Foreword

The Office of Health Technology Assessment (OHTA) evaluates the risks, benefits, and clinical effectiveness of new or unestablished medical technologies that are being considered for coverage under Medicare. These Assessments are performed at the request of the Health Care Financing Administration (HCFA). They are the basis for recommendations to HCFA regarding coverage policy decisions under Medicare.

Questions about Medicare coverage for certain health care technologies ared directed to HCFA by such interested parties as insurers, manufacturers, Medicare contractors, and practitioners. Those questions of a medical, scientific, or technical nature are formally referred to OHTA for assessment.

OHTA's assessment process includes a comprehensive review of the medical literature and emphasizes broad and open participation from within and outside the Federal Government. A range of expert advice is obtained by widely publicizing the plans for conducting the assessment through publication of an announcement in the Federal Register and solicitation of input from Federal agencies, medical specialty societies, insurers, and manufacturers. The involvement of these experts helps assure inclusion of the experienced and varying viewpoints needed to round out the data derived from individual scientific studies in the medical literature.

After OHTA receives information from experts and the scientific literature, the results are analyzed and synthesized into an assessment report. Each report represents a detailed analysis of the risks, clinical effectiveness, and uses of new or unestablished medical technologies considered for Medicare coverage. These Health Technology Assessment Reports form the basis for the Public Health Service recommendations to HCFA and are disseminated widely. Individual reports are available to the public once HCFA has made a coverage decision regarding the subject technology.

OHTA is one component of the Agency for Health Care Policy and Research (AHCPR), Public Health Service, Department of Health and Human Services.

• Thomas V. Holohan, M.D.
• Director
• Office of Health Technology Assessment
• J. Jarrett Clinton, M.D.
• Administrator
• Copies may be obtained at no charge from:
• Center for Research Dissemination and Liaison
• Division of Information and Publications
• AHCPR
• 5600 Fishers Lane
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• Rockville, MD 20857; (301) 443-4100

Introduction

The automatic implantable cardioverter-defibrillator (AICD) is an electronic device that is implanted in patients identified as being at high risk for sudden cardiac death (SCD) due to ventricular tachyarrhythmias (ventricular tachycardia/ventricular fibrillation, VT/VF) (1) Although the indications for AICD have not been clearly delineated, the device is commonly used in patients with primary ventricular arrhythmia, coronary artery disease with resuscitation from SCD, cardiomyopathy, or survivors of otherwise fatal cardiac arrest due to ventricular tachyarrhythmias not associated with myocardial infarction. These resuscitated patients, when evaluated during a programmed electrophysiologic study (EPS), exhibit inducible tachyarrhythmias uncontrollable by drugs or antiarrhythmic surgery.(2-7) A 1985 Public Health Service assessment of the AICD(8). concluded that in patients with inducible VT/VF during EPS, the device is safe and clinically effective. This assessment will evaluate the additional use of AICD for patients in whom arrhythmias cannot be induced.

The AICD continuously monitors heart rhythm, automatically senses malignant tachyarrhythmias, and aborts VT/VF by means of a transcardial electrical countershock (usually 25-30 J), which restores normal rhythm.(9,10)

The basic system consists of a pulse generator, sensing electrodes, and an anode and cathode used for cardioversion or defibrillation.(11-13) The device has the capability of waveform analysis, rate counting, and R-wave synchronization.(14)

In the decade since its introduction into clinical use by Mirowski in 1980, (9). and AICD has been increasingly utilized and is referred to by some clinicians as the emerging gold standard for the treatment of recurrent life-threatening VT/VF. In survivors of SCD, its use has dramatically reduced arrhythmic mortality from 27-66 (based on historical experience with alternative treatments) to approximately 2 per year.(9,15-19) There are currently more than 400 centers regularly implanting these devices in numbers now totalling more than 14,000.(20)

The original device was designed to sence and correct only ventricular fibrillation. Newer devices introduced since 1982 respond to a full range of ventricular tachyarrhythmias and include additional capabilities such as pacing, internal memory, programmability, and telemetry.(21)

Background

In the United States, more than 300,000 persons die annually outside of hospitals of presumed SCD.(22) Survivors of SCD who have no correctable cause for these events are at high risk for recurrences and are most commonly treated with pharamacologic agents.(22-27) Guidance of treatment by EPS (which delivers appropriately timed ventricular depolarization impulse to induce VT/VF) is generally accepted as te primary approach to the management of the majority of these patients.(28)

Treatment to prevent a recurrence of symptomatic VT/VF or SCD in patients with drug-resistant VT/VF has included investigational drugs, antitachycardia surgery, catheter ablation techniques, antitachycardia pacing, internal low-energy cardioversion, high-energy de-fibrillation, and the AICD.(29-31)

The induction of a sustained monomorphic ventricular tachyarrhythmia during EPS is widely accepted as being indicative of the presence of an arrhythmic substrate or pathway and a marker of increased risk of SCD.(32) However, the natural history of the inducibility of ventricular tachyarrythmia has not been well characterized, and controversy exists regarding the prognosis and optimal therapeutic approach for patients who are not inducible to VT/VF at EPS.(29,33-36) Recurrence rates of VT/VF or SCD have been reported to vary between 0 and 50.(38) The percent of noninducibility in various studies(23,32-34,37-46). can be seen in Table 1.

