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Is verapamil and beta blockers really contraindicated in AV reentry tachycardias of WPW syndrome ?

January 9, 2010 by dr s venkatesan

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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What is the simplest way to differentiate pseudo normal mitral infow doppler from normal ?

January 8, 2010 by dr s venkatesan

Diastolic dysfunction  as concept  has  come a  long way after  initial hiccups . Now,  it is a well established  left ventricular pathology  , and has   a  sound physiological and molecular basis. Even though there are variety of methods available to quantify  LV diastolic function,  echocardiogram is the simple method to identify and grade diastolic dysfunction.

There are 4 grades of diastolic dysfunction

1.Impaired relaxation  (without elevated filling pressure)

Some  describe another grade  1 a  with elevated filling pressure

2.Pseudonormal mitral inflow

3.Restrictive -Reversible

4.Restrictive -irreversible

What is pseudo normal pattern ?

The grade 1 is the  most common type  diagnosed  . It is diagnosed when the  A  velocity is more  than E velocity . This  simply implies ,  ventricular filling needs greater assistance from atrial contraction than in resting conditions. It is so common , especially in elderly ,  many thought it should not be considered a pathology . In youngsters it is definitely pathological especially if it is persistent.

The issue that  really concerns  us  is  this  : When the diastolic dysfunction  progress  from grade 1  to grade 2  ,  the mitral the inflow  doppler pattern ,  instead of showing any  new changes simply nullifies the changes that occurred in grade 1 and  records a normal E : A velocity .

So , a person with grade 2 diastolic dysfunction will have a near normal pattern .Of course  deceleration time, and IVRT is shorter than in grade 1 but it is not very useful in differentiating it from normal .

Pseduonormal is  actually  equivalent to moderate diastolic dysfunction , but the abnormality is masked  as near normal  filling is restored with atrial assistance . So,  technically it a  assisted LV filling . A  superficial  look at the doppler pattern may exactly mimic normal . But there will be a  2 D echo  abnormality  that makes the patient  pathological . Our eyes need to look  beyond  doppler  ( in coherence with  2 D ) to differentiating  normal or pseudo normal.

It is learnt  ,  2D abnormality of LV or LA occurs in nearly 90 % of grade 2 diastolic dysfunction .(There can be a pure functional grade 2 diastolic dysfunction  without structural changes in LA/LVH in minority -This is poorly understood form of silent sub clinical CAD manifesting only as diastolic dysfunction  )

Traditionally  there are few methods taught  in echocardiaographic schools  all over the world to differentiate normal from pseudonormal

1.Pulmonary vein  doppler

2.Response to valsalva maneuver

3.Tissue doppler etc

One simple echo feature  that is   often forgotten , that can be really useful in differentiation of  normal from pseudo normal is    left atrial dimension

While patient with pseudonormal who  have  progressed   into  stage 2  will show a  definite left atrial abnormality .

When does a left atrium begins to enlarge in diastolic dysfunction?

  • It depends  on LA thickness  and  LA afterload (LVEDP is the afterload for LA)
  • It is generally believed  LAE  will be there in almost all cases of grade 3  diastolic dysfunction.
  • It is present in  majority of patients  with grade 2 as well . But the degree  of LAE may be less  ( 4-4.5cm)

It is yet unclear ,  the onset of LA enlargement in diastolic dysfunction .This is potentially a research topic for the fellows !

It is not uncommon  to find   LA enlarge  like a balloon even in stage 2  of diastolic dysfunction. So , in patients who are suspected to have  pseduonormal  doppler profile , look for the presence of LAE  , (however mild it may be !)  , there is no business for LA to enlarge in normal persons.

Ofcourse , if  you are a echo expert one can measure A reversal in PV doppler, tissue doppler echo etc .But remember a simple 2D echo feature like a LA dimension / LVH   may score over the sophisticated (Also read complex  . . .) parameters  in the grading of diastolic dysfunction

Final message

While  we  immerse  ourself  in   sophisticated doppler methods  to differentiate normal from psedunormal pattern, the fact that  , normal persons will  have normal hearts  is often forgotten , and    presence of left  atrial enlargement (Which is all too common in pseudonormal !)  straightaway   settles the issue . Detailed diastolic function studies are warrented only if the LA size is normal .

