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Archive for the ‘Cardiology -Interventional -PCI’ Category

Doing multivessel PCI during acute STEMI is forbidden except in cardiogenic  shock . (or in some very unstable patients without cardiogenic shock)

The reason

  • During acute MI   hemodynamics  are precariously balanced.We do not know yet how  emergency multivessel plasty alters this .
  • Our  initial aim should be   confined to myocardial salvage in the IRA . Total myocardial revascularization is niether  the  priority nor its desirable.
  • The more  time  you spend  within the inflamed coronary artery , more its  hazardous.
  • Multiple stenting  is prone for thrombus   and  migration  into side branch .
  • Stent opposition is sub optimal in many thrombus infested lesions.

 

Still  . . .  in real world it is extremely difficult to curtail the urge to stent  all eligible lesion during primary PCI !

 

multivessel angioplasy during stemi

 

How to avoid it ? 

If the patient is poor or the insurance limit is low , the issue  of multi vessel stenting does not arise at all  !

Always  ignore  complex  non IRA lesions  during primary  PCI. Be happy if a non IRA has a bifurcation lesion !

Still , some lovely looking lesions in non IRA  would be  tempting  and inviting .  Indulge at your own risk !

* Please remember if  the proximal  LAD  has a non IRA lesion , it may be sensible to attempt  simultaneous revascularisation even if the patient is stable !

Other unrealistic advice

  • Keep the professional fee and other benefits   fixed whether  we do a single or multiple   vessel stenting (Realise  . . .  surgeons do not charge more for a  4  vessel by-pass graft  than a single  ! )
  • Keep the current AHA/ACC/ESC guidelines pasted right next to the fluroscopy monitor .
  • Ask your subordinates to repeatedly caution   you  about the possible  excesses and ask them to wave a red flag !
  • You may  empower the   senior staff nurse   with a veto power  to shut off the cath lab once IRA plasty is  completed and the patient  is stable.
  • In extreme  situations , keep a cath  marshal ready to manually evacuate  the primary operator  from cath lab !

Reference

multivessel angioplasty during stemi

ACC GUIDELINES FOR STEMI 2013

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The link between brain and the  hand  starts right from fetus .  It is a well known fact  vertebral artery   competes with hand blood flow  . In the right side , there  is one more  vascular issue !  .Bracho cephalic  artery  arises  directly  from aorta and supplies the  right  hand and  right half of brain.

It remains a mystery  why left brain  is   blessed with a  separate  origin ,  while right has to share it with blood meant for hand  .It is beyond science  . . . isn’t

It is possible the left hemisphere  of brain   has more   purpose   to be alive  ,  with bulk of the cognition work to do . Hence   God created a  separate  supply to it !  Of course , he  would   have never  thought ,  the  possibility of  his ” mean” creations   adventuring  within the   arterial tree  !

Click over the Image for animation

right radial artery coronary angiogram  pci  risk of stroke 002

Please remember  whenever  we   play with   catheters and wires  through   radial route , we  are  hugging  and scraping   the artery meant  for cerebral circulation !

Final message

Femoral Interventions  enjoys a proven  track record. Currently ,  radial route has virtually taken over with  few  advantages . However , the  overall stroke risk in the two approaches  remain  low but genuine (.4 %) .It may be true , arch manipulation is more  with  femoral but  the threat to  vertebral and brachiocephalic circulation  is more with radial .  When the available evidence are  not conclusive  and  new ones are not forth coming  . . . it is wiser to rely on common sense !

