The case for explantation of the automatic implantable cardioverter-defibrillator

The case for explantation of the automatic implantable cardioverter-defibrillator

1210 BRIEF REPORTS VTl3OBPM/CL460 cw I AICD DISCHARGE NSR II 1037 BD FIGURE 2. Discharge of the automatic implantable cardioverterdefibrillator ...

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VTl3OBPM/CL460 cw




1037 BD FIGURE 2. Discharge of the automatic implantable cardioverterdefibrillator (AICD) during chest wall stimulation. Discharge is synchronous with the chest wall stimulus. The chest wall stimulus artifact can be seen superimposed on the patient’s ventricular tachycardia (VT). The sudden deflection corresponding to the AICD discharge is simultaneous with and thus obscures the chest wall stimulus artifact. CL = tachycardia cycle length in milliseconds; CWS = chest wall stimulation; NSR = normal sinus rhythm.

The delivery of asynchronous cardioversion is a potentially important difficulty [Fig. 2). In a prior report, the AICD typically required about 5 seconds, [range 3.4 to 7.8) to sense an arrhythmic event.j Once sensed the device is committed to a discharge, which will not occur for the additional 5 to 15 seconds re-

The Case for Explantation of the Automatic Implantable Cardioverter-Defibrillator PETER R. KOWEY, MD TED D. FRIEHLING, MD ROGER A. MARINCHAK, MD RUTH ANN KLINE, RN JANE L. STOHLER, RN LOUISE A. YEAGER, RN


e cared for a patient whose malignant ventricular arrhythmia improved as a result of a remission of the underlying cardiac disease. Based on a thorough reevaluation, we recommended not replacing her pulse generator after battery depletion. This case illustrates the importance of periodic reevaluation of the need for device therapy. A 58-year-old woman was well until Iuly 3984, when she began to have symptoms of congestive heart failure and idiopathic dilated cardiomyopathy was diagnosed. During hospitalization, she had syncope caused by a very rupid monomorphic ventricular From the Cardiac Arrhythmia Service, Department of Medicine, Medical College of Pennsylvania, 3300 Henry Avenue, Philadelphia, Pennsylvania. This study was supported in part by a grant from the Fannie Rippel Foundation, Madison, New ]ersey. Manuscript received October 6, lY86; revised manuscript received and accepted December 19, lY86.

quired to charge the capacitors6 Thus, most events will be sensed in less than 8 seconds, but the device will rarely respond within this period. This provides a relatively safe window for chest wall stimulation, lasting about 8 seconds, during which the AICD becomes committed to shock. Chest wall stimulation terminated within this window will no longer be present when the AICD charge cycle is complete and synchronization occurs, resulting in cardioversion appropriately synchronized to the QRS complex. All recent cardioversions have been performed synchronously using this approach. 1. Mirowski M. ‘The automatic impluntable cardioverter-defibrilJator: an overview. jACC 1985;6:461-466. 2. Ruffy R, Smith P. Laseter M, Lal R, Kim SS. Out-of-hospital automatic cardioversion of ventricular tachycardia. [ACC 1~85:6:482-485. 3. Kim SC. Furman S, Mates ]A. Waspe LE, Brodman R, Fisher ID. Automatic implantable cardioverter/defibriIlotor: inadvertent discharge during permanent pacemaker magnet tests. PACE, in press. 4. Langer A, Heilman MS, Mower MM, Mirowski M. Considerations in the development of the automatic implantable defibrillator. Med Instrument 1976:1U:lti3-167.

5. Winkle RA, Bach SM. Echt DS. Swerdlow CD, Imran M, Mason ]W, Oyer PE, Stinson EB. The automatic implantable defibrillator: local ventricular bipolar sensing to detect ventricular tachycardia and fibrillation. Am 1 Cardiol 1~83:5~%i-27t~. 6. Intec Systems, Inc. Physician’s manual AID-H implantable defibrillator. April, 1982.

tachycardia. She was resuscitated, but had recurrences despite treatment with various antiarrhythmic agents. Electrophysiologic testing was carried out and included introduction of up to 3 extrastiumuli at multiple ventricular sites (including the left ventricle) during multiple cycle lengths of drive and no ventricular arrhythmia was induced. Several investigational drugs, including amiodarone, were administered, to no avail. The patient was then referred to our hospital for implantation of an automatic implantable cardioverter-defibrillator (AICD). Two epicardial patches and rate-sensing electrodes were inserted through a median sternotomy without complication. The device was tested by inducing ventricular fibrillation using alternating current. Defibrillation threshold was 10 to 35 1 less than than the maximum energy of the AICD (30 I]. The patient made an uneventful recovery and no further episodes of spontaneous arrhythmia were observed despite the cessation of all antiarrhythmic therapy. Two months after discharge, the patient, although asymptomatic, received a series of 4 defibrillator shocks without loss of consciousness. She returned to the hospital and the device was deactivated. Nonsustained ventricular tachycardia lasting up to 6 seconds was observed during monitoring, associated with palpitations but not loss of consciousness. A11repetitive ventricular ectopic activity was suppressed with lidoCaine or tocainide. The device was reactivated, tocainide therapy was continued, and the patient had no further shocks. Over the next year, exercise tolerance improved and the patient gradually resumed normal activities. Ejection fraction, which had been 15% during the acute illness, increused to 56%. 7’he patient under-