Table

Table 1. Noninducibility during EPS.

Some investigators(47-50). report long-term freedom from recurrent VT/VF in patients in whom arrhythmias cannot be induced, while others(2,23,31,37,41). report a high rate of such recurrences and SCD. Direct comparisons of the prognosis for patients with or without inducible VT-VF have not been made. The predictive value of the failure to induce VT/VF may well depend on differences in patient populations, the differences in the type of arrhythmia, the nature of the underlying heart disease, and the use of nonstandard-ized EPS protocols and varied therapies.(6,29,40,51,52)

Although the prognosis of patients whose arrhythmias cannot be induced during EPS is better than for those having inducible VT/VF, significant mortality exists for both groups.(23,37,41,46) There is no firm evidence that the empirical use of antiarrhythmic drugs can improve the known poor prognosis of patients with a history of VT/VF or SCD.(53) However, long-term control of VT/VF is more likely to be successful with those drugs selected during EPS using inducibility as a marker.(23) If inducibility can be suppressed by drugs during EPS, the risk for recurrent VT/VF or SCD is reduced from 25-40 to approximately 7 at 1 year and from 12-20 at 2 years to approximately 5.(41,44,45,54)

Rationale

Recognition of the significant risk of death in survivors of SCD who have noninducible arrhythmias during EPS, prompted the use of empiric drug therapy for these patients.(23,55). The most effective drug therapy, amiodarone, is associated with a 12 recurrence of VT/VF at 1 year.(6) However, the failure of such treatment to substantially reduce mortality has led to considerations of more definitive therapy including antitachycardia surgery (e.g., endocardial resection) or the AICD. Surgical therapy for those patients with an identifiable disease focus has been associated with both a high failure rate and significant morbidity and mortality.(13,56)

On the basis of success of AICD in the treatment of patients with inducible VT/VF, and in the absence of effective alternative therapies, proponents of AICD suggest that it is the treatment of choice for all patients with a history of symptomatic VT/VF or SCD without an identifiable and/or reversible cause, independent of inducibility during EPS.(3,4,15,57-61)

Review of Available Information

In a study of 38 patients who were survivors of VF, Kehoe et al(39). reported that 22 patients (58) had inducible VT at EPS and 16 patients (42) did not. It remains unclear why some patients exhibits inducibility and others do not. Patients with VF have much lower inducibility rates than those with sustained VT as the presenting arrhythmia. Ventricular fibrillation has been documented to be the proximate cause of most cases of SCD.(22,24-27) Patients with inducible arrhythmias are more likely to exhibit left ventricular (LV) dysfunction. Patients in whom arrhythmias cannot be induced are more likely to have ischemic heart disease.

Buxton et al(40). performed EPS in 172 consecutive patients with documented sustained VT or SCD. The inducibility rate was higher in VT patients (97) than in survivors of SCD (81).

Wellens et al(40). performed EPS in 100 patients divided equally into groups with a documented history of either sustained or unsustained VT. Inducibility was common in patients with a prior myocardial infarction (approximately 100), idiopathic VT (75-90), and cardiomyopathy or mitral valve prolapse (50-60). Inducibility was very difficult to achieve in patients without prior VT/VF or absent structural heart disease (approximately 10).

In evaluating the role of EPS in predicting the response to therapy in survivors of SCD, Benditt et al(41). studied 34 consecutive patients who required cardiopulmonary resuscitation and countershock. Of the four patients who were not inducible at EPS, two had a recurrence of SCD during a mean followup of 25 months. Skale et al(42). studied 62 survivors of SCD. Only 2 of the 15 patients who were not inducible at EPS had a recurrent SCD during a 22-month mean followup.

In a study of EPS in patients with idiopathic dilated cardiomyopathy (IDC), which is known to be associated with high rates of VT/VF and SCD, Milner et al(43). found that 6 of 19 patients were not inducible. There was no difference in recurrence of arrhythmia between patients who were or were not inducible (54 and 50 respectively)

In another study of EPS and the clinical outcome of patients with IDC, Poll et al(44). evaluated 47 patients who presented with VT/VF or SCD and had a mean ejection fraction of 28. Of the 23 patients who were not inducible, 9 had recurrent VT/VF or SCD during a mean followup of 18 months.

