Archive for September, 2014

One of oldest hospital  in the world , is now an  UNICEF heritage site. Santa Creu , Sant Pau original hospital built in 1400 AD rebuilt in 1900 by Catalonian modern architect Montaner.

sant pau hospital barcelona unicef

Architecture by Lluís Domènech i Montaner

sant pau hospital barcelona


sant pau hospital unicefReference

Hospital de Sant Pau

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TVI  (or VTI)  is a hemo-dynamic  echo parameter measured from Doppler spectrum  across the valves ,usually in the outflow.This parameter is used to calculate cardiac output .VTI times the cross sectional area gives the stroke volume.


time velocity Integral  TVI

A correction: TVI is multiplication of velocity into time not division as suggested in the cartoon   

Time velocity Integral

What is time velocity integral  TVI echocardiography


*VTI is a Doppler parameter described in cm , it can be referred to as Stroke distance.This stroke distance when multiplied by  valve area gives the stroke volume from LV/RV  (or flow volume across AV valves or through any conduit)

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One of  the hottest debate in  the recent  world  cardiology forum in Barcelona WSC 2014 , was  about  how to tackle incidentally detected non IRA lesions  during primary PCI.

So far , the dictum is , one should not meddle  the non culprit lesions unless demanded by hemodynamic instabilty .The next option is to do a staged PCI for these  lesions. (Few days later). or just forget about these lesions unless they are critical.

Now new studies are appearing that suggest  doing all  “do-able” lesions must  be stented  in one go ! This is obviously inviting trouble .The worry is not  in the concept but with the  dubious  track record , fragile guidelines and potential  ethical debacle of the cardiology community !

Stent “As you want and as you please”  has  already  invaded our mindset in  the chronic coronary  scenario. Now in 2014 , we want more freedom  in acute coronary  syndrome as well ! We  can’t ask for a  referee less game of soccer !

We clearly know coronary  arteries  are to be respected and do not deserve indiscriminate stenting  especially  in ACS  where  the early hazard is  more.

A recent story  which I heard  was a  height of  futility . A semi experienced cardiologist in the suburbs of a big southern Indian city , opened  successfully a LAD  which was the IRA  and  subsequently caused  acute  LCX  STEMI , while trying  to tackle an insignificant  non culprit lesion due to procedural mishap ! (Some suggested migration of LAD thrombus !)

What a pity , when we are supposed to  arrest the culprit, in reality it is simply  chased  down to another territory !

 Here comes  unique  advantage of thrombolysis , you need not locate  the culprit  artery the drug chases it wherever it is , even if they are  multiple ! Read in this link :

 Final message

We call it as fate when  thrombus suddenly occlude  a coronary artery  and the IRA becomes  a  culprit . We  need not compete with fate and end up creating  potential new culprits.Let the  sixth sense prevail over the five .Use judicious discretion when trying to stent muti-vessel  CAD  during PCI. Please  realise ,the concept  of  multivessel stenting during pPCI is not wrong .  How we interpret is the issue !

There is no excuse  to indulge as you like  , simply because your intentions are good !


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One of my favorite quote  about Happiness from Buddha !


Happiness quote from Buddha

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When a patient comes with angina at rest , it could mean two things .Either a  STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the  character of chest pain alone ?

Very  tough task isn’t  ? But there are some definite clues .

Infarct  pain

  • Is mostly sudden .
  • Likely to be crescendo , lasts more than 20-30 minutes .
  • Fails to get relived by rest or even  Nitrites.
  • Sweating due to sympathetic activation is more pronounced.

Unstable angina

  • Is rarely  sudden .Often has a pro-drome.
  • UA is  mostly precipitated by an increased demand situation or a stress.
  • It has  a typical waxing and waning  pattern . Rarely assume a true  crescendo character  as myocytes  does not necrose (Just threaten to die !)
  • The chest pain radiation   to  shoulder is less  conspicuous , instead it  tends to  reach  the  jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is   due to subtotal occlusion and  endocardial ischemia , while STEMI is  sudden total occlusion  and the resultant  transmural  ischemia . In STEMI  epicardial  surface is always involved (Which lifts the ST segment in ECG .).We know epicardium  is same as  visceral layer of pericardium which is well innervated .Hence  pain  of STEMI   acquires  more of somatic character  than a  predominately visceral type pain  that occurs with  UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue  to differentiate the  chest pain of  STEMI and NSTEMI  .A significant overlap can occur  in  real coronary care scenario . We know   chest pain  that occurs in both   pre and post infarct  phase  is considered  as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating  them may even be termed as futile.

