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 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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What is  the most important factor that  will decide  the revascularsation following a  STEMI  ?

  1. Patient’s  symptoms
  2. Residual Ischemia documented by stress  test /Perfusion scan
  3. Presence of  significant  LV dysfunction
  4. Coronary anatomy and lesion profile
  5. Wealth  of the  patient (Insurance  limit  and  other  financial  resources )

Response  2  is   academically correct ,   but    practically  and politically   response 5  would be   the right one  for most cardiologists . At  any given day  ,  affordability and availability  of PCI  will prevail over all other factors  .

Affluence based cardiology

Image courtesey : Jupeter images

What is the  height of  inappropriateness in modern cardiac care ?

This world will never forgive the medical profession , if they do not fight  against  grossly inappropriate medical  care system especially in the life saving situations  .While one  cardiologist    just watches   a  left main disease patient  with unstable angina die peacefully in a Govt institution ,  while  another  patient with asymptomatic  distal PDA lesion gets a 3rd generation drug eluting stent in a  nearby corporate hospital !

Please note : Harm is the ultimate outcome in both rich and poor.One suffers with non availability while the other is the victim  of   affordability .

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A patient  walks  into the consultation suit in an  upscale cliniq  of  a  south Indian Metro.

Good evening doctor !

Welcome . . .   what brings you here ?

Doc ,  I  have a vague chest  and back pain since two days . It  had been a  strenuous   week  . . .  I  had to travel a lot ,

I am worried  it could be a heart attack

Let me examine you ,

(After  the examination )

Will you please  lie down for an  ECG  ( Records it  in a minute , Glances it )

Every thing looks fine , i believe  you are under some stress and  I am sure it  is  a  pain from your muskulo – skeletal system

You should  be alright by few days . I will  prescribe  some pain killers .

It is not uncommon to find a  patient wear a doctor’s mask

Doctor , why don’t  you prescribe  a 10 second 64 slice heart scan*, I just saw  an  ad in yesterday’s  “Times of India”

I want to confirm every thing is fine with my heart doc  ,   I believe  there is  a  special   World heart day offer too !

You will  not need a scan for that ! I can confidentially rule out a heart problem right now , and  you can schedule a  exercise stress test later.

You may sure doctor ,    but  I am not !

Please ,  will  you advice  a  scan for my satisfaction ?

It is not correct  for patients to demand investigation  . . .  thinks for a moment   . . .umhh   .. yeh  . . .ok . . .  any way   I  will do just that   . . . after all  we are here to satisfy you.

By the way , you  take  the  scan  in this a particular  centre  , (Let me also benefit  by your foolishness  ! )

Thanks doc ,  you are  really great   !   upholding the dignity of  the noble profession !

(* A single 64 slice CT scan of heart  is equivalent to radiation of 100 chest  x rays , which is equal to   a  life time dose of medical radiation)

Can a patient demand an investigation and a prescription ?

It is an  awkward question .  Our medical schools do  not teach about these issues. If the answer is yes , it would be  diagonally opposite  against  the  principles of practice of  medicine  ,  It is same as self medication  with a  non academic  ratification  by the doctor !

The patient   guided medical practice  has a niche market by itself . Now patients tend to  ch0ose  not only  hospitals  and  doctors   but also  they want to  decide the  investigation and treatment as  well  , fueled by crazy  mass  media advertising  . It  all started with  from simple master health check now extended into  all common disorders.

And  no wonder  . . . future looks  bright for medical  practice .

**Please note  : When the treatment  is debatable and outcomes are not clear in certain complex  diseases ,  one has to involve  the patient and their relatives  with an informed consent and allow them to make a  learned decisions.This is an acceptable form of patient and family guided disease management.

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This is an  RCA of   a  patient who had chronic stable angina  , class 2  with moderate anti anginal medication.

What shall we do ?

  1. The RCA needs  multiple stenting
  2. Multiple plain balloon angioplasty
  3. CABG to PDA
  4. No intervention ?
  5. It depends upon status of LAD  and LCX

The correct response would be 5

Without knowing  the status LAD and LCX . . .  RCA should not be touched . Further,  the concept of tackling  the  coronary artery  by itself  is   fundamentally wrong !  We are supposed to tackle patient’s symptom ,   reduce future risk of  events and   not merely  their coronary artey !

