Figure 9A.1.1

Questions

1. What is this rhythm, and what information can you infer about the arrhythmia?

2. Why is the QRS morphology changing? What is the location of his myocardial infarction?

Discussion, Interpretation, and Answers

The ECG rhythm strips show evidence of sinus P waves marching through the tracing (Figure 9A.1.2, red arrows) with a dissociated and faster ventricular rate (102 bpm) suggesting ventricular tachycardia (VT). There is a repetitive pattern of interspersed fusion beats between conducted sinus and VT (F) and purely conducted sinus beats (C). These “capture beats” demonstrate a narrow QRS complex with a sharp initial deflection in lead V₁.

Figure 9A.1.2

In general, the QRS complex in VT is negative in ECG leads corresponding to the site from where activation spreads out to the bulk of the ventricle (inferior leads corresponding to the inferior wall in this case). However, for a VT from an endocardial site in a structurally normal heart, there will be a small initial r wave, representing transmural activation in direction of the ECG lead, before the vector becomes predominantly negative. Presence of QS complexes (without initial r wave) suggests either an epicardial site with the entire activation wavefront (including local transmural depolarization) moving away from the corresponding ECG lead, or, as in this case, point to the presence of transmural infarction. Presence of an inferior infarction is further confirmed by q waves in the conducted beats in leads II and III (arrowheads).

The VT morphology demonstrates an “Rs” configuration in leads V₁–V₃ transitioning to “rS” in leads V₄–V₆ suggesting spread of activation from a site in the left ventricle (atypical right bundle branch block morphology in lead V₁), closer to the apex than the base (predominantly negative in leads V₅ and V₆). It has a superior axis (upright in aVR and aVL; “QS” in inferior leads), further localizing to the inferior apical wall. The QRS width during VT is relatively short (approximately 120 ms) suggesting the depolarization wavefront spreading centrifugally from the septum to activate both ventricles at the same time. A narrow QRS also suggests activation spreading from the endocardium with early access to fascicular conduction system, as opposed to spreading from the epicardial surface that has a slurred initial component (pseudodelta wave) and overall wider QRS complex. Put together, the VT morphology suggests activation spreading from the left ventricular apical inferoseptal region to the rest of the ventricles.

On careful measurements, other interesting phenomena can be noted in Figure 9A.1.2. First, the PR interval for the sinus capture beats is longer for F and shorter for C (blue arrows). The prolongation of the PR interval for F is explained by concealed retrograde penetrance of VT into the AV node. Therefore, the AV node is relatively refractory and antegrade AV nodal conduction encounters more decrement with PR prolongation. Second, the conducted complexes F and C reset the tachycardia so that the subsequent VT beat (asterisk) is slightly advanced. Both focal and reentrant mechanisms of tachycardia can be reset with premature beats. Reset with a fused QRS complex, however, proves reentry. Comparison with conducted QRS complexes during normal sinus rhythm (not available) can help determine if the complex C is purely a conducted sinus beat or demonstrates some evidence of fusion with the VT. Regardless, a stable monomorphic VT in the setting of structural heart disease has overwhelmingly high odds of being a reentrant arrhythmia.

Identical QRS morphology achieved during rapid atrial pacing (Figure 9A.2.1 Left) and left posterior fascicular ventricular tachycardia (VT)—also called “Belhassen VT”—(Figure 9A.2.1 Right) in a young patient with a normal heart. In both instances, an identical pattern of complete right bundle branch block and left axis deviation is observed. Atrial pacing is initiated during sinus rhythm showing a normal QRS configuration and is associated with left bundle branch block aberration on the first paced beat. This tracing suggests that a tachycardia with right bundle branch block-left axis deviation in a patient with a normal heart and normal baseline electrocardiogram may have (albeit exceptionally) a supraventricular origin.

Figure 9A.2.1

Patient History

A 44-year-old female patient presented with rapid palpitations. Clinical and echocardiographic examination reveals a structurally normal heart. Her basic ECG shows no abnormality. ECG during tachycardia is shown in Figure 9A.3.1. Patient was admitted to electrophysiology lab for diagnosis and radiofrequency ablation of the tachycardia (Figures 9A.3.2, 9A.3.3, and 9A.3.4).

