Archive for the ‘cardiology journal club’ Category

The current  fad called EBM has lots of lacunae. Though evidence based approach is  considered  the ultimate  journey  towards  truth  ,lot of non academic factors contaminate it .In it’s  current form , it is difficult to comprehend it.

This is an attempt to decode the mystery of EBM  expressed in a simplified  lay person’s term .They are the ones  from whom we learn  medicine. They are our teachers in the true sense.

evidence based cardiology guidelines evidecne levelBy the way ,it  is also my approach  to   EBM .Sorry , if  this post  sounds  arrogant ! It is not the intention .Truths often times appear brutal .

And   . . . the  Genius  approach to EBM  for comparison






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Few Innovations are real breakthroughs in cardiology . Here is an imminent technology waiting to explode in the  permanent pacing . Expected to hit market next year (2014 in Europe ) FDA approves clinical studies .


Click over for the animation video  of the procedure .

  • The wireless pacemaker has many advantages. (It’s devoid of all those pocket and wire related issues.)
  • The ability to change batteries is  a  going to be a  new paradigm shift in the filed of electro physiology. .
  • Down side would be,  right now it can be only VVI pacing . All that hype about    physiological pacing  will go to the background !

Future directions in Permanent pacing.

The only threat for this technology is the  concept of biological pacemaker Converting ordinary myocytes into  pacing cells by genetic engineering.This is expected to happen within few decades.

biological pacemaker

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I stumbled upon this  web   site . I think this  can be  glorified as the  standing  example  for     “Democracy  of science”

INTECH open science  open mind


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If you are a doctor  and  whatever  be your specialty   . . .  if you do  not read this article  and understand the nuances  probably you  will not become a   complete medical professional !

Master health check up futility general health check

master health check up geenral health checks bmj british medical journal cohcrane nordic


While  BMJ  struggles to  propagate  a vital truth , this  banner on a  Indian  high way   tempted the public  to go for 64 slice CT scan   . . .just like that !

Master health check up 2

Final message

Accruing medical knowledge and skills is only one aspect of medical profession. Applying it properly in our patient population is entirely  different ball game . Let us be disease curers and not disease hunters . This is important because disease  hunting is  a dangerous  game ,  where victims can be innocent  bystanders. This  is exactly same thing  Hippocrates  refered to as  Primum non nocere  1000 years ago.  It  has required  a huge statistical study to RE-INVENT  this universal fact !

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  • How do you classify  stent thrombosis ?

  • What is target vessel revascularisation ?

  • How do  you define  peri-procedural MI ?  Is  troponin elevation alone  enough ?

Want answers for all these ? Your search ends here  . . . The academic research consortium criteria committee provides everything free .

A must read for both  mature and immature  cardiologists . http://circ.ahajournals.org/content/115/17/2344.full.pdf+html

Here is a cartoon for classifying  stent thrombosis (Time based )

There is another etio-pathological /Geographical classification for  stent thrombosis  that will be discussed later.

( Entry block , exit block  , diffuse thrombosis  etc  Read -Geographical miss.)

A word about Academic research consortium

ARC is a consortium of clinical research  from the  Harvard medical school and their associates . The aim of which is  to bring clarity in the  definition of  medical  terminologies and study endpoints.A universal  criteria is being prepared  so that  the study results are comparable which currently use  different criteria  and end points.

For cardiology ARC came out with standardized definition in the year 2007.

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 Hypertension  ranks  number one  in the risk for future  stroke . Surprisingly this is true  for ischemic  as well as  hemorrhagic strokes.

 What  causes  thrombosis or  rupture of small cerebral arterioles ?

 It is somewhat similar to coronary events . ( With one major exception,  coronary vesels  are   not prone for rupture ) .It is  believed   sudden spikes of   blood pressure  and the resultant endothelial injury are responsible. Atherosclerotic plaque fissure and inflammation  also  contribute. 

Is embolic stroke related to hypertension ?

The vast majority of embolic stroke are believed to  arise from heart .This belief is getting gradually eroded , as we now know aortic arch and carotid arteries vie for this honour . .(This was indirectly proved in AFFIRM trial  when rhythm control failed  to reduce the incidence of  stroke inpateints with AF ,   implying much of the strokes arise  in the upstream rather than within the cardiac chambers )  

Meanwhile , there is no controversy  in  SHT  promoting  both cardiac  and non cardiac embolus to brain

Systolic ,  Diastolic or Mean pressure   which is  important  in the genesis of stroke  ?