His LAD and LCX was near normal. In the weekly  cath   meet   PCI to mid RCA  covering  the critical segment was  strongly debated but  lost a close race .

The final decision was to allow the patient to continue   intensified   medical management (Statin 80mg /Metoprolol 100mg ) . He is comfortable with that .

Medical management  in a tight  single vessel disease  can never be digested by  any   Interventional cardiologist  whatever   may be  the guidelines !

Final  message

Do not decide PCI on the basis of   how ugly a coronary artery looks , rather spend some time on true  symptomatology ,  optimise baseline therapy  and re assess risk profile

One learned dictum is ,  do not  meddle a RCA ,  however severe the lesion may be   if  LAD and LCX are fine.*

*This  rule is not applicable in ACS

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Human coronary artery anatomy would  rank  top among  all human biological mysteries. The variations in their branching pattern is next only to palmar creases and cerebral gyri !

The left coronary artery can divide in to two , three  or even four branches occasionally.The trifurcation  occurs in upto 20 % of population .The ramus intermedious  can some times be a major division .Usually it supports the diagonal or OM territory.

It is very rare to see a ramus  take a long course . Here  is a patient whose LAD is small  which  falls  short of LV apex . Sensing this , the ramus travels all the way to apex and support the LAD in distress !

RAO caudal view shows the Ramus reaching all the way to LV apex! Note the diminutive LAD and absence of true OMs from LCX.

* Technically  this can  also be  referred to as a rare form of dual LAD system .

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Ventricular tachycardia can be classified in a variety of ways. Monomorphic VT  and polymorphic VT  is one such classification based on VT morphology.Polymorphic VT  generally conveys a meaning of origin from multiple focus .But in reality  bulk of the polymorphic VT originate from a single focus .

How does a single focus have a multiple QRS  morphologies ?

This is possible because ,  even though VT arises from a single focus , the route it takes to exit  from the myocardium is different and hence they inscribe different QRS morphology for each  beat. It is also possible ,  as the conduction time varies with each  exit route  the VT  becomes  irregular. This  phenomenon   is called  polymorphic VT.

It is assumed the VT focus  is often located in the sub endocardium and breakthrough occur in the epicardial side as  we record  the activity  in the surface ECG. Electrophysiology of VT is not that simple ,  focus  of VT can be anywhere ,  the focus can be single or multiple and exit pathways  can also be multiple it and  it may even exit into endocardial cavity . Please note , even  a single  electrically abnormal cell  shall  act as a  focus . To confuse us further ,  some of  VTs  may not exit at all , extinguishes before reaching the surface.

It is  a  difficult  job to fix  a given  polymorphic VT  to arise   from a single focus or from multiple focus  .  Multifocal VT  can be  diagnosed  with  confidence only  after a through electro physiological  study.Clinically few clues are there. Electrolytic disorders and ischemia  are usually  multifocal,  while scars VT gives single focus .Other famous  example  of polymorphic VT are Torsedes de pointes .

Polymorphic VTs are  usually hemodynamically unstable but it is not a rule. Surprisingly ,some of the polymorphic  VTs are well tolerated . This is especially common in  multi focal polymorphic  VTs  which are hemodynamically and electrically  better off  . Ironically ,   presence of  multiple focus may be  a blessing  as they    compete with each other ,  in the process  pulling  down the other focus from triggering a VF . It  is possible  one focus acts like a natural anti tachycardia pacing for a  VT from another focus.

Ventricular fibrillation can be termed as an extreme form of irregular polymorphic VT as the wavefront breaks into innumerable fragments  each exiting the myocardium at will in a random fashion bringing ventricles to a standstill.

Final message

The term multifocal polymorphic  VT  is generally been abandoned at the bedside  as distinguishing  it from single focal  polymorphic VT  is a difficult task*.Still  the concept of  multifocal VT  is alive and  kicking in the EP labs ,  giving sleepless nights to  our Electro-cardiologists!

*Please note , multi focal VPDs can be recognised  with ease by different coupling intervals, but  it is difficult to identify during a  run of VT .

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Venous access for permanent pacing can be troublesome . Especially with anomalous subclavian ,  second implantation  ,obese patients with upper limb DVT . Temporary pacing through femoral vein is a well known concept.