Denniss et al(62). studied the prognostic significance of inducible VT/VF in 403 survivors of acute myocardial infarction (MI) and found that inducible VT but not VF predicted a higher risk of SCD or recurrent VT/VF.

In a group of 144 patients with documented VT/VF, Henthorn et al(63). reported a very high incidence of subsequent VT/VF (46) despite noninducibility at EPS. Five of 23 patients who were not inducible had subsequent sudden death. In a study of 239 patients with VT/VF, Swerdlow et al(64). found the two strongest predictors of SCD to be a higher New York Heart Association class and the failure to identify an effective suppressive therapy during EPS.

One of the largest studies of survivors of SCD involving 119 patients showed no difference in recurrence rates between inducible and noninducible patients.(37). In another large study (108 patients), Eldar et al(23). concluded that noninducibility following SCD is not predictive of a subsequent favorable outcome. In this study, 75 inducible and 33 noninducible survivors of SCD were followed for 26 months. No differences were seen in the rates of recurrent VT or SCD (25 and 24 respectively).

During a long-term (3-year) followup of his previous study, (38). Bonnet et al(36). reported no significant difference in the rate of recurrent arrhythmias between 58 patients in whom arrhythmias were noninducible (27 patients) or unsustained (31 patients) at baseline EPS and 87 patients in whom arrhythmias were inducible.

In the largest series of patients treated with an AICD (163 patients) with the longest followup (6 years), Veltri et al(6). concluded that the risk of recurrent VT/VF or SCD in survivors of a prior SCD can not be predicted on the basis of inducibility during EPS. During a mean followup of 22 months there was approximately a 50 recurrence rate, independent of inducibility.

McLaren et al, (65). studied 59 survivors of SCD who were treated with various drug regimens. They found that a prior myocardial infarction was the only predictor of recurrent SCD in this group of patients, and noninducibility was of no predictive value for response to drug therapy.

In a review of five studies involving 186 survivors of SCD who had no inducible VT at baseline EPS, Bardy et al(66). concluded that prognosis was generally very good, averaging only a 6 rate of recurrent SCD during a mean followup of 16.5 months.

Freedman et al(45). studied 150 survivors of SCD, only 37 of whom were not inducible at EPS. The recurrence rate of VT/VF or SCD was respectively three and six times greater for inducible patients.

Wilber et al(46). evaluated EPS for the prediction of long-term outcome in 166 survivors of SCD. The 35 patients who were not inducible were significantly younger and less likely to have coronary artery disease that those with inducible VT/VF. Recurrent SCD was seen in 6 of 35 (17) noninducible patients during a mean followup of 21 months.

In a study of 124 survivors of SCD, Zheutlin et al(34). observed 40 noninducible patients who were not given prophylactic treatment during a mean followup period of 32 months. No arrhythmic recurrences were seen in 37 of 40 patients (92).

A summary of the rate of recurrent VT/VF or SCD involving patients who did not exhibit inducible arrhythmias during baseline EPS is seen in Table 2.

Table

Table 2. Prognosis for recurrence of VT/VF or SCD in patients in whom arrhythmias were not inducible during EPS.

Discussion

Although there have been no prospective, randomized clinical trials of the safety and efficacy of AICD compared with pharmacologic or other nonpharmacologic therapies, its use has been widely documented to achieve dramatically lower rates of recurrent VT/VF or SCD than any other therapy.(3,6,62,67,68) The earlier controversy concerning the optimal therapy for patients who were not inducible during baseline EPS was addressed in the previous assessment of the AICD.(8) The present assessment's data have now shown that the results of EPS have failed to reliably identify subsets of patients at high or low risk for recurrent life-threatening VT/VF based on inducibility of VT/VF. Additional experience has confirmed the thesis that the prognostic significance of noninducibility is by no means benign.(13,28,33,38,46,69) The reported incidence of recurrent VT/VF or SCD for these patients ranges from 8 to 50, and up to 50 of them die at the time of recurrence. In most series, the recurrence rate of these events in patients in whom arrhythmias cannot be induced is lower than that of patients who have inducible arrhythmias, but this rate remains significantly high, and according to some investigators, would logically obligate therapy.(6,23,52) Increasingly, some physicians are recommending AICD for patients regarded as high risk, independent of inducibility at baseline EPS, (6). and sometimes without EPS, believing that very little except the AICD can improve the prognosis of these patients (personal communication, Richard Fogoros, Allegheny General Hospital, 1990).

