Byron K. Lee, MD, and Jeffrey E. Olgin, MD
A 90-year-old man with a history of previous myocardial infarction (MI), coronary artery bypass surgery, and recurrent right side pleural effusions was admitted for effusion drainage. During his hospitalization, he developed sudden onset of a wide complex tachycardia (Figure 64-1) requiring cardioversion. IV amiodarone was started. Troponins were found to be borderline positive. Catheterization showed total occlusion of both the right coronary artery and a saphenous vein graft to the LAD. Although neither occlusion appeared to be acute, both vessels were stented. Following percutaneous coronary intervention, despite continued IV amiodarone and multiple external cardioversions, the wide complex tachycardia was recurrent and then became incessant. At heart rates in the 140 to 180 bpm range, he maintained his systolic blood pressure at 90 to 110 mm Hg. He was transferred to our hospital for EP study and ablation.
FIGURE 64-1 ECG of the wide complex tachycardia. There are more QRS complexes than P-wave complexes (arrow), essentially clinching that the mechanism of the wide complex tachycardia is ventricular tachycardia.
• The differential diagnosis for a wide complex tachycardia include:
Ventricular tachycardia (VT)
Supraventricular tachycardia (SVT) with aberrancy (ie, LBBB or RBBB)
Antidromicatrial ventricular reciprocating tachycardia (AVRT)
SVT with a bystander accessory pathway
• Patients with previous MI or impaired ejection fraction are at higher risk for VT.
• Paced tachycardias should have pacing spikes before each QRS.
• Antidromic AVRT and SVT with a bystander accessory pathway are seen in Wolff-Parkinson-White patients who should have a delta wave on baseline ECG.
• In this patient, VT was suspected based on the history of MI. Furthermore, there were more QRS complexes than P waves seen on the presenting ECG (see arrows in Figure 64-1), essentially clinching the diagnosis of VT. Rarely, SVTs such as AVNRT with upper common final pathway block or junctional tachycardia with retrograde block in the AVN can have more ventricular depolarizations than atrial depolarizations; however, one would not expect a wide QRS complex different than the native QRS in that case.
• For patients with incessant VT, antiarrhythmics are typically tried first to suppress the VT.
• When antiarrhythmics are not successful, emergent ablation is necessary.
• Although ICD implantation may be eventually necessary, it is not the next step in management of patients with incessant VT since it would lead to multiple shocks.
PATHOPHYSIOLOGY AND MANAGEMENT
• The patient was brought to the EP Laboratory in stable VT.
• A diagnosis of VT was confirmed with intracardiac recordings.
• Mapping of the tachycardia started in the LV since the patient had a scar in the LV from a previous anterior wall MI.
• Voltage mapping of the LV showed low voltages in the apical septum corresponding to scar from the previous MI (Figure 64-2).
FIGURE 64-2 Voltage map of the LV during VT. The gray color indicates an area of low voltage in the apical septum corresponding to scar from the previous MI.
• Activation mapping showed the VT was likely from a small circuit exiting from the mid septum basal to the scar (Figure 64-3).
FIGURE 64-3 Activation map of the LV during VT. The white color indicates that the earliest site of ventricular activation is the mid-septum just basal to the scar. The reentry circuit is exiting from this region.
• Mapping in this region discovered a site with a mid-diastolic potential (Figure 64-4), indicating that the catheter tip is at a protected area of slow conduction.
FIGURE 64-4 Activation mapping at the successful ablation site. The mid-diastolic potentials (arrows) indicate that the catheter tip is at a protected area of slow conduction, suggesting a good site for ablation.
• Pace-mapping at this site led to conduction delay and a pace map matching perfectly the clinical VT (Figure 64-5), indicating that catheter tip is in a region of slow conduction that exits from the same region as the VT.
FIGURE 64-5 Pace-mapping at the successful ablation site. Conduction delay and a perfectly matching pace map indicate that catheter tip is in a region of slow conduction that exits from the same region as the VT, suggesting a good site for ablation.
• The postpacing interval after pace-mapping matched the VT cycle length, indicating that this site was in the circuit.
• Ablation at this site promptly terminated the tachycardia. No VT was inducible after ablation.
• The patient had no recurrent VT subsequently.
• An ICD was placed prior to discharge.
FEATURES OF VENTRICULAR TACHYCARDIA IN ISCHEMIC CARDIOMYOPATHY
• VT in ischemic cardiomyopathy is typically due to a reentrant circuit involving the scar from a previous MI.
• When the VT is stable (not leading hemodynamic collapse), ablation of the targeted VT is successful in 71% to 79% of patients.1-5
• Three-dimensional mapping and more powerful ablation catheters have improved the ablation of VT.
• After acutely successful VT ablation, 31% of patients during follow-up of 9 to 25 months have recurrence of either the original VT or a new VT.1-5
• It is controversial whether patients with ischemic cardiomyopathy and ejection fraction >35% who have had successful VT ablation should get an ICD.1-3
• Even though the recurrence rate of VT is relatively high after ablation, most VT recurrences are not fatal.1-3
• ICDs are very effective in terminating VT. Frequently, the ICD can terminate the VT with antitachycardic pacing rather than a shock that might cause pain.
• Patients with frequent or incessant VT, even if they meet guidelines for ICD implantation will need therapy for the VT (either drugs or ablation) to prevent frequent ICD shocks.
1. Borger van der Burg AE, de Groot NM, van Erven L, Bootsma M, van der Wall EE, Schalij MJ. Long-term follow-up after radiofrequency catheter ablation of ventricular tachycardia: a successful approach? J Cardiovasc Electrophysiol. 2002;13(5):417-423.
2. Delacretaz E, Stevenson WG. Catheter ablation of ventricular tachycardia in patients with coronary heart disease. Part II: Clinical aspects, limitations, and recent developments. Pacing Clin Electrophysiol. 2001;24(9 Pt 1):1403-1411.
3. Della Bella P, De Ponti R, Uriarte JA, et al. Catheter ablation and antiarrhythmic drugs for haemodynamically tolerated post-infarction ventricular tachycardia; long-term outcome in relation to acute electrophysiological findings. Eur Heart J. 2002;23(5): 414-424.
4. Nabar A, et al. Echocardiographic predictors of survival in patients undergoing radiofrequency ablation of postinfarct clinical ventricular tachycardia. J Cardiovasc Electrophysiol. 2002;13(1 Suppl):S118-121.
5. Strickberger SA, et al. A prospective evaluation of catheter ablation of ventricular tachycardia as adjuvant therapy in patients with coronary artery disease and an implantable cardioverter-defibrillator.Circulation. 1997;96(5):1525-1531.