Here is a concept of implanting the PPM  through femoral vein ,    in the upper thigh and the pacing  lead all the way reaches the right ventricle .There were few  issues which were  thought to be critical .As patients ambulate   there could be more  generator motion  than the sub pectoral location .(By the way , upper limb movement is equally common daily living is isn’t !)

Surprisingly excess  motion is  rarely an issue .  Even dual chamber  pacers were implanted  through femoral approach.Implantation  procedure  are simpler than one would have thought  and  complications are less as well .Since most of the leads are now screwing type  and  actively fixed   dis-lodgement  is never an issue.

Final message

The femoral venous access can be considered in all in whom SVC approach is difficult or not possible . 85cm lead is ideal . It is routinely available.

Always consider trans-femoral approach  whenever you encounter difficulty in subclavian .  Falling back on  epicardial  approach in such cases should be avoided at all cost. After all , epicardial approach is a major procedure.

Unfortunately,  very   few centers   practice transfemoral modality  for PPM right now . Brazil has some experience I understand.Royal Brompton  hospital ,London , Memorial  heart institute ,Long beach , California  have advocated this approach with good success.

We Indians , have a huge potential to propagate this useful concept.I wonder  why Femoral –  IVC approach  could  not be a  first choice for permanent pace maker implantation  especially in small children and adults ! The  main issue is  not technical , it is more of   perceived  fear  and reluctance to change the tradition.

Reference

The  article  by Ellsted  http://onlinelibrary.wiley.com

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ST segment depression is a fairly common observation in anterior precardial leads. It   is  due to

  1.  Pure electrical phenomenon (Referred to as reciprocal changes)*
  2.  Additional  ischemia in LAD territory
  3.  It could imply  the IRA  is  a critically occluded  LCX and STEMI is actually an   infero -posterior STEMI
  4.  Simply  indicate a  multi vessel disease.
  5. Many times  reciprocal changes may simply indicate extensive nature of the  index  inferior MI.

How to differentiate reciprocal ischemia from true  remote ischemia ?*

  • Logically true ischemia patients  should suffer from double dose of angina (Infarct pain plus ischemic). Most of these patients will present in a   scenario of  post infarct persistent  angina . Patients with   pure electrical reciprocal  changes are relatively  quiet and  severe distress is uncommon.
  • In true ischemia  , both patterns are  not temporally related  in time. If its a  pure electrical phenomenon they should be linked in time .
  • Disproportionate ST segment depression  (ST elevation  in inferior lead  is  2 mm  while ST depression in v1,v2, v3 is >  3 mm )
  • Persistence of ST depression even after thrombolysis  or PCI to IRA.
  • Worsening with thrombolysis would suggest ST depression in V1V2 and v3  is indeed an  episode of  true NSTEMI  of LAD , where thrombolysis is contraindicated. (Also  read  – A  related article  dual acute coronary syndrome in this site )
  • Echocardiogram will give us a clue .One can  detect ischemic the wall motion defect in the segment in dispute .(Reciprocals do not show WMA )
  • Coronary angiogram   would provide   definite  answer to the speculations in most  . Still , it may   require a FFR  to confirm ischemia in the contra lateral artery.

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This RIFLE  shoots without  bullets . Yes ! it  helps the cardiologist to  trouble shoot  the kidneys which often  suffer from  cath lab cross fires .

As  the cardiologists indulge in sophisticated cardiac procedures ,  in more and  more  sick and co- moribund  patients , it is becoming increasingly  important  for them ,  to   give due  respects  to  other organs as well !

Renal function is an important determinant   in the  over all outcome  in any cardiac patient.

  1. How to assess  the baseline renal function ?
  2. How to measure  the impact  of the  cardiac procedure ?
  3. How to  follow  up and monitor the  progress of  renal function   in coronary  care unit.
  4. How to  reduce the enhanced renal  risk ?
  5. When do you call for  the Nephrology consult ?

Every step becomes  vital . Do not ever think , a  cardiologist’s job is over  once few  stents are deployed . Wheeling   out a  sick  and fragile diabetic  with borderline  creatinine    out of the cath lab  may be  considered   as a procedural success  , but the real success happens only after  every organ of the  your patient  comes  out  unscathed  after the procedure .  In this  context  , we should first aim to  become a nephron  savvy and a nephron friendly cardiologist .

