  2. RVOT
  3. Aortic root
  4. Any of the above

Answer :   RVOT.

RVOT is the classical site of TOF  murmur , but  there is  a  rider . The murmur of TOF is  inversely proportional to the degree of RVOT obstruction. (Contrary to VPS with intact IVS) .In severe TOF especially during spells the murmur attenuate dramatically and may disappear altogether. Hence a silent and quiet heart do not necessarily  indicate  a mild form of TOF .

Other possibilities also  exist.

  • The VSD in TOF is  large and do not restrict  blood flow on either direction . Rarely  restrictive VSD can generate a murmur across VSD.
  • Aortic flow is increased in all severe cases of TOF ( Highest in pulmonary atresia and VSD)   Hence there is always a possibility of a soft systolic flow murmur across Aortic valve .
  • Other rare  cause for systolic murmur is due to  prolapse of   tricuspid  valve  that occludes the VSD  potentially causing  TR  and in the  process may  convert the  VSD  into restrictive type.
  • One more cause for  systolic murmur is sub Infundibular anomalous  muscle bundles criss crossing the RV body .
  • Peripheral pulmoanry arterial stenosis is recognised cause for distant faint systolic murmur.
  • Diastolic murmurs can also occur in TOF . Absent pulmonary valve and aortic regurgitation can result  in diastolic murmurs .

Question for analysis

What happens to TOF murmur during squatting  ?

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Aorta  is connected to the left ventricle  like a hose pipe.The energy  generated within the LV myocardium is efficiently delivered to  the root of the aorta. Mechano -coupling of LV with  aorta  is important means by which  blood is  is ejected into systemic circulation .

Even though aorta  has  mainly passive  contraction and ( The  wind- kessel effect) ,  the most  powerful contractile force  of aorta comes from   the  transfer of kinetic energy from  left ventricle .

This helps  us to  measure the LV function  simply by  looking at the aortic wall motion.Since aorta is the final common exit for LV  it effectively represents the global LV  function . The  ubiquitous errors during  LV border tracing  and it’s subsequent mathematical  amplification  can be avoided. Here is a  patient with severe LV dysfunction  whose  aortic  motion is depicted . We refer to this as   ” rail roading” sign of Aorta  which  implies  a critically dysfunctional LV . His EF was 23 %  The aortic motion is esepcailly useful in categorizing severe LV dysfunction  from moderate LV dysfunction (The sensitivity we feel is as high as sophisticated tissue motion Doppler protocols .Of course  it may lack specificity !* as hardened  aorta due to aging can confound the aortic motion )

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Mark E Jospehson  is the man who single-handedly carried  the burden of teaching  generations  of electro-physiologists  from  Harvard  Thorndike electro physiology services , Boston USA. Today , whatever  we know  about the mechanisms of VT , it is because of such great men who  spent thousands of hours  in the  first generation EP labs in early 1970s and 80s  , meticulously analysing   the data emanating  from  over  600   scar mediated VT with complex circuitry .

He along with  Miller published this seminal paper  in circulation 1988 , which gave us  the  algorithm  that localises  Post MI VTs.

Following table summarises their finding.

VT localisation in Infero-posterior MI

The general principles  of localisation of VT  

  • Localising VT following myocardial infarction  is difficult but distinctly  possible with  about 60 % accuracy.
  • Whenever we locate a focus we generally refer to epicardial site of exit not the focus of  origin.
  • Ischemic VTs with complex scars are difficult to locate .
  • The rule  that RBBB VT arise from  LV and LBBB VT from RV is too simplistic  in scar mediated VT.
  • The fact  that IVS is common to both RV and LV confounds the issue .Further, in a given  clinical VT  the origin  , course   and exit points of VT can considerably vary .For example  septal VT can exit  on  either side and  result in  either RBBB or LBBB morphology (Epicardial break thorough )
  • Multiple exit points are also possible.
  • VT induced in EP lab may not be reproducing the same clinical VT. So we have to be careful in what  we ablate and claim success !
  • VT with  structurally normal heart  has   more predictable behavior  , for  example RVOT VT  almost always have LBBB morphology.

Other important rules of thumb are

  • LBBB VT has more localising value .
  • Superior  axis is the most common  axis.
  • Bulk of the ischemic VT are located within the septum either in the apical or basal region .(75%)
  • Infero posterior MI has more complex scars , hence VT morphology is heterogeneous.

The purpose of localising VT is important  only with reference to  ablation.(Of course for academic reasons  as well )   With advent of electro anatomic imaging (Carto ) it is becoming   easier  to locate and track them . Still only a minority of VTs are amenable for RF ablation .

Please note ,  the most common modalities we use  in the management of VT  ,   Amiodarone  and ICDs   simply do not   bother  about   focus of origin  for it’s action !  That makes our job easy !



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Benjamin Gasul  is a well-known name  in  cardiology community especially  among the old generation . He and  his team from  Cook  county children’s hospital  Illinois,  Chicago,  created a stir among pediatric cardiologists  in late 1950s and 60s . His concept  was rather controversial .He suggested   Tetrology of Fallot can be an  acquired  defect as a sequel to  large   peri-membranous VSD.

He and his team published a series of papers one in 1957 and other in 1963 (JAMA and circulation ) .Later in 1970s  Kieth  and  Tyrrell  from children’s hospital Toronto tried to confirm this. Though they were not fully agreeing with  Gasul  they could not dispute the concept either !

