Posts Tagged ‘wpw syndrome’

 Delta waves  are initial 20 ms  (or is it up to 40ms ?)  segment of  qrs complex that is  inscribed due to pre-excited depolarisation of the ventricle due to an accessory pathway .

It is more of a  fusion complex with  native normal qrs complex. The leads in which appear , the polarity and magnitude of these delta waves are determined by

  • Site of APs
  • Rapidity of  conduction through this AP
  • The quantum of native AV conduction
  • Influence of Autonomic tone  and the  refractory period of these accessory pathways .
  • Heart rate , distal conduction velocity , also can influence .

Can delta occur without AP ?
Like any other variation  isolated delta waves are reported in routine ECG finding.   It can be  be present in 0.15% to 0.25% of the general population. A higher  prevalence of 0.55% has been reported in first-degree relatives of   patients with accessory pathways.

How do you account for delta in general population ? We know concealed pathways can not record delta  . . . then it is possible some from of accelerated AV conduction  with twin pathway should be quiet common . ( It is very much possible  dual AV nodal pathway with grossly different conduction properties and distal insertion sites  inscribe a delta wave .)

  The crux of the discussion  of WPW syndrome revolves around  identifying delta wave and its direction .  If  the delta wave is well inscribed this job is easy  but at times  it  can be really difficult .

Many moods of delta wave

  • Positive delta  wave inscribes  above baseline. (See the above ECG  showing different delta in same patient )
  • Negative below baseline  and  iso-lectric on the baseline .
  • Please note , delta wave polarity and QRS polarity need not be in the same direction . If  they are in  the opposite  direction many time it appears as  small a pathological “q”  or pathological  “r”
  • It is likely  a delta wave can also drag  and  change the direction of qrs depolarisation  if  the  quantum pre-excitation  is large and with a fast conduction property.
  • It is also possible  the combined contribution of  negative delta with negative qrs together make a  deep  q waves . (Typical example is the LBBB type ECG in type B WPW in Ebstein anomaly )
  • Rarely the entire QRS can be  due to pre-excited  tract and native AV conduction contribute less.(This exactly happen in anti-dromic tachycardia ) but  this phenomenon is extremely rare to occur without tachycardia.

Final message

WPW  syndrome is such a dynamic  entity ,  one can realize how futile it will be to formulate fixed rules for ECG localization based on this wave .In fact,  we suffer from a  fundamental  electrical ignorance .How often delta wave polarity is discordant with qrs polarity and what is the  mechanism ? Standard text books do not discuss this issue . Many of the EPs skirt this question ! For this , we need  to critically decode the mechanisms of delta wave generation . Hope our youngsters take up the job !

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Pectinate muscles are specialized Intracardiac  muscle

  • Pectinate muscles are located mainly in the right atrium  , more  in right atrial  appendage , sparse in left atrium
  • Has muscle fibers arranged in a  comb like fashion.
  • Has less mechanical activity, no significant contribution to atrial contractility.
  • Can stretch and improve the voluminous nature of right atrium
  • The pectinate muscle  folds act as RA volume reserve  during adverse loading conditions . It helps RA dilate with out much wall stress.
  • Rarely it can be a cell of origin for focal atrial tachycardia

Image Source : Greys anatomy

The concertina like effect of pectinate muscle .

The atrial infolding increases the surface area of atrial chamber at times of dilatation , like  the music instrument .So,  these macro  folds ( like intestinal villi )  help overcome the  constantly changing volume status of right atrium.Since the  variation  left atrial blood flow is  not that much ,  the pectinate muscles  are not well developed  in the left atrium.

The same rules would apply for  why  there is excess  trabeculations  in right  ventricle  than  left  ventricle .

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WPW syndrome remains as  a   fascinating ECG entity ,  ever since it was described by Wolf , Parkinson and White in the year 1930.It is  primarily a  disorder of cardiac embryology . Heart is an organ made up of  tissues from mesoderm and neuro ectoderm.The muscle which comes from mesenchyme has to be incorporated with specialized conducting system. This is a complex  process .It is determined by the bio-genetic forces. When errors happen in the embryonal  tissue  flow  congenital anomalies occur.

In  WPW this  error   happens  exclusively in the conduction  tissue movement  . Normally the specialized conducting system    pierces  the  entire  AV ring and connect atrium  and ventricle  .Later ,   it regresses in  all areas  except in the AV nodal zone  . When  It  fails  to regress ,  these  remnants of  conductive  tissue act as AV accessory tissue  and create electrical  short circuiting .This is the reason , all these pathways are located in the close vicinity of AV ring.

