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Workshop #5 VT and ICD Unknowns. Chair: David J. Wilber, MD Faculty: John P. DiMarco, MD, PhD Francis E. Marchlinski, MD. CASE #1.

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Workshop 5 vt and icd unknowns l.jpg

Workshop #5VT and ICD Unknowns

Chair: David J. Wilber, MD

Faculty: John P. DiMarco, MD, PhD

Francis E. Marchlinski, MD


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CASE #1

A 74 year old man with an implantable defibrillator placed 4 years ago was admitted for multiple defibrillator shocks. Device interrogation revealed VT at a cycle length of 370 ms. Shocks were delivered following failed attempts at ATP.

During EP evaluation, a right bundle right superior axis tachycardia was induced at a cycle length of 370 ms. Electrograms were recorded and pacing performed from multiple sites in the left ventricle during VT.

  • Should RF be given at this site?

  • Yes

  • No


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ACTIVATION

PACING


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CASE #1 – Question 1 Answer

  • Should RF be given at this site?

  • Yes

  • No

The purpose of this question was to test the ability to recognize optimal sites for RF energy application based on the findings of entrainment mapping at multiple sites during the same tachycardia. Pacing is performed at a CL of 350 ms.

.


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The EGM during VT is not very early (-44 ms). Pacing accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.


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Case 1: Question 2 accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

  • Should RF be given at this site?

  • Yes

  • No

ACTIVATION

PACING


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Case 1: Question 2 Answer accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

  • Should RF be given at this site?

  • Yes

  • No

RF is unlikely to be effective at this site. There is a middiastolic potential preceding the QRS by 111 ms during VT. During pacing the tachycardia is accelerated to the pacing rate with an S-QRS similar to the EGM-QRS interval. However, the morphology of paced QRS is quite different in several leads, thus the entrainment is manifest rather than concealed. This site is within the reentry circuit, but is an “outer loop” site. Focal RF application is unlikely to eliminate the VT.


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Case 1: Question 3 accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

  • Should RF be given at this site?

  • Yes

  • No

ACTIVATION

PACING


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Case 1: Question 3 Answer accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

  • Should RF be given at this site?

  • Yes

  • No

Yes. There are multiple middiastolic potentials, the earliest of which precedes the QRS by 180 ms, or approximately 50% of the tachycardia cycle length. During pacing, the tachycardia accelerates to the pacing rate, the QRS morphology is identical in all 12 leads, and the S-QRS interval is nearly identical to the EGM-QRS interval during tachycardia. Thus there is concealed entrainment with activation time - stimulus time matching. This site is most likely within a protected isthmus, and RF application here is associated with a good probability of terminating and eliminating VT.


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Case 1: Question 4 accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

  • Should RF be given at this site?

  • Yes

  • No

ACTIVATION

PACING


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Case 1: Question 4 Answer accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

  • Should RF be given at this site?

  • Yes

  • No

During tachycardia, there is a middiastolic potential, preceding the QRS by 148 ms. At first glance, pacing appears to capture the ventricle with a similar QRS configuration, but on closer inspection, it can be seen that the pacing stimuli are not capturing the ventricle. The probability of successful ablation based on the presence of middiastolic potentials alone, without corroborative pacing data is relatively low.


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CASE accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective. #2

A 24 year old woman had a 10 year history of tachycardia. She has no other structural heart disease. She recently underwent evaluation elsewhere and was found to have AV nodal reentry and underwent slow pathway ablation. She now presents with recurrent sustained palpitations and undergoes electrophysiologic evaluation. A wide complex tachycardia is initiated during atrial pacing.


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12 Lead of Induced Tachycardia: accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.


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Case 2: Question 1 accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

At which location is the site for successful ablation most likely to be found?

  • Left ventricular outflow tract

  • Slow AV nodal pathway

  • Inferoapical septum

  • Subeustachian isthmus

  • Posterior mitral valve annulus


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Case 2: Question 1 Answer accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

At which location is the site for successful ablation most likely to be found?