Clinical importance of Gasul VSD

This entity was suspected based on a  curious observation  in children with large VSDs ,  who initially struggle with the defect and   show signs of  failure   . After a critical time frame  (If  they survive )  they  begin to stabilise and some of them do extremely well  in functionality too !

For this to happen , we presume the  quantum of  shunt  must  reduce by any means. Ironically ,  we also know , even patients who are destined to develop dangerous Eisenmenger reaction also live a blissful life for a decade or so  before it strikes  and  take  their life . This is one aspect of the natural history   . . .

While  some ther  children did well without developing  pulmonary hypertension  .This bothered  Gasul .When he analysed those patients (Mind you  there was no echocardiography  those days !)   he found something curious  was happening in the RVOT area. (It was almost like TOF !) This he documented in few patients  who showed progressive infundibular narrowing   acting as a check dam (Artificial banding ? ) and resulted in improvement of  VSD hemo-dynamics  .In extreme situations there was  a significant  right to left shunt as well. It was so tempting  to label it as acquired TOF !

Who are likely  to develop  Gasul  like reaction ? (Reference : Kieth 1978  Heart disease in Infancy and child hood.)

  • Persons with  oblique RVOT angle normal <40 ( 40-60 degrees)
  • Aortic override ride > 30%
  • Patient with anomalous muscle bundle
  • Children with right aortic arch

Why the concept of  Gasul was disputed ?

Gasul  concept primarily relied on the fact that  there  would be  some resistance at RVOT  for all those dramatic improvement in failure  as  the children grows .  This he consistently documented in many children who had significant regression of cardiomegaly .

There can be other mechanisms for  the signs of stabilisation in large VSDs.

Relative  reduction  of VSD size as child grows  could be an  important factor .  The falling pulmonary vascular  resistance  allows to  accommodate   the shunted  blood  without  any major issue as RV  after- load regress .

Is concept of  Gasul  alive   in the year 2012 ?

Since  it represent the natural history  of the defect  , most VSDs are closed surgically ,  one may not get an occasion to see a Gasul VSD today . More intriguing is the fact  we will ever get an oppurtunity to  confirm the concept .

Special  situations in  VSD / PS . Can RVOT obstruction  exist with raised pulmonary  arterial pressure ?

This  is a challenge to the traditional teaching . Logically pulmonary obstruction   and  high  pulmonary pressure  does not go hand in hand.Do not get fooled by logic .(We know aorta can record  even  200mmhg  in critical aortic stenosis ).

The respect and command  we give to clinical medicine   even  today is because ,  it can defy logic in  any random patient .

If a  patient with Eisenmenger  develop  Gasul reaction what will happen ? PAH will persist  as do the RVOT obstruction .They are the  blessed  ones and  belong to the category of   Eisenmenger surviving into 4th  5th decades . (Batisda of  Brazil extrapolated this and suggested huge benefits with  PA banding in adult Eisenmenger !)

Summary and verdict

TOF is a cono-truncal anomaly due to defective genes. The Mal-aligned  conal  septum is responsible for RVOT obstruction . Hence  this defect can not be termed as  acquired  , by  any  sort of imagination .

Still , a subset of patient with large VSD  can mal-align their conal  septum for hemo-dynamic  reasons .This  is  especially likely to occur  if the flow is heavy the infundibulum  slides horizontally to generate the obstructive  gradient .  Hence  Gasul was  indeed right when he pointed  to us some of the   grown children with VSD  mimic  TOF .

However,  the controversy remains  whether  the equation  “Adult VSD + IPS” = Adult  TOF  is  true or  false !

Incidentally , the classic book on congenital heart disease by J.K Perlof has a chapter on VSD with PS  and not  on TOF  !  Does it light  a spark ?  Is it worth pondering this question ? Probably not ,  instead we may use our resources to  correct these anomaly  .


Gasul’s  original article published in 1957 (Only abstract )



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Mechanism of chest pain in mitral valve prolapse  include

  1. Mitral valve  has pain fibers , the myxomatous degeneration  of the valve tissue generates pain .* (Not much evidence )
  2. Mitral valve stress, strain ,  stretch and bending.
  3. Mechanical stretch  of papillary muscle or LV free wall (dimple ?  ) as the mitral valve prolapse into LA.
  4. It is a central pain perception disorder .Panicky and anxiety reactions included
  5. It is not chest pain  at all it is simply a feeling of palpitation .
  6. Associated ischemic  heart disease

The commonest mechanisms  are   response  4 and 5 .

The evidence  lies in the fact ,  many of  these people  begin to complain of chest pain only after being aware this problem. MVPS is  often a  fancy entity created by cardiologists  which  unfortunately has  labeled  many of the normal  general population as cardiac patients. Barlow who described this entity  decades ago  would have never imagined  it  would be  so popular and subjected to mis-use . We have proposed a solution for this . The diagnosis of MVPS shall not be mentioned unless it is obvious  and fulfill a strict criteria . The commonest error we make is  an elongated , redundant , hyper mobile mitral leaflet   at   as  MVPS.

It is expected  ,  true MVPS must have all of the following  three criteria

  • Thickened leaflets
  • Clear prolapse of  at least one leaflet in long axis view beyond the plane  of  mitral annulus
  • At least some degree of mitral  regurgitation must be present

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