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Archive for March, 2016

One of my fellows gave a discharge summary  for a 62 year old patient with stable diabetic  CAD  who had Triple vessel disease with a final advice reading as CABG / PCI/or OMT .

There was a near fury over his angiogram report in the cath meet. How can be  eligible for all the three Intervention at the same time ?.(PCI -Percutaneous coroanry Inervention ,CABG-Coroanry artery by-pass graft, OMT-Optimal medical therapy )

The lesion in question was , Triple vessel disease(Non critical LAD) and significant LCX and again a non critical RCA .Syntax was less than 22 for sure , however the patient  had class 2 angina (now reducing ) .When asked to explain  , the fellow  argued since the patient  is symptomatic , has DM with TVD  he is eligible for CABG , since  LCX lesion was discrete and PCI was distinctly possible , of course as all three  lesions would be  eligible for OMT on any given day  ! he inferred .

How can  a cardiologist be so casual and non-commital in an important medical decision where a life of a heart is at stake.There was a unanimous condemnation about the report. As a consultant he has to be specific , one can’t leave the decision to  your patient’s whims  . . . rather it’s our scientific whims  that should prevail  !

 

MEDICAL VS PCI VS CABG OMT COURAGE BARI 2D FREEDOM FAME STUDY MASS 2 CASS OPTOMAL MEDICAL MANAGEMENT SYNTAX ACC AHA ESC GUIDELINES PTCA STS EUROSCORE NEJM

The curiosity continued and looked amusing for many. I was the only one supporting  his argument ! After all , he is being frank and understood the futility of  applying  evolving knowledge base in critical decision making. But, I  asked him to grade the choices .In my opinion  OMT should be the first choice if it can be administered , but reality tells me  true OMT is rare as a modality  at-least in  this  part of world . However every one should insist for it.

Apart from poor  compliance for OMT , pressure  mounts for a procedure from peers and non peers . I am  sure  many  patients  will end up with an  invasive modality sooner or later  backed by a  second or  third opinion  driven by that elusive googled intellect !

Final message

When clinical decision making is debatable with available knowledge (Especially with futile and evolving knowledge base !) , please include your patient into the debate and you may even consider giving him the veto power.If Hippocrates is alive today , I am sure he will argue for medical  knowledge and ignorance should be equally shared with their  patients.

Counter thoughts

Don’t give the choice to your patient  . . . that would mean you lack  clarity, wisdom and confidence !

No, I don’t agree , I know there are  some  patients who are  well informed , rational , more focused than even a professional  !

 

 

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Junctional tachycardia(JT) is often a misunderstood arrhythmia. Technically,  any tachycardia arising from the AV junction could be termed as JT.Even AVNRT was considered as a form of Junctional tachycardia till recently.The crux of the issue is , true anatomical extent and borders of  so called AV junction is  yet to be clearly demarcated .The common perception that  AV node is a discrete  structure is  an anatomical illusion  , rather its collection of  condensed fibers with proximal  nodal approach and distal fanning .

Now , we have a  proper definition by the apex scientific bodies  ACC/AHA/HRS 2015)

definition of junctional tachycardia

Source :2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: Executive summary A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society April 2016Volume 13, Issue 4, Pages e92–e135

Please note :The key point is , JT by definition  should  be a focal  /automatic tachycardia either due to triggered activity or after depolarisation and the boundaries of  junctional tissue is liberally extended up to  His bundle.

Read  related post  :What does the term junctional tachycardia mean in current era?

Reference

http://www.heartrhythmjournal.com/article/S1547-5271%2815%2901188-1/pdf

 

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I don’t know the answer, rather I am afraid to answer that question.

Read this article , that may  help find answer to this forbidden question.

medical ethics inappropriate medical care

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100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component’s  contribution in the genesis of  STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thromotic STEMI with  just a residual endothelial  erosion and hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion  seems to be biased and misunderstood scientific fact .

What happens once 100 % occlusion take place ?

Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of  tissue plasminogen system. In this aftermath  few succumb . ( Re-perfusion arrhythmia  generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus ,  and the elasticity of fibrin mesh , location of  platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3  flow !)

thrombus propgation
What happens to the natural history of thrombus in STEMI ?
Thrombus formed over the culprit lesion can follow any of the following course

  •  Can remain static
  •  Get lysed by natural or pharmacological means
  •  Progress distally (By fragmentation or by moving en-mass )
  •  Grow proximal and and involve more serious proximal side branch obstruction
  • Organise and become a CTO

Factors determining thrombus migration

The interaction between the hemodynamic  forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by  platelet vs RBC / fibrin core,  totally of obstruction,  reperfusing forces , re-exposure of raw areas and  the distal vessel integrity all matters.

While, logic would tell us,  thrombus more often migrates  distally  assisted by the direction of blood flow, an  opposite concept also seeks attention , ie since the blood flow is sluggish  in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.

(In fact, its presumed  in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to  queue up proximaly and  clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)

What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?

If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still  we don’t  know why thrombus aspiration in STEMI is not consistently useful. We also know little about  the length of the thrombotic  segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like  “cutting a slice of  butter” in some , while in few we struggle and  end up with severe no-reflow inspite of great efforts .Why ?

What is the Impact of distal collateral flow in flushing fresh thrombus ?

The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it’s soft and fail to get organised early that would help cross the lesion easily.

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