I have witnessed  cardiologists  spend hours  together  in cath lab with liberal injections of contrasts  even in  elderly  who have delicate kidneys .Cardiologist should realise  kidneys are soft and gentle  organs  which unlike the heart  , do not  know  how to cry  (Angina) at times of stress  as they lack  well developed pain fibers  (unmedulated  type c fibers to be precise!) .Only thing they  know  is ( like touch me not plant !)   they  strike work  the next   next morning (What we refer to  technically as Acute renal  shut down !)

Now , we see little  interaction  occurring between a  cardiologist and nephrologist  prior to PCI , even though  those two organs ( The   respective experts behold )  are  constantly in touch  with each other , every minute ,  by neural and hormonal mechanisms. The new generation organ  specialists  has to learn  a lot   from these sincere , interactive  , democratic  human   biological system.

Coronary arteries can gulp any amount of dye but  not the renal  arteries .The   future looks still more frightening ,  as we have a variety of devices lined  up  to invade human vascular tree (TAVI, Renal ablation, per cutaneous aortic pumps etc)

So what should we do ?

  • Patients  prone for  CIN should be promptly  recognized .
  • Ask repeatedly  the question .  Am  I   sure  ?  . . .does this patient  require this  procedure at all ?  If  so , have I taken all the precautions ?
  • Use the nephrologist’s services more liberally

Finally ,  read the basics of  nephrology   lessons  once again .  The international consensus group has  classified   the Acute kidney  injury  (AKI)   with a  simple and lovely criteria  for  risk  triaging .     It is a  five faceted ,  inverted  (Tip less ) triangular  cartoon called  RIFLE .

The beauty of  RIFLE   lies in its  simplicity . All  it requires  is  serum  creatinine   (eGFR)  levels  and urine output.  Let  every  cardiologist  master this scheme of AKI . It will immensely  help  our  patients   and make us  a  complete  physician   instead of   being  labelled as a  “master of  an  organ”   or   ” An accessory sub physician”

The CIN prevention recipe.

Source Catheterization and Cardiovascular Interventions 69:135–140 (2007)

References

For review about Contrast nephropathy (CIN)  there are lots of excellent articles.

One company is trying to find a new  solution for  this complication . Let us welcome it ! The device is called rena  guard .

Renal Guard : A new technology to prevent CIN

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Interventional cardiologist are excessively  talented  guys .They always  lead ahead in innovations  .The only issue is , their  enthusiasm  (   many times  overtake  the pace of science .  In the name of off label indications  they indulge   in drug and device extravaganza   in uncharted territory .

Even as we boast of practicing evidence  based cardiology   scientific  adventures  happen  without  proper  evidence  . . .   rather  we  have wait for evidence to come later .” A clear case of  cart pulling the horse “

The wide-spread of use of  second generation DES in STEMI has not been found to superior to BMS in the  EXAMINATION trial just released in ESC 2011 Paris. It failed miserably ,  when every one took  the superiority  for  granted.( Some may claim  non inferiority is  not a failure , but for a DES which was perceived a revolution,  it is definitely a failure in the  STEMI subset )

Further,  what  EXAMINATION  trial did not  address  is  acute and sub acute  stent thrombosis .Even as the DES is credited  with a dubious  record for  sub acute stent thrombosis ,   there is every reason to  suspect , in  the milieu of STEMI the thrombotic risk of DES  would increase many fold.

The  seemingly  low   incidence  of stent thrombosis with DES  in STEMI ,   in  EXAMINATION  trail  is a statistical mirage .This  trial was  neither  planned  nor powered to address the issue of stent thrombosis.

In the  ultimate  analysis of EXAMINATION ,   One could conclude   Cobalt chromium BMS,  has  cemented  its place ,  more firmly for use in primary PCI.

DES  at best ( *With all those conditions apply , Dual antiplatelet etc) can be equal to BMS,  while  BMS at any  day ,  would  casually will  win over DES without any conditions at a  huge cost advantage.

The above analysis is diagonally opposite to that of general  perception  that  emanated  from Paris  ESC meet 2011   trial   .

Please remember EXAMINATION trial did not reach its desired primary end point  !

That is  a strong point  against it  .What do you think ?

Reference

http://www.theheart.org/article/1272077.do

A  TV  debate on Examination  trial from EURO PCR

http://www.oxfordjournals.org/our_journals/eurheartj/ehjvideo.html

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