Figure 9A.3.1 Surface ECG of the tachycardia. A 12-lead surface ECG showing wide complex tachycardia having right bundle branch block (RBBB) morphology. Tachycardia apparently seems irregular due to multiple narrow complexes that appear as captured beats. The normalized beats have no terminal delay on as seen in V₁, giving the impression of a significant irregularity. Note that the extreme right axis, monophasic R in V₁, predominantly negative V₆, and dominant R in aVR is in favor of VT.

Figure 9A.3.2 Intracardiac interpretation of the tachycardia. Intracardiac recordings show His bundle electrode (proximal and distal), coronary sinus (proximal and distal) and RV apex. As shown, there is gradual conduction delay over three beats, then it normalizes. There is a minor delay in the HH timing due to variable AV nodal conduction time, thus giving time for the right bundle to recover in the normal beats. Note that in the aberrant beats there is delay in the RV activation, especially the apical activation to approximate the LV activation, giving the irregularity seen in the RVa electrode. Also note the infra-Hisian delay results in earlier activation of the A wave, resulting in pseudo q wave on the surface ECG in the aberrant beats [rather than the usual pseudo S].

Figure 9A.3.3 Surface ECG of another morphology of the tachycardia. Intracardiac recording showing normalization of the RBBB in the same session, with fixed HH interval of 440 ms.

Figure 9A.3.4 Intracardiac findings for tachycardia 2. Intracardiac recording shows concentric AV activation, with early RV activation, consistent with typical AV nodal reentrant tachycardia.

Questions

1. Using the differentiation algorithms, what is the diagnosis of the wide complex tachycardia?

2. What is the cause for the irregularity of the tachycardia?

Discussion, Interpretation, and Answers

Although the right bundle branch block (RBBB) is not wider than 160 ms, the morphologic criteria of the RBBB favors ventricular tachycardia (VT). The monophasic R wave in V₁, the predominant S in V₆, and R in aVR together with the pseudo-capture beats favors the diagnosis of VT; however, the presence of two successive capture beats in VT is very unusual, unless there is simultaneous supraventricular arrhythmia (atrial fibrillation/atrial flutter).

Two interesting phenomena appear in the intracardiac recordings: the mechanism of pseudo capture beats and the earlier appearance of the A wave in the aberrant beats. The HH variation with its later entrance in the right bundle gives it more time to recover. The variation of the autonomic input to the AV node during tachycardia is responsible for that phenomenon, with more rapid conduction resulting in aberration. Interestingly, the earlier appearance of the A wave in relation to the QRS and its disappearance in the nonaberrant beats disrupts the appearance of VA association, giving the impression of VA dissociation.

Patient History

A 62-year-old patient with an old inferior myocardial infarction complains of near syncopal episodes. His ECG (Figure 9A.4.1) shows atrial fibrillation and a right bundle branch block, and episodes of ventricular fibrillation (VF).

Figure 9A.4.1

Question

What is the electrophysiological mechanism of VF onset?

Answer

VF is induced by short-coupled PVCs, but not every short-coupled PVC induces VF. Induction occurs each time after a long RR interval (long-short sequence), usually described in patients with a long QT and torsades de pointes. This sequence of VF onset has been also described in patients with an ICD and a low pacing rate. The underlying mechanism proposed is a different change in refractory periods between myocardium and Purkinje in response to an abrupt change in cycle length, allowing reentry to occur.

References

1. Denker S, Lehmann M, Mahmud R, et al. Divergence between refractoriness of His-Purkinje system and ventricular muscle with abrupt changes in cycle length. Circulation. 1983;68:1212–1221.

2. Sweeney MO, Ruetz LL, Belk P, et al. Bradycardia pacing-induced short-long-short sequences at the onset of ventricular tachyarrhythmias: A possible mechanism of proarrhythmia? J. Am. Coll. Cardiol. 2007;50(7):614–622.

Patient History

A 30-year-old male presented with wide complex tachycardia at 200 bpm with a blood pressure of 90/60.