*Correction: in table A reversal in normal is less than 35cm/sec

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What is the therapeutic approach for failed primary PCI ?

January 5, 2010 by dr s venkatesan

” This is post is 5 years old , Newer developments should be given considerations”

STEMI is the “Numero Uno” of  cardiovascular emergency .The  treatment has evolved over decades,  right from   the primitive  arm chair approach to the  air dropping of  patients  over the cath  lab  roofs  for primary PCI ! We realise by now ,both are extreme forms of treatment and  may  have unique  hazards. What we forget is the , the natural history of STEMI is too  much dependent on the degree of initial damage to the myocardium , and it is very difficult to alter this,  however good is the therapeutic strategy .  We are yet to find an answer regarding the mechanism of primary VF and modes of preventing it. We also have no answer for  ,  why  some  develop myocardial damage  very fast and  the  cardiogenic shock occur in an  accelerated fashion. (Fate ?)

Many would consider  ” non availability of   infrastructure and expertise ”  is the major issue  for  primary PCI . But the real problem is much more than that .When an  illusion of knowledge is  created by constant bombardment of data  , it is natural for human beings to believe whatever is told or printed in books and journals. We cardiologists are made to believe thrombolysis is a far . . .  far  inferior treatment than primary PCI in STEMI .  It is not so in any stretch of imagination !

The fact that,there is no entity called ” Failed primary PCI ” in cardiology literature  , would  suggest how biased we are against thrombolysis. Every cardiology  resident will  recognise  thrombolysis fails  at least 40% of time .Yes , it is  a  fact  , but the irony is , this   is  often  used   to convey a surrogate  meaning , that  is , primary PCI is  near 100% successful !

How  do you assess success of primary PCI ?

Unlike elective PCI where the criteria is too liberal, we can not afford to adopt the same in an emergency PCI. Here the aim of the procedure is entirely different (Salvaging dying myocardium vs pain relief  ).

It’s still a  mystery ,  while  thrombolysis is vigorously assessed  for it’s  effectiveness   primary  PCI is rarely  subjected to the same scrutiny  . A check angiogram  after the procedure ,  is all that is done . . . and every one  leaves the cath lab happily. The  effect of primary PCI on ST segment ECG resolution must be documented immediately after PCI. While ,  It is mandatory to take ECG after 60 -90 mts after thrombolysis , this sort of protocol is rarely  followed after PCI.

If the ST segment  fails to retract  > 50% immediately  following PCI  the procedure  should be  deemed to have failed . Further , unlike thrombolysis  in primary PCI , the ST segment has to regress within 10  mts , as IRA patency occur instantly .If we apply this criteria , the success rate of primary PCI would be far less than what we believe*

* Not withstanding the official lesion , hardware, related failure. If we encounter a severe triple vessel disease , with a bifurcation lesion and thrombus it’s  a tough exercise as we are racing against time .

Primary PCI  Camouflaging  in semantics

  • A successful but  delayed   primary PCI  is actually a failed PCI
  • A  complicated  primary PCI  often  reach the equivalence  of   failed PCI
  • No  reflow is almost synonymous with failed primary PCI as successful correction of no reflow occur in minority.
  • Not all TIMI 3 flow is converted into myocardial flow.
  • Renal dysfunction following excess dye has a  high  morbidity
  • If patient  develops significant  LV dysfunction following primary PCI it is a failed PCI.
  • Finally if the cost of primary PCI exceeds the insurance limit it is  economically a  failed primary PCI as the patient  has to spend double or triple  the amount of sum insured .This stress has resulted in many recurrent coronary events .

Why is it important to recognise failed primary PCI ?

For failed thrombolysis we have a strategy . Unfortunately , even in this modern era  we have  no useful  strategy for failed primary PCI . Handing over a patient to a surgeon in a such a situation is considered by many as a great rescue strategy but in real world it does no good in most of the patient.