Reference

I think  this 2011  study  from the  prestigious stroke journal  has convincingly answered the issue

cholesterol and ateromatous emboli following coroanry intervention 2

cholesterol and ateromatous emboli following coroanry intervention  radial vs  femoral 2

It concludes , the right radial approach  is indeed risky  to develop cerebral  micro embolism   when compared to right femoral

A Review article in  Circulation

cholesterol and ateromatous emboli following coroanry intervention 2  radial vs  femoral 2

Other references

1.http://stroke.ahajournals.org/content/38/7/2176.full.pdf+html

2.Transient Cortical Blindness after Coronary Angiography Journal of International Medical Research. 2009;37:1246-1251,

3. Stroke and Cardiac Catheterization Circulation. 2008;118:678-683,

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For STEMI management there are  6 management protocols available

  1. Thrombolysis
  2. Primary PCI
  3. Rescue PCI
  4. Facilitated PCI
  5. Pharmaco -Invasive approach
  6. CABG

*CABG is rarely used except in  severe mechanical complication.

There is some  issues in differentiating  facilitated PCI and  Pharmaco Invasive Approach.

What do we facilitate ? How we do it ?

PCI in acute STEMI is done in a thrombotic milleu. So we get sub optimal results .Hence to facilitate it we try using

either 2B-3A antagonists, Newer Heparins, or even thrombolytic agents before submitting them for PCI

Where is this facilitation done ?

Facilitated PCI is done in small hospitals where  there  is no cath lab or cath lab is available only during office hours.

Facilitation can be done in either in same hospital or on the way to big hospital

Is there a time window to start  this ?

The main aim was to was to facilitate the PCI .Hence time window was not considered vital in few studies (Wrongly though !) ideally it should be started as early as the first contact . Since facilitation can be started earlier the time window is 0-24 hours .

What happened to the concept of f-PCI ?

It died a premature death  and  last rites were  completed when the FINNESE trial was out .

But it left behind a daughter concept ie in selected patients if the facilitation is done early , especially in those patients who are going to get the subsequent PCI late ,or in high risk individuals  , the initial  pharmacological facilitation* was indeed useful.)

*If  facilitation was with   fibrinolytic agents (Not 2a/2b )  .It is very important the benefits of facilitation is mainly  attributed to the time gain in achieving partial opening of IRA  making it more complete salvage of the subsequent PCI .

This aspect later on named as PIA .

Pharmaco- invasive approach(PIA)

We know p PCI is a race against time .We also  know fibrinolytic therapy  fares well in this race  but   pPCI  beats in   effectiveness  .

So what prevents us to combine the swiftness the fibrinolysis and the robustness of pPCI ?  That is  like getting the best of both world .( It is not that easy thing accomplish after all 1+1 in medicine is rarely 2 !)

In it’s core principle it  is same as f-PCI . But facilitation is done only with fibrinolytic agent (Not 2B-3A) . Pharmaco Invasive strategy can be started in any small hospital/ In the ambulance /. It  is routinely followed by PCI whether the initial thrombolysis is successful or not . PIA should not be done before 3 hours window if  a timely pPCI is feasible.  Hence PIA has a typical time window of 3-24 hours .

Summary

f-PCI is combining  various anti-platelet and fibrinlytic strategy prior to PCI . It was found  to be useless if it is used routinely in all cases of pPCI. (Rather 2B-3A  was useful  if  only the facilitation was done within the cath lab to prevent procedure related issues) .Time window can be between 0-24h .

Pharmaco Invasive approach (PIA)   is actually a type of f-PCI where  fibrinolytic agents are used routinely which is followed by mandatory angiogram and PCI in all deserving cases.Many still  believe the facilitation in PIA is primarily accured in  shortening the   time to reperfusion  rather than altering the thrombus load and morphology  ! Time window is usually between 3-24 hours.

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Those who answered  “Yes” ,  can leave this article . Those who answered  “No” read further .

* Logic would tell us myocardial revascularisation should correct  stress induced ischemia and it  should disappear promptly  . This does not happen in all cases  real world  ! That is  why medicine is  different  from mathematical science .

Some of the  reasons for  persistence of stress positivity even after an apparently successful PCI are  . . .