Figure 9A.5.1

The ECG revealed:

1. Bicuspid aortic valve with marked calcification

2. Mean atrioventricular (AV) gradient of 25 mmHg (moderate aortic stenosis)

3. Moderate aortic regurgitation

4. Normal left ventricle size and systolic function

5. Mild concentric left ventricular hypertrophy (1.4 cm wall thickness)

Figure 9A.5.2 Panel A: Resting 12-lead ECG shows right bundle branch block (RBBB)/RAD and first-degree AV block. Panel B: The bottom panel shows RBBB/RAD tachycardia with similar but not identical morphology as the sinus rhythm ECG. There are retrograde P waves (asterisk) in some beats but not others.

Figure 9A.5.3 Left bundle branch block (LBBB) ventricular tachycardia (VT) with a cycle length of 360 ms (165 bpm). Later on after medical therapy with flecainide, the patient went into a LBBB tachycardia with a cycle length of 360 ms.

Figure 9A.5.4 RBBB tachycardia with a cycle length of 360 ms (165 bpm). The LBBB tachycardia terminated spontaneously, and soon after the RBBB tachycardia recurred with the identical cycle length. In the electrophysiology lab, both of these arrhythmias could be induced. The LBBB tachycardia was induced with programmed stimulation from the right ventricle and was confirmed to be bundle branch reentry using the RBB in the antegrade direction and the LBB in the retrograde direction. The RBBB tachycardia was induced with atrial programmed electrical stimulation and was demonstrated to be bundle branch reentry using the LBB in the antegrade direction and the RBB in the retrograde direction. Ablation of the right bundle eliminated both tachycardias.

Patient History

A 50-year-old male with known coronary artery disease and normal left ventricular function presented to emergency for recurrent chest pain and dyspnea. A remote non-ST segment elevation myocardial infarction (NSTEMI) had been treated with angioplasty and stenting of the right coronary artery. His initial ECG (Figure 9A.6.1A) was unremarkable and the first set of troponin was negative. Given his history of previous angioplasty and his ongoing chest pain, a coronary angiogram was performed that demonstrated a patent stent and no other flow-limiting lesion. The ECG of Figure 9A.6.1B was recorded after the coronary angiogram. The patient was completely asymptomatic. Echocardiogram and cardiac magnetic resonance imaging (MRI) showed a normal biventricular function and no evidence of myocardial scarring. Exercise treadmill testing resulted in complete suppression of the ECG findings displayed in Figure 9A.6.1B.

Figure 9A.6.1 Intermittent accelerated idioventricular rhythm with likely RV outflow tract (RVOT) origin. A. Initial ECG at emergency. Normal sinus rhythm at a rate of 65 bpm. Isolated, nonspecific QRS fragmentation in lead III, otherwise normal ECG. Intrinsic sinus beats have a normal QRS duration. B. There are three different types of QRS complexes: wide QRS complexes with left bundle branch block pattern and inferior axis at a rate of 75 bpm (black arrows); narrow QRS complexes at a rate of 65 bpm (blue arrows); and QRS complexes with intermediate width and similar morphology compared to the wide complexes (dark red arrows). There is AV-dissociation (dashed arrows) with more R than P, suggesting an underlying ventricular rhythm. The QRS complexes with intermediate width represent fusion beats between conducted sinus beats and idioventricular rhythm. Note the slightly shorter PR interval of fused beats. The most likely diagnosis in this asymptomatic patient is intermittent accelerated idioventricular rhythm with likely origin from the posteroseptal RVOT (precordial transition at V₄ and V₅, leads I and aVL positive).

Interpretation

(A) Normal sinus rhythm at a rate of 65 bpm. Isolated, nonspecific QRS fragmentation in lead III, otherwise normal ECG.

(B) Intermittent accelerated idioventricular rhythm at a rate of 75 bpm. Underlying sinus rhythm at a rate of 65 bpm, with presence of fusion beats. The idioventricular rhythm most likely originates from the RVOT.

