Archive for September, 2009

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Medical profession has  evolved over centuries with humble discoveries by genuine researchers in the past . As we  pursued  science vigorously  , we  looked  for innovations , when innovation  work ( or many times shown to work !) we jump to sky , even as  some of these  innovations fail and crash down  to earth , many times  we continue to be in the clouds . This is the fundamental problem of modern medical science . When  our expectations reached  unrealistic proportions ,   we tend to lose the common sense . Prolonging life and reducing human suffering may be the ultimate aim of the medical  profession , but  If we try to fight the death with science and money without application of mind , our current  life may become  miserable ! Thats what is happening for the majority of the population of this planet . After all ,  death is an essential and final  component of life !

Coming to the issue of CAD ,  in our country , a  rich gets a 4th generation drug eluting stent for a insignificant  asymptomatic PDA lesion , and poor fellow with left main dies without any intervention .This is  fairly acceptable   to this uneven world  , where a rich westerner  dies due to obesity related disease and a  poor African dies to malnutrition .

This article is in   response to  my  recent  experience  when  . . . I advised

Simple life style modification &   few drugs   for a patient with chronic multivessel   CAD  , I was  made to look   ordinary , inferior  and funny   by  many of the current generation cardiologists .

Further , the term optimal medical therapy(OMT)  for chronic stable angina has evoked laughter in one of the interventional cardiology  conferences  I  attended !

It is a sorry state of affairs  for the whole cardiology community , a  genuine scientific  fact , proven by  real life experience  as well,   is  being  ridiculed.

Richard  Conti tells in this excellent editorial in his journal   Clinical cardiology about the issue of medical management of CAD

“Respect in clinical trials”

Chronic stable angina pci vs cabg vs medical courage trial oat trial ethics in cardiology

Click here to reach the article  http://www3.interscience.wiley.com/cgi-bin/fulltext/122512853/PDFSTART

A similar study which  suggested  exercise  could be  better than PCI in the recent 2009 ESC is suffering the same fate !

What if regular exercise were as good as a stent for stable angina?


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Internet has revolutionised  in sharing our knowledge . But  , the  freedom it gives  has a trade off .Identifying   genuine  knowledge  in the  vast cyberspace is like searching for lost treasure in the ocean bed.

Have a look at this site which innovates medical teaching

great medical videos top cardiology web site drsvenkatesan

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Normal P waves

normal p wave ecg rae lae

What are the components of Pwave ?

RA component : The SA node depolarises the RA first  , so the initial part of  P wave represents  RA  current .After about 40msec  the wave front reaches LA and it begins it’s depolarisation .LA component :By the time LA is maximally depolarised the RA  already starts its repolarisation.So there is  overlap and also a short time lag between these two wave forms . This is very important to recognise as , even if the RA conduction is prolonged in pathology the RA component of P Wave still falls within the LA wave .Hence it is not shown in the ECG and P wave is not widened in RA enlargement. This is in contrast to LA enlargement , when the terminal half of P vector delayed it stretches the P wave wide beyond the normal 110ms .Hence LAE widens the Pwave.

Why P wave becomes taller in RA enlargement ?

In classical P pulmonale , the P waves are  tall >2.5mm. It is easy to explain why it not getting wide than  why it is getting taller ! The atrial vector has two components .The initial RA vector  is directed  anteriorly .The main reason for tall p with RAE is  due to the anatomical proximity of RA to the chest wall Further ,the  Initial atrial  electrical dp/dt is steep . Any RA voltage increase is easily picked up by the chest leads and P wave voltage increase and becomes tall. We need to realise LA is not only left of RA its equally posterior of RA. Hence LA enlargement rarely brings (Never ?)  it closer to chest wall ,and hence high voltage tall P is almost unheard of with LA . Note , deep negative late P wave activity is typical of LAE , consistent with its posterior location as well its late depolarisation compared to RA)

rae right atrial enlargement ecg tall p p pulmonale p tricuspidaleright and left atrial enlargement how to differentiate lae rae

Why LAE can not produce tall P wave ?

The Left atrial vector which  follows RA vector  is mainly directed posteriorly and hence inscribe a  descending  limb of   P wave . This causes the P terminal force .  So  the direction of vector forces  and the anatomical locality  make a  tall & positive P  deflection highly improbable in   LAE .

