Archive for July, 2012

A 38 year old man presented with  acute breathlessness  and chest pain .His ECG is  posted  below . The ER in charge   medical officer promptly handed over the patient to   STEMI  alert    group (This is how  cardiologists are   referred to !   in one of the leading corporate hospital in India )

Note Atrial fibrillation , ST segment elevation, in pre-cardial leads

A team of  white coated  humans  in  various  gender and ages  swarmed the patient . ECGs and text where shared  among  the  STEMI alert group  through  I pad 3 which transmitted  HD  quality ST elevation with a  retinal  precision . A senior consultant   insisted   to shift the patient to cath lab direct  . Since he had  signs of cardiac failure , one of  the wise Junior fellow wanted  to correct the failure with Nitroglycerine  and  Dobutamine before rushing him to cath lab . Hence he was put on hold in the side room of ICU .

Echo examination showed LVH and wall motion defect could not  either confirmed or ruled out .  Initial  Troponin was negative . In the mean time the bio chemistry results came. He had a creatinine of  5.2 and Potassium of 6 meq . Hence the patient was diverted to Nephrology unit  and  dialysis was done. The next day morning  his ECG   looked like this .

It  may  sound a  pessimistic , but  still I would consider   the above  episode  is  a rare  example of appropriate care happening  ! This patient was diverted in a timely fashion from cardiology  care  to the  Nephrology . Please note , it is not the  the  clinical acumen that   helped  here.  If  he had  not presented with  LVF   he would have been a victim of inappropriate care  and landed on the cath-lab table directly  !

Final message

Every moment in clinical medicine is important , especially during the genesis of  diagnosis.  Where the patient lands  . . . in a frighteningly  large  hospital is as important  as the disease process itself. In this scientifically arrogant medial atmosphere  most of us, are  tuned  to view every problem as their own  ! This is  the default mode of modern medical  thinking process . How faulty  we are ?

The future is worrisome  as the field of  Internal medicine is  at risk of dying a premature death (or is it dead already !)

By the  way  what is the mechanism of ST elevation and Tall T waves in hyper-kalemia ?

Many factors contribute .

  1. Is it a true ST elevation  ? There is reason to believe   the tall T waves drag the fag end of ST segment along with it .
  2. Next is  related to QT interval . Hypo-kalemia widens while hypo-kalemia does  the opposite .(  though not classically) .
  3. When QT is shortened the segment gets squeezed in within a limited space ,  in order to accommodate the  ST segment it   gets rolled up and elevated . (Like an up sloping ST segment  in extreme tachycardia during stress  testing)
  4. Whatever  be the mechanism it is something to do with potassium ion flux .Transient intra-cellualr hyper-kalemia.
  5. Another possibility is diffuse uremic peri-carditis , which is a common accompaniment  of renal failure.In fact this patient did have a peri-cardial rub

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Doppler Mitral Inflow velocity profile   is the key to  assess LV diastolic function . The ratio between  E and A has become most popular parameter .

In the absence of atrial contraction what shall we do ?

The answer is simple .  We have 2 D parameters of LV diastolic function.

LA dimension ( > 30 % basal dimension which is  usually >  4 cm  ) is a most specific marker of diastolic dysfunction in the absence of   mitral regurgitation or stenosis.

The only available  velocity E wave profile  can help .A short  E deceleration time in a short cycle  would suggest  significant diastolic dysfunction.High amplitude   E  wave  > 2  M/sec in the absence of MR  will suggest diastolic dysfunction .

Curiously  ,   it can be  assumed    an episode of   lone AF  per-se   ,  be an indicator of diastolic stress for the left atrium .

After all ,  why should a person all of a sudden develop an episode of AF .(Hypoxia, Ischemia ,  excluded )

Other parameters.

Mitral annular velocities / E propagation velocity   / E/E’  are other tissue Doppler parameters  can be used.

Pulmonary venous flow velocity is  largely not useful  (Since A reversal does not occur )

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Medical science and commerce grow hand in hand .  Many believe   the field  of   medicine has  ceased to be a pure  science long ago . Both are mutually inclusive . We have no other option ! If there is no commercial interest   . . .Who will fund cardiology research ?  Then  . . . How are you going to  develop a biological pacemaker or  the  eagerly  awaited  total artificial heart ?