  1. Incomplete  correction of ischemia. (Ideally  to be referred as failed PCI )
  2. Error in Identifying culprit 9Angina related artery ) .Common feature of poorly worked up  multivessel CAD.
  3. Re-stenosis /Re-occlusion
  4. Doing very early stress test without giving time for revascularisation to work *
  5. Rapid progression of non culprit lesions .(Sub -optimal medical management )
  6. Chronic N0-Reflow phenomenon  surrounding  area of infarct .(Especially in  PCI of CTOs)
  7. Dyskinetic  or grossly remodeled ventricular segments  can result in non ischemic positive EST response (ST drag **)
  8. Associated systemic conditions especially  Anemia/ SHT & LVH -(False positive )
  9. Many diabetic patients may  continue to show stress ischemia due to  small vessel disease.
  10. A  patient with  syndrome X  characters  can have incidental  epicardial lesion as well . In such a patient EST will always be positive .

* Optimal time to do  EST  for assessing the  efficacy of  PCI/CABG is not established .Six months may be the reasonable point .If done within 2- 3 months it may  end  up  in embarrassment for the Interventionist . (So only it is kept at 6 months , this also help us  greatly  as  we can always blame it on poor life style control and progression of  the disease !)

** No reference  for this  , a  personal observation .We know  Q leads following MI ,  will show ST elevation during stress test especially if the segments are dyskinetic  . In leads diagonally opposite to q leads ,  ST depression is observed . This may not be  a evidence for true  ischemia . It probably represents   ST drag due to mechanical stretch .

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bifurcation angle

  • At any branch point three angles are possible .True bifurcation angle is formed between LAD and LCX .
  • The angle between LM and LAD or LM and LCX can also be important in specific situations ,especially when we encounter short left mains and Medina 1,1,0 lesions .
  • Major bifurcation angle can  occur in mid  segments  as well ,  between LAD / major Diagonal  , LCX and OM.
  • Logic would tell us the  left main  bifurcation  angle is relatively fixed by the anatomical AV and IV grooves. Still early course of LAD and LCX can be out of grooves.
  • Further ,the bifurcation angle is imparted some amount of dynamism by cardiac cycle . It can vary between 80 -120 degrees (LAD/LCX).
  • Most importantly various  angiographic views can alter the true angle (by illusion ) in dramatic fashion . RAO caudal view appear ideal to measure it. (LAO caudal make every bifurcation angle obtuse !)
  • Acute angled bifurcations are prone for stent related mechanical issues both during deployment and in the long term outcome . (When two stent technique is used) This is because ,  acute  angled bifurcations has a tendency to drift the carina , and  encroach  the lumen  which can create new  turbulence . Of course final kissing balloon is expected to reduce this hemodynamic side effect at least on paper !

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In the early 1980s , when cardiac physicians were confronting how to tackle intra coronary thrombus , one man from Japan  was  looking directly at the ground zero with fiber-optic coronary angioscope .He  provided live images  of coronary plaques and thrombus (long before the IVUS and OCT era) because of technical difficulties it did not get into  clinical utility  but gave us vital information like plaque morphology and behavior.

  • The concept of red and white thrombus
  • The yellow lipid enriched vulnerable plaques
  • Post lytic  clot surface
  • The fibrin strands within the clot etc.

coronary angioscopy Yasumi Uchida

The angioscopes have now given way to IVUS and OCT which provide indirect vision of the coronary arteries .Uchida has written a book tilted coronary angioscaopy which is a must read for all clinical cardiologists.

I think Japanese are  leading in this aspect of cardiac Imaging .Yasunori Ueda is another person who has  done lot of work on angioscopy . here is an  Image from his paper. Exciting  stuff  is isn’t !

coronary angioscopy  Yasunori Ueda www.invasivecardiology

Image source : Yasunori Ueda http://www.invasivecardiology.com

  Reference 

http://circ.ahajournals.org/content/104/24/e143.full

http://www.invasivecardiology.com/article/5571?page=3

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Answer :

In cardiogenic shock it is A . In all others it is probably  C.