*Of  course  when LAE is   huge , where a antero -supero vector from  roof of LA may inscribe a positive wave .

What happens in bi atrial enlargement ?

It can have features of both . Tall & wide P waves .

Can RA generate a Q wave ?

Yes . When RA assumes a huge  size  , especially if the RV is also at high pressure as  in severe PHT or valvular PS   a  q wave is generated in the lead V1 .This q wave is nothing but the intra cavitary potential of the enlarged RA.

What is the difference between atrial enlargement, atrial dilatation, atrial hypertrophy, intra atrial block and inter atrial  block  ?

The p wave morphology has no  specificity to identify the various entities. In any pathology of atrium the first thing that happens is a conduction delay ! It is now realised the bulk of the changes we see in atrial enlargement especially in LAE is due to intra and inter atrial  blocks or more subtly conduction delay.

It is  obvious , a wide P wave can occur either  due to LAE or simple conduction delay .In elderly  hypertensive patients atrial fibrosis is more common , one can not confirm LAE  without echocardiogram .

A notched P wave  can be a very specific sign of   inter atrial block .Which is more common in severely diseased left atrium. A notch , slurred p wave is a good marker for impending AF or atrial flutter.


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Pharmacology is a major discipline in medicine where we learn how a drug acts in our body for various ailments . Now  in this era ,  doctors need not only how a drug acts but also how a drug company acts ! This has become vitally important   for the welfare of the mankind .

In this context one of the best books on medical pharmacology is from the

Famous Editor of New England  journal of medicine

A must read for all genuine medical professionals

ethics hippocrates ebm

Watch Marcia Angell  talk http://www.youtube.com/watch?v=ouF3ISihHLM

Full lecture of Mercia Angell  http://videos.med.wisc.edu/videoInfo.php?videoid=940

Click to buy/read the book  http://www.amazon.com/Truth-About-Drug-Companies-Deceive/dp/0375508465#reader

A Review  about the book  http://calitreview.com/176

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Wide qrs tachycardia has a unique place in clinical electrocardiography .It is  a much fancied and glamorous entity for the simple reason , it continues to be the  cardiologist ever solved puzzle .For over three decades of research, clinical debates , symposiums , seminars have effectively failed to take away the uncertainties in decoding the wide  QRS  tachycardia . (Specifically ,  VT vs SVT with aberrancy)

Some wondered , should we really waste our efforts in differentiating the two . In emergencies it never matters , in fact one need  not attempt to do this often futile exercise !

Few dedicated criterias like Brugada etc have helped us .

While the difficulties in differentiating between VT and SVT with aberrancy remain over the decades .A less reported  , but more common issue is  confronting  us .

It is  the big question of  differentiating a  wide  QRS tachycardia from a narrow QRS  tachycardia

wide qrs tachycardia vt svt aberrancy

This  occurs  more often than we realise  ,because we define wide  QRS  tachycardia in a vague manner

  • Normal qrs width between Up to 80 / up to 100 ms acceptable  ?*
  • Narrow qrs tachycardia 80 ms?
  • Wide qrs tachycardia i> 120ms  ?
  • Definitely wide qrs >140msec

* The confusion is mainly because 20ms difference between limb leads and chest leads .

In reality one may not be able to all  tachycardia into narrow or wide .

There is big  overlap zone that need to be labeled a intermediate qrs tachycardia

If we can  triage the tachycardias into three instead of two it may help us arrive  fast  ,  to the  correct diagnosis

Narrow QRS tachycardia ( qrs 80ms)

  • Sinus
  • All svtS (avnrt etc)

Intermediate QRS tachycardia 90-120

  • Most of the SVT with  aberrancy  ( Except antidromic SVTs which are really to wide !)
  • Septal VTs*
  • Fascicular VTs*
  • VT in PPM and ICD /CRT patients **

*  Any VT that arise near the major conducting system of ventricle conduct  fast and hence qrs are relatively narrow.