Without involvement of the commercial forces ,  no break through is possible . If you take medical science  , majority of growth has occurred by the motivational force of  medical industry  . Here is an  exclusive website for sub specialty called cardiopulmonary business .

But do we  have  the  medical research in safe hands ?

Why  a  hastily  developed  cardiac  device enter  the human domain and recalled within 2 years  fearing grave Injury   ?

Why a drug known to cause serious side effect was purposefully  blinded with a hidden agenda  till the drug earns a  billion or two ?

What is in store for future generations  ?

When the profession is at the mercy of  forces other than  patient care as a primary aim  there is every reason for it  go awry and  become   a dangerous health hazard  . If any medical professional   who does not see this , as an important issue  for man kind ,  requires a rebooting for reality  !

Public should realise , what they often get  in the name of science  is  a huge  human body trial and victims of   biological  shopping  . It has   wide-ranging  Implication . It is ironical , we are in a piquant  situation , where   our bio-system   has to  fight not only against  the  diseases but also  the misplaced scientific methodology  and fraudulent practices.


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ICDs have revolutionizes the management of refractory VT   and in the  prevention of  sudden cardiac deaths in vulnerable population.Every year  100s of  thousand    ICDs are    implanted . Three  industry leaders are providing  state of  art  machines. The technology is evolving . Till recently , the  shocking leads of ICD has  a separate connectors  called DF1 .

Now,  we have all 4 leads incorporated into one lead  connector called  DF 4 . It has gained tremendous interest  among cardiologist and stand alone electro-physiologists  . The reason is simple  – Ease  of   implantation !

Does the  ease of implanting  do compromise   the  efficiency of ICD  system ?

I am surprised by this article . Here is an  excellent analysis by a truth seeking   electro-physiologist  about the   genuine issues of ICD implantation  especially to potential problems with  DF 4 interface .


A related article .


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A patient with  extensive anterior STEMI  presented 18 hours  after onset of  chest pain . He  was  other wise stable and free from angina but had persistent ST elevation (5mm in V 1 to V 5 ). He had a  total occlusion of LAD  with TIMI zero  flow . He had a  tight PDA lesion  as well . A bed side echo revealed LV EF  of 50% . The septum was hypo-kinetic but did not appear severely dysfunctional .

So , it was decided to open up the LAD. The moment  LAD was opened he developed severe acute LVF  /   flash pulmonary edema   .  Even after a 30 minutes of  heart (Fire )  fighting  he could not be resuscitated .

What is the mechanism of death here ? Expert  STEMI interventionist  from core  labs  may answer this !

An acute ischemic MR with myocardial disruption was suggested . Why it  was triggered after opening the IRA ?

Three mechanisms were discussed

  1. Re-perfusion injury
  2. Collateral  damage
  3. Physiological  de-stabilisation of  Contra -Lateral lesion (Remote lesions )

Re-perfusion Injury ?  How relevant it is in cath lab ?

Is re-perfusion injury  electrical  ,  mechanical or  both ?

In this particular patient even though there was a total LAD occlusion , the segments supplied   by  the LAD  was partially functional and  it was contributing to LV  pump function.  The moment  a trickle of   flow was established  , some thing happened and the whatever  little mechanical function  his LV  had  was also interrupted  . The LV came to standstill and the patient died .

If re-perfusion Injury is  simply an   electrical  event   like VF ,  it can be resuscitated . If it is mechanical  outcome is bad ! This is not a new concept  . It is  part of the  once famous  concept called myocardial stunning . There are  lots of reasons   for stunning  to be a  clinically relevant phenomenon .Unfortunately   if any cardiologist talks about it in 2012 ,  he is at risk of  labeled  as old fashioned !

Collateral damage.

One more mechanism which we feel that  might have contributed to death here  is   the  “collateral damage” .(This is not cross fire !)

We know collaterals can be recruited within 12 hours in many STEMI patients . In some  it can even salvage  significant mass of  myocardium . The acute collaterals to LAD may be interrupted  during primary PCI . Once you poke the lesion the coronary  vascular  bed which had dilated  (as a response to total occlusion ) may react with inappropriate vasoconstriction . This raises the local hydrostatic pressure (Myocardial edema)  and further impede  the   incoming  micro collateral flow . This a very  critical time  for the myocardium  where antegrade and retrograde flow are kept in a fine balance .