Doing an emergency CABG in a sinking patient with a battered coronary artery is no easy job /Many times it only rescues the cardiologists from the embarrassing situation of facing the relatives who ask for explanation.

So , what can be done at best , in failed primary PCI ?

  • CABG can be an option but still questionable !
  • Most times  there is  no other option except to fall back on the medical management.
  • Intensive anticoagulation and one need to consider even a rescue thrombolytic treatment !
  • Some times we can only prey !  Failed primary PCI for a patient in cardiogenic shock with IABP support is near death sentence !

Final message

  • Remember ,  success of primary PCI   is  not in  wheeling out a  patient  alive out of cath lab   , with a TIMI 3 flow  in the IRA ,  but in  garnering significant   myocardial salvage   which  should have an impact on   intermediate and long term  outcome .
  • Do not ever think primary PCI is a sacred treatment modality in STEMI  and the job of the cardiologists ends there. It is vested with  lots of important complications – defined, undefined , recognised,  unrecognised, reported, and unreported ,  concealed ,denied, poorly understood, etc etc.
  • There are  equally  effective, less dangerous treatment modality available .
  • Decision  to do primary PCI  must not be based   only on the  “affordability and  availability”  of  cath lab and expertise !
  • In  clinical cardiology practice,  no  procedure  is  great   & nothing is inferior either  !  Every thing has to be used judiciously , appropriately  and  intelligently (Intelligence is synonymous with common sense many times!)

Coming soon

Surgeon’s real time experience of operating  on a failed primary PCI. To our surprise , only a handful of surgeons  have this experience

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How common is persistent ST elevation in inferior leads following STEMI ?

January 5, 2010 by dr s venkatesan

Persistent ST elevation is the  general technical term for  failed thrombolysis.Regression of 50%  of admission ST elevation is the required criteria for susccesful thrombolysis .

Thrmobolysis fails in about 40-50% .

Main determinant is the timing of thrombolysis – not the thrombolytic agent ! do not get carried away with all those curent hoopla  about Tenecteplase stuff

If we take 100 patients with persistent ST elavation 90-95 will be in anterior LAD territory .

This is a stunning a cardiology secret no book of cardiology address . . . Implication of which could be very significant . Primary PCI  will always struggle to  prove it’s superiority over thrombolysis  in the right coronary artery .(Note LCX STEMI is different , infact it is more tricky than even even LAD .This issue will be addressed seperately in my blog.)

Read the following link  for  answer to the title question .

How common is persistent ST elevation in inferior leads following STEMI ? https://drsvenkatesan.wordpress.com/2008/09/22/why-thrombolysis-rarely-fails-in-right-coronary-artery/

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Why revascularisation promptly relieves angina but rarely relieves dyspnea ?

December 30, 2009 by dr s venkatesan

It is a well known fact  ,   CABG and PCI  provides immediate relief  for patients with angina ,  which is refractory to medical therapy. Of course , this happens only if a critical occlusion of  at least one epicardial coronary artery is  opened . It need to be realised ,  angina  due to  microvascular  disease can not be cured by maintaining  epicardial  patency .

While angina  relief is prompt ,  dyspnea is not ! . If we  believe,  opening  up a  coronary artery  in a patient with LV dysfunction will  restore the LV function  ,  it  is grossly mistaken !

Why is it so ?

Angina  relief requires  simple  restoration  of  oxygen supply and correction of local ischemia .  This happens without any issue as the blood  seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals   . While  ,  for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this,   there need to be an intact  cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is  zig zag  orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of  extracellular matrix  namely the collagen frame work is also vital . Note ,  angina relief  is not concerned with any of the above .

And now ,  we also realise  dyspnea  in failing ventricles  is vitally  dependent on diastolic function ,  which is also very much  impaired in ischemic DCM .There is little proof for  PCI/CABG  to correct the  molecular   mysteries in  diastolic dysfunction !