All parameters  are  important , but the   systolic blood pressure  is vested with more  vigour  to damage the  cerebral arterioles. The reason  systolic pressure is more important lies  in the  fact ,  it  can  attain  high pressure peaks instantly ,  unlike diastolic or pulse pressure which  slowly builds up. Further , systolic BP  carries  leading edge of the pressure  curve with high Dp/Dt and hits  the target  first !

At what pressure the cerebral artery becomes  uncomfortable ?

We do not know  the answer as yet , but any systolic pressure above 180 mmhg is a huge stress for the cerebral arterioles.The rapidity with which the BP  raises  (Dp/Dt) also becomes  important  . High blood pressure increases the shearing stress .It  interferes with nitric oxide synthesis and promotes endothelin release which precipitates  cerebro vascular event.

How do you identify people who are at risk for stroke ?

While  cardiac physicians are obsessed with exercise stress test to predict CAD  very  few  are worried about  stroke . In fact the same exercise stress test can be used to stratify stroke risk. The exercise induced systolic blood pressure  raise  is a useful risk stratifying  tool. This concept is there for more than a decade without reaching the clinical domain.

The following paper was  published in stroke journal (2001)  from the picturesque university of  Kupio Finland.(See below )  It is a wonderfully done study and throws great insight into the  new  emerging  science of  Intra cerebral hypertension .


The following can be summed up as risk factors for stroke during EST  (Derived from   various sources  and  . . .  with   liberal dose of personal  logic !)

  • Raise of 20 mmhg  SBP  at  2  minutes .
  • Increment of >  20mmhg in SBP any subsequent minute.   
  • Any  SBP  above 200mmhg during  EST
  • Failure to  reach baseline SBP  at 6 minutes recovery .
  • SBP  or DBP remaining high  even  after  the heart rate reaches baseline.


 Final message

For the kind attention  of all  cardiac physicians . . .  whenever you do an  EST for a cardiac indication ,  please spend the first  few  minutes  carefully ,and   look at the  blood pressure response . It is encouraged ,  to  specifically mention about the  behavior of  SBP  and write a remark about the propensity for  stroke in  every EST/TMT report .   Let us grow our brain  sense as well   . . .  for   the sake of our patients !

Thanks again  to Dr S.Kurl et all from Finland  for their  nice article which  stimulated  me to write  this post .




Further queries

How common is stroke following a EST procedure ?  Can high blood pressure dislodge a carotid plaque during a stress test ?

The answers will be posted soon once I  get it . ( Of course you can do it if you know !)

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The much published TRANSFER -AMI study  has few important queries to ponder about.It was supposed to test the role of routine PCI following  thrombolysis. In other words it compared  rescue only strategy with routine strategy.The caveat is , even among  failed thrombolysis, the   rescue strategy has not convincingly proven superior to medical management  (if the time is lapsed ) as much of the damage is done .

In essence , Acute MI is  more about time management than drug or cath lab management

  1. Why the 67 % of  standard therapy cohort underwent PCI. Technically , you are supposed to transfer for rescue only if there is a  failed thrombolysis ?That is the standard approach , if  most of the cases are any way land up in cath lab , then you are trying to compare two similar groups .
  2. Why the rate of   failed thrombolyis with TNK-TPA in both arms not disclosed ?
  3. How can a 92% of study population be in class 1 Killip still considered to be high risk group ?
  4. Why the recurrent ischemia  was very vaguely  defined and still included and clubbed with primary end point along with deaths. If only recurrent ischemia was removed from primary end point . . .this study will straight away land in a regret bin.
  5. Why there were 6 additional deaths at 30 days  in routine early  PCI group ,  What was he cause of death ? Mind you these deaths have happened in a 92 %  Killip class  one cohort . Is it  not important ? The trend looks vitally   significant .We can not afford take refuge under a false  statistical roof .
  6. How many patients died or  developed MI  because of the early PCI in-spite of having  successful thrombolysis.This again could be vital . Complications during intervention  for a failed thrombolysis may be acceptable. While ,complications , when we try to  improve upon the already  successful thrombolysis is simply not acceptable .

Will the investigators share their experience ?


Why the title of the paper says it is about “Routine angioplasty” and  the conclusion emphasizes  it is indeed   “high risk subsets ofangioplasty” (While the study itself involves a 92 %  least risk Killip class 1 ) .  Why this double dose of confusion ?  (Is it deliberate  ! Which i think is unlikely )

NEJM please take note of this  . . .

All that glitters  are  not natural glitter . . .some are made to glitter !

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