Accessory pathway shows   varying conduction velocity , but generally devoid of  decremental conduction properties .  The presence of such pathways make these individuals prone for variety of cardiac arrhythmias .It can range from  simple AVRT  to  malignant antidromic  AVRTs  that can end up in  VT /VF.

Resecting  these  pathways surgically was once popular.  Effective blocking  of  the pathways with  drugs  is a good option. Currently ,  it is possible to  locate and  ablate  most of these  pathways   successfully.

Even though there are many protocols to locate accessory pathway the one that is very popular is  simple   Type A and type B  WPW , which locates the pathway either in the  left  or  right  ventricle  respectively.

Huge data base  has been accumulated over the past 80 years  regarding WPW syndrome,  still   many questions are unanswered.  One of the important clinical issue is  multiple  accessory pathways , scattered  at  random  across the  tissue planes of atrium and ventricle  .

The other issue is intermittent pre-excitation and shuffling  of path ways during tachycardia  .

It is very rare to see a patient who manifests both Type A and type B pattern during sinus rhythm .Here is an  article from  unexpected  quarters  , Colombo Sri-Lanka in the year 1972  candidly  describes a patient with classical  combination  of  Type A and  B  WPW . It is great to see such an interesting  observation in the pre  EP/Echo era from a remote island nation.

Now , let us ponder over  these questions

    1. Can a pre-excitation  happen simultaneously in both right and left free wall pathway ?
    2. How will the ECG look like  when impulse travels over multiple pathway ?
    3. When dual pre-excitation combines   with  normal AV  conduction  ,     will  it not make  a  triple AV pathway ?
    4. How does a supra-ventricular impulse decide ,  which pathway it is going to travel  when confronted with a choice of  three or  four pathways ?
    5. How do you plan ablation for such a patient  ?

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Echocardiography is an imaging tool . Can it  be used as a non invasive  EP lab ?

Heart is an  electromechanical organ . For every mechanical activity there must be a electrical event preceding it . So, when we analyse the cardiac contraction and relaxation it indirectly provide us clues how the electrical activity spreads across the heart.

The concept of using echocardiography for diagnosing cardiac arrhythmias have never been popular for the simple reason we have a cheap and best modality : The ECG.  But, it  does not give us the temporal relationship with the cardiac contraction. When these two are combined it can be a really powerful tool to analyse many cardiac arrhythmia.

  • In fact ,  for every brady and tachyarrhythmia there has to be an unique pattern of IVS motion and mitral , tricuspid valve movement.
  • Almost all bradycadias can be diagnosed with echocardiogram by virtue of analysing the timing of  atrial vs  ventricular  contraction.
  • We know echocardiogaphy is the only modality available to diagnose fetal cadiac arrhythmias.* (How can  this modality becomes useless when the baby comes out of the mother’s womb  !)
  • Apart from this there is an  unique use for echocardiography to locate accessory pathway in WPW syndrome

The premature contraction of LV can be seen in few as  an early systolic dip in IVS movement -Type B WPW.

Image courtesy :  Helmut F. Kuecherer Circulation 1992;85:130-142

Abnormal jerky movement of LVPW indicate left accessory pathway -Type A WPW

Newer modes of echo like tissue doppler will improve the phase analysis of tissue motion and may provide us accurate information about preexcitation

Final message

The future looks bright . Time is not  far off . . .  where ,  we shall  use ultrasound as an adjunct  EP  study .


*Fetal Echo  =  to  Fetal electro cardiogram

WPW syndrome




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It is often said , old thoughts  die hard ! It is more so in medical science as we realise ,  perceived fears and  physician phobias  have a long shelf life . A  few  case reports of  verapamil induced acceleration of accessory pathway conduction  was enough , to create a   global  perception among physicians and cardiologists  that any drug which acts on AV node is dangerous in the management of AV nodal reëntry tachycardia (AVRT)

This is a gross perception problem due to dispropotinate importance given to a remote possibility  . Thus ,  a  great therapeutic concept was  put on the back burner.

AVRT is a macro reentrant tachycardia that traverses both AV node  , accessory  pathway  ventricle & atrium .This  tachycardia can be terminated by interuppting  the path way  any where in the circuit .

The most easy and simple option is  to block the   AV node ( Verapamil, beta blockers, even digoxin !)

