Archive for January, 2012

AV dissociation is  the most specific diagnostic clue in VT.But this is not a constant finding. In fact one  would be  lucky to spot a fusion beat  which denotes AV dissociation . It occurs in less than 30% of patients with VT .

Technically ,  for AV dissociation to occur atria and ventricle should  not be related in either direction .

If there is  a retrograde VA association ante grade AV conduction   is not possible  and hence one can not get a  fusion beat or so.

What happens to p waves during VT ? How does atria depolarise during VT ?

Atrial chambers can not sit idle during  VT .It has to somehow get depolarized  and contract   but  the  timing    may not be appropriate .

P waves  during VT can either be antegrade or retrograde .

Theoretically both can be present   but most times  it is   the  retrograde  p waves we see.

The occurrence and timing of p waves  is related  to the VA conduction .

If there is  1 :1  VA conduction during VT there can not be AV dissociation  for the simple reason  we have VA association.In fact there is constant vigil to depolarise the ventricle  through the normal AV node and his purkinje  in spite of the VT .SA  node is aware of this fact ,  how difficult it is going to be  confront the upcoming  rapid ventricular impulse . Usually the ventricular impulse   prevails  over the atrial impulse and much part atria is controlled by the VT . In fact  the VT reaches  all the way to SA node and simply  overdrive it . At these fast heart rates  retrograde p waves are not visible. ( But surprisingly one may see a regular  cannon wave in the neck with 1: 1   VA conduction.

Mean while ,  the SA  is always under look out for a opportunity to sneak into the ventricles thorough AV node. This happens  when the VT focus slightly slows down or shifts to a new site . this sis the time  we are able to  witness the AV dissociation . When the atrial impulse capture fully or partially the ventricle fusion beats occur confirming  AV dissociation .

Final message

AV dissociation is present in  less than 30% of VT because in  70%  there is a VA  association.(Retrograde  VA conduction ) . When V is associated with A there can not be AV dissociation.

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We do come  across ,  even  senior  cardiologists , who  tend to undermine  the importance  of  poster  presentations in scientific  conferences   (I know a  few ,  who  ridicule it as well  ? ) .

                      Is  it not a meanly  job   for  a  cardiologist  to paste a  poster  and stand  beside  it  for hours  , waiting for scientifically motivated audience !

But , what really matter is the thoughts ,  concepts  and often the hard work   that brings  these  posters to  big league  conferences .

Please remember   abstract posters  must cross the hurdle of  the conference peer review  committee’s scrutiny . Often times   the poster arenas   has  launched  some crazy ideas  ,  transform  them to  great  discoveries.

If   only  , Gruentzig had shied  away from the poster  he famously  pasted on lawns of   ACC  , Annual scientific sessions ,Florida

1975     .  .  .  the    revolutionary  concept  of  PTCA   would still be  in utero  !

Final message

I argue the young  fellows in cardiology to send as many  scientific  abstracts as  possible   in their  national or international  meets  . This is  where the  the future of cardiology lies ! Simply don’t  bother about the critics  .

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There are many  organic causes of mitral regurgitation. ( Ischemic , degenerative , valvular , cardiomyopathy etc.) It is not  rare for  pure  electrical events to result in valvular regurgitation.   A 70year old  man  with SHT   presented  with palpitation  and exertional dyspnea  .He was  later referred  for  Echocardiography.  Echo revealed LVH with intermittent MR and moderate LV dysfunction.

His ECG looked like

Ventricular ectopic recorded in bi-geminal rhythm

His  echocardiogram showed


His echo showed randomly timed mitral regurgitation was detected .See the Doppler MR jets below.

We know ventricles are integral  part of mitral valve apparatus  .Hence  it  wouldn’t  be a surprise to note  abnormally timed ventricular contraction  can  have a major impact  on mitral valve function.

