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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 !

Reference

http://europace.oxfordjournals.org/content/12/4/567.full.pdf+html

http://europace.oxfordjournals.org/content/12/4/466.full.pdf+html

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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  ?

Reference

http://circres.ahajournals.org/content/107/6/728.full.pdf+html

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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  !

Management

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

Reference

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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