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Electrophysiology Corner
Incessant Ventricular Tachycardia
June 2002
Intractable ventricular tachyarrhythmias (IVTA) have been defined as frequent, recurrent and recalcitrant ventricular tachyarrhythmias and/or ventricular fibrillation (VF), which may result in significant symptoms potentially associated with hemodynamic compromise.1 IVTA is classically associated with a poor prognosis.2 We present a multi-tiered approach utilizing advanced cardiac life support guidelines, current pharmacological regimens, ventricular burst pacing with overdrive suppression, intra-aortic balloon counterpulsation (IABCP), coronary revascularization and implantable cardioverter defibrillator (ICD) insertion to successfully achieve a favorable outcome.
Case Report. An 87-year-old woman with a history of myocardial infarction and aortocoronary artery bypass graft surgery [saphenous vein grafts to the left anterior descending coronary artery (LAD) and right coronary artery (RCA) with subsequent insertion of the left internal mammary artery (LIMA) into the occluded LAD graft] was referred for evaluation of near syncope secondary to ventricular tachycardia (VT). The patient presented to the hospital with palpitations, nausea, vomiting, lightheadedness, dizziness and diaphoresis in VT. Synchronized cardioversion successfully terminated the VT to normal sinus rhythm (Figure 1). She later ruled in for a non-ST segment elevation myocardial infarction and was transiently placed on intravenous lidocaine. Her home medications included digoxin, levothyroxine, atenolol and an enalapril/hydrochlorothiazide combination. A left heart catheterization was performed on the third hospital day; it showed severe native triple vessel disease, with a widely patent LIMA to LAD insertion and RCA graft. The proximal LAD had a 70% stenosis just prior to the insertion of the first diagonal. Left ventriculography showed a calculated ejection fraction of 29% with moderate to severe global hypercontractility. Since the patient was without chest pain, percutaneous coronary intervention was not performed at this time.
Upon arrival at the electrophysiology laboratory on the fourth hospital day, the patient was in relatively asymptomatic incessant VT with a right bundle branch morphology at a cycle length of 280 ms, which was terminated by ventricular overdrive pacing (Figure 2). The VT was then induced via stimulation requiring cardioversion for termination. The patient was loaded with 150 mg intravenous amiodarone and sent to the coronary care unit for monitoring. She was started on an intravenous amiodarone load of 900 mg over 24 hours and an oral load of 400 mg amiodarone four times daily.
During the night, the patient developed a hemodynamically stable, morphologically identical VT. The tachycardia did not respond to 2 additional intravenous 150 mg boluses of amiodarone and 75 mg of intravenous lidocaine. The patient eventually became hemodynamically unstable and required synchronized cardioversion, which only transiently terminated the VT (200 J, 200 J, 300 J, 360 J, 360 J, respectively). During the periods when the VT broke, an underlying junctional rhythm with a heart rate of approximately 40 beats per minute was present. A transvenous ventricular pacing wire was inserted via the left subclavian approach into the right ventricle and ventricular burst pacing was performed at a cycle length of 270 ms terminating the VT into asystole (Figure 3). Ventricular pacing at a cycle length of 800 ms was promptly initiated, but failed to suppress the tachycardia. Burst pacing was again employed at the same cycle length with termination of the VT followed again by asystole. Complete suppression of the VT was achieved via titration of ventricular pacing to a cycle length of 600 ms (ventricular overdrive suppression). IABCP was used to minimize myocardial oxygen demand and treat potential ischemia. The patient was stable without recurrent VT with IABCP, ventricular pacing at 100 beats per minute, and amiodarone.
Due to the recurrent and incessant nature of the VT and suppression thought partially due to IABCP, the patient underwent successful stenting of the proximal LAD leading into the insertion of the first diagonal artery (Figure 4). On the tenth hospital day, the patient underwent a repeat electrophysiology study. The patient had easily inducible VT with both a left bundle branch pattern (cycle length of 560 ms) and a right bundle branch pattern (cycle length of 500 ms) both terminated with ventricular overdrive pacing (Figure 5). An implantable cardioverter-defibrillator was inserted the following day and the patient was discharged on amiodarone 400 mg orally per day.
