26. Managing Ventricular Tachycardia

Published on 26/02/2015 by admin

Filed under Cardiovascular

Last modified 22/04/2025

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History

In September 2000 the patient was referred to a cardiologist because of premature ventricular contractions. The 12-lead surface electrocardiogram (ECG) showed sinus rhythm with atypical right bundle branch block (RBBB), a fragmented QRS, and negative T-waves in III, aVF and V1-3. Echocardiography, a 24-hour Holter ECG, and stress test were reported to be unremarkable. An expectant strategy was adopted.
In December 2009 the patient was hospitalized for sustained monomorphic ventricular tachycardia, with a heart rate of 254 bpm. A coronary angiogram did not show atherosclerosis. Magnetic resonance imaging (MRI) revealed marked thinning and hypokinesia of the basal anterior and anteroseptal wall. The left ventricular end-diastolic volume was 169 mL, left ventricular ejection fraction (LVEF) was 48%. Right ventricular volumes and systolic function were normal. An implantable cardioverter-defibrillator (ICD) was implanted, complicated by pneumothorax.
The patient experienced life-threatening electrical storm as a result of recurrent sustained monomorphic ventricular tachycardia in June 2010. When the emergency service arrived, the twelfth ICD shock was administered for monomorphic ventricular tachycardia resulted in ventricular fibrillation, and the patient lost consciousness. ICD therapy was disabled by a magnet and the patient resuscitated. After successful external defibrillation, acute ventricular tachycardia recurrence was prevented by intravenous amiodarone. However, despite amiodarone, ventricular tachycardia recurred during admission in her local hospital. The patient was referred for ventricular tachycardia ablation.
The patient’s cousin died suddenly at the age of 37. At autopsy a pale and mottled heart was found.

Comments

Although the ECG in 2008 was suspicious and the patient had symptomatic premature ventricular contractions, the echocardiogram, 24-hour Holter ECG, and stress test were reported to be unremarkable. However, contrast-enhanced MRI could have been considered at this time, based on the suspicious ECG.

Current Medications

The patient was taking thiamazole 30 mg daily, metoprolol Zoc 100 mg twice daily, calcium carbasalate (Ascal) 100 mg daily, ramipril 2.5 mg daily, oxazepam 10 mg three times daily, and clorazepate 5 mg if needed.

Current Symptoms

The patient received 12 ICD shocks for monomorphic ventricular tachycardia. In the hospital the patient was highly anxious because of the multiple ICD shocks. She did not report chest pain or dyspnea on exertion. The history was otherwise unremarkable.

Physical Examination

Laboratory Data

Electrocardiogram

The ECG recorded sinus rhythm (Figure 26-1) and sustained monomorphic ventricular tachycardia (Figure 26-2) on the first day of admission at the cardiac care unit of the referring hospital.

Findings

The ECG in Figure 26-1 shows sinus rhythm at 72 bpm, pulse rate 140 ms, RBBB QRS 160 ms, QT/QTc 448/469 ms, a fragmented QRS with Q-waves in V1, I and aVL, a fragmented S-wave in lead II, V4 and V5, a fragmented R-wave in leads V2 and V3, and an R′ wave in leads I and aVL.
The ECG in Figure 26-2 recorded monomorphic ventricular tachycardia at 216 bpm, RBBB-like morphology (defined as dominant R in precordial lead V1), left superior axis, transition V3, and QRS width of 280 ms.

Echocardiogram

Findings

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FIGURE 26-1 

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FIGURE 26-2 

Magnetic Resonance Imaging

Findings

Based on cine magnetic resonance imaging (MRI) images, the LVEF was 40%, with marked hypokinesia of the basal anterior and anteroseptal wall, and the left ventricular end-diastolic volume was 182 mL. The right ventricle showed normal function and dimensions. The short-axis contrast-enhanced MRI slices (Figure 26-3, A) demonstrated a transmural scar in the basal anterior and anteroseptal wall. Using custom software, the contours were traced (see Figure 26-3, B) to create a three-dimensional scar reconstruction (see Figure 26-3, C and D).

Comments

The scar distribution is not typical for prior myocardial infarction, because the apical segments are completely spared. However, a scar distribution, involving in particular the basal septum and the adjacent basal anterior wall, has been previously described in patients with nonischemic dilated cardiomyopathy presenting with ventricular tachycardia.