When ventricles  prematurely begin  to contract  ( As  during  VPDs) it  interferes with  opening of mitral valve. In other words every VPD  technically imparts a  sort of  diastolic dysfunction !

VPDs occur in which part of cardiac cycle ?

VPDs  occur  either in early   or mid  diastole . Thank fully VPDs can not occur in systole . (Refractory period )

What would be the status of mitral valve at times of  VPDs?

Though it depends upon the timing of VPD ,  generally it interrupts the rapid inflow period of diastole .

In fact ,  it converts the cardiac  cycle from diastole to a partial systole or  a combination( fusion ) of diastole   and systole ! *

More MR jets are visualised than LV filling waves . Note the some of the E waves are sandwiched between two MR jets. ECG gating should have made this image more interesting .Any way , we have good MR jets to time systole nicely

* Is that a funny  imagination  ?

During   diastole ,  if  LV suddenly  begins  to contract   instead of  receiving the blood  ,  what will happen ?

VPDs are such a common arrhythmia , we  rarely  wondered  ,  it can have a dramatic  consequence  in a any  given cardiac cycle .While   the cardiologists think too  technically  their  patients observe with  shrewd  sense and tell us clearly  what  they feel  is  actually a   missed beat !

(Yeh  . . .  how simple  they describe the complex  hemo-dynamics  of  missing  diastole !)  .They also tell  us ,  next systole is felt as big thump as palpitation . (Post VPD potentiation )

Just imagine ,  if a patient  has  multiple VPDs  with  different  coupling intervals   that fall in different location of diastole  also  interspersed with sinus beats ,   how chaotic  would be the  the  mitral   filling .

This is what  is recorded in the above patient with multiple random MR jets .

Why all VPDs do  not cause MR ?

The timing is critical .We know all VPDs do  not generate a powerful contraction to cause MR. Atrial fibrillation, Prolonged PR intervals , heart blocks , critically raised LVEDP all can influence the trans mitral gradient . In fact these situation can result in  an  entity called diastolic MR that would be discussed later.

Can  VPD induced MR be  referred to  as diastolic MR ?

When VPDs  occur  in  diastole  , it  interrupts the diastole  and a new systole begins. In any  particular point of time there will be  leak into the LA  if the mitral valve is open .This is technically a new systole but in true sense it is the diastole of  the  previous beat . I wonder , whether   VPD induced MR  may be referred  to as one  form of  diastolic MR.  Of course ,  this MR can spill over to true  systole as well .

This also  makes  sense (Non !) as many of the VPDs do not open the  aortic valve ,   hence technically we can’t call the phase reset  by  all  VPDS   as a true systole !

What is the effect of VPDs  on pulmonary venous flow ?

Left atrial  cannon waves can occur that can elevate PCWP .This is the prime reason for resting or  exertional  dyspnea in these patients. Some may get a paradoxical relief  during exertion   as  exercise  suppress VPDs which are frequent at rest.

If VPDs can seriously interfere with mitral valve function , why  they are  often  considered benign  ?

VPDs are well tolerated* as long as  the  LV function is intact.  If VPDs are associated with  LV dysfunction  it  can initiate a vicious cycle of   hemodynamic deterioration .  Multiple VPDs  if left untreated can lead to progressive LV dilatation  in a  significant population .  Hence patients with  recurrent VPDS need some sort of  follow up. It  makes good medical sense to suppress VPDs in the long run. (Of course the  available anti VPD  drugs  are not very safe  !  The search for non toxic ,  ideal drug should go on !)

*”Well tolerated VPDs”   in no way  means  normal physiology.  Read a related article in my site.  “3 minutes crash course on VPDs”

Final message

VPDs  though considered  largely benign , can lead to dramatic  alterations in the  functions  of mitral valve , especially in diseased hearts.

We  must  realise  when ventricular  ectopic beats occur frequently  , it  interfere with the  both opening and closing of mitral valve.