Still,clinical cardiology  can be  made  fascinating by indulging in such exercise !


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Most of my students were  struggling to answer this  seemingly simple question . I  realised  later it is indeed a difficult one !

tall t waves

Some thoughts

Tall T waves are observed in very early phase of STEMI .(Within 30 minutes ?)  What is the mechanism ? Since ST shifts occur little later than T elevation ( considerable overlap may occur)  it may not be related to current of Injury.It is an  inherent alteration in the T wave genesis .T wave is inscribed when rapid phase 3 K+ efflux happen (Mainly by Iks and also  IKr )

What is the effect of ischemia on K + channels ?

No uniform answer.(Blocks, stimulates, irritates, Bi-phasic, variable ?)

There are 6 important K  channels in every cardiac myocyte adding to the complexity.

Does  the  Ischemic cells leaks potassium or accumulates it ? 

Though It does both ,  predominantly it should leak .If it’s leaking there is local extracellular hyperkalemia . Is that the explanation for tall T waves ?

What is the influence of QT interval on T wave morphology ?

Long QT as occurs in hypokalemia  pulls the  T down  and it may even  invert it.  .Short QT tends to push it up as in ERS .The effect of ischemia on QT interval is again unpredictable.Further regional and remote ischemia in a given patient can alter this.

Once the ST begins to elevate  the T  waves  losses it power to grow tall .It only can regress. I think this is the time the QT is sort of prolongs .

Effect of reperfusion on T waves

The tall T tend to regress as some form perfusion takes place as  K+ Is pushed back into the cells or  flushed away  from the vicinity.

The dynamic nature of reperfusion  makes the behavior of T wave amplitude further complex. But one thing is certain , a well perfused IRA  is associated with inverted  T wave  which we call it as completion of the process of evolution of MI .

Finally and most importantly this hyper acute T phase is not a constant  phenomenon. In fact it is uncommon in  persons who  have baseline T inversion .After analysing many things we are back to the original state of ignorance .


Researchers with intra-myocardial micro electrodes try to decode the mysteries in electrophysiology . Still there is a huge disconnect  between  clinicians and physiologists.

In simple terms  I would  believe the mechanism of   ischemic tall  T waves are almost similar to renal  hyperkalemia. (A local , transient  extracellular k + excess ) The base of the T waves are not narrow and tented as in CKD because  some degree of ST elevation (that always is expected )  widens the base of T wave. Further  ,the  prolonged QT interval in  renal hyperkalemia  stretches the QT and encroach   the base of the T wave to the left making it  appear narrow.

A simplest  version for  students

Tall T waves  are due to  transient  local extra cellular hyperkalemia , when K + leaks due to cellular  Ischemia.

Caution: This is  a superficial scientific attempt .I need inputs from more scientific  brains and electrophysiologists.


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I got this alert from World health organisation  yesterday .Click over the image to read more .

dr s venkatesan who sucide alert cardiology heart transplantation

Why should  a cardiologist   affected about this ?

When we are fighting in cath lab day in night day out  to  extinguish the  myocardial fire set by  coronary thrombosis and the resultant STEMI  . . . the  solemn attempt to  salvage  whatever myocardial cells we can !

See . . . what is happening elsewhere  every 40 seconds a healthy heart  in toto  is executed by weak minds !

What should the WHO do ?

Just publish these data and forget . No,they should organise the world leaders to take a resolve !

Either , we should prevent these unnatural deaths or else we should  have world organ net work. Why can’t we use these weak hearts  for those courageous  men and women  who lose their life daily with end stage  cardiomyopathy  who  long for living !

Is this  possible ?

Why not ?  Ain’t  the world leaders group  together periodically  to impose a sanction or bomb other countries  for personal reasons !


WHO sucide prevention

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