**These are rare entities where  base line wide QRS getting narrower with the onset of VT . (Ref : http://europace.oxfordjournals.org/cgi/content/full/eun254v1)

Wide qrs tachycardia >120ms

  • Most of the genuine VT (Ischemic , myocardial origin)
  • Post MI VTs
  • SVT aberrancy especially AVRT
  • Any SVT with preexisting BBB
  • Marked electrolytic disorders

Unresolved questions

  • Which lead we should look for measuring the width of qrs ?
  • Should we take the narrowest qrs or widest qrs or should we take the average ?
  • Should we calculate how much the tachycardia has widened the qrs from the baseline  width of a given patient ?  Is it not possible , what is wide for some may be normal for another !
  • If  there is no isoelectric line  and ST segment  blends with qrs complex  how to mark end of qrs ?
  • If  limb leads show a narrow qrs and chest leads shows  wide qrs what is the significance  ?
  • In precardial leads  if one lead alone shows a narrow qrs , what is the significance ?
  • Can a narrow qrs VT conduct  with aberrancy and making it  really  wide ?

Final message

When we are  able to solve   complex electrophysiological  problems  , we must also realise  even   simple  tasks can be demanding in medicne ! It is proposed to create a  new  group “Intermediate QRS tachycardia “that can help solve the issue where we have difficulty in labeling these  tachycardias which fall  in the  greyzone .We can try &  apply the modern EP based VT criterias  to this group and find out the hidden truths !

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The most popular criteria to differentiate VT from SVT aberrancy is  formulated by Brugada in 1991.

The greatness of  this  criteria is that  a single question asked  is able to confirm VT in vast majority of cases.

Is RS complex absent all  of the pericardial leads ? If  the answer is  yes  it is VT 100%

How is that,  we have been struggling for so long , a single question is able to solve the issue quite easily ?

wide qrs tachycardia vt svt aberrancy brugada

This is because , the term  “Absent RS complex ” actually means

Presence of  one of the  following three typical complexes Of VT.

  1. QS
  2. QR
  3. Monophasic R

Two of them  actually imply ,  q waves throughout   V 1-V6 .This  means a badly damaged ventricle and  with  little electrical activity coming towards the chest wall .This situation  almost always occur in VT.*

The third complex is Monophasic R .

A  monophasic , wide  QRS  complex  again indicate VT  as monophasic aberrancy is very rare as the supraventricular  impulse invariably conducts with  RSr’  (The right bundle  refractory period sees to that  at least a small r’ is inscribed however fast the SVT is !  )

So if there is no RS complex  it must be VT !

What  are the  difficulties  faced in applying this   first step of Brugada criteria ?

It is funny to note , in medicine criterias  often work perfectly in  text books only !

Is there a RS complex seems to be a very easy question ? There lies the catch !  .Even though this criteria may be 100% specific , differentiating RS from QS complex even by an experienced cardiologist may be difficult in a significant number of VT tracings.This  realistically ,  reduces    supposedly  100% specificity  of this criteria !

In fact we expect Brugada to develop an  another limb  to his now famous algorithm

Is there  absence  RS complex in precardial leads  ?  Yes / No / May be ,  not sure !

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Left main disease  is an important subset of CAD , and it has special interest for the interventionist. Traditionally cardiologist have   a fear to touch this lesion , as they thought a sudden occlusion within this vessel is life threatening   . Later on as  they gained experience  it was thought  we could intervene safely at least in protected left main . Subsequently  it was realised this fear was largely unfounded  , after all  the proximal LAD is equally  dangerous and we spend hours together inside an LAD ! .Now we have technology and expertise to do successful PCI any where in LM. And  unfortunately , the same expertise is not applied in selecting the ideal patients who will benefit the most . LMD has become a glorified indication for PCI.

The terminology of protected and unprotected LMD is in vogue for many years . Unfortunately it do not convey a uniform meaning . In next few minutes ,  I shall share  my views on the nuances of protected and unprotected LMD .

The term   protected was  not  coined by  cardiovascular physiologists   but by   interventional  cardiologists . Hence it connotes a  anatomical  meaning rather than physiological.  Protected LMD  meant there must be a at least one  graft to either LAD or circumflex . And this graft should be functional . The presence of this graft is supposed to increase the comfort levels of the interventionist as well as  the patient.