It is really surprising  ,  the literature is  devoid of  major studies  about the  impact of  VPDs on  mitral valve  physiology . . . rather pathology !

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This  is the ECG  of  a  45 year old man with  H/O hypertension  and  chest pain .The general practitioner who first saw him alerted this  patient about a possible  heart  attack  asked to meet a cardiologist immediately. The cardiologist who  saw  this ECG   tended to confirm  the diagnosis  and advised admission in  a coronary  care unit .

The patient   defied  both  and  somehow landed in my echo lab  .  Looking at the ECG   I also  expected  it to be a  STEMI  evolving into a  Non Q  MI .

I was surprised  to find  only LVH with absolutely no wall motion defect  . There was no evidence of ASH,  HOCM or apical cardiomyoapthy as one of my fellows initially  suspected . His  EF was 70 %.   Cardiac enzymes were sent by then. When  I spent few minutes  with him ,  listening the history , it was very clear  what  he had was  non cardiac pain . In the anxiety ,  no one  got it right  about the character of pain ,which  was localised , lasted  for few seconds and  least suggesed angina.

The moral of the story is   listen to the patient  however dramatic the ECG may look !

What is special in this ECG ?

It is common for LVH with ST depression to be  mistaken for  ACS/NSTEMI

Here , there were  other  observations that  added  more  complexity .

  • Presence  of  ST/T changes in inferior leads(ST elevation in lead 3)
  • Bi-phasic  T wave in v1 to v3
  • ST elevation  in precardial leads

In LVH  it is usual  to note  ST depresion , how do you explain ST elevation in LVH ?

ST elevation in LVH   may occur in  leads  v1 to v3   . It is very rare  for LVH to inscribe  ST  elevation in   v4 v5 v6  .   Why certain  leads elevate the ST segment while others depress  in LVH  is not clear. It may represent  incomplete LBBB pattern where the ST segment deviates opposite to the  dominant QRS  complex. Septal  hypertrophy often elevate  while free  wall  hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads  record  classical  ST depression .

Importance of Bi-Phasic T waves

Please remember  Bi phasic T waves are notorious for it’s  unpredictability. An  innocuous looking bi-phasic T waves  (especially  with dynamic behavior )   is a  harbinger of proximal  LAD or even left main disease.

Finally , what will be ECG  changes if a patient with classical  LVH  who  develops a  real  STEMI ?

  • LV strain  pattern normalises ?
  • Further ST depression  occurs ?
  • No great changes . ECG  Looks near normal ?

Answer : ?

What is the significance  of   Bi-phasic T  waves : A  link to  a related post

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The mechanism of pedal edema in Amlodipine

Note : I lost track , the source of this Image .I thank with courtesy whoever has created this Image .

It is primarily a  local phenomenon . The calcium channels  are primarily  arteriolar dilators . Since the  venules  lack much muscle they  are not much affected by the Amlodipine   .  This  facilitates flooding of  venules and leaks into the peri venular interstitial space. It may be apt to call Amlodipine induced edema  as a form of   local venous edema .

This results in near permanent  collection of fluid  especially  near  the ankle . Systemic fluid retention has no major role . However few patients may  show an  augmented   RASS  response due to sudden arteriolar dilatation  .  In these patients   addition of ACEI or ARB may help relieve  edema legs .The Amlodipine  induced edema is  dose  and  time dependent .(Cumulative)  . It is mostly benign in nature ,  rarely warrants withdrawal of the drug.  The edema can  occasionally be generalised   and weight  gain is  possible .

Other factors that increase the chance of edema is age , women  , obesity. They have loose  interstitial  tissues.Many especailly women complain tingling feeling in the edematous zone.

The calcium blocker induced edema is  an  exclusive feature of dihydrpyridine group  .(For some reason  , Verapamil and Diltiazem do not  share  this side effect  as  theya balanced Arteriolar and venous dilator . )

Can we use diuretics to treat Amlodipine induced edema legs ?