As a consequence of this review of the literature and an analysis of current data, the risk of recurrence of VT/VF or SCD in survivors of SCD in the subgroup of patients in whom arrhythmias cannot be induced justifies the consideration of an AICD, especially for those patients who have no other reasonable treatment options.

In response to the Federal Register notice of this assessment, (70) and the solicitation of information and opinions from individuals and groups having experience with the AICD, OHTA has received a number of letters concerning this technology:

• The University of Texas Health Science Center at Houston, Division of Cardiology (personal communication, 1989) states that AICD may be the treatment of choice for survivors of SCD not associated with an MI who are not inducible during EPS because of the significant rate of recurrence for these patients.
• The Sinai Hospital of Baltimore (personal communication, 1989) states that baseline EPS should not be a discriminant factor in the selection of AICD therapy. Patients that should not be considered for AICD are those that:

  1. Respond to drug or surgical therapy;
  2. Have incessant VT;
  3. Have class IV heart failure;
  4. Have other illnesses and a life expectancy of less than 6 months;

• The North American Society of Pacing and Electro-physiology (personal communication, 1989) states categorically that the implantation of the AICD is the treatment of choice for patients resuscitated from VT/VF with no inducible ventricular arrhythmias. Recommended patient selection criteria are as follows:

  1. Reversible causes of VT are not present.
  2. A history of cardiac arrest or hypotensive VT that is not associated with a myocardial infarction or correctable ischemic event.
  3. The patient's life expectancy is greater than 6 months.
  4. The patient is a cardiac transplant candidate.
  5. Adequate psychological resources are present.

• The Wayne State University, Division of Cardiology (personal communication, 1989) states that the AICD is the treatment of choice in noninducible patients who are survivors of SCD or VT and have cardiomyopathy, primary electrical disease, or those with arteriosclerotic heart disease and a poor ejection fraction, where an acute ischemic factor cannot be implicated.
• The University of North Carolina, Division of Cardiology (personal communication, 1989) states that because noninducibility implies the lack of a marker to assess drug therapy, this category of patient may have the greatest need for an AICD.
• The Penn State College of Medicine, Cardiology Division (personal communication, 1989) regards patients with prolonged QT syndrome who are inadequately controlled by beta-blockers and all patients with dilated cardiomyopathy as being at high-risk for VT/VF and SCD and, therefore, are considered candidates for AICD.
• The University of Utah Medical Center, Division of Cardiology (personal communication, 1989) states that the available evidence suggests that noninducibility alone should not deprive survivors of SCD of an opportunity to have an AICD.
• The Medical College of Wisconsin, Division of Cardiology (personal communication, 1989) has reviewed their experience in 106 patients with AICD who were survivors of SCD and found no difference in arrhythmic episodes or mortality between the inducible and noninducible groups during a mean followup of 27 months.
• The Mayo Clinic, Division of Cardiology (personal communication, 1989) states that in the absence of clinical data allowing selection of patients who might benefit from an AICD (i.e, a negative EPS), it remains necessary to consider this device for all survivors of SCD.
• The Minneapolis Heart Institute (personal communication, 1989) recommends the AICD for all noninducible patients in whom there are no correctable structural or metabolic faults.
• The Lahey Clinic Medical Center states (personal communication, 1989) that the implantation of an AICD in noninducible patients is most appropriate in SCD survivors who also have structural heart disease with reduced left ventricular function.
• The University of Wisconsin Medical School, Department of Medicine states (personal communication, 1989) that the lack of inducibility during EPS makes the AICD the only appropriate therapy in a situation where surgical or medical therapy cannot be instituted.
• The Hospital of the University of Pennsylvania states (personal communication, 1989) that EPS can only induce arrhythmias that develop by the mechanism of reentry. Other mechanisms causing arrhythmias resulting in SCD are associated with conditions in which inducibility will not be achieved during EPS. The lack of inducibility is a limitation of the technology of EPS and not an indication that patients are not at risk for arrhythmia. A history of prior SCD itself implies a significant risk for recurrent cardiac arrest and a consideration of an AICD.
• The University of Washington Harborview Medical Center states (personal communication, 1989) that survivors of SCD who are not inducible at baseline EPS have high-risk subgroups that are candidates for AICD. These include being male, having a history of congestive heart failure or of a remote MI, and having no Q-wave development after cardiac arrest.
• The University of Iowa, Department of Internal Medicine has noted (personal communication, 1989) that fully one quarter of patients are at risk for recurrent SCD for whom no treatment can be selected based on a negative EPS. In this group of patients, AICD implant is lifesaving by preventing recurrent cardiac arrest.
• The University of Alabama at Birmingham, Division of Cardiology states (personal communication, 1989) that because the risk of recurrent cardiac arrest is significant for survivors of SCD or those with symptomatic arrhythmias, the AICD is the treatment of choice for these individuals.
• The Vanderbilt University Medical Center Cardiac Arrhythmia Service states (personal communication, 1990) that in the absence of a reasonable reversible cause, all patients with documented sustained VT/VF or SCD are at risk for recurrence at a level that far exceeds the risk of implantation of an AICD device.
• The University of Miami School of Medicine, Division of Cardiology (personal communication, 1990) considers the following subgroups of patients who are not inducible at baseline EPS as being at high-risk for SCD: Patients with low ejection fraction (less than 30-35), those with coronary artery disease or cardiomyopathy, or those patients with long Q-interval syndrome if there is a failure of drug treatment or autonomic surgical therapy.
• The American College of Cardiology states (personal communication, 1990) that the AICD is reasonable in certain patients in whom VT/VF is not inducible during EPS. Included in the category for which they believe there is little or no controversy regarding the indications for AICD are patients who have had one or more documented episodes of hemodynamically significant VT/VF and in whom EPS and Holter monitoring cannot be used to accurately predict the efficacy of therapy, and mapping-directed therapies are not appropriate. Recurrent syncope of undetermined cause is generally not regarded as a sufficient indication for AICD.