A left main coronary artery disease angiographically  can be  classified  as

Common types of Left main lesion

  • Asymptomatic , non flow limiting , angiographically insignificant disease(< than50%)
  • Ostial
  • Ostio proximal
  • Shaft : Mid, distal or diffuse Left main
  • Bifurcation

Unprotected left main

  • All the above lesions
  • Non functional GABG grafts ( eg: LIMA occlusion makes LAD unprotected)

Protected left main

  • Post CABG  with atleast one functional graft to LAD /LCX
  • ? Left main   with total  LAD and very good LAD collaterals from RCA /LCX

Partially protected Leftmain

It could mean any of the following,     Left main Plus  .  . .

  1. Incomplete occlusion of single  LIMA graft
  2. Occlusion of  SVG-LCX and patent LAD-LIMA
  3. Occlusion of LIMA-  LAD graft but patent SVG-LCX  graft
  4. Patent LIMA-LAD  but a  critical  LM / LCX  bifurcation lesion with no grafts for LCX*

The above 3  situations may demand a  PCI .But logic would  suggest one would try to open up the partially occluded graft rather than open the left main . Of course the decision involves status of RCA .

*The only indication for a  PCI  in protected  LMD could be 4

Unusual ( Crazy !) questions  about  left main disease

Can left main be protected by collateral circulation ?

It is very common to find Left main   bifurcation  lesion   with LAD having  very good collaterals from RCA sometimes filling up to proximal  LAD .This can be considered   “protected left main equivalent”

As on today , cardiologists would rather   believe  a surgeon’s graft  rather than a naturally grown  collateral from RCA however extensive it may be !

But logics and real case experience would indicate in a patient  with LMD and an  extensively collateralised LAD can in fact be  considered a protected left main.

If a  left main is well protected by a functional LAD graft , why should we do a PCI for left main at all ?

This question was risen in one of our cath conferences , a patient   who had functioning  LIMA to  LAD graft.His   RCA had a functioning  venous graft  and his circumflex had a partially functioning  graft.The left main had a near total  obstruction and the proximal  LAD was  faintly visible .

Since the  patient  had class  2 angina Options were discussed .He  satisfied  the  current criteria of protected LMD .Just because he fulfils the criteria of protected left main , he  does not  become eligible for  left main    PCI .  After all he is having this LMD for many years. Protecting again the left main which is already protected is not a big deal in terms  of outcome .  Double protection is waste of resource at additional risk. It was decided to attempt a PCI to SVG graft to LCX. If it does n’t work leave him with medical management.

Does  every patient  after a CABG   has a high chances of developing LMD ?

What is accelerated atherosclerosis of Left main following LAD /LCX  grafts ? It is  true  left main  has high risk of  accelerated atherosclerosis and it   undergoes  gradual obstruction once the LAD and LCX is grafted.This is due to low flow across the native left main as distal grafts maintain the flow . This is all the more likely in good bulk of patients who had undergone  CABG  where   LMD  was the indication .

A typical scenario

A left main patient   who undergoes a CABG  a follow up for a suspected  angina  angio after 5 years show the  totally  or near totally occluded native left main . Sudden   Visualisation of worsened leftmain disease    makes this patient eligible for  a  PCI as he fulfills the criteria for  protected leftmain .

Final message

A well protected left main  with a good  functioning graft especially to LAD   most often do not require a fresh revascularisation  procedure  irrespective of the tightness of left main disease . Most of such patients will be candidates for medical therapy .Contrary   to the popular belief ,   left main  intervention   could  be    confined  to   ” unprotected LMD   rather than well protected LMD” as the  potential benefits are more .Further interventional resources need not be wasted in giving second alternate protective channel  for an already protected vessel !

Of  course it should be remembered  in any given patient  with  protected or unprotected  LMD  the indication for  revascualrisation  is based on  the severity of lesion , symptoms,  LV function ,  residual ischemia, viability  etc .

Suggestions  , comments  and  corrections  welcome

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CHB and AV dissociation are often confused with one another . While CHB is an important cause for AVD , there are distinct differences  which have clinical implications. This table is an attempt to simpify the understanding of the two. Corections and suggestions welcome.