Dysfunctional LV means what ? (read the link )

It is a collection of  variety of myocardial tissues . Viz : Fully  necrosed , partially necrosed ,  ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments   may  also be perfused normally by  spontaneous reopening of an IRA.

One can imagine the complexity  of events in these segments  once we do the  PCI /CABG . The response  is highly variable and unpredictable. The major concept we  , the physicians  believe or ( to be precise made to believe !) is  the  sanctity  devoted to  the viable myocardium .For  many us ,  it is considered a  holy  exercise  to identify viable myocardium in patients following MI and then revascularise them if  found to have significant viable myocardium (Atleast 20% of infarcted area )

A full 2 decades were lost or (shall  we   say wasted on this futile exercise !) as   we have since  realised most of the cardiologists do not follow this rule .

Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where  there is no contradiction for not doing a PCI /CABG   with reference to LV dysfunction.

Now every  patient  with post MI  LV dysfunction  is considered to  have  some amount of viable myocardium that is  fit   enough  for revascularization

Are we justified in doing  this ?

Many clinical  trials  have revealed  , the  recovery of LV function  in these segments  has not been consistent at all .

The most surprising discovery is  a viable myocardium need not  be ischemic   .It might get adequate blood supply either  from invisible collaterals or trickle of antegrade flow .  Hence an adequately  perfused myocardial segment can  still be   non contractile . This shatters the myth  that  revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.

The other major finding is  ,  even ischemic   viable   myocardium ( documented by metabolic activities PET etc)  need not regain it’s original contractility  after the ischemia is fully corrected .

*reference for  both the above statements are available from variety of sources including real life experiences .(Type C evidence )

Final message

  • Do a PCI/CABG promptly for patients with refractory angina.
  • Never  advocate PCI/CABG  for  a primary relief of dyspnea .  (Never is a harsh word,  let it be  “use it  with caution ” ! and  the  patient  should be  revealed  the whole facts  about  what we know and what we do not know regarding the complex  hemodyanmic events  in  revascularisation   )

Counter point

If  the above statements are really true ,   How does PCI/CABG   help  relieving  dyspnea  and functional class  what is your answer for thousands of patients  with CAD and ischemic DCM who have greatly benefited from CABG ?

The answer could  be  simple , The revascularization  piggybacks  over the   medical management (which , these patients pursue vigorously)     like  ACEI,  statins, salt restriction, betablockers  , optimal diuretics and tend to hijack the credits from the poor  drugs !

Read a related blog

Revascularisation for ischemic DCM

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Less discussed issues in coronary care : Preinfarction angina vs Acute MI – problems in estimating Time window in STEMI

December 30, 2009 by dr s venkatesan

Acute MI is a major medical emergency encountered in ER . Prompt adminstration of thrombolytic agents or rapid   triaging for a  primary PCI   may be required . The whole concept of management of STEMI  revolves around time as a therapeutic   target .Every minute counts . The beneficial effects of  reperfusion   and the resultant  myocardial salvage  rapidly declines over time . Hence ,  the symptom to door time  remains the ultimate determinant of  outcome in most situations.

So , estimating the  time window of  “Symptom to door time ” becomes an all important parameter. This is often done by paramedics .

The apparently  simple  job  measurement of time window  can be  misleading at times especially in elderly, diabetic and alcohol abusers .

When  a patient  says he has chest pain since yesterday straightaway he is excluded from reperfusion strategies as 12 hours  would have elapsed

When a patient  describes  chest  pain since two days , but  more intense  only since today morning what does it imply ?

  • The first episode of pain could  either  preinfarction angina or infarct
  • The second episode of pain could again be the continuation of same  angina or conversion of that angina into infarct

So ,  calculating the time window  when a  patient has recurrent episodes of angina prior to an MI is a real difficult issue.For the benefit of doubt, we have to take the last episode of chest pain  which was continuous and more severe as the infarct pain.

How does ECG help to time STEMI ?

When it is difficult  , to differentiate pre infarction angina from infarct pain, the ECG may give  useful clues to time the STEMI.

