Clinical characteristics and long-term follow-up in 119 survivors of cardiac arrest: Relation to inducibility at electrophysiologic testing

ARRHYTHMIAS AND CONDUCTION DISTURBANCES

Clinical Characteristics and Long-Term Follow-Up in 119 Survivors of Cardiac Arrest: Relation to lnducibilityat ElectrophysiologicTesting DENIS ROY, MD, HARVEY L. WAXMAN,

MD, MICHAEL G. KIENZLE, MD,

ALFRED E. BUXTON, MD, FRANCIS E. MARCHLINSKI, MD, and MARK E. JOSEPHSON, MD

Electrophysiologic studies were performed in 119 survivors of cardiac arrest. Sustained ventricular arrhythmias were initiated by programmed ventricular stimulation in 72 patients (61%). Coronary artery disease patients with induced sustained ventricular arrhythmias had a higher incidence of prior myocardial infarction (95 versus 72%) and ventricular aneurysm (59 versus 26 % ) and a lower ejection fraction (37 versus 50% ) than those with no inducible sustained ventricular arrhythmias. Of the 72 patients with inducible ventricular arrhythmias, 11 (15 %) died suddenly during a mean follow-up of 16 months (range 15 days to 56 months). In this group, 6 of 41 patients (15 % ) discharged on a successful antiarrhythmic regimen and 5 of 27 patients (19%) discharged on an unsuccessful regimen or without a predischarge study have died suddenly. Of these 27 patients, 1 of 12 patients treated with amiodarone and 4 of 15 (27%) with conventional antiarrhythmic therapy died suddenly.

The remaining 4 patients died of nonarrhythmic causes in the postoperative period. Of 47 patients without inducible sustained ventricular arrhythmias, 15 (32%) died suddenly at a mean follow-up of 20 months, 10 (34%) with and 15 (26%) without empiric therapy. It is concluded that sustained ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Patients with inducible arrhythmias have greater left ventricular dysfunction than those without inducible arrhythmias. Medical or surgical therapy that prevented the induction of sustained ventricular arrhythmias was predictive of a successful outcome in 65% of the patients. Patients with persistence of inducible sustained ventricular arrhythmias despite conventional drug therapy and patients without inducible arrhythmias in whom therapy cannot be guided by electrophysiologic testing have a higher incidence of recurrent sudden death. (Am J Cardiol 1963;52:969-974)

Survivors of out-of-hospital cardiac arrest who are discharged without treatment or receive empiric antiarrhythmic therapy have a high risk of recurrent sudden death.1-4 Recently, several investigators have demon-

strated that using programmed ventricular stimulation, ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Furthermore, it has been suggested that electrophysiologic testing can identify survivors of cardiac arrest who require antiarrhythmic therapy and predict which antiarrhythmic regimen is likely to prevent recurrent sudden death.5-g However, the benefits of this approach have been evaluated in relatively few patients and follow-up periods have often been short. This study describes the clinical and electrophysiologic characteristics and long-term follow-up in 119 survivors of cardiac arrest, relates these findings to inducibility or noninducibility of sustained ventricular arrhythmias by electrophysiologic testing, and determines if therapy guided by electrophysiologic testing

From the Clinical Electrophysiology Laboratory, Hospital of the University of Pennsylvania, Cardiovascular Section, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania. This study was supported in part by grants from the American Heart Association, Southeastern Pennsylvania Chapter, Philadelphia, Pennsylvania, and grant #HL24278 from the National Heart, Lung, and Blood Institute. Bethesda, Maryland. Manuscript received February 18, 1983; revised manuscript received July 11, 1983, accepted July 12. 1983. Address for reprints: Mark E. Josephson, MD. 656 Ravdin Building, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104.

969

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ELECTROPHYSIOLOGIC

TABLE I

STUDIES

ARREST

SURVIVORS

Cardiac Dkagnosis in Patients with Inducible and Noninducible Sustained Ventricular Arrhythmias

Atherosclerotic coronary artery disease Myocardial infarction Left ventricular aneurysm Cardiomyopathy Rheumatic heart disease Mitral valve prolapse Long QT syndrome Wolff-Parkinson-White syndrome Hypertensive cardiovascular disease Coronary arterial spasm No heart disease

is effective tients.