Hydrochorthiazide  is rarely useful as the primary problem is not in the renal  retention.

How to  treat Amlodipine induced edema ?

Unfortunately the popular combination with diuretics do not work . Angiotensin  inhibitors which has some veno dilatation is shown to reduce this edema  . ( COACH study . Olmesartan / Telmisartan combination  is an option ) .It defies logic ,  to  add  another anti HT drug for the sole  purpose of reducing  the side effect of the initial  anti HT drug . Ideally if  your patient is not tolerating  Amlodipine due to edema ,  switch to  an another group of  anti HT drugs.



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Aspirin under attack  . . . not by  Gastro-enterologists  this time ,  but by cardiologists themself  !

Aspirin , after all may not be safe ,  as a primary prevention drug against CAD . It  seems ,  it considerably increases  the risk of   bleeding . The  new meta analysis just published in Archives of internal medicine  says so !

Be cautious it concludes  !  Since the  track record of evidence  based  medical science  ( and its reproducibility  )   looks   pathetic  in recent times  ,  we may expect another  stunning  study  very soon , with an exactly opposite conclusion  !

After thought

So , we have a  “vacancy  in  the top slot”  for primary prevention of CAD . Mind you ,  makers of  Prasugrel and  Ticagrelor  are already  fastening their seat belts !

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RVOT obstruction is the  sine qua non of TOF. It is  traditional to believe the obstruction  in TOF   is dynamic and is located in the infundibulum. It may be true in a broad sense .But  in reality  the  blood flow faces  too many hurdles within the RV before it reaches the pulmonary artery  and lungs  there after.

The commonest and most important one being the mal-aligned conal septum encroaching the infundibulum .(This anterior migration of conal septum is responsible for the aortic  over ride and  VSD as well) .It is erroneous to  think  the RVH in  TOF is simply an after effect of RVOT obstruction .There  can be  intrinsic defects in the RV trabecuale  that hypertrophies and  traverses the RV cavity  in  randon fashion.

Soto described 6 types of obstruction in TOF in elegant anatomic and pathologic study in 1981. Every cardiology fellow must read this original article before going to the Board examination. http://circ.ahajournals.org/content/64/3/558.full.pdf+html

For some reason  God  has  not  arranged  the   RV inflow , body  and out flow  in a linear  fashion . ( ? Meant  for haemic  acceleration in the low pressure venous circuit  )  .In  TOF this becomes important.  It is curious to note even minor  muscle bundles that  criss cross the RV body  act  as a speed breaker and alter the stream and direction of blood flow  .This  is why ,  TOF  can generate   systolic murmurs in various shapes and  time  over the left para-sternal area .(In TOF one can get a murmur right from left  2nd space to well down the lower sternal area )

What are the fixed obstruction in TOF ?

The  resistance  to  blood flow  within the RV  is often multiple ,  extend  from RV body to  pulmonary arterial branch points. It is important to realise few of the obstructions are fixed in nature.  Differentiation of dynamic vs static obstruction  is important in therapeutic aspect also. The efficacy of beta blockers is directly related to the ratio of dynamic vs fixed resistance .

Hypertrophied  trabecuale sept0 margianlis (TSM) usually offers fixed resistance. The infundiubulm is the only place where one can expect a dynamic component . If the annulus and valvualr PS  caused more of a  fixed obstruction

Final message

So,  fellows beware if some one asks this  question “Where is the site of obstruction in TOF ”  .Be ready with an elaborate answer . It is better to classify according to sites  of obstruction   with specific  reference to  dynamic or static nature .


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Who is the father of interventional cardiology ?

William Rashkind a cardiologist from Children’s hospital, Philadelphia in 1966  probably is the first person who thought it was indeed possible to use a wire and balloon as cardiac therapeutic intervention .When surgeons were groping in dark with  sick cyanotic new borns with dTGV , He along with Miller executed their idea.