Discussion

The term accelerated idioventricular rhythm (AIVR) describes an ectopic rhythm originating from the His-Purkinje system or the ventricular myocardium.¹ The underlying mechanism is automaticity, and AIVR usually manifests during increased vagal tone.² This ectopic rhythm is typically monomorphic with rates between 50 and 120 bpm and creates no or minimal symptoms.¹ AIVR has traditionally been reported in the context of acute myocardial infarction, but can also occur in the context of drug intoxication, chronic cardiomyopathies, electrolyte disorders, or pregnancy.^1,3,4 The presence of AIVR in the setting of acute myocardial infarction with ST-segment elevation gained widespread interest in the era of thrombolysis because it was initially thought to be a marker of successful reperfusion. However, more recent studies have demonstrated that AIVR is not reliably associated with reperfusion, but rather is a marker of extensive myocardial damage and abnormal myocardial microcirculation.^3,5 In the present case, intermittent increase of vagal tone appears to be the sole explanation for his AIVR in the absence of active ischemia or other reversible causes.

The ECG suggested an RVOT origin based on widely accepted morphology criteria for outflow tract arrhythmia.^6–9

References

1. Riera AR, Barros RB, de Sousa FD, et al. Accelerated idioventricular rhythm: History and chronology of the main discoveries. Indian Pacing Electrophysiol. J. 2010;10(1):40–48.

2. Castellanos A, Jr., Lemberg L, Arcebal AG. Mechanisms of slow ventricular tachycardias in acute myocardial infarction. Dis. Chest. 1969;56(6):470–476.

3. Bonnemeier H, Ortak J, Wiegand UK, et al. Accelerated idioventricular rhythm in the post-thrombolytic era: Incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention. Ann. Noninvasive Electrocardiol. 2005;10(2):179–187.

4. Navarro V, Nathan PE, Rosero H, et al. Accelerated idioventricular rhythm in pregnancy: A case report. Angiology. 1993;44(6):506–508.

5. Terkelsen CJ, Sorensen JT, Kaltoft AK, et al. Prevalence and significance of accelerated idioventricular rhythm in patients with ST-elevation myocardial infarction treated with primary percutaneous coronary intervention. Am. J. Cardiol. 2009;104(12):1641–1646.

6. Betensky BP, Park RE, Marchlinski FE, et al. The V(2) transition ratio: A new electrocardiographic criterion for distinguishing left from right ventricular outflow tract tachycardia origin. J. Am. Coll. Cardiol. 2011;57(22): 2255–2262.

7. Dixit S, Gerstenfeld EP, Callans DJ, et al. Electrocardiographic patterns of superior right ventricular outflow tract tachycardias: Distinguishing septal and free-wall sites of origin. J. Cardiovasc. Electrophysiol. 2003;14(1):1–7.

8. Hutchinson MD, Garcia FC. An organized approach to the localization, mapping, and ablation of outflow tract ventricular arrhythmias. J. Cardiovasc. Electrophysiol. 2013;24(10):1189–1197.

9. Yoshida N, Yamada T, McElderry HT, et al. A novel electrocardiographic criterion for differentiating a left from right ventricular outflow tract tachycardia origin: The V2S/V3R index. J. Cardiovasc. Electrophysiol. 2014;25(7): 747–753.

Patient History

A 52-year-old male with a history of coronary artery disease (CAD), coronary artery bypass graft surgery, and left ventricular dysfunction (ejection fraction of 28%, inferior aneurysm) underwent primary prevention implantation of an implantable cardioverter-defibrillator (ICD). The baseline ECG showed sinus bradycardia with a remote inferior myocardial infarction. The patient was followed in the heart failure clinic; during follow-up, his ECG showed atrial pacing with ventricular sensing and an increase of the PR interval to 250 ms (Figure 9A.7.1). Eight years following ICD implantation, the patient was admitted with VT storm. He required multiple ICD shocks and was treated with amiodarone.