The National Institutes of Health (NIH) concluded that the implantation of the AICD should no longer be considered a treatment of last resort and is appropriate in noninducible patients in the following circumstances:

1. Existence of a documented episode of symptomatic VT/VF or SCD unrelated to an acute myocardial infarction
2. Presence of poorly controlled myocardial ischemia at the time of the arrhythmic event or ischemia that is not medically or surgically correctable
3. Documented patient life expectancy of at least 6 months
4. Demonstration of adequate patient psychological resources

Summary

The AICD is an electronic device that is implanted in patients identified as being at high risk for SCD due to VT/VF. The AICD continuously monitors heart rhythm, senses malignant-VT/VF, and aborts the arrhythmia by means of a electronic shock. Recent clinical experience and data have indicated that the risk of recurrent VT/VF or SCD in survivors of prior episodes is significant, and that inducibility at baseline EPS cannot reliably discriminate all patients who might be at either high or low risk or who might respond to any therapy. Pharmacologic therapy, the historic first-line treatment for the prevention of recurrent VT/VF or SCD, has been shown to be less than adequate, especially for noninducible patients. The AICD is indicated in patients who are resuscitated from SCD unassociated with concurrent myocardial infarction, and in whom a sustained monomorphic ventricular tachycardia cannot be induced in the electrophysics laboratory.

The frequency of subsequent SCD can be quite high and unpredictable in patients with noninducible arrhythmias during EPS. Therefore, arrhythmia inducibility is not a rational criterion for implantation of AICD.

References

1.

Myerburg RJ, Luceri RM, Thurer R, et al. Time to first shock and clinical outcome in patients receiving an automatic implantable cardioverter-defibrillator J Am Coll Cardiol 1989 14:508–514. [PubMed: 2754136]

2.

Fogoros RN, Fiedler SB, Elson JJ. The automatic implantable cardioverter defibrillator in drug-refractory vertricular tachyarrhythmias Ann Intern Med 1987 107:635–641. [PubMed: 3662277]

3.

Manolis AS, Tan-DeGuzman W, Lee MA, et al. Clinical experience with the automatic implantable cardioverter defibrillator Am Heart J 1989 118:445–450. [PubMed: 2773768]

4.

Cannom DS, Winkle RA. Implantation of the automatic implantable cardioverter defibrillator (AICD): Practical aspects PACE 1986 9: 793–809. [PubMed: 2432482]

5.

Hargrove WC III, Josephson ME, Marchlinski FE. Surgical decisions in the management of sudden cardiac death and malignant ventricular J Thorac Cardiovasc Surg 1989 97:923–928. [PubMed: 2724998]

6.

Veltri EP, Mower MM, Mirowski M, et al. Follow-up of patients with ventricular tachyarrhythmia treated with the automatic implantable cardioverter defibrillator: Programmed electrical stimulation results do not predict clinical outcome J Electrophysiol 1989 3:467–476.

7.

Roy D, Waxman HL, Krenzle MG, et al. Clinical chroraclinistics characteristics and long-term followup follow-up in 119 survivors of cardiac arrest: Relation to inducibility at electrophysiologic testing Am J Cardiol 1983 52:969–974. [PubMed: 6637850]

8.

[no authors listed] Health Technology Assessment Report 1985 No. 16,Implantable Automatic Cardioverter Defibrillators .