This is a high resolution image , to read better  right click on the table  copy image and open in any image viewer


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Atrial fibrillation and CHF are close companions. Either it   precipitates  CHF  or  follows it.In advanced heart failure of any etiology  the incidence of AF can be up to 40% .Medical therapy of AF is fairly effective in patients with normal LV function  .But when associated with refractory cardiac failure  it becomes  too complex to control .

Currently CRT with ICD  is becoming the standard OF care for advanced CHF. The efficacy of CRT is being rigorously being assessed . Even as the controversy  about  the wideness of QRS is being settled , the issue of optimal  timing of CRT has risen  . Now ,  the MADIT-CRT has answered this issue “Earlier it  is better , it can be  indicated even for  class 1 patients”

While MADIT -CRT will increase the number of CRT implants , we  have no clear cut answer for the  efficacy of CRT in patients with AF .( Of course , the MUSTIC and CARE HF sub group analysis suggested AF has no significant impact on CRT efficacy )

atrial fibrillation crt cardiac resynchronisation therapy icd madit crt care chf

Why is AF important in CRT ?

There are two issues that need analysis

  1. A patient who  has chronic AF at the time of CRT
  2. Development of  new onset AF after CRT implantation.

Impact of AF during CRT

  • Inter atrial synchrony is lost. ( Significance not clear . . . makes AF permanent)
  • AV synchrony is lost
  • Rapid AV conduction : May trigger   too much of Bivi pacing if sensed by LV lead

Presence of AF at the time of CRT gives us an opportunity to tackle this issue.

How to tackle  sudden AF induced CRT response ?

There are variety of algorithms available to

  • Ventricular sense response
  • Conducted AF response
  • Atrial tracking recovery

In dual chamber pacing mode switching converts DDD into VVI  .This happens  at the cost of loss of AV synchrony .This may have profound implication in CRT .

Then the big question comes  . What is the use  of  having Intraventricular  and interventricular  synchrony without AV synchrony ?

When nothing works .The best strategy is ( Rather deemed to be best ! )

  • To ablate the  AV node  pace  the atrium and ventricle  (RV & LV)  .

Note : Ablation of AV node and putting a dual chamber pacing can never guarantee a physiological pacing as the atrium continues to fibrillate and AV synchrony is rarely there .

Final message

For CRT is to be successful , there should be maximal Bi-Vi capturing , of course this capture has to optimally timed , and must reverse the three pathological asynchronies , namely intraventricular , Interventricular  and  atrio  ventricular  asynchronies.

It is obvious , presence of AF complicates the issue as it demands  constant monitoring and programming of the device (Of course  now most  of them are automated) . It may   require  knocking down of AV node , which  not only carries a risk of SCD *  ,  it also make these  patients   permanently  dependent   on the RV pacing  . This  adds on ,  another  risk ,  for an  acute complication   if the RV lead fails for some reason.

Reference :

*Sudden death after radiofrequency ablation of the atrioventricular node in patients with atrial fibrillation
Journal of the American College of Cardiology, Volume 40, Issue 1, Pages 105-110

EP experts generally take  too much liberty in adopting this  strategy for the simple reason it solves the nuisance of atrial impulses  interfering with   ventricular  leads  function that result in  inappropriate ventricular capture fusion or ultimately poor BiVi pacing . But it is not an easy decision  atleast for the patient ! This article , emphasises the dangers involved in ablate and pace strategy for uncontrolled AF.

Further reading

  • Fung, J. W H, Yip, G. W K, Yu, C.-M. (2008). Does atrial fibrillation preclude biventricular pacing?. Heart 94: 826-827 [Full Text]
  • Khadjooi, K, Foley, P W, Chalil, S, Anthony, J, Smith, R E A, Frenneaux, M P, Leyva, F (2008). Long-term effects of cardiac resynchronisation therapy in patients with atrial fibrillation. Heart 94: 879-883 [Abstract]
  • Buck, S., Rienstra, M., Maass, A. H., Nieuwland, W., Van Veldhuisen, D. J., Van Gelder, I. C. (2008). Cardiac resynchronization therapy in patients with heart failure and atrial fibrillation: importance of new-onset atrial fibrillation and total atrial conduction time. Europace 10: 558-565 [Abstract] [Full Text]

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