Europace (2000) 2, 346–349 doi:10.1053/eupc.2000.0122, available online at http://www.idealibrary.com on
CASE REPORT
Prevention of recurrent ventricular fibrillation by ventricular rate stabilization W. Grimm, J. Hoffmann, V. Menz and B. Maisch Clinical Electrophysiology Laboratory, Cardiology Division, Department of Medicine, Hospital of the Philipps-University of Marburg, Marburg, Germany
This report describes a post-infarct patient with recurrent ventricular fibrillation in the absence of acute ischaemia, in whom arrhythmia recurrences could be prevented by ventricular rate stabilization of a third-generation cardioverter defibrillator. Review of the literature and clinical implications are discussed.
Introduction The high efficacy of implantable cardioverter defibrillators for termination of ventricular tachyarrhythmias by overdrive pacing, cardioversion or defibrillation has been well documented[1–4]. In contrast to overdrive pacing, cardioversion and defibrillation therapy for termination of sustained ventricular tachyarrhythmias, little information is available regarding the role of pacing in tachycardia prevention. This report describes a patient with recurrent ventricular fibrillation in whom arrhythmia recurrences were prevented by ventricular rate stabilization provided by the implantable cardioverter defibrillator (Medtronic Gem 7227Cx). The ventricular rate stabilization feature of this device has been described in detail elsewhere[5]. Briefly, ventricular rate stabilization was designed to eliminate long pauses following short ventricular intervals. Ventricular rate stabilization (programmable ‘on’ or ‘off ’) is based on a programmable minimum interval and an incremental value. When the duration of an interval following a premature ventricular complex exceeds the previous interval plus the programmable interval incremental Manuscript submitted 20 September 1999, revised 23 June 2000, and accepted 28 June 2000. Correspondence: Wolfram Grimm, MD, Philipps-University Marburg, Department of Cardiology, Baldingerstrasse, 35033 Marburg, Germany. 1099–5129/00/020346+04 $35.00/0
(Europace 2000; 2: 346–349) 2000 The European Society of Cardiology Key Words: Implantable defibrillator, ventricular fibrillation, rate stabilization.
value, a series of ventricular pacing pulses is delivered. As soon as the ventricular rate stabilization pacing slows to the intrinsic heart rate or to the programmed antibradycardia pacing rate, the implantable cardioverter defibrillator returns to normal operation[4].
Case report A 72-year-old post-infarct patient with a history of documented ventricular fibrillation in the absence of acute myocardial infarction underwent implantation of an implantable cardioverter defibrillator Model Medtronic Gem 7227Cx at our hospital in February, 1998. The postoperative course was uneventful and the patient was discharged from hospital with the ventricular rate stabilization feature of the implantable cardioverter defibrillator programmed ‘on’. The 3-month routine implantable cardioverter defibrillator follow-up visit revealed no spontaneous arrhythmias and the ventricular rate stabilization feature was programmed ‘off’. All other features of the device as well as the patient’s medication remained unchanged. The patient returned to our defibrillator outpatient department on 2 September, 1998, and on 11 November, 1998 for device interrogation after he experienced spontaneous implantable cardioverter defibrillator shocks which were not preceded by angina. Stored electrograms showed 2000 The European Society of Cardiology
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(a) Ventricular flutter (300–350 bpm)
Short–long–short sequence (420–810–430 ms)
V S
V S 8 2 0
V S 4 2 0
V S 8 1 0
V T T T F F F F F F F F F F F F F F F F F F V V V V V V VV V V V V V V V V V V S S S S S S S S S S S S S S S S S S S S S DS S S S S S S S S S S S S S S S S S 4 2 2 2 1 1 1 2 2 2 2 2 2 1 2 1 1 1 2 1 1 1 1 1 1 1 1 1 1 11 2 2 2 1 1 2 2 1 1 1 3 8 4 6 7 9 8 0 2 0 0 0 1 9 1 7 7 9 0 8 8 8 8 8 8 8 7 6 9 47 0 0 1 7 9 1 0 5 8 8 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 00 0 0 0 0 0 0 0 0 0 0 VF Rx 1 Defib.
