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Archive for August, 2018

Thousands of delegates* converge annually in glittering convention centers on a regular basis to present high quality research. It’s all about overflowing seminar halls, stunning speeches , Intense questions , adoring debates , cozy discussions in grand dinner nights . The meet continues further, as news breaks in global TV shows, spreads in non-stop handles of twitter after igniting the face books.

Finally , it ends over the week-end ! (It has to you know ! ) . . . Every one flies back, only to come back next year to ponder “almost the same issue”  all over again. (Some times the questions are left unanswered for decades ! Not getting an answer is okay , after all research is a  journey towards  truth   but sustaining a confusion or creating new one has been a norm in recent times.)

*Sorry , If am provocative , I need to be genuine in my expression.

Coming to the topic, Aspirin is one wonder drug which made a big impact on CAD risk . We know there is something great with this cheapest and humble Dual COX  blocker.The only weak point is ,it lacks the glamor quotient like that of newer antiplatelets, NOACs  and their clones.

Its my perception ,big breaking research has tried to ditch this drug for quiet a while .But ,it was all too difficult to go for the kill.So these studies circumnavigate the real issue. and end up with  suspicious conclusions  (or Inconclusions !) always trying to hide behind sinister statistics of course with a questionable caveat !

What’s new in the topic of Primary prevention of CAD ?

Two major studies were released recently in August 2018

Both studies suggest caution for Aspirin. If Aspirin is really  bad it would (and should) have buried long ago. We should be thankful even in these testing times for truth ,this humble drug is fighting  back and forth .(Digoxin is another close  cousin of Aspirin fighting for the existence  crisis in cardiology  ! ) 

So what is the role of Aspirin in primary prevention of CAD ?

This question doesn’t make sense in many clinical situations.

Primary and secondary prevention are defined with reference to manifest vascular event. We will not know how much of silent CAD exist in asymptomatic persons.Primary prevention of CAD itself could be a misnomer as most elderly do carry at-least some form of CVD. For example, If a patient with manifest peripheral arterial disease (PAD) and takes Aspirin , its  secondary prevention for PAD but becomes primary prevention for CAD . . . isn’t  ?

Final message

We know Aspirin  continues to be the flag bearer of  all DAPT regimen.I wish it remains a star in primary prevention as well. It looks like(for me)  these studies  are another attempt to pull down Aspirin in primary prevention .I think ARRIVE failed to reach the desired conclusion. Aspirin is a warrior and it will never allow that to happen and ASCEND to glory again !

Postamble

Modern drug research appears to pursue a study till the desired conclusion is reached. We need important  drugs in many vital areas of cardiology .Our energy should be focused to find new molecules. It is worrying trend(if its true !) if efforts are wasted to finish off humble generic drugs with proven worthiness. Doing research in established concepts is the most silly thing to do. Its duplication of knowledge.

Counterpoint

It’s scientific blasphemy to criticise  studies without analysing it in a professional manner.It appears all too brutal to take a biased view and questioning the motive of researchers. Yes agreed , I may be prejudiced , . . but , why a doctor of this caliber make a statement of this sort ?

Its a fact  , there are so many true scientist doing their job right, my query is simple why we are not getting clear answer in many common issues In spite of great research ?

Is it the limitation of science or vagaries of research ? I think it’s more of a  Intellectual insufficiency  aided by  malfunctioning regulators !

 

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This 70 year old man in routine check up showed up this ECG.

What is it ? a  quick debate ensued !

Is this

  1. RVH
  2. RBBB
  3. Or Both ?
  4. Neither RBBB nor RVH
  5. Wrong lead placement
  6. Is it a normal ECG after all ?

Incidentally the ECG shows a Wenkebach AV block in the bottom strip lead 2.

I thought it was RVH. (do considered RBBB) but since lead V 2 showed tall R , I was more than sure RVH was likely . Many voted for RBBB. .Some others said RBBB can never occur in monophasic form.I said it’s possible.

Some body challenged me without Echo Imaging a  monophasic RBBB can never be differentiated from RVH. After a mini argument I reluctantly agreed.Yes, it seemed there is no way to differentiate the two.

What do you think ?

Curious to know the Echo finding in the above patient  ? Yes , your guess was right /wrong. There was no RVH.He had normal Echocardiogram.

How to diagnose RVH in RBBB ?

  1. Look at the r’ wave if its taller than initial r by more than 5mm suggest RVH (Not absolute evidence though)
  2. Look for other evidence like Right axis , RV strain etc.

How to diagnose RBBB in RVH ?

Sorry.I don’t know the exact answer.It could be masked within Qrs complex of RVH.RVH could convert biphasic  RBBB into monophasic RBBB.

Some more about this RVH/RBBB duo

  • The term incomplete RBBB is liberally used with minor rsr’ pattern.It is not advisable to do so.
  • RBBB is classically multiphasic (To be precise RBBB can be complete to incomplete  rsr’ with various combinations of small r and big s big R or big S).
  • But more than the morphology of Qrs in V1 the S wave in lead V 6 or Lead 1 could be Important.It should be delayed slurred.
  • QRS width has no great use to diagnose RBBB as it can be narrow or wide.

Final message 

To diagnose monophasic RBBB( in V1 ) by itself requires some guts.However ,the entity do exist.

Finally , please recall there is a traditional list for  tall R in V1 other than RVH.

  • Wrong lead placement
  • RBBB
  • Some cardiomyopathy(RV myopathy)
  • Systemic Duchenne’s muscular dystrophy
  • Pre-excitation
  • Posterior MI
  • Normal variant*

*Why should normal guys grow a tall R in V1 , it mystifies ! but true.

What is the rarest cause of tall R in V1 ?

Localised cardaic tumors over RVOT. Cagli K , Tok D, Basar FN   .An unusual cause of tall R wave in lead V1: cardiac lipoma.Heart Asia. 2013 Mar 7;5(1):33. 

 

Annexure : Further questions in RBBB

 

1.How does AV bundle penetrate to become bundle of HIS and branches ?
Note AV node is fully Intra atrial structure , while part of His bundle is atrial , after crossing the membranous septum second part lies within the ventricle at the crest of muscular septum .Then the bundle of His goes for the famous division. Left fans out  tow streams, while right descends on right side of IVS. Note : Applied anatomy 1.Its this small portion of HIS we are trying to physiologically pace the ventricle 2.In proximal LAD lesions both RBBB and LBBB is common still LBBB can’t be used to localise but RBBB can be.Guess why ? Read the next question and find the answer..

 

2.What is the blood supply of bundle branches ?

 

3.What is the mechanism of RBBB in ASD ?

Is it true RBBB or Right bundle delay ? Students should know there need not be conduction system pathology to cause RBBB. Simple delayed conduction in RVOT can cause a RBBB. (The concept of central RBBB vs Peripheral RBBB) This is what happens in ASD.

In fact , true pathological damage due to right bundle branch due to necrosis, Ischemia, Infiltration is much rarer than pathological LBBB.

4. What are the  structural , histological  difference between right and left bundle branches that has electrophysiological Importance ?

Wait . . . I am trying to collect info for this .Meanwhile ,Why don’t one of the energetic young  fellows in cardiology find the answer and post here !

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