It was published in JAMA

How the Rashkind  has revolutionized  our approach to congenital  heart disease  is evident from the current guidelines in 2011.

The procedure has since evolved with improving hardware and we are able to ferry a blade into the IAS for cutting .

Current  recommendations for Atrial  septostomy

It is primarily useful

1. Atrial septostomy  to enhance atrial  mixing (eg, transposition of the great vessels with restrictive/intact atrial communication) or to decompress the left atrium
2.During Extra corporeal membrane oxygenation (ECMO)   to decompression   of left atrial hypertension

3.If there is poor cardiac return from ECMO  circuit  low venous saturations  (Class 1 Evidence  C)
It may also be tried in  (Class 2 )
1.  Hypoplastic left heart syndrome  with  restrictive atrial communication.

2.  Static balloon dilation of  l synthetic / bioprosthetic  IAS  (eg, Gore-Tex)

3. Tricuspid atresia with restrictive atrial  communication

4 .Pulmonary atresia with intact IVS

5. TAPVC with  restrictive atrial communication.

6. Primary pulmonary hypertension / Eisenmneger VSD/PDA .(Occasionally useful )



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 21’st  century  Human beings  on the road !

                              A scene  from  Jaipur’s   main commercial  road

Lame  ducks on the road !

             My all time  favorite  news photograph taken  from a Tamil  daily Dinakaran

An After thought

In this fast and furious world ,  the medical profession  too suffers from the same disarray like  the  Jaipur traffic !

  • Let  us prey  for the   Noble professionals  to be  blessed with  more   discipline,  character , conduct  and  knowledge ( yeh . . .knowledge  ranks  last and least !)  .
  • Let us be focused on task .
  • Let us  also  prey for the strength to differentiate  facts from fiction,  distinguish trivia from  the momentous.
  • And finally let us  have the courage to follow the truth !

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How to manage multi -vessel CAD in STEMI ?

In this era of explosive information  , we rarely get clear-cut answers to  our  problems.

There are rare  exceptions . Here is an wonderful  review article on the issue of multi-vessel CAD  during STEMI. (http://www.ncbi.nlm.nih.gov/pmc/articles)   Especially  heartening ,   is the way the article concludes . It can not be more crisp than this !

Conclusion (Reproduced from the above article )

  •  Single-vessel acute PCI should be the default strategy (to treat only the IRA during the acute phase of STEMI).
  • Acute multi-vessel PCI can be justified only in haemo-dynamically  unstable patients with multiple truly critical (90%) lesions.
  • Significant lesions of the non-culprit arteries should be treated either medically or by staged revascularization procedures— both options are currently acceptable.

In-spite of the clearest possible guidelines   there  are frequent   debates  going on  for aggressive approach  to non IRA  lesions in hemo-dynamically  stable patients  as well  !  Many of the  learned cardiologists are calling for a  a  “legal violation”  of above guidelines !

The term staged primary PCI (Non IRA)  is often misused  . One such strategy is  rescheduling the non IRA PCI by 24 to 48 hours  later  than  the primary  ira PCI.  This  enables  us to violate the guidelines silently   . Please mind , the excess morbidity of non IRA PCI is due to the altered hemo -rheology which is expected to persist for at least few weeks !

I have recently come across a  cardiologist performing RCA PCI on Monday and LAD PCI (A 70 % lesion )  on Wednesday in a hemo-dynamically stable inferior STEMI ( Incidentally , he  felt  no guilt  , as  he was   ignorant about  existence of such  guidelines . In fact ,  he wanted to finish both angioplasties  on the same sitting  . It seems  he had to defer  the LAD  PCI   to Wednesday as the initial insurance  limit was exceeded   .

I do not want to dwell into another  unfortunate story  , as  this   patient had  to borrow  Rs 1.25lakh for  his life saving second stent  !

Final message

Come on   . . . let us violate the primary PCI guidelines . . . after all , our patients do not know the reality !


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