OF CARDIAC

in the long-term

Inducible (72 Patients)

Noninducible (47 Patients)

56 (76%)

29 (62%)

53 (95%)

2; 1;;;; 0

“f (!j9%) 3

: 4 2

0” 2

:,

!

1 4

management

of these pa-

Methods Patients: Electrophysiologic studies were performed between July 1976 and December 1981 in 119 consecutive patients resuscitated from cardiac arrest. Patients were excluded from this study if the cardiac arrest occurred in the setting of an acute (572 hours) myocardial infarction. There were 84 men and 35 women, aged 16 to 75 years (mean 55). Organic heart disease was present in 112 patients (Table I). The earliest arrhythmia recorded at the time of any cardiac arrest was ventricular fibrillation (VF) in 70 patients (59%) and ventricular tachycardia (VT) in 34 (28%). In 15 patients (13%), the arrhythmia was not documented before cardioversion. Thirty-three patients had >l cardiac arrest; in 23,11 multiple arrests occurred in the hospital. The cardiac arrest occurred in the hospital in 21 of the 86 remaining patients who had only 1 arrest. Overall, the earliest arrhythmia observed in the 44 patients with in-hospital cardiac arrest was VF in 20 patients (45%) and VT in 23 (52%); in 1 patient the arrhythmia was not documented before cardioversion. At the time of the initial cardiac arrest 63 patients were receiving antiarrhythmic medication. Electrophysiologic studies: After they gave informed written consent, the patients underwent electrophysiologic testing in the nonsedated, postabsorptive state. Antiarrhythmic agents were discontinued 24 to 48 hours before the control study in 116 patients. Procainamide was continued for the control of recurrent and rapid ventricular arrrhythmias in 3 patients. Three or more electrode catheters were inserted percutaneously or by venous cutdown and positioned in the heart under fluoroscopic guidance. Routinely, quadripolar catheters were positioned in the high right atrium, coronary sinus, right ventricular apex and a tripolar catheter at the atrioventricular junction for His bundle recording. Our protocol used during programmed ventricular stimulation has been previously described.lO Stimulation techniques for initiating ventricular arrhythmias during control and subsequent studies included the introduction of 1, 2 or 3 ventricular extrastimuli during sinus rhythm or ventricular pacing at multiple cycle lengths from the right ventricular apex. The introduction of 3 ventricular extrastimuli was routinely performed only in the 70 patients studied after July 1979. Rapid ventricular pacing at cycle lengths of 400 to 250 ms was also performed for 10 to 30 seconds. If VT was not induced by these techniques, stimulation was performed at the right ventricular outflow tract. In 14 patients, right ventricular stimulation was also repeated during isoproterenol

infusion (increasing sinus rate to 100 to 150 beatsimin). Left ventricular stimulation was performed in 34 patients in whom right ventricular stimulation had failed to initiate sustained ventricular tachyarrhythmias. Electrical stimulation was performed with a specially designed digital stimulator and isolated constant current source (Bloom Associates, Ltd). The stimuli were rectangular pulses 1 ms in duration at twice diastolic threshold. Intracardiac recordings were filtered at 30 to 500 Hz and simultaneously recorded with 3 electrocardiographic leads (I, aVF and VI). Ventricular tachyarrhythmias were defined as sustained if they lasted longer than 30 seconds or required termination by programmed stimulation or cardioversion because of hemodynamic compromise. Ventricular tachycardias were considered nonsustained if they persisted for 4 beats or more and if they terminated spontaneously within 30 seconds. Patients with inducible, sustained ventricular tachyarrhythmias underwent short- or long-term drug studies, or both, using a method previously described in detail.‘* Serial electrophysiologic studies were performed with conventional drugs (procainamide, quinidine, disopyramide, phenytoin, propranolol or lidocaine) or experimental antiarrhythmic agents (mexiletine, aprindine or amiodarone), alone or in combinations. Plasma drug concentrations, if available, were measured after acute intravenous administration and after long-term oral therapy. Therapy was determined effective if the sustained ventricular arrhythmia observed at the time of the control study could no longer be induced by programmed ventricular stimulation. In 22 patients with inducible sustained ventricular arrhythmias, a successful drug regimen could not be found and in each, surgical treatment was attempted. The surgical procedures included 1 or more of the following: left ventricular endocardial resection, left ventricular aneurysmectomy and coronary artery bypass grafting. Endocardial excision guided by endocardial and epicardial mapping has been described previously.“*‘” Patients without inducible sustained ventricular arrhythmias were empirically treated with drugs (22 patients), treated surgically (7 patients), or were discharged without antiarrhythmic therapy (18 patients). The surgical procedures in this group included coronary artery bypass grafting, left ventricular aneurysmectomy, left ventricular endocardial excision and septal myotomy. Statistical analysis of the data was performed using an unpaired Student t test or chi-square test. Data are expressed as mean f standard deviation.