Continuous
35 Joules shock
V V V V V V V V V V V V V V V V V V V V V V V V V V V VC V V C S S S S S S S S S S S S S S S S S S S S S S S S S S S SE RS D 1 1 2 1 1 1 1 1 1 11 2 1 1 1 1 1 1 2 1 1 2 11 2 11 3 1 1 8 7 1 8 8 8 8 8 8 85 1 8 7 8 9 9 9 2 7 5 2 59 0 689 2 5 8 0 0 0 0 0 0 0 0 0 00 0 0 0 0 0 0 0 0 0 0 0 00 0 000 0 0 0
V S 8 1 0
V S 4 0 0
V S 3 6 0
V S 3 7 0
V S 3 5 0
V S 3 7 0
V S 3 7 0
V S 3 7 0
V S 3 8 0
34.7 J
Figure 1
(a).
two episodes of sustained polymorphic ventricular tachycardia which were preceded by short–long–short intervals in the absence of ventricular rate stabilization by the device (Fig. 1). Laboratory tests after each implantable cardioverter defibrillator discharge revealed normal electrolyte levels ,including potassium and magnesium. Recurrent myocardial infarctions as a cause of these two ventricular tachycardia episodes could be ruled out by repeated determination of normal values of cardiac enzymes in the absence of changes in the 12-lead echocardiogram. QT intervals and rate-corrected QT intervals were also found to be normal in the 12-lead ECG in the absence of antiarrhythmic drug treatment. Since both episodes of polymorphic ventricular tachycardia leading to implantable cardioverter defibrillator shocks were triggered by short–long–short sequences as shown in Fig. 1, the ventricular rate stabilization feature was programmed ‘on’ again on November 11, 1998. Throughout the following 15 months, the patient remained completely free of ventricular tachycardia until the patient died at home in February 2000 due to end-stage heart failure. The patient’s medication during follow-up included an angiotensin-converting enzyme
inhibitor, diuretics and digitalis for treatment of heart failure symptoms, and coumadin for prevention of thromboembolic events in the presence of severely depressed left ventricular function. Importantly, the patient did not receive class I or class III antiarrhythmic drugs at any time during follow-up. In addition, the patient did not receive -blocker therapy because of the presence of chronic obstructive lung disease.
Discussion This report demonstrates that preventive pacing with ventricular rate stabilization by third-generation implantable cardioverter defibrillators may be a highly effective tool to prevent recurrent ventricular tachycardia in selected patients in whom ventricular tachycardia is triggered by short–long–short intervals. Short–long–short intervals have been described to precede sustained ventricular tachycardia or ventricular fibrillation in 14–64% of patients in whom the tachycardia onset was documented by Holter ECG or device stored ECG[6–10]. An increase in the dispersion of Europace, Vol. 2, October 2000
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(b) Ventricular flutter (300–350 bpm)
Short–long–short sequence (370–860–460 ms)
V S 4 3 0
V S 6 4 0
V S 3 7 0
V P 8 6 0
V V F F F F F F F F F F F F F F F F F F V V V V V VV V V V V V V V V V V V V V V V S S S S S S S S S S S S S S S S S S S D S S S S S SS S S S S S S S S S S S S S S S 4 3 2 1 2 2 1 1 1 2 1 1 1 2 1 1 1 1 1 1 1 1 1 1 11 1 1 1 1 1 1 1 1 1 1 2 2 1 1 1 1 1 3 1 2 8 0 0 9 9 9 0 9 9 9 0 7 8 8 7 7 7 7 6 7 7 87 5 7 7 7 7 7 9 7 6 5 1 0 6 9 8 7 7 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 00 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 VF Rx 1 Defib.