Figure 9A.7.1

The patient presented two years later with two shocks from his ICD. The patient underwent VT ablation; multiple morphologies were also induced during mapping, showing a narrower morphology (Figure 9A.7.2) and another very wide complex morphology associated with left bundle branch block morphology (Figure 9A.7.3). The patient had a ventricular aneurysm, which has been associated with pleiomorphic VT (i.e., >1 morphologically distinct VT during the same episode of VT, while the QRS does not continuously change) Figure 9A.7.4.^2,3 This patient had different morphologies of induced VT, rather than pleiomorphic VT. During VT ablation, using activation and pacemapping, homogenization of the extensive inferior wall scar was associated with no inducible VT post ablation. During > 2 years of follow-up in ICD clinic, the patient has not had recurrence of VT, while his follow-up ECG continued to show atrial pacing with prolonged AV conduction.

Figure 9A.7.2

Figure 9A.7.3

Figure 9A.7.4

Question

Pleiomorphic ventricular tachycardia refers to:

1. Ventricular tachycardia associated with atrial fibrillation

2. The change of morphology of ventricular tachycardia during continuous recording, showing two distinct morphologies

3. Ventricular tachycardia associated with ventricular fibrillation

4. Ventricular tachycardia showing multiple morphologies at different times, but without distinctly showing a change from one morphology to another morphology

Answer

2

References

1. Josephson ME, Horowitz LN, Farshidi A, et al. Recurrent sustained ventricular tachycardia. 4. Pleomorphism. Circulation. 1979;59(3):459–468.

2. Liu E, Josephson ME. Pleomorphic ventricular tachycardia and risk of sudden cardiac death. Circ. Arrhythm. Electrophysiol. 2011;4:2–4.

Patient History

A 59-year-old female without a previous cardiac history developed sudden and intermittent palpitations associated with lightheadedness. During one of her episodes, she was found to have heart rates in the 160 seconds. Her ECG is shown in Figure 9A.8.1 (initiation) and Figure 9A.8.2 (termination). Her echocardiogram showed a structurally normal heart.

Figure 9A.8.1 12-lead ECG showing initiation of ventricular tachycardia. Note the presence of dissociated P waves (arrows).

Figure 9A.8.2 12-lead ECG showing termination of wide complex tachycardia. Note the capture beat (arrow) revealing diagnosis of ventricular tachycardia.

Questions

What type of arrhythmias is this? Where is the site of origin?

Discussion

The presence of A-V dissociation and capture beats indicates that this is ventricular tachycardia rather than supraventricular tachycardia with aberrant conduction. The ventricular tachycardia (VT) has a left bundle branch block morphology and an inferior axis, suggesting an outflow tract origin.

In localizing outflow tract arrhythmias, it important to remember that the posterior wall of the right ventricular outflow tract (RVOT) is adjacent and immediately anterior to the right coronary cusp (RCC) and part of the left coronary cusp (LCC).¹ A precordial transition after lead V₃ suggests a right-sided origin, whereas an early transition (≤ lead V₂) with a right bundle branch block (RBBB) morphology usually indicates a left-sided focus. However, outflow tract arrhythmias on the posterior aspect of the RVOT or the anterior aspect of the left ventricular outflow tract (LVOT) may have similar ECG characteristics. This case shown here has a precordial transition in V₃, indicating that the arrhythmia focus could originate from either the RVOT or LVOT.

The RVOT wraps around the anterior aspect of the LVOT.^2,3 The plane of the pulmonic valve is approximately 1–2 cm more superior to that of the aortic valve (Figure 9A.8.2). Therefore, the crest of the posterior RVOT myocardial wall is adjacent to the aortic sinuses, generally the RCC and a portion of the LCC. Because the LVOT is positioned more posteriorly in the chest compared to the “septal” RVOT, arrhythmias from this region are associated with larger anterior forces and therefore an earlier precordial transition. Thus, idiopathic LVOT PVCs with a precordial transition in lead V₃ show an earlier transition compared to sinus rhythm. This is confirmed by computing the percentage R wave during the PVC/VT in lead V₂ (R/R+S)_VT divided by the percentage R wave in sinus rhythm (R/R+S)_SR. A V₂ transition ratio ≥ 0.60 predicts an LVOT origin with a sensitivity of 95%, specificity of 100%, positive predictive value of 100% and negative predictive value of 95%.⁴

The case shown has a PVC precordial transition that occurs later than sinus. The V₂ transition ratio is 0.5, suggesting that the origin is from the RVOT rather than LVOT.⁵ The VT was mapped and localized to the posteroseptal region of the RVOT. It was adenosine-sensitive, indicating that the mechanism was due to triggered activity. The arrhythmia was eliminated with radiofrequency ablation.