May 1. 1987




Volume 59


went elective cholecystectomy during that year without complications. AICD evaluation during this time showed satisfactory battery and capacitor function. Because of the patient’s clinical recovery, an assessment of the continued need for the device and for antiarrhythmic drugs was arranged. This evaluation was performed 20 months after implantation and consisted of 5 days of computerized monitoring in a cardiac telemetry unit, 48 hours of ambulatory monitoring, exercise testing and repeat electrophysiologic testing, all carried out in a drug-free state. Rare g-beat salvos of a slow polymorphic ventricular rhythm were observed on monitoring. The patient exercised for more than 9 minutes on a Bruce protocol, and ventricular ectopy was mostly overdriven. Programmed stimulation using up to 3 extrastimuli at 2 right ventricular sites during multiple cycle lengths of drive yielded no inducible ventricular arrhythmia. Based on these results, we discontinued antiarrhythmic therapy and considered device deactivation or removal. However, the patient requested that the AICD be left in place and in an active state and simply not replaced at AICD end of life. Four months later, the patient was readmitted to hospital after receiving 7 consecutive AICD discharges. She denied symptoms compatible with an arrhythmia before, during or after the device discharges. In-hospital monitoring with the device deactivated again revealed infrequent salvos of nonsustained ventricular tachycardia. After device reactivation, no arrhythmia was provoked with exercise, nor did the device fire inappropriately. Since AICD discharge was likely due to nonsustained ventricular tachycardia, and there was no evidence of a sustained or life-threatening arrhythmia, strong consideration was again given to generator deactivation or removal. However, the patient wished to continue with the original plan to leave the device in place and in an active state and not to replace it at end of life. Tocainide therapy was restarted to suppress the nonsustained arrhythmia.

lar arrhythmia in these patients is prone to marked variability, remission is difficult to prove.4 The improvement in our patient’s symptomatic state and left ventricular function led us to suspect that the arrhythmia substrate had changed. This conclusion was supported by a comprehensive evaluation, which included both invasive and noninvasive testing. The encouraging results of these studies were corroborated by a long symptom-free interval. Our decision to reevaluate the need for the AICD was also motivated by a desire to spare our patient the complications of long-term device therapy that occur in many patients.5 Our patient had received several shocks as a result of nonsustained ventricular tachycardia that required chronic antiarrhythmic drug therapy.6 Because we could find no tendency for development of sustained arrhythmia, the AICD was providing little benefit and in fact was causing significant disability. In lieu of having the capability to reprogram the AICD to a longer sensing period, a potentially toxic antiarrhythmic drug was required to suppress an arrhythmia that was not in itself life-threatening. Furthermore, without hard evidence of arrhythmia remission, generator replacement would have been required, with the attendant risks of another surgical procedure. In effect, the results of our arrhythmia evaluation obviated some of the problems inherent in chronic use of a sophisticated antitachycardia device, but not all, since device discharge continued thereafter. Psychological considerations provided an added impetus to reassessthe continued need for device therapy. Our patient had been an active, independent woman who had raised a family and pursued a career. After AICD implantation, she became dependent on friends and family members, especially since operating a motor vehicle had been proscribed. She was further plagued by fear of loss of consciousness but was greatly relieved to have objective evidence of arrhythmia remission and particularly pleased to have the opportunity to return to gainful employment.

An antitachycardia device is implanted only after a painstaking evaluation, which includes the systematic evaluation of conventional and investigational antiarrhythmic drugs and consideration of surgical therapy.l Using this approach, investigators have conclusively proved that the AICD improves patient survival and quality of life.2 However, experience with these devices is relatively recent and the question of arrhythmia improvement has not been addressed. Very little has been published regarding remission of cardiac arrhythmia. Ventricular tachycardia induced in the electrophysiology laboratory in patients with coronary artery disease is chronically reproducibleP Our patient had malignant ventricular arrhythmia unrelated to coronary artery disease. Since spontaneous ventricu-

1. Reid PR. Griffith LSC, Mower MM, Platia EV. Watkins L, Juanteguy J, Mirowski M. Implantable cardioverter-defibriIlator: patient selection and imolantation protocol PACE 1984:7:1338-1344. 2. Mirowski h. Reid PR, Mower’MM, Watkins L, Platia EV, Griffith LSC, Guanieri T, Thomas A, Juanteguy JM. Clinical performance of the implantable automatic defibrillator. PACE 1984;7:1345-1350. 3. Schoenfeld MH, McGovern B. Garan H, Ruskin JN. Long-term reproducibility of responses to programmed cardiac stimulation in spontaneous ventricular tachyarrhythmias. Am J Cordial 1984;54:564-568. 4. Pratt CM, Delclos G, Wierman AM, Mahler SA, Seals AA, Leon CA, Young JB, Quinones MA, Roberts R. The changing base line of complex ventricular arrhvthmias. A new consideration in assessine lone-term antiarrhvthmic drug’therapy. N Engl J Med 1985;313:1444-144;. ” 5. Marchlinski F, Flores BT. Buxton AE, Hargrove C. Addonizio VP, Stephenson LW, Harken AH, Doherty JU, Grogan Efi. Josephson ME. The automatic implantable cardioverter-defibrillator: efficacy, complications, and device failures. Ann Intern Med 1986;104:481-488. 6. Chapman PD. Troup P. The automatic implantable cardioverter-defibrillatar: evaluating suspected inappropriate shocks. JACC 1986;7:1075-1078.