Results Electrophysiologic results: Sustained ventricular tachyarrhythmias were initiated in 72 of 119 survivors of cardiac arrest (61%). The induced arrhythmia was VT in 63 patients (of uniform morphology in 45 and multiple morphologies or polymorphic in 18 patients), and VF in 9. Spontaneous degeneration into VF occurred in 8 of the 63 patients with inducible VT. The mean VT cycle length was 277 ms (range 190 to 530). Sustained ventricular arrhythmias were initiated by right ventricular stimulation in 63 patients, and required 1 premature stimulus in 10 patients, 2 premature stimuli in 38 (during isoproterenol infusion in l), 3 premature stimuli in 14 and rapid ventricular pacing in 1 patient. Left ventricular stimulation was required in 9 patients, with 2 premature stimuli in 2 patients, 3 premature stimuli in 4 (during isoproterenol infusion in 1) and rapid ventricular pacing in 3 (Table II). The

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TABLE II

Ventricular Stimulation Protocol in Patients with and Without Inducible Sustalned Ventricular Arrhythmlas Inducible (72 patients)

Right ventricular stimulation 1,2VESRVP 3 VES Left ventricular stimulation 1,2VESRVP 3 VES t isoproterenol RVP = rapid ventricular

:: 14 : 4 2

pacing; VES = ventricular

Noninducible (47 patients) 22 15

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TABLE Ill

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Relation Between Clinical and Induced Ventricular Arrhythmia

Earliest Rhythm at Cardiac Arrest

No. of Cases

VF

70

2: 15

No. of Cases

Induced Rhythm ZLstained VT (degeneration to VF in 5) l’$;~e;uwd VT

;: extrastimuli.

induced arrhythmias were terminated by 1 premature stimulus in 2 patients, 2 premature stimuli in 3, rapid ventricular pacing in 19, 1 extrastimulus after a burst of rapid ventricular pacing in 1 patient, cardioversion in 42 patients and thump-version in 1 patient; in 4 patients the arrhythmias terminated spontaneously. In 47 patients no sustained ventricular arrhythmias were induced by programmed stimulation. The stimulation protocol in these 47 patients included the delivery of 3 premature stimuli in 17 patients and 2 extrastimuli and/or rapid ventricular pacing in 30. Left ventricular stimulation was performed in 25 patients and isoproterenol was administered in 12 (Table II). A maximum of 3 repetitive ventricular responses were observed in 36 of these patients. Nonsustained VT was induced in 11 patients. The tachycardias terminated spontaneously within 6 seconds in 10 patients and lasted 23 seconds in 1 patient. The nonsustained tachycardias were of uniform morphology in 7 patients and were polymorphic in 4. Relation between clinical and induced ventricular arrhythmias (Table III): Sustained ventricular arrhythmias were initiated in 36 of 70 patients (51%) whose earliest arrhythmia recorded at the time of cardiac arrest was VF. Nonsustained VT was induced in 8 patients and 53 complexes were observed in the other 26 patients who had VF at the time of cardiac arrest. Sustained ventricular arrhythmias were induced in 26 of 34 patients (76%) in whom VT was documented during cardiac arrest. Nonsustained VT was induced in 2 of these patients and 13 complexes were observed in the other 6. Sustained VT was initiated in 10 of 15 patients (67%) whose arrhythmia at the time of cardiac arrest was not documented. Nonsustained VT was induced in 1 patient and 13 complexes were induced in 4 patients. Clinical and anatomic characteristics in relation to inducibility or noninducibility of sustained ventricular arrhythmias: The cardiac diagnosis in patients with and in patients without inducible sustained ventricular arrhythmias is shown in Table I. Hemodynamic catheterization was performed in 96 patients, 61 with and 35 without inducible sustained ventricular arrhythmias. Patients with inducible arrhythmias did not have a significantly higher incidence of atherosclerotic coronary artery disease than those with noninducible sustained ventricular arrhythmias (78% versus 62% of patients) and the extent of coronary