References

1. Lerman BB. Outflow tract ventricular arrhythmias: An update. Trends Cardiovasc Med. 2015;25(6):550–558.

2. Asirvatham SJ. Correlative anatomy for the invasive electrophysiologist: Outflow tract and supravalular arrhythmia. J. Cardiovasc. Electrophysiol. 2009;20:955–968.

3. Ho SY. Anatomic insights for catheter ablation of ventricular tachycardia. Heart Rhythm. 2009;6:S77–S80.

4. Betensky BP, Park RE, Marchlinski FE, et al. The V(2) transition ratio: A new electrocardiographic criterion for distinguishing left from right ventricular outflow tract tachycardia origin. J Am Coll Cardiol. 2011;57:2255–2262.

5. Yoshida N, Yamada T, McElderry HT, et al. A novel electrocardiographic criterion for differentiating a left from right ventricular outflow tract tachycardia origin: the V2S/V3R index. J Cardiovasc Electrophysiol 2014;25:747–759.

Patient History

A 72-year-old female developed ventricular tachycardia after cardiac catheterization.

The patient presented with profound sinus bradycardia with heart rates in the 20–30 bpm range. Cardiac catheterization showed a stenosis of the right coronary artery, which was stented. A temporary pacing wire was placed before the intervention given her bradycardia. Soon after the catheterization, the patient developed ventricular tachycardia (Figure 9A.9.1). She received a 150 J shock externally that was successful in terminating the arrhythmia. Post-shock, the patient is complaining of chest soreness. She received 150 mg of amiodarone bolus but remains with frequent runs of nonsustained ventricular tachycardia post shock. The rhythm strip from the event is shown in Figure 9A.9.1.

Figure 9A.9.1 Rhythm strip showing the onset of the ventricular tachycardia that converted to sinus after a 150 J external shock.

Question

What should be the next step in this patient’s management?

1. More amiodarone boluses

2. Lidocaine boluses

3. Take her to the catheterization laboratory and recheck the RCA stent for possible occlusion

4. None of the above

Discussion, Interpretation, and Answers

The correct answer is 4. The morphology of the PVCs (Figure 9A.9.2, arrows) and first beat of the ventricular tachycardia are very similar to the paced complex, suggesting that the ectopy is induced by mechanical stimulation by the temporary pacing wire. After repositioning the temporary pacing wire, there was no more ventricular tachycardia. The patient received a permanent pacemaker. During the pacemaker implant, there were multiple runs of ventricular tachycardia during the implant of the right ventricular lead.

Figure 9A.9.2 The morphology of the PVCs and first beat of the ventricular tachycardia (marked with red arrows) are very similar to the paced complex.

Patient History

A 32-year-old male arrived at the emergency department for evaluation of persistent fatigue. He had a viral illness some weeks earlier and had not recovered his energy. On routine vital signs, his pulse was rapid and irregular, and an ECG (Figure 9A.10.1) was obtained as shown.

Figure 9A.10.1

Question

What does his ECG illustrate and how might it relate to the cause of his fatigue?

Discussion

The ECG shows a very irregular wide complex tachycardia, which at first glance appears to be atrial fibrillation with left bundle branch block aberration. This would be unusual in an otherwise healthy young male (right bundle branch block being the more common type of aberration in young people) and should raise suspicion that the arrhythmia is not aberrantly conducted (instead, conduction to the ventricles using an accessory pathway, or ventricular tachycardia [VT]). On closer inspection, it is evident that the atrial rhythm is not fibrillation, but discrete P waves are visible (most are inverted, suggesting retrograde conduction; P = sinus P wave, P’ = retrograde P waves, ? = uncertain atrial activity). Application of algorithms to differentiate among potential causes of wide QRS tachycardia in this case yield mixed results, as indicated in the table (SVT = supraventricular tachycardia):

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