  • Left ventricular outflow tract

  • Slow AV nodal pathway

  • Inferoapical septum

  • Subeustachian isthmus

  • Posterior mitral valve annulus


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CASE #2 Comments accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

The purpose of this exercise was to test knowledge regarding the diagnosis and localization of idiopathic LV tachycardia (Belhaussen’s VT or posterior fasicular reentry). The tachycardia appears to be due to reentry involving incorporating the purkinje fibers in the inferior apical septum of the left ventricle, although the exact elements and dimensions of the circuits remains the subject of ongoing investigation. The tachycardia is often induced by atrial pacing, and typically has a right bundle, superior axis. During atrial pacing in the example, the QRS complex prior to the onset of tachycardia is most likely a junctional beat. The tachycardia begins with a fusion beat without preceding PR prolongation. Subsequently, the tachycardia continues at the atrial paced cycle length, suggesting (though not of itself conclusively proving) that is entrained by atrial pacing (also reported with this form of VT). As in this example, the QRS is often relatively narrow (<0.14 ms) due to early engagement of the His-purkinje system and rapid activation of the ventricles. This may be misinterpreted as SVT with aberration. The 12 lead also shows QRS alternans, not uncommonly observed.


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CASE #3 accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.

A 62 year old man with a history of chronic atrial fibrillation (left) develops a regular wide QRS tachycardia (right). He has no other structural heart disease.

The most likely mechanism of tachycardia is:

  • AV nodal reentrant tachycardia

  • Bundle branch reentrant tachycardia

  • Nodofasicular reentrant tachycardia

  • Junctional ectopic tachycardia

  • Atrial flutter with 1:1 conduction


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3-1 accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.


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3-2 accelerates the tachycardia to the paced cycle length, with close reproduction of the spontaneous VT QRS in all 12 leads. During pacing, the stimuli appear to capture the immediately following QRS with a 10-20 ms delay. However, close inspection reveals that the last pacing stimulus actually captures the first QRS complex not immediately preceded by a pacing spike with a very long delay of approximately 350 ms, identical to the paced cycle length. Thus there is concealed entrainment, but a pronounced mismatch between the EGM-QRS and the S-QRS. This site is likely a “blind loop” bystander. RF is unlikely to be effective.



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Case 3: Question 1 following tracings were obtained:

The most likely mechanism of tachycardia is:

  • AV nodal reentrant tachycardia

  • Bundle branch reentrant tachycardia

  • Nodofasicular reentrant tachycardia

  • Junctional ectopic tachycardia

  • Atrial flutter with 1:1 conduction


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Case 3: Question 1 Answer following tracings were obtained:

The most likely mechanism of tachycardia is:

  • AV nodal reentrant tachycardia

  • Bundle branch reentrant tachycardia

  • Nodofasicular reentrant tachycardia

  • Junctional ectopic tachycardia

  • Atrial flutter with 1:1 conduction


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Question 3 Comments following tracings were obtained:

  • The best answer is B.

  • In this example, the tachycardia has a 1:1 association between the ventricle and the His, though AV dissociation may also be seen.

  • The HV interval is approximately 90 ms, similar to that seen in sinus rhythm.

  • The RR intervals are regular, so that one cannot search for the relationship between the HH and RR intervals as a potential clue.

  • In the left panel, the His and the QRS following the premature beat are advanced without changing their relationship or changing the QRS morphology, indicating that the circuit has been engaged in an orthodromic fashion, and that the right bundle is part of the circuit.

  • An intramyocardial circuit in left ventricle with passive retrograde activation of the His is excluded, because one would not have expected the next QRS to be advanced along with the His potential.

  • A slightly more premature beat, given at the time of His bundle refractoriness terminates the tachycardia, excluding a supraventricular or junctional origin. It is likely that the tachycardia terminated because concealed retrograde penetration of the left bundle. The only mechanism compatible with these tracings are bundle branch reentry.


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Case 3 Comments following tracings were obtained:

  • The purpose of this exercise was to test knowledge of the physiology of bundle branch reentry and the maneuvers required to confirm the diagnosis.