Continuous
35 Joules shock
V V V V V V V V V V V V V V V V VV V V V V V V V V V V V V V V V V V V V V V V VC V V C S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S SE R S D 4 3 3 3 3 4 4 4 1 1 1 1 1 11 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 1 2 1 2 1 1 1 1 1 4 1 1 6 0 9 8 9 8 1 0 5 7 7 7 6 6 69 2 8 7 7 7 8 5 8 7 4 9 7 0 7 6 7 7 9 8 0 7 6 8 7 1 1 5 7 3 0 0 0 0 0 0 0 0 0 0 0 0 0 00 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 34.4 J
Figure 1
(b).
Figure 1 Stored electrograms showing two episodes of spontaneous ventricular flutter in a patient with a Medtronic Gem 7227Cx defibrillator. Of note, both episodes were initiated by short–long–short sequences while the ventricular rate stabilization feature of the implantable cardioverter defibrillator was programmed ‘off ’. Subsequently, the ventricular rate stabilization feature was programmed ‘on’ and the patient remained free of arrhythmias during the next 15 months of follow-up.
ventricular refractoriness caused by short–long–short intervals is thought to be the major mechanism by which short–long–short intervals facilitate induction of reentrant ventricular arrhythmias in the late myocardial infarction period[11]. As in the present case, with recurrent rapid polymorphic ventricular tachycardia as shown in Fig. 1, short–long–short sequences have been found to be a trigger of polymorphic ventricular tachycardia or ventricular fibrillation more often than monomorphic ventricular tachycardia[8,11]. The clinical utility of rate-smoothing pacing techniques for the prevention of monomorphic ventricular tachycardia in patients with a remote myocardial infarction as the arrhythmogenic substrate is limited by the observation that the majority of these monomorphic ventricular tachycardias are not initiated by short–long–short intervals[9,10]. In addition, many factors besides short–long–short intervals contribEuropace, Vol. 2, October 2000
ute to arrhythmogenesis in the human heart including the type and severity of the arrhythmogenic substrate, influences of the autonomic nervous system, ischaemia, wall stress, electrolyte status and antiarrhythmic drugs. Therefore, a single preventive therapeutic tool such as ventricular rate stabilization in third-generation implantable cardioverter defibrillators is unlikely to prevent ventricular arrhythmias in the majority of implantable cardioverter defibrillator patients with any certainty. Nevertheless, the present case report suggests that selected patients may benefit from this new preventive therapeutic tool of third-generation implantable cardioverter defibrillators. Prospective multicentre studies[12] are currently underway to clarify the role of rate-smoothing algorithms for ventricular tachycardia prevention in implantable cardioverter defibrillator recipients.
Rate stabilization for prevention of ventricular fibrillation
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[7] Bayes de Luna A, Coumel P, Leclercq J. Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases. Am Heart J 1989; 117: 151–9. [8] Gomes JA, Alexopoulos DSL, Deshmukh P, Fuster V, Suh K. The role of silent ischemia, the arrhythmic substrate and the short-long sequence in the genesis of sudden death. J Am Coll Cardiol 1989; 14: 1618–25. [9] Roelke M, Garan H, McGovern BA, Ruskin JN. Analysis of the initiation of spontaneous monomorphic ventricular tachycardia by stored intracardiac electrograms. J Am Coll Cardiol 1994; 23: 117–22. [10] Meyerfeldt U, Schirdewan A, Wiedemann M, Schuett H, Zimmermann F, Luft FC, Dietz R. The mode of onset of ventricular tachycardia. A patient-specific phenomenon. Eur Heart J 1997; 18: 1956–65. [11] El-Sherif N, Gough WB, Restivo M. Reentrant ventricular arrhythmias in the late myocardial infarction period: mechanism by which a short–long–short cardiac sequence facilitates the induction of reentry. Circulation 1991; 83: 268–78. [12] Fromer M, Wietholt D, on behalf of the Prevent Investigators. Algorithm for the prevention of ventricular tachycardia onset: The Prevent Study. Am J Cardiol 1999; 83: 45D–47D.
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