These drugs have cured many thousands of AVRTs  in the past  .As our knowledge progressed , we  found  , it may not be safe to block the AV node in WPW as it could  divert incoming signals through accessory pathway and result in 1:1 conduction and  possibility of  VF

As soon as this concept was flashed all over the cardiology journals in early 1980s cardiologists  took it as sermon . At the same time, lots of new anti arrhythmic drugs were developed  and this concept came in handy to promote all these new class 1 c and class 3 drugs which are supposed  to act more on the accessory pathway and hence projected to eliminate the risk of  VF.  

It was never  minded ,  all these new group of drugs has it’s own pro arrhythmic  properties  like  prolonging   QT interval   and has a potential to precipitate dangerous ventricular arrhythmias 

So, by the turn of   millenium calcium blockers and beta blockers have been removed form the  cardiologist mind in the management of WPW/AVRT

What is the reality ?

Verapamil or betablocker induced sudden death in WPW is a grossly exaggerated concept in clinical cardiology .Treatments and procedures with many fold risks is being practiced in every walk of cardiac patients.

Complete heart block  and related morbidity  during RF ablation of WPW syndromes can easily exceed the   of verapamil induced  side effects  in WPW.

 How to  identify potential patients who are likely  to develop complications  with AV nodal blockers in WPW syndrome ?

The key determinant is the accessory pathway refractory pathway . If it is < 250ms  the chances of accelerated conduction is considered high. EP study is needed to measure accessory path refractory period.If it is > 300ms the accessory pathway is unlikely to condcut fast .

Is there a  non invasive bedside method  to estimate  accessory pathway refractory period?

NO, It is not possible , but some clinical clues are available .

  • All concealed accessory pathway have very high RP *thats why they are concealed .Since they can not conduct antegradely   resting  baseline ECG do not show any evidence for preexcitation . They  are  safe .
  • These patients can develop only orthodromic tachycardias as the accessory pathways allow only a retrograde conduction  and AV nodal blockers are ideal in them as there is no purpose to use Amiodarone and  related drugs as antegrade  condction thorough accessory pathway is naturally blocked .
  • Intermittent WPW syndromes  have negligible risk of fast antitrade conduction. As episodes of  disappearance of delta wave indicate the antitrade conduction has a tendency to get blocked so no great worries.This is especially important if the WPW disappears at higher heart rates .

This clearly tells us  , many times  accessory pathway  shares some of the decremental properties of AV node (Applying automatic  electrical  breaks at higher  heart rates ) and it is a safety mechanism .The exact incidence of such property is not known . So , it may be a good idea  to subject patients with WPW on a treadmill and look for it’s  influence on delta waves and degree of pre excitation  .Even a few normalised beats  or prolonged PR intervals can give us assurance  against  rapid rates at times of  AF .

*One should  also remember , if a concealed WPW , manifest only during excercise it is the most dangerous group of patients in whom AV nodal blockers are absolutely contraindicated . They are immediate candidates for ablation . The above phenomenon  tells  us  , during excercise  the  AV node expresses the decremental conduction properties while accessory pathway  does not !

 Final message

Verapamil and betablockers are not  the  drugs to fear upon in WPW syndrome.In fact ,  even in this era of  hi tech cardiac care , it has a  useful role to  play  in the chronic management of WPW .

May be ,  it need to be  used with  caution . Atleast  , some  efforts  must be taken to estimate the refractory period of accessory  pathway before prescribing these drugs.

Using with caution is not synonymous with contraindication   

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Looks very much a infarct of  infero posterior territory is it not ?

Have a look at her 2D echo still picture . . .

Are you convinced ?

This women had normal LV systolic and diastolic function with no evidence of constriction.

The explanation for the asymptomatic pericardial thickening is due to a healed  chronic pericarditis .This sort of localised thickening in the posterior aspect is all the more likely following a loculated pericardial effusion.Tuberculosis is a very likely etiology.But this women do not have any markers for tuberculosis.Since she is symptomatic no treatment was offered.She is being followed up.

Discussion .

Q waves are not ” sacred waves” to diagnose myocardial infarction.It simply indicates the  direction of current flow is away from the  recording lead of the ECG .Any thing  electrically inert , that come in the interface between the heart and the recording electrode   can record a q waveWhat are the pathological entities that can produce q waves other than infarct ?

  • Fibrotic myocardium(DCM-Cardiomyopathy)
  • Myocardial Scars
  • Myocyte dis array(LVH, HCM)
  • Air,fluid in pericardium /pleural space
  • Pericardial thickening (As in this patient)
  • Electrical shortcircuits (WPW syndrome)
  • Rarely pure ischemia without necrosis can produce q waves (Electrically stuned myocardium)

Final message

Localised pericardial thickening is  a rare  (?unrecognised) cause for pathological q waves , that may mimic a MI.

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