  • Degree  ST elevation
  • T wave inversion
  • Q waves

Among the  above three ,T wave inversion is most useful to time an infarct. If T wave begins to invert, it can generally assumed the acute  infarct process is  almost complete . Q waves are less reliable  to time a acute MI as ischemic stunning can in the  very early phase of STEMI   inscribe a q wave over the infarct territory.

How will you time a STEMI in silent MI ?

There is no symptom to door time in patients with silent MI . Many do not even reach the door , for the simple reason there is no symptom that drives them to hospital. Those who are refered  have vague non cardiac symptoms and incidental ECG  which shows STEMI like changes. Here , the decision to thrombolyse is taken entirely on the basis of ECG *finding .

Note : Cardiac enzymes are can also be  used  to  diagnose  to estimate the time window .

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Why we rarely diagnose junctional ectopic beats ?

December 26, 2009 by dr s venkatesan

Ectopic beats , other wise called premature depolarisaton are one of the common ECG abnormalities  diagnosed by physicians.

  • Atrial premature beats (APDs)
  • Ventricular premature beats(VPDs) 

APDs and VPDs  form  the bulk of all clinically important ectopic beats.

Heart has a specialised electrical conducting system , every cell in this system is capable of firing on it’s own. But why then only the atrium and ventricle produce ectopic beats .Other structures like AV node, His bundle , purkinje are relatively rare to produce ectopic beats .

Is the AV junction relatively immune to develop JPDs?

The answer to this question would be  “May be yes” . Yet, we need to recognise they may not be as rare as we think , many times we fail to  diagnose  it or rather recognise it !

Certain observation about Junctional premature depolarisation are made .AV junction has unique properties than any other parts of the heart.The basic purpose of AV junction ( AV node is not a preferred word as it has no anatomically distinct demarcation)  is to apply a electrical break on the incoming electrical signal .Nature does this with a purpose .   It is essential for the ventricles to fill adequately . We call it as PR interval.

So, when the basic purpose of AV junction is slow down the conduction it is logical to expect it won’t get irritated that  easily  and  result in ectopic beats. So JPDs are less common than other forms of ectopic beats.

What is invisible JPD and HIS ectopics ?

We should realise many of the JPDs  & his bundle ectopics are not conducted ,  the impulses simply dissipate down hill .  Unlike the atrium and ventricle the junctional and his tissue has no associated chambers to depolarise , hence they are not  often visible in the surface ECG.The only evidence in the surface ECG may be an unexpected pause which represents concealed conduction. A EP  study  of the bundle  ECG often unmask these silent JPDs and His VPDs.

 JPDs are  less common  , while  junctional escape beats are the  hall mark of any  severe supraventrcualr bradycardia . How  does  that occur ?

AV junctional cells have  an unique behavior in that , it comes to the rescue of the heart whenever the native SA node becomes too slow  . This happens as a passive response .We call this as junctional escape beat.The major difference between a JPD and Junctional escape beat (JEP or JED )  is in the initial timing of the beat . Escape beat comes late .The coupling interval of escape beat (We generally use coupling interval for ectopic beats only , but  it helps to understand )  will be longer than the previous sinus cycle. So escape beat is never premature (Rather a  post mature beat !) .Ectopic beats are always premature ,( except Interpolated ) and occurs earlier than the next anticipated beat.

The other difference is escape beats are tolerated well as the primary purpose is to rescue back up.Their rate is generally equal to the  intrinsic rate  of AV junction ie around 40-50.

General characters  of  Junctional  premature beats and tachycardia

  • Fortunately rare,  fires at a  higher rate.(Unlike junctional escape beats )
  • Enhanced automaticity is a common mechanism
  • Reentrant JPD is rare , unless the patient has AVNRT or it’s variant  physiology.
  • Manifest as narrow qrs complex . JPD with aberrancy is distinctly possible .In that case differentiation from VPD may be difficult.Retograde  P wave morphology may help.But it is non specific as VPDs also have varied atrial capture depending upon the VA conduction .
  • Causes include Hypoxia,  (Rarely ischemic junctional tachycardia. ) common causes include  digoxin induced , post operative states, incessant JT
  • JTs are Difficult to control.Overdrive pacing may be needed. May lead onto tachycardic cardiomyopathy.
  • A benign form of junctional ectopic tachycardia is also reported .

