Archive for the ‘excercise stress test .EST’ Category

Any new ST depression occurring during  EST is sine qua non for inducible ischemia.But,this rule does not uni-formally apply  in all 12 leads .ST depression occurring is certain leads is more important. While severe global ischemia can depress  ST segment  in most leads ,factually  only the leads V 5 and V6  predict true Ischemia.This because , bulk of LV muscle mass faces these two leads.

Isolated ST depression in inferior leads  during exercise

  • Is a frequent issue occurring at the peak exercise.
  • Is least predictive of significant CAD.
  • The exact mechanism is not clear.
  • Some continue to  believe it is indeed significant .
  • We have  observed  isolated  ST  depression > 2mm in inferior leads with significant CAD.
  • What really matters is the quantum of ST depression , symptoms, and exercise time and preexisting CAD .

Probable mechanism

  • Apart from true ischemia ,ST depression may indicate relative sub endocardial strain rather than ischemia.(By the way can simple stretch can cause ST depression ?)
  • The Infero posterior surface of heart represent  right ventricle .RV volume overlooked peaks exercise.Some think it represents acute raise in RV load during peak exercise.

How to report such EST ?

You can report it as such,  what you have observed.

  • ST depression noted in Inferior leads at peak exercise.
  • Mention whether it was angina free,
  • At what METS,
  • Total exercise time .

If you are statistically inclined  you can also mention the likely hood of CAD by positive predictive value (PPV) of the test (Low with isolated Inferior ST depression )

If you are really confused , and do not want to scratch your brain we have the most convenient terminology  invented by cardiac physicians ie Borderline EST, or Mildly positive EST “

Should we do Angiogram for such patients ?

In this era of catching normal people  who attend master health check ups  for a day care CAG  . . . it is not all  a crime to do angiogram in a  patient who shows suspicious  ST depression in three of his leads (2,3,AVF) especially if he also complains of vague chest pain.

Alternate investigation

Of course , we  always have the luxury of using  MDCT  that can stunningly  photograph the coronary arteries.

It is a mystery investigation, if it comes entirely normal every one is happy.Even slightest  defects in the photography  has a potential to confuse both physician and the patient .

What I do ?

I hesitate to  do routine CAG  if ST depression occur exclusively at  peak exercise beyond 10-12  METS , which disappear fast.(Many times we can apply this rule  to classical ischemic ST depression of lead V4 as well !)

ST  depression  in any leads (with any degree) following an episode of  ACS seems to be important.

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  1. The concept of  FFR is based on pressure gradient  alone.In any hydraulic model (Both biological and non biological systems ) pressure difference  is the least   important parameter  that determines flow.
  2. FFR  is unphysiological  as hyperemia   is  artificially induced one .(Adenosine  is not the only parameter that determines it !)
  3. Serial obstructions and branch point hemodynamics are  conveniently ignored.
  4. Reproducibility  remains a big question mark .
  5. On safety  issues  FFR  is a suspect.( Often times , it  requires expertise comparable to  that of a  complex  PCI !) .Beware , the FFR unit has stiff catheter system and is an additional health hazard .  I have witnessed   atleast two cases  where  insignificant lesions were  made significant by  FFR related Injury .
  6. And  now the  knock out punch ,  ! Probably the most vital  issue for which FFR should be banished * , it is not taking into account of vulnerabilty of a plaque .( An FFR > .9 with a hanging , eccentric , mid LAD lesion was left alone by one of the  academically up to date ,  evidence  based interventional cardiologist!  )
           (*If perfomed  in isolation without IVUS/OCT  )
I am still wondering how this concept came into cardiologist domain and into the cath lab .It should have  never been let out of theoretical physics labs !
Final message
The best way to assess physiological significance of an anatomical obstruction is  to  do  exercise  stress test .
If  the lesion is  able to sustain good exercise capacity , it  can be deemed physiological unimportant.
While , this is an explicit  proof  in single vessel disease  ,  even  in   multivessel  CAD ,   EST  is   a  collective  measure of  coronary  reserve flow .( Something like instantaneous equivalent of virtual  multivessel  FFR  )
Moderated After thought
FFR is a highly specialized theoretical  tool , that has very limited role in cath lab .
The two major practical (Non academic)  use of FFR   is to shun away  those   internet fed ,  annoying, pseudo  intellectual patients ,  who constantly ask for  angioplasty  for  obliviously insignificant lesions !
FFR comes very handy  to  bail out  cardiologists at  times of distress   ! (To escape  from the wrath of our patients   after a sub optimal &  technically inferior   PCIs   and   in  the  long term confabulations  in   restenosis  after stenting !  )


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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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