  • While the clinical presentation is unusual, with antegrade conduction down the left bundle and retrograde conduction up a diseased right bundle (the reverse of the usual circuit), the electrophysiologic evaluation of this tachycardia is straightforward and permits unequivocal diagnosis provided that the diagnosis of bundle branch reentry is considered.

  • Bundle branch reentry in patients with structurally normal hearts may occur in the presence of previous His-purkinje disease, and atrial fibrillation with its accompanying long-short intervals is a common initiator of the tachycardia.

  • If the right bundle was completely blocked in both antegrade and retrograde directions, the tachycardia could not occur. However, patients with complete antegrade block may have persistent retrograde conduction. In this case, even antegrade block in the right bundle is not always complete (note the difference in width between the first and subsequent complexes of the ECG during atrial fibrillation.


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CASE #4 following tracings were obtained:

A 71 year old man with a previous extensive anteroseptal MI, prior CABG, and ICD implantation is referred for multiple shocks for recurrent VT not successfully terminated by ATP. A 12 lead of the ECG is shown below:


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Case 4: Question 1 following tracings were obtained:

Which is the most likely site of origin of the tachycardia?

  • Apical septum

  • Right ventricular septum

  • Anterobasal septum

  • Inferobasal septum

  • None of the above


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Case #4: Question 1 Answer following tracings were obtained:

  • Apical septum

  • Right ventricular septum

  • Anterobasal septum

  • Inferobasal septum

  • None of the above

Which is the most likely site of origin of the tachycardia?

The purpose of this exercise is to test your understanding of electrocardiographic localization of ventricular tachycardia

The left bundle suggests an origin on the septum, the inferior axis suggests a superior site, and the positive QRS in V4-V6 suggests a basal site.

.


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CASE #5 following tracings were obtained:

  • A 39 year old Hispanic man presents with recurrent palpitations. His baseline ECG and the initiation and adenosine termination of a tachycardia are shown in the next 3 figures.

  • Ablation at which site(s) should be performed?

    • RV below the pulmonic valve

    • RV inferior apical

    • Right atrium at lateral tricuspid annulus

    • Right bundle

    • Right atrium at lateral tricuspid annulus and in slow pathway region


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CASE #5 Answer following tracings were obtained:

  • Ablation at which site(s) should be performed?

    • RV below the pulmonic valve

    • RV inferior apical

    • Right atrium at lateral tricuspid annulus

    • Right bundle

    • Right atrium at lateral tricuspid annulus and in slow pathway region

This tracing shows sinus rhythm with a normal QRS complex. In the second tracing, an atrial premature beat causes a change in the QRS morphology with a long A to V time and loss of the His potential. This is consistent with a atriofascicular tract. The premature stimulus starts tachycardia. In the third tracing, the tachycardia is terminated with block in the antegrade direction. This is also a characteristic more frequently seen with atriofasicular tracts.


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CASE #6 following tracings were obtained:

  • A 15 year old African-American man is evaluated because of exertional dyspnea. His heart is enlarged on chest x-ray and his echo shows decreased function. His baseline ECG is shown. At electrophysiologic study, a VPD was introduced during tachycardia as shown in the second figure.

  • Which of the following is the most likely tachycardia mechanism?

    • AV reentry (accessory pathway)

    • Atypical AV nodal reentry

    • Atrial tachycardia

    • Low atrial rhythm (automatic)

    • Sinus tachycardia with dextrocardia


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CASE #6 Answer following tracings were obtained:

  • Which of the following is the most likely tachycardia mechanism?

    • AV reentry (accessory pathway)

    • Atypical AV nodal reentry

    • Atrial tachycardia

    • Low atrial rhythm (automatic)

    • Sinus tachycardia with dextrocardia

A long RP tachycardia is shown. The patient is a young man with a persistent tachycardia who probably has a tachycardia related myopathy. The His synchronous PVC slightly advances the A suggesting that there is an accessory pathway present.