9.

Mirowski M. The automatic implantable cardioverter-defibrillator: An overview J Am Coll Cardiol 1985 6: [PubMed: 3894475]

10.

Luceri RM, Thurer RJ, Palatianos GM. The automatic implantable cardioverter-defibrillator: Results, observations, and comments PACE 1986 9:1343–1348. [PubMed: 2432560]

11.

Thomas A. Automatic implantable cardioverter-defibrillator J Cardiovasc Nurs 1988 3:77–81. [PubMed: 3199163]

12.

Wood M, Ellenbogen KA. Brachyarrhythmias Bradyarrhythmias, emergency pacing, and implantable defibrillation devices Crit Care Clin 1989 5:551–568. [PubMed: 2670093]

13.

Manolis AS, Rastegar H, Estes NAM III. Automatic implantable cardioverter defibrillator. Current status JAMA 1989 262:1362–1368. [PubMed: 2668575]

14.

Deluca SA, Girard M. The automatic implantable cardioverter-defibrillator Am Fam Phys 1989 39:141–143. [PubMed: 2911954]

15.

Lehmann MH, Steinman RT, Schuger CD, et al. The automatic implantable cardioverter defibrillator as antiarrhythmic treatment modality of choice for survivors of cardiac arrest unrelated to acute myocardial infarction Am J Cardiol 1988 62:803–805. [PubMed: 3048073]

16.

Cohen AI, Wish MH, Fletcher RD, et al. The use and interaction of permanent pacemakers and the automatic implantable cardioverter defibrillator PACE 1988 11:704–711. [PubMed: 2456550]

17.

Tullo NG, Saksena S, Krol RB. Technological improvements in future implantable defibrillators Cardiology 1990 7:107–111.

18.

Borbola J, Denes P, Ezri MD, et al. The automatic implantable cardioverter-defibrillator: Clinical experience, complications and follow-up in 25 patients Arch Intern Med 1988 148: 70–76. [PubMed: 3337605]

19.

Moss AJ, Benhorin J. Prognosis and management after a first myocardial infarction N Engl J Med 1990 322:743–751. [PubMed: 2407955]

20.

[no authors listed] Cardiac Pacemakers Inc,, Minneapolis, MN. 1990.

21.

Mower MM, Reid PR, Watkins L Jr, et al. Automatic implantable cardioverter-defibrillator structural characteristics PACE 1984 7:1331–1337. [PubMed: 6209679]

22.

Liberthson RR, Nagel EL, Hirschman JC, et al. Pathophysiologic observations in prehospital ventricular fibrillation and sudden cardiac death Circulation 1974 49:790–798. [PubMed: 4828598]

23.

Eldar M, SuaveSauve MJ, Scheinman MM. Electrophysiologic testing and follow-up of patients with aborted sudden death J Am Coll Cardiol 1987 10:291–298. [PubMed: 3598002]

24.

Nikolic G, Bishop RL, Singh JB. Sudden death recorded during Holter monitoring Circulation 1982 66:218–225. [PubMed: 7083510]

25.

Kempf FC Jr, Josephson ME. Cardiac arrest recorded on ambulatory electrocardiograms Am J Cardiol 1984 53:1577–1582. [PubMed: 6731302]

26.

Panidis IP, Moganroth Morganroth J. Sudden death in hospitalized patients: Cardiac rhythm disturbances [detected] by ambulatory electrocardiographic monitoring J Am Coll Cardiol 1983 2:798–805. [PubMed: 6630760]

27.

Myerburg RI, Conde CA, Sung RJ, et al. Clinical electrophysiologic and hemodynamic profile of patients resuscitated from prehospital cardiac arrest Am J Med 1980 68:568–576. [PubMed: 7369235]

28.

Zipes DP, Akhtar M, Denes P, et al. [no authors listed] Guidelines for clinical intracardiac electrophysiological electrophysiologic studies. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee to Assess Clinical Intracardiac Electrophysiological Electrophysiologic Studies) J Am Coll Cardiol 1989 14:1827–1842. [PubMed: 2584574]

29.

Swerdlow DC, Freedman RA, Peterson J, et al. Determinants of prognosis in ventricular tachyarrhythmia in patients without induced sustained Am Heart J 1986 111:433–438. [PubMed: 3953349]

30.

Kelly PA, Cannom DS, Garan H, et al. The automatic implantable cardioverter-defibrillator: Efficacy, complications and survival in patients with malignant ventricular arrhythmias J Am Coll Cardiol 1986 1988 11:1278–1286. [PubMed: 3367002]

31.