Catheterization

The decision was made to perform ventricular tachycardia ablation to prevent recurrence of ventricular tachycardia and a potential life-threatening electrical storm. During endocardial ablation, multiple different ventricular tachycardia morphologies could be induced by programmed electrical stimulation (ventricular tachycardic cycle length 200 to 270 ms, most RBBB with inferior axis, one with RBBB and superior axis, and one with LBBB and superior axis). An electroanatomic map of the left ventricle was created, which revealed a low bipolar voltage area in the basal anteroseptal wall with fragmented electrograms, but no late potentials. For several episodes of ventricular tachycardia, early activation was identified in the basal left ventricle, but only 1 of 11 could be abolished. Although potential ablation target sites could be identified in close proximity to the bundle of His and the proximal left bundle, radiofrequency energy applications were withheld, considering that parts of the reentry circuits may be located deep intramurally or epicardially. The patient was rescheduled for a combined endocardial and epicardial procedure.
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FIGURE 26-3 Based on short axis contrast-enhanced MRI slice (panel A) and semi-automatic detection of late enhancement (panel B), a 3-dimensional scar reconstruction was created (panels C and D). The core scar is displayed in red, borderzone in yellow. LAO denotes left anterior oblique; RAO, right anterior oblique.

During the same admission, the patient underwent combined endocardial and epicardial ventricular tachycardia ablation. Arteriovenous access was obtained, and subxyphoidal puncture was performed. During the procedure, low-voltage areas and fragmented electrograms were identified at the basal and mid-anteroseptal wall, both on the endocardium and the epicardium overlying the septal region and the adjacent basal anterior wall (Figure 26-4, A to D). Of note, the endocardial low unipolar voltage area was much larger than the endocardial low bipolar voltage area, suggesting a more extensive mid-myocardial or epicardial substrate. Indeed, this area corresponded to the location of an MRI-derived scar (see Figure 26-4, E). The epicardial low bipolar and unipolar voltage area could not be explained by epicardial fat, as demonstrated by CT-derived meshes color-coded for epicardial fat thickness (see Figure 26-4, F).
During the procedure a total of 17 different ventricular tachycardia morphologies could be induced (the first 9 ventricular tachycardia episodes are shown in Figure 26-5), all related to the scar in the basal septum and basal anterior wall. Several ventricular tachycardia reentry circuit isthmuses were mapped to an area in close proximity to the bundle of His or proximal left bundle. In Figure 26-6, diastolic activity and concealed entrainment are demonstrated at the right ventricular side of the septum for one of these ventricular tachycardic episodes. Despite extensive mapping at the endocardium and epicardium with radiofrequency applications limited to potential entrance or exit sites that were considered to be at safe distance from the bundle of His and left bundle, ventricular tachycardia remained inducible.

Focused Clinical Questions and Discussion Points

Question

Should iatrogenic total atrioventricular block with consecutive pacing be accepted to potentially prevent ventricular tachycardia recurrence in a patient with nonischemic cardiomyopathy who has experienced a life-threatening electrical storm requiring resuscitation despite ICD therapy?
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FIGURE 26-4 Electroanatomic maps of the left ventricle and epicardium, color-coded for bipolar and unipolar voltage. A low bipolar and unipolar voltage area is present in the left ventricular basal anteroseptal and anterior wall (A to D). The part of the epicardial low unipolar voltage area that was overlying the right ventricle is likely to be caused by the thinner right ventricular wall. The magnetic resonance imaging–derived three-dimensional scar reconstruction reveals scar in this area (E). The anterior basal wall is covered by no or little epicardial fat as visualized from the computed tomography–derived three-dimensional reconstruction of epicardial fat distribution (F).

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FIGURE 26-5 The first nine sustained monomorphic ventricular tachycardia episodes that were induced during catheter ablation. Two beats are displayed for each ventricular tachycardia episode.

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FIGURE 26-6 Electroanatomic maps of the left and right ventricles during sustained monomorphic ventricular tachycardia number 5 (A; for 12-lead electrocardiograph morphology, see Figure 36-4). The earliest activated region is displayed in red. A diastolic potential was found at the mid-septum remote from the bundle of His, as indicated by the yellow tag (B). Entrainment mapping was performed, demonstrating concealed entrainment with a postpacing interval of 280 ms, equaling the tachycardia cycle length (C). The 180-msec interval between the stimulus and the peak of lead II suggests that a small potential (black arrows) slightly before the larger potential has been captured. A radiofrequency energy application at this site resulted in slowing of the ventricular tachycardia and termination after 7 seconds.