While D may be  considered as  an  essential target criteria  for completing the  rescue PCI

Read also

Why-we-often-follow-a-reckless-time-window-for-rescue-angioplasty ?

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Myocardial salvage is like  coronary fire fighting.When fire is fought  very early after the accident  , benefits are accrued  more . Text book primary angioplasty is . . .  fire engine arriving at the scene when the house is on fire .

Rescue angioplasty is asking for more force ,  when the initial fire fighting  was inefficient to control the fire. So , it is obvious the rescue efforts should be fast and brisk.In fact the pace should me more than the primary (The the second engine should  reach the ground zero  faster than the first !  – Read as  door -balloon time ! )

But what happens in real world ? We would tell  time window for primary angioplasty even in sleep ! but will struggle to come   with clear cut  answer for the  same in  rescue angioplasty  even in a  fully awake state !

CaptureWiz

It is  an overwhelming fact , we have  not taken enough efforts to define strict time limit  for rescue .( Even though guidelines say it should not be beyond  24  hours , common sense will tell us rescue PCI should not go beyond 12-15 hour window ! .One more definition for rescue PCI could be within 3 hours after diagnosing failed thrombolysis. In real world  it is a race against time in a different perspective .In many centers  rescue angioplasty “enjoys time less windows “

I was funny witness in a big private  hospital  when a  colleague  of mine  has posted  a case for  “elective rescue angioplasty” and was  waiting in the side cabin  for his turn !

Coming back to the title question

Why we often follow  a reckless time window for rescue Angioplasty ?

The reason is simple

Time is not only  muscle . . . time  is  money too !

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Acute MI kills a few million people world-wide every year .It does not differentiate rich from poor. Logic would  tell us  , principles of management  should  not differentiate  the people  when  dealing with a myocardium in distress .

Unfortunately , we scientists do it with passion !

The problem is enormous  . . . the rich is suffering from too much* care and the poor is suffering from want of care !

The following flow chart  is a result of my observation from close quarters  about the management strategies in corporate as well as Govt hospitals .

The first chart exposes the problem .The second one tries  to address the issue

Please bear with me . . .  if the  stuff  sounds  too crazy !

* Too much care is also referred to as inappropriate care

Practical and ethical guidelines for stemi management corporate

And for the solution  . . . try this

Practical and ethical guidelines for stemi management

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Soft skills in pPCI 

Experience  would tell  us only about 70-80 % of STEMI are truly eligible for a  good  quality pPCI .(Multivessel CAD, Complex bifurcation lesion, difficulty in identifying IRA, No IRA-sapsms , complete spontaneous reperfusion )  The remaining 20-30 %  should , logically  be included in the failed pPCI category .This fact is largely concealed in the literature .

Beware of huge thrombus load in every patient with STEMI .The  contribution of  mechanical occlusion  vs thrombus  (in the total occlusion )  is the single most important factor in determining the intervention strategy.

Deploying a stent in a poorly  prepared (debrided of thrombus  ) lesion confers  further continuous  risk of a STEMI .Stents smartly jail  even large thrombus against the coronary vessels and they release it into the lumen in a controlled fashion  and prolong  the  acute coronary  risk phases

If thrombus aspiration  does a neat job and establishes a good   flow , if the   lumen  appear   good , think twice or even thrice before deploying a stent .It is akin to stent a  zero % lesion and we know it is foolish to do that at any stretch of imagination .(Stenting has never been proven to convert a vulnerable ulcerated lesion into stable one )

IVUS, OCT are not the answer in the above situations  as we are dealing with  emergency coronary  fire fighting !

Of course the intensive anti-platelet   protocols , will take care of  potential after effects of the intra coronary contact sport we play  !    . But . . . there is a limit for every thing. So spend as little time as possible when attempting catheter based reperfusion during STEMI.

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