Reid PR, Griffith LSC, Platia EV, et al. The automatic implantable cardioverter-defibrillator: Five year clinical results in Breitghart G, Brogrefe M, Zipes DP (Eds): Nonpharmacologic Therapy of Tachyarrhythmias. , New York: Futura Publishing, 1987 pp. 477–486.

32.

Wellens JHH, Brugada P, Stevenson WG. Programmed electrical stimulation of the heart in patients with life-threatening ventricular arrhythmias: What is the significance of induced arrhythmias and what is the correct stimulation protocol? Circulation 1985 72:1–17. [PubMed: 4006120]

33.

Kim SG. The management of patients with life-threatening ventricular tachyarrhythmias: Programmed stimulation or Holter monitoring (either or both)? Circulation 1987 76: 1–5. [PubMed: 3594762]

34.

Zheutlin TA, Steinman RT, Mettioni TA, et al. Long-term arrhythmic outcome in survivors of ventricular fibrillation with absence of inducible ventricular tachycardia Am J Cardiol 1988 62:1213–1217. [PubMed: 3195483]

35.

Fonger JD, Guarnieri T, Griffith LSC, et al. Impending sudden cardiac death: Treatment with myocardial revascularization and the automatic implantable cardioverter defibrillator Ann Thorac Surg 1988 46:13–19. [PubMed: 3382280]

36.

Bonnet CA, Elson JJ, Fogaros RN. Prognostic significance of noninducibility during baseline electrophysiology study vs. noninducibility during serial drug testing in cardiac arrest survivors J Am Coll Cardiol (Abs) 1990 15:

37.

Roy D, Waxman HL, Kienzel MG, et al. Clinical characteristics and long-term follow-up in the 119 survivors of cardiac arrest: Relation to inducibility at electrophysiologic testing Am J Cardiol 1983 52:969–974. [PubMed: 6637850]

38.

Bonnet CA, Elson JJ, Fiedler SB, et al. The prognostic significance of inducing nonsustained ventricular tachycardia in patients presenting with sustained ventricular tachycardia or cardiac arrest J Electrophysiol 1989 3: 435–446.

39.

Kehoe R, Tommasco C, Zheutlin T, et al. Factors determining programmed stimulation responses and long-term arrhythmic outcome in survivors of ventricular fibrillation with ischemic heart disease Am Heart J 1988 116:355–363. [PubMed: 3400561]

40.

Buxton AE, Waxman HL, Marchlinski PE, et al. Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias Circulation 1984 69:532–540. [PubMed: 6692515]

41.

Benditt DG, Benson DW, Klein GJ, et al. Prevention of recurrent sudden cardiac arrest. Role of provocative electropharmacologic testing J Am Coll Cardiol 1983 2:418–425. [PubMed: 6875106]

42.

Skale BT, Miles WM, Heger JJ, et al. Survivors of cardiac arrest: Prevention of recurrence by drug therapy as predicted electrophysiologic testing or electrocardiographic monitoring Am J Cardiol 1986 57:113–119. [PubMed: 3942053]

43.

Milner PG, DiMarco JP, Lerman RB. Electrophysiologic Electrophysiological evaluation of sustained ventricular tachyarrhythmias in idiopathic dilated cardiomyopathy PACE 1988 11:562–568. [PubMed: 2456534]

44.

Poll DS, Marchlinski FE, Buxton AE, et al. Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy Am J Cardiol 1986 58:992–997. [PubMed: 3776856]

45.

Freedman RA, Swerdlow CD, Soderhold-Difatte V, et al. Prognostic significance of arrhythmia inducibility or noninducibility at initial electrophysiologic study in survivors of cardiac arrest Am J Cardiol 1988 61:578–582. [PubMed: 3344682]

46.

Wilber DJ, Garan H, Finkelstein D, et al. Out-of-hospital cardiac arrest. Use of electrophysiologic testing in the prediction of long-term outcome N Engl J Med 1988 318:19–24. [PubMed: 3336381]

47.

Morady F, DiCarlo L, Winston S, et al. Clinical features and prognosis of patients with out-of-hospital cardiac arrest and a normal electrophysiology study J Am Coll Cardiol 1984 4:39–44. [PubMed: 6736452]

48.

Ruskin JN, DiMarco JP, Garan H. Out-of-hospital cardiac arrest: Electrophysiologic observations and selection of long-term antiarrhythmic therapy N Engl J Med 1980 303:607–613. [PubMed: 6772952]

49.

Winkle RA, Stinson EG, Echt DS, et al. Practical aspects of automatic cardioverter/defibrillator implantation Am Heart J 1984 108:1335–1346. [PubMed: 6388295]

50.