Importance of Junctional escape rhythm

The role of AV junctional escape is vital in extreme bradycardia , as if the junction fails to escape the dangerous ventricular cells take  over  electrical control  and that’s  bad news for the heart  with  sinister consequence.The situation can rapidly degenerate to VT  , what we call  as phase  dependent or brady dependent VT. The treatment for which is increasing the proximal heart rate. By isoprenaline or pacing. So the AV junction does  a delicate balancing act .At times of tachycardia it blocks unnecessary impulses.At times of extreme  bradycardia it assists the heart as escape rhythm . The problem here is many of the disorders that affect SA node , affect the AV node as well .So ,  AV node may not be able to help the SA node always.That is the reason many extreme myocardial end up with VT straightaway.

Final message

JPDs are not very uncommon as one would believe.It has some unique properties. There are vital difference between JPDs and junctional escape beats.JPDs can trnasform into JTs in local pathological milleu and as a rule they are difficult to control.

AVNRT is also a type of  junctional  tachycardia  but,  it  is delinked from  the ( unofficial  ! ) classification of JT  , not  with  any  academic purpose  but by tradition.

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When knowledge becomes a disease !

December 26, 2009 by dr s venkatesan

When we get contaminated with excess  knowledge , we lose our ability to think !   &  Common sense is the casuality . . .

Human beings differ from other forms of life by their sixth sense . Our planet is  few billion years old . Life came into existence over a million years ago .Our life has  evolved over many  thousands of years .The average life span of  human race   is  75 years . We need to realise , our life constitutes  only a fraction of our planet’s life (<.0000001% ) . A  may fly , which lives a life of  less than a  day ,   does it in style  , looking for the light  throughout  the night ,  says good bye ,  to earth by morning  leaving  it  unharmed . Actually ,  in terms of time , the life of the fly is  just a  fraction less than  human life span , when compared  to  our planet’s life !

When these children are  longing for food , some of  earthly humans go to  spend millions for  obesity surgery ! That is  the progress of knowledge driven society . . .

It is  extremely common to  experience the following  scenario  in any corporate hospitals of  both developing and developed country .A   uninsured  or half insured !  person is  refused entry into a hospital even for an  emergency care  while a wealthy person is lying comfortably watching TV in a five star suit of the same hospital after an inappropriate coronary angioplasty for  an   innocuous   lesion of his heart !

The irony is ,  in this short span  of  earthly life  ,  we want to prevail over the nature and conquer the planet . God is watching  this human  behavior silently . And he is smiling  . . .

With all our knowledge base ,  modern science  have done the maximum possible  damage to our  planet  .We have made many lives extinct. If  we  tend to  think , with the help of  6th sense  we can become immortal , it would be the ultimate foolishness. When every one of us ,  is  obsessed with our own  health  , we are deaf  to  the silent cries  of  our beloved planet earth .

Now , all of a sudden we realise all the accumulated knowledge & development has actually worked against us. We find our knowledge is dissociating our thoughts   and now , we are fighting  vigorously  over acquiring the rights to damage our planet  .

So it seems ,  the more we learn,  less wisdom we have  ! We may need to  learn important lessons  of living  from  all those  species   which  do not  boast to have  the  6th sense  !

Read a related article , excellent one published in British medical journal  nearly 2 decades ago

Knowledge disease BMJ. 1993 December 18; 307(6919): 1578.

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Pericarditis can be regional just like STEMI !

December 25, 2009 by dr s venkatesan

The commonest cause of ST elevation is  STEMI .

The non infarct causes of ST elevation include

  • Pericarditis
  • Early repolarisation syndrome
  • Hyperkalemia
  • Brugada syndrome
  • CNS injury

What is the mechanism of ST eelvation in pericarditis ?