Discussion

As demonstrated in this case, electrical storm can be life-threatening. Patients with nonischemic dilated cardiomyopathy are at high risk for ventricular tachycardia recurrence after ablation in contrast to patients after myocardial infarction.5 Two small studies suggest that this risk can be significantly reduced if patients are rendered noninducible for sustained monomorphic ventricular tachycardia.1,5 Thus it may be worthwhile to pursue complete noninducibility of ventricular tachycardia. On the other hand, ablation in close proximity to the bundle of His and the left bundle is likely to result in total atrioventricular block, particularly in patients with preexisting RBBB requiring permanent ventricular pacing, which may have deleterious effects, as outlined in the following section.
Based on inducibility by programmed electrical stimulation, diastolic potentials, and concealed entrainment, the mechanism of the ventricular tachycardia in this patient was likely reentry, and thus another part of the reentry circuit may be at a safe distance from the bundle of His and left bundle, allowing abolishment of the ventricular tachycardia without damage to the conduction system. However, this approach was not effective and several radiofrequency applications at a safe distance from the His bundle and left bundle did not abolish the ventricular tachycardia.
Iatrogenic persistent total atrioventricular block and left bundle branch block (LBBB) has been reported to occur in 16% of patients who undergo ablation of ventricular tachycardia associated with septal and anterior basal scars.3 In some patients, benefits may outweigh disadvantages. After unsuccessful ablation, patients are at high risk for ventricular tachycardia recurrence, in particular after prior electrical storm. In a study by Carbucicchio and colleagues,2 electrical storm recurred in 8 of 10 patients with ablation failure, in contrast to none of the 85 patients with complete or partial procedural success. Of 8 patients with electrical storm recurrence, 4 died suddenly despite appropriate ICD intervention. Thus ablation failure in patients with prior electrical storm seems to carry a high risk not only for recurrent electrical storm but also for sudden death even when an ICD is implanted. Based on these risks, the decision was made to target all ventricular tachycardia reentry circuits, also at the location of the proximal conduction system.

Question

In the case of total atrioventricular block after ablation of the bundle of His and left-sided proximal conduction system, is permanent right ventricular pacing likely to affect left ventricular function?

Discussion

During right ventricular pacing the ventricles are activated relatively slowly through the myocardium, instead of fast activation through the His-Purkinje conduction system in physiologic conditions. As a result, early activated regions “prestretch” late activated regions, whereas late activated regions “poststretch” early activated regions that are already in the relaxation phase. The resulting dyssynchronous contraction pattern is less effective and may reduce ventricular function. Other potential deleterious effects of right ventricular apical pacing include left ventricular remodeling, functional mitral regurgitation, and left atrial remodeling.8 In the Mode Selection (MOST) trial, which compared dual-chamber “physiologic” right ventricular apical to pure right ventricular apical pacing in patients with sinus node dysfunction,6 a strong association was found between high percentages of ventricular pacing and increased rates of heart failure hospitalization. In patients with bradycardia and a normal LVEF, Yu and associates9 demonstrated that right ventricular–apical pacing results in adverse left ventricular remodeling and a substantial reduction in the LVEF of 7.4%.
Although the adverse effects of right ventricular pacing are well-documented in patients with bradycardia and normal LVEF, only scant data exist on the effect of right ventricular pacing in patients with total atrioventricular block and moderately impaired left ventricular function in the setting of a nonischemic dilated cardiomyopathy without symptoms and signs of heart failure. In the Dual Chamber and VVI Implantable Defibrillator (DAVID) trial, patients with an implantable cardioverter-defibrillator (ICD) with LVEF 40% or less and no indication for ventricular pacing were randomized to ventricular backup pacing at 40/min or dual-chamber rate-responsive pacing at 70/min.10 The composite end point (death or heart failure hospitalization) occurred more frequently in dual chamber–paced patients than backup-paced patients (84% vs. 73%), suggesting that deleterious effects of right ventricular pacing also may apply to patients with reduced LVEF.

Question

Should right ventricular pacing or biventricular pacing be initiated in case of total atrioventricular block after ablation of the bundle of His and left bundle with preexisting RBBB?