Garan H, Ruskin JN, DiMarco JP, et al. Electrophysiologic studies before and after myocardial revascularization in patients with life-threatening ventricular arrhythmias Am J Cardiol 1983 51:519–524. [PubMed: 6600577]

51.

Prystowsky EN, Miles WM, Evans JJ, et al. Induction of ventricular tachycardia during programmed electrical stimulation: Analysis of pacing methods Circulation 1986 73(Suppl 11):1132–1138. [PubMed: 3943174]

52.

Marchlinski FE, Buxton AE, Waxman HL, et al. Identifying patients at risk of sudden death after myocardial infarction: Value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction Am J Cardiol 1983 52:1190–1196. [PubMed: 6650407]

53.

Mitchell LB, Duff HJ, Manyari De, et al. A randomized clinical trial of the noninvasive and invasive approaches to drug therapy of ventricular tachycardia N Engl J Med 1987 317:1681–1687. [PubMed: 3320747]

54.

Mason JW, Winkle RA. Accuracy of the ventricular tachycardia-induction study for predicting long-term efficacy and inefficacy of antiarrhythmic drugs N Engl J Med 1980 303:1073–1077. [PubMed: 7421912]

55.

Liberthson RR, Nagel EL, Hirschman JC, et al. Prehospital ventricular defibrillation N Engl J Med 1974 291:317–321. [PubMed: 4853730]

56.

Evans GT Jr, Scheinman MM, Zipes DP, et al. Catheter ablation for control of ventricular tachycardia: A report of the percutaneous cardiac mapping and ablation registry PACE 1986 9:1391–1395. [PubMed: 2432568]

57.

Olinger GN, Chapman PD, Troup PJ, et al. Stratified application of the automatic implantable cardioverter defibrillator Thorac Cardiovasc Surg 1988 96:141–149. [PubMed: 3386288]

58.

Thurer RJ, Lucedri Luceri RM, Bolooki H. Automatic implantable cardioverter-defibrillator: Techniques of implantation and results Ann Thorac Surg 1986 42: 143–147. [PubMed: 3741011]

59.

Cox JL. Patient selection criteria and results of surgery for refractory ventricular tachycardia Circulation 1989 79:1163–1777. [PubMed: 2655975]

60.

Luderitz B, Manz M. Role of antitachycardia devices in the treatment of ventricular tachyarrhythmias Am J Cardiol 1989 61:75J–78J. [PubMed: 2596414]

61.

Fogoros RN, Elson JJ, Bonnet CA. Actuarial incidence and pattern of occurrence of shocks following implantation of the automatic implantable cardioverter defibrilliator PACE 1989 12; 1465–1473. [PubMed: 2476775]

62.

Denniss AR, Richards DA, Cody DV, et al. Prognostic significance of ventricular tachycardia and fibrillation induced at programmed stimulation and delayed potentials detected on the signal-averaged electrocardiograms of survivors of acute myocardial infarction Circulation 1986 74:731–745. [PubMed: 3757187]

63.

Henthorn RW, Mesa A, Epstein AE, et al. Prognosis of ventricular fibrillation patients with a negative electrophysiologic study: What does initial non-inducibility mean? (Abs) Circulation 1984 70:

64.

Swerdlow CD, Winkle RA, Mason JW. Determinants of survival in patients with ventricular tachyarrythmias tachyarrhythmias N Engl J Med 1983 308: 1436–1442. [PubMed: 6855814]

65.

McLaren McLaran CJ, Gersh BJ, Sugrue DD, et al. Out-of-hospital cardiac arrest in patients without clinically significant coronary artery disease: Comparison of clinical, electrophysiological, and survival characteristics with those in similar patients who have clinically significant coronary artery disease Br Heart J 1987 58:583–591. [PMC free article: PMC1277309] [PubMed: 3426894]

66.

Bardy GH, Packer DL, German LD. Utility of electrophysiologic studies in the management of tachycardia, sudden death, and syncope Ann NY Acad Sci 1984 427:16–39. [PubMed: 6378012]

67.

Kowey PR. CAST and paranoia Cardio 1990 7:3–47.

68.

Tchou PU, Kadri N, Anderson J, et al. Automatic implantable cardioverter defibrillators and survival of patients with left ventricular dysfunction and malignant ventricular arrhythmia Ann Intern Med 1988 109:529–534. [PubMed: 3262325]

69.

Buxton AE, Marchlinski FE, Waxman HL, et al. Prognostic factors in nonsustained ventricular tachycardia Am J Cardiol 1984 53:1275–1279. [PubMed: 6711427]

70.

[no authors listed] Federal Register: May 10, 1989 54:20209.

AHCPR Pub. No. 91-0041