The mechanism of ST elevation in STEMI  is  injury current coming towards the recording lead. In pericarditis  we are not  sure  about the presence of  injury current  because pericardial cells are not  capable of depolarising and repolarsing .But ,  the fact that  epicardium and visceral layer of pericardium are anatomically  are almost same entities .Attempts to rip off visceral pericardium from myocardium ie epicardium is often futile .This makes it very obvious  any true pericarditis  must involve epicardial layers of the heart.

How does inflammation of epicardium  lifts the ST elevation ?

This again is a mystery .The   effect of   inflammation   on the polarity of ST segment  is  complex one. Diffuse and global ST segment elevation with concavity upwards  is the hall mark of pericarditis. This makes us believe pericarditis has to be diffuse  and involve  the entire  circumference of the heart.

Logically and realistically  this happens rarely . Many of the pericarditis are localised and regional . Even regional constrictive pericarditis are reported .The factors that determine the ST elevation in pericarditis  depend on the  spread of the inflammatory process beneath the epicardium .If the inflammation is active  andeep  ST elevation is likely to be  prominent.

The ECG is  that of a 15 year old boy  with a febrile illness .  He developed  severe myopericarditis .The echocardiogram showed  global hypokinesia and severe LV dysfunction .Patient failed to respond  with  medical therapy and succumbed  after 48 hours of onset of shock .

Can we localise pericarditis with the help of ECG ?

It is possible. But there is no clinical purpose to do it.

Can troponin be elevated in pericarditis ?

No it should not happen in pure isolated pericarditis.But , epicardial involvement can result in inflammatory damage  to muscle and troponin can be elevated. When pericarditis occurs as an accompanying manifestation of pancaritis troponin  is bound to elevate (Fulminant pan carditis of acute rheumatic fever)

Final message

Pericarditis need not be diffuse and global infact pathologically it is rare to have global pericarditis  . Localised pericarditis especailly adhesive type , which involves the  posterior  /anterior  epicardial layers can mimic an  either inferior  or anterior  STEMI  . This has important clinical implication as unneccssary coronary interventions can be avoided.

Do not expect  text book descriptions for any ECG pattern in clinical cardiology .

We will be rarely  correct . . .

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Pulmonary artery pulse pressure : A simple parameter to predict reversible PAH In Eisenmenger syndrome

December 20, 2009 by dr s venkatesan

PAH  is  the major determinant of surgical outcome of left to right shunts. In this  modern era of cardiac care  allowing a child  with   left to right shunt   to progress to a  stage of   Eisenmenger syndrome  is  considered  as a  huge medical failure . But  , this is still rampant in many of the developing countries .

Cardiologists are divided over the issue of  operability of Eisenmenger syndrome .The confusion is largely due to the conflicting data of outcome in these patients. While  there is strong   data  when  PVR exceeds  SVR  ,  the death is imminent in the post operative period .

What has complicated the issue is   there are  many case reports  where severe PAH patients have been successfully operated. Most would think it is a statistical exception and one can  not alter the traditional criteria based on few case reports.

But ,it remains an irony as on 2009 ,  we do not have a proper methodology to assess reversibility of PAH in Eisenmenger syndrome . Further ,  there is a  significant number of  patients with high PVR  , who continue to experience  an  unabated left to right shunting .  We do not have an answer  for either the mechanism of such shunts and  how to manage these patients.

Click over the slide  to view full  PPT  presentation in PDF format .

This short paper was presented in the Annual scientific sessions of cardiological society of India 2009 regarding the usefulness of a new parameter to assess reversibility of PAH. This may not be called as  a study rather a report of  our experience  in  five  patients  with eisenmenger syndrome

Download the full PPT presentation in PDF  format.

pulmonary artery pulse pressure

Posted in cardiac surgery, Cardiology -Interventional -PCI, Hemodynamics, Uncategorized | Tagged , , , , , , , , , , , , , , , , , , , , , , , , , | Leave a Comment »

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