Interference with remote lesion Hemodynamics .

Another possibility  is  the  opening the  LAD lesion some how  impact on remote lesional  flow as well (PDA  in this patient  )

Please remember ,

Even a transient hypo- tension can have  devastating effect in  the  hemo -dynamics   of  non IRA  territory  especially if it harbors a critical lesion !

Final message

Coming to the title question  , Is no – flow better than  slow- flow in late presenters of STEMI ?

Common sense dictates whenever  an artery is obstructed  just get rid of it.  When  it  comes to the heart it must be done in an urgent basis That is the essence of primary angioplasty  . . .  agreed . But in this  patient  I believe ,  the  common sense  was proved wrong !

Truths are always hidden.  The  science of  myocardial re-perfusion is a perfect example . We need to learn a lot still !

This I  call as  Para cardiology : Heart  facts without  evidence !

Counter point

One may argue this   is an  exceptional case  in STEMI  intervention. Don’t  hype   exceptions  and undermine the importance of a great concept ! Exceptions  and rules  are directly related to our  experience  we have accrued.  Exceptions are the great  knowledge substrates  and help  crack  medical  mysteries !

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Ventricular septal rupture is a major mechanical complication of STEMI . Excruciating  chest pain ,  is the sine qua non of  any myocardial tear , dissection and rupture . It is surprising ,   VSR  following STEMI  is rarely a painful event . I can recall number of  such events  , when a  stable   patient with persistent ST elevation  in the  coronary care unit ,   wakes up next morning  with a systolic murmur.And echo reveals a septal defect promptly.

Three  reasons  can be  proposed  for relatively  pain free rupture of IVS in STEMI.

  1. Typically  VSR  occurs in 3rd or 4 th day of infarct . By this time myocardium  can be as  soft as an ice cream ! . There is not much stress and strain at the site. The necrotic  debri just gives way to spikes of   LV systolic pressure .
  2. For rupture to occur there   must be  transmural infarct  .The pain nerve terminals also die in the process .
  3. Further , it is a cavity to cavity rupture  (LV to RV ) . Direct pericardial  stretch  does not occur .

* Ventricular free wall tear   is a near fatal event is extremely painful .This  often occurs  in the first 24 hours when  the nerve terminals are  alive . The free wall rupture is more of  a  tear in the plane of  myocardium . The  pericardial  (epicardium)  layer has  rich   somatic  nerve supply .

In summary

Early  myocardial  tear   involving the epicardial  surface can be severely  painful  .  Late giving way  of softened  , necrotic  often  hemorrhagic muscle ( especially in the IVS ) is less painful or totally painless.

Coming soon   . . .

By the    . . .  what happens  to  pieces of  septal myocardium as it  gives way  and enter the right ventricle   ?

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A pulse wave is generated  with each heart beat  when  the potential energy is converted into kinetic energy.

  • For the pulse wave  to travel from the heart to periphery  Aortic integrity is vital.
  • The pulse wave travels through the walls of arterial tree  , in the process the wall itself is set into oscillations .
  • Whether the  moving blood imparts the  pulse  on the walls or the walls itself  vibrate  independently is not clear .

The following   M -Mode  echocardiogram  of  aorta from young man   stunningly  documents  the  morphology  of  central aortic  pulse  wave . Note how closely it resembles the  Intra- aortic  pressure curve recorded with a catheter.

The anterior aortic wall motion was sliced from the above motion image  to create a non invasive recording of aortic   pulse wave

This simple observation was made in  a crowded  echo lab our hospital. Cardiology fellows can explore  further  ,  the link between aortic pulse transduction (From mechano -hemodynamics)

Further studies are warranted regarding the  rate of raise (Slope)  of aortic  wall motion  , and the quantum of motion ,its correlation with central aortic pressure etc. This would unravel the the mechanisms  of Isolated systolic  hypertension  , where a stiff aorta amplifies  the systolic pressure due to loss of elasticity .

Read also

Rail roading of  Aorta in Severe  LV dysfunction

Wind Kessel effect

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