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Posts Tagged ‘scar induced vt’

Management of recurrent ventricular tachycardia has developed a lot in recent times. Anti-arrhythmic drugs(AADs) were a cornerstone for most recurrent and refractory VTs till recently. Surgeries including CABG,  repair of the aneurysm, and subendocardial resection has helped to control many post-MI ischemic VTs. Soon they became obsolete. Realistically, PCIs had little impact on post-MI VT for some unknown reasons. However, with the advent of ICDs and RF, ablation, a new dimension is added to this field. 

ICDs, though an attractive device, don’t prevent a VT but vow to nullify the consequence of VT. This is problematic. ICDs in spite of their ability to prevent SCD effectively, it has little say in preventing non-sudden deaths of in any form of cardiomyopathy. (In fact, there is some evidence ICDs might increase myocardial damage with inappropriate shocks )

Hence, RF ablation can be called as true curative therapy by extinguishing hot spots of VT genesis. Still, we need to understand ablation is technically creating new dead myocardium (in alreadly  damaged myocardium) and hence, can’t avoid a consequence. More importantly, ablation as a modality is technically more demanding. We have accumulated huge experience with the help of electro-anatomic imaging and cutting-edge hardware in the last few decades. Still, we find it difficult to zero in the target area of RF ablation, with all available techniques of mapping (Activation, substrate, entrainment, and pace mapping) The reason is,  VT circuits can be really complex ones. Not only different loops but also it can travel deep into the myocardium (Intramural or epicardial) making a single approach endocardial often futile. Success rates vary between 60 -70% (Some may claim 90 +)

This post wants the young fellows to take on this fundamental issue and learn in-depth about the arrhythmia circuit.(Get Inspired by Dr. Samuvel Asirwatham of Mayo clinic work )

What is the best site to ablate ventricular tachycardia?

  1. Exit point 
  2. Central isthmus
  3. Entrance 
  4. Inner loop
  5. Outer loop
  • Though logic would tell us we can intercept an arrhythmia by ablating anywhere in the circuit. But the issue here is we need to permanently ablate it. not just interrupting. 
  • The best site to ablate is the exit point or entry point. Maybe isthmus. I am not really sure. But, one thing is clear, the outer and inner loops are not important. Further, live tissues are the culprits and not the scars and infarcted zones. 
  • One more possible answer is to try to ablate all (or maximum) points in the circuits.

How to identify entry points and exit points?

Not a simple answer .EPs apply their life experience to do that, assisted by technology. Not everyone who has a Carto -GPS can do that.

One simple answer for the fellows is, in entrainment mapping,  critical sites can be somewhat arbitrarily labeled as exit, central isthmus, or entrance on the basis of the Stimulus-QRS interval relationship to the TCL. Exit sites will show an S-QRS interval < 30% TCL (QRS onset shortly after pacing), central isthmuses will show an S-QRS interval of 30% to 50% TCL (some delay in QRS onset after pacing), and entrance sites will show an S-QRS interval of 50% to 70% TCL 

Ruairidh Martin et all Circulation: Arrhythmia and Electrophysiology. 2018;11:e006569

Final message 

Key to the successful ablation of VT is the accuracy in choosing the target site. Locating the target is meaningless if we can’t reach that site. Reaching the site is again futile unless we are able to deliver adequate burning or icing with sufficient contact.

Meanwhile, AADs can never be ignored in spite of the apparent side effects, for the simple reason they reach the VT circuits without any fuss. The Pharma industry has almost lost its interest in AAD research and the hyper-talented EP guys are squarely responsible for this unintended consequence.

Future directions

RF energy modification and newer catheter designs will help. While cryoablation shows a promising advantage over RF, it is still to prove its sustained efficiency. Meanwhile, other ablation modes are being tried. Transvascular ethanol ablation and stereotactic radio ablation have both shown promise for arrhythmias that fail other ablation strategies.

Some more questions

  • What is the difference between arrhythmia focus of origin and entry point? 
  • Once the VT is set in, what is the relevance of its origin? 

Reference

One of the very good reviews on the topic.

1.Gustavo S. Guandalini, Jackson J. Liang, Francis E. Marchlinski, Ventricular Tachycardia Ablation: Past, Present, and Future Perspectives,
JACC: Clinical Electrophysiology, Volume 5, Issue 12, 2019, 1363-1383,
2;,W.G. Stevenson, H. Khan, P. Sager, et al.  Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction Circulation, 88 (1993), pp. 1647-1670










3.M.E. Josephson, L.N. Horowitz, H.L. Waxman, et al.Sustained ventricular tachycardia: role of the 12-lead electrocardiogram in localizing site of origin Circulation, 64 (1981), pp. 257-272

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Myocardial scars remain forever ! It forms the focus for many chronic  ventricular tachycardias following MI. A healed scar is not often benign . It blocks the electrical wavelets and deflects into multiple directions some of them may reenter and form re-entrant VT .

This scar fascinated  one man from Holland -De Bakker . . . his quest for myocardial  scars produced this excellent paper .

No one  can do  such a meticulous work  today !

He did a extraordinary  study with the scarred  papillary muscle of infarcted myocardium . It included stunning histo-pathological analysis .He found for the first time , how the scar  even though mechanically idle conducts in multiple directions that precipitate the arrhythmias

 

We need to classify myocardial scar for understanding better the VT circuits. The newer imaging like Carto system can help us in imaging the ventricular scars.