Discussion. IVTA have been defined as frequent, recurrent and recalcitrant ventricular tachyarrhythmias and/or VF, which may result in significant symptoms potentially associated with hemodynamic compromise.1 Assessment of the patient with IVTA mandates an investigation into its etiology including a detailed history and physical examination (including potential culprit medications), a 12-lead electrocardiogram, serum laboratory values (electrolytes), a drug screen (if warranted), and a work-up of myocardial ischemia.2
Monomorphic VT usually has a reentrant mechanism and may be suppressed by intravenous antiarrhythmic drug therapy. If the VT is hemodynamically unstable, prompt cardioversion/defibrillation is the first-line treatment. Lidocaine may be useful in the peri-infarct setting; however, its first-line use has recently been surpassed by amiodarone, a class III antiarrhythmic drug (potassium channel blocker).3–7 This medication in combination with lidocaine (or its oral congener mexiletine, a class IB drug, or sodium channel blocker) can help suppress arrhythmias that are refractory to single dose regimens. Other antiarrhythmic drugs and drug combinations have a secondary role in the management of IVTA.7–12
In experienced hands, external antitachycardia (burst) pacing is another method for terminating stable IVTA without electrical cardioversion/defibrillation. Ahern et al.13 reported the use of bedside external burst pacing for termination of sustained monomorphic recurrent VT via temporary transvenous pacing leads in the critical care setting. Over 3,000 VT episodes were successfully terminated over a 25-day period in 8/10 patients who previously failed a number of antiarrhythmic medications (mean, 4 medications) and required electrical cardioversion.
The treatment of choice for IVTA may be direct intervention to alter the substrate; however, safety must be the foremost consideration.14 In hemodynamically stable patients, radiofrequency catheter ablation (RFA) may be useful in reducing the frequency and potentially eliminating the IVTA. This option is preferred over ablative surgery for substrate alteration in select patients in whom the benefits of this procedure outweigh the potential risks. The success rate of RFA in VT in patients with structural heart disease ranges from 45–75%.1,15,16
Lee et al.17 demonstrated a 67% non-inducibility rate for VT post-surgical cryoablation; however, an 8% operative mortality rate was noted. Shumway et al.18 reported similar results.
Persistently inducible and poorly tolerated VT not amenable to RFA can be successfully treated with an implantable cardioverter-defibrillator. However, because it delivers multiple shocks without preventing recurrence, its use is contraindicated as a sole therapeutic option.15
IABCP has been shown to increase peak aortic diastolic pressure and to decrease peak left ventricular systolic pressure, therefore augmenting coronary blood flow and myocardial oxygen supply as well as reducing wall tension and oxygen demand. However, arrhythmia termination has also been demonstrated in patients with normal coronary arteries. Other mechanisms include a reduction in adrenergic drive and perhaps via mechano-electrical feedback. The latter mechanism states that ectopy and tachycardia increase with increasing afterload, whereas increasing preload results in a reduction of action potential duration and spontaneous depolarization.19
Hanson et al.20 reported an 86% improvement and 55% total resolution of post-infarction VT/VF in 22 patients with IABCP. Bolooki et al.21 noted 50% resolution and survival in a group of 24 patients with VT/VF after IABCP. Fotopoulos et al.19 reported a reduced frequency of VT/VF and stabilization of overall medical condition in 18/21 patients with medically resistant ventricular arrhythmias using IABCP. Furthermore, in all 10 patients in the series with IVTA, IABCP terminated the arrhythmia. Patients with severely impaired ventricular function with arrhythmia suggesting end-stage cardiac failure and those in whom arrhythmia itself or the administration of antiarrhythmic drugs compromised a normally stable hemodynamic state appeared to most likely benefit from IABCP in the setting of VT/VF. Similarly, left ventricular assist devices (load-bearing assist devices) have been reported to stabilize refractory ventricular arrhythmias in patients awaiting cardiac transplant, but data are limited.22
Improved medical regimens, ICDs and RFA have reduced the need for surgical management of IVTA (most notably, endocardial resections and other map-directed surgical procedures).23 Dor et al.24 reported on 100 patients with either left ventricular aneurysm or large apical scar resection and endoventricular patch repair. Cryotherapy was also performed in 37 of the patients who had pre-operative ventricular arrhythmia. Hospital mortality was 12%, but all survivors had significant improvement in left ventricular function and ventricular arrhythmias.
Conclusion. This case illustrates a multi-tiered approach to the treatment of incessant ventricular tachycardia. IVTA is classically associated with a poor prognosis.2 Utilizing advanced cardiac life support guidelines, current pharmacological regimens, ventricular burst pacing with overdrive suppression, intra-aortic balloon counterpulsation (IABCP), coronary revascularization and implantable cardioverter-defibrillator insertion achieved a favorable outcome.
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