Discussion

In patients who are not in heart failure, without the need for ventricular pacing, insufficient data exist to support a role of biventricular pacing to improve ventricular function. In patients who require frequent ventricular pacing, however, adverse effects of right ventricular pacing may be expected, as outlined earlier. In the study by Yu and colleagues,9 these deleterious effects could be prevented by biventricular pacing in patients with a normal LVEF who required a pacemaker because of bradycardia. In patients with an LVEF 40% or less, and an indication for ventricular pacing, the small Homburg Biventricular Pacing Evaluation (HOBIPACE) trial demonstrated biventricular pacing to be superior to right ventricular pacing in terms of left ventricular function, quality of life, and exercise capacity.4
This patient was considered to potentially benefit from cardiac resynchronization therapy (CRT) because female gender, nonischemic cardiomyopathy, and QRS duration greater than 150 msec consistently have been found to predict greater benefit from CRT. A positive response to CRT has been associated with a reduced risk for ventricular arrhythmia.7 Thus biventricular instead of right ventricular apical pacing may reduce the risk for recurrent ventricular tachycardia and perhaps electrical storm.
Based on the expected negative effects of right ventricular pacing and the potential higher risk for recurrent ventricular tachycardia or electrical storm, it was decided to implant a biventricular ICD in case of total atrioventricular block.

Final Diagnosis

Electrical storm resulted from sustained monomorphic ventricular tachycardia in this patient with nonischemic dilated cardiomyopathy, with ventricular tachycardia reentry circuit sites located in close proximity to the bundle of His and left bundle.

Plan of Action

The plan for this patient was to perform ablation at the location of the bundle of His and left bundle to abolish all ventricular tachycardia episodes and implant a biventricular ICD in case of total atrioventricular block.

Intervention

All episodes of ventricular tachycardia were abolished and, as expected, complete atrioventricular block occurred. A biventricular ICD was implanted, and biventricular pacing was initiated.

Outcome

During 2 years of follow-up, the patient did not develop heart failure and had no recurrence of ventricular tachycardia.

Findings

After 6 months, echocardiography was repeated. The LVEF had increased from 35% to 50%, and the left ventricular end-systolic volume had decreased from 111 mL to 61 mL. Left ventricular function and dimensions were stable during 2 additional years of follow-up, and the patient remained in New York Heart Association class I. The biventricular ICD was interrogated at 6-month intervals, with no ventricular arrhythmia recorded.

Comments

The decision to perform ablation at the location of the bundle of His and left bundle to abolish all ventricular tachycardias has resulted in arrhythmia-free survival, which would have been unlikely in the case of persistent inducibility of the ventricular tachycardia. The impressive increase in LVEF and reduction in left ventricular end-systolic volume at 6-month follow-up and the lack of symptomatic heart failure during further follow-up may be the result of biventricular pacing.

Selected References

1. Arya A., Bode K., Piorkowski C. et al. Catheter ablation of electrical storm due to monomorphic ventricular tachycardia in patients with nonischemic cardiomyopathy: acute results and its effect on long-term survival. Pacing Clin Electrophysiol. 2010;33:1504–1509.

2. Carbucicchio C., Santamaria M., Trevisi N. et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverter-defibrillators: short- and long-term outcomes in a prospective single-center study. Circulation. 2008;117:462–469.

3. Haqqani H.M., Tschabrunn C.M., Tzou W.S. et al. Isolated septal substrate for ventricular tachycardia in nonischemic dilated cardiomyopathy: incidence, characterization, and implications. Heart Rhythm. 2011;8:1169–1176.

4. Kindermann M. et al. Biventricular versus conventional right ventricular stimulation for patients with standard pacing indication and left ventricular dysfunction: the Homburg Biventricular Pacing Evaluation (HOBIPACE). J Am Coll Cardiol. 2006;47:1927–1937.

5. Nakahara S., Tung R., Ramirez R.J. et al. Characterization of the arrhythmogenic substrate in ischemic and nonischemic cardiomyopathy implications for catheter ablation of hemodynamically unstable ventricular tachycardia. J Am Coll Cardiol. 2010;55:2355–2365.

6. Sweeney M.O., Hellkamp A.S., Ellenbogen K.A. et al. Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRS duration in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation. 2003;107:2932–2937.

7. Thijssen J., Borleffs C.J., Delgado V. et al. Implantable cardioverter-defibrillator patients who are upgraded and respond to cardiac resynchronization therapy have less ventricular arrhythmias compared with nonresponders. J Am Coll Cardiol. 2011;58:2282–2289.

8. Tops L.F., Schalij M.J., Bax J.J. The effects of right ventricular apical pacing on ventricular function and dyssynchrony implications for therapy. J Am Coll Cardiol. 2009;25(54):764–776.

9. Yu C.M., Chan J.Y., Zhang Q. et al. Biventricular pacing in patients with bradycardia and normal ejection fraction. N Engl J Med. 2009;361:2123–2134.

10. Wilkoff B.L., Cook J.R., Epstein A.E. et al. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA. 2002;288:3115–3123.

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