 

A rough approach for myocardial scar classification could be .

Location

  • Epicardial
  • Endocardial
  • Transmural

Combined

  • Predominantly endocardial
  • Predominately epicardial

Septal scars

Anterior

Apical

Posterior scars

*With or with out Pap Muscle

Based on thickness and volume**

Small< 2CC  >5CC

Intermediate up to 10cc

Large >20cc

**Scar volume

Based on electro-physiological properties

  • Inert
  • Inducible
  • Spontaneous with clinical VT

Based on Metabolic activity

PET matched

Mismatched

Scars with reference to vascularity

  • Vascularised scars
  • Avascular scars
  • Revascularised scars

Further modification of the scheme by the readers are welcome

 

Clinical implication of scars apart from arrhythmias ?

CRT lead positioning

 

 

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Acute MI and ventricular tachycardia are closely related entities.In fact ,  the earliest response to ischemia could be a VT .But what  is peculiar about this VT is,  it  almost always degenerates into VF  within a minute or so.(Unlike idiopathic VTs /RVOT/LVOT VTs)

This arrhythmia in  every sense  can be called as  “primary VT which is the cause for “primary VF”

It is strongly  believed VF cannot occur without  a  brief episode of VT preceding it .Logic would also suggest  the ischemic myocardium  can not suddenly  become chaotic  “with the first  beat  “. There is little documentation available to unprove this presumption.

In spite of  this intimate relationship between VT and STEMI ,  it is very rare for a STEMI patient   to enter  ER with a sustained stable  ventricular tachycardia .  While  many VTs are known for it is hemodyanmic stability and immunity against degeneration   into  VF  , it is extremely rare  for  VT to remain as VT  in acute STEMI.

*Note : NSVT can be common   in  hospitalised patient in the coronary care unit . In our experience a sustained  VT in STEMI  will enter the VF mode within 60 seconds .If not , it is a highly  unusual phenomenon .

“But surprise is the other name of medicine ”

Here is  case report, a patient walked into coronary care unit with sustained( relatively stable) VT with LBBB morphology .We thought  it was   a  non- ischemic VT  (cardiomyopathy  , RVOT etc) .As we were examining him,  he became  unstable  and  was shocked 50 J biphasic .To our surprise a classical STEMI was unmasked and he was immediately  thrombolysed.

* It is possible ,  the patient had  suffered a  old MI  which got infarcted again and the VT  was scar mediated .

But it is still uncommon  for  it  not to degenerate into VF  with fresh  STEMI

Final message

Nearly all episodes of  ventricular tachycardia , that occur in the early minutes/ hours of  STEMI would degenerate into VF.This includes  VTs  that  occur within the CCU . Most  of the times , the CCU physicians and staffs  revert this VT  promptly and deny the  ventricles  from performing the dance of death !

It is extremely rare for an acute ischemic VT associated with STEMI to walk in to the hospital,  which our patient did !

Further reading and unanswered questions

  • What determines a VT to degenerate into VF ?
  • Why macro-reentrant , scar dependent VTs  often  are well tolerated ? ( In spite of LV dysfunction !)

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Ischemic ventricular tachycardia is a  too well recognised clinical  entity  . But , ischemia triggered atrial arrhythmias are less often encountered .

Does that mean , atria are relatively protected from the effects of ischemia ?

Not really  . . .  It  is possible  it may not be  that rare ,  as we think .

And then ,  the semantics play  a major  role !

Atrial fibrillation  is the commonest supra ventricular  arrhythmia  in human ,  we also know CAD is the leading cause of the AF apart from HT & Cardiomyopathy . So technically , ischemic SVT  is  more common than Ischemic VT ,but we do not call it so !

If we analyse the triggers for AF it is more often hypoxia  (than ischemia )  . . .yes there is huge difference between the two .In the ventricles it is more often ischemia that  trigger a VT.

Atrium is very sensitive to systemic  oxygen saturations especially in elderly and COPD patients. This is the reason we get many of the complex atrial arrhythmias in hypoxic situations ( Ectopic atrial, Multi focal atrial , etc) .These arrhythmias are difficult to control unless oxygen saturation is corrected. While  many of AF episodes are transient and disappear after correction of hypoxia.

If the ventricle also  responds with fibrillation  at times of systemic  hypoxia ,  one can  imagine the disastrous consequence ! God is kind enough , systemic hypoxia per se  rarely trigger a VF ,  though  it can maintain a VT which was initiated by some other mechanism.

So what are the causes of  narrow qrs tachycardia in the coronary setting

Apart from AF ,  Ischemic SVT  can occur in the following situations

  • STEMI -RVMI
  • Atrial infarction -Focal AT -Atrial flutter /AF
  • Post Pericarditis
  • Refractory , ischemic JT (Junctional tacycardia ) in elderly , perioperative , hypoxic patients

*Atrial arrhythmias are very rare during unstable angina for some unknown reasons . Atrial scar induced ischemic focal AT is underdiagnosed.

** Never  diagnose AVNRT /AVRT in a patient   who has an ACS. It is likely you will be 99.9% wrong.

*** Preexcited AVRTS are very rare in elderly CAD patients even in those with a history of SVT  .This is because as the age advances the accessory pathways undergo degeneration either by ischemia or  the wear and tear  and get self ablated .

Many times the associated , HT and diabetes may contribute to the arrhythmia.

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