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T

Not recorded

34

15

VF Sustained VT (degeneration to VF in 1) Nonsustained VT 13 beats Sustained VT (degeneration to VF in 2) f$rrpe;swd VT

2; 6 26 2:

: 10

: VF = ventricular

fibrillation;

VT = ventricular

tachycardia.

artery disease was similar in both groups of patients (2.2- versus 2.3-vessel disease). However, coronary artery disease patients with inducible arrhythmias had a higher incidence of prior myocardial infarction than patients with noninducible arrhythmias (95 versus 72% of patients, p <0.02) and a higher incidence of left ventricular aneurysm (59 versus 28% of patients, p <0.02). A few patients with miscellaneous cardiac diseases or no heart disease were found in both groups. Mean ejection fraction was lower in patients with than in those without inducible sustained ventricular arrhythmias (37 f 17% versus 50 f 16%, p
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;;EDlSCHARGE

SUDDEN

DEATHS

ALIVE

FIGURE 1. Outcome in 72 patients with inducible sustained ventricular arrhythmias at control electrophysiologic study. EPS = electrophysiologic study; I = inducible: ND = not done; NI = noninducible.

Management of follow-up in patients with inducible sustained ventricular arrhythmias (Fig. 1): Fifty of the 72 patients with inducible sustained ventricular arrhythmias were treated medically. Antiarrhythmic drug therapy prevented the induction of sustained ventricular arrhythmias in 24 of these patients. Eighteen patients remained with inducible sustained ventricular arrhythmias despite serial drug evaluations and were discharged on amiodarone therapy or a drug regimen that slowed the tachycardia or rendered its induction more difficult. A predischarge electrophysiologic study was not performed in 8 medically treated patients. Twenty-two patients in whom medical therapy had failed to prevent the induction of sustained ventricular arrhythmias were treated surgically. Left ventricular endocardial resection was performed in 20 patients, 17 of whom also had coronary artery bypass grafting. Coronary bypass grafting alone was done in 2 patients. Postoperative electrophysiologic testing failed to induce sustained ventricular arrhythmias in 17 patients (3 patients also receiving antiarrhythmic drugs). Persistence of inducible ventricular arrhythmias was observed in 1 patient, and 4 patients died of nonarrhythmic causes 1 to 4 weeks after surgery. Overall, patients with inducible sustained ventricular arrhythmias were followed for 17 months (range 15 days to 58 months). Eleven patients (15%) had recurrent sudden death, 14 (19%) died of nonarrhythmic causes (congestive heart failure in 5 patients, myocardial infarction in 3, postoperative deaths in 4 and cancer in 2), and 48 patients are alive. There have been 4 (17%) recurrent sudden deaths among the 24 patients discharged on a drug regimen that prevented the induction of ventricular arrhythmias. One patient was resuscitated from VF 2 weeks after he was discharged on beta-blockade therapy. He was thereafter treated with amiodarone and is alive without recurrent sudden death at 17 months of follow-up. There have been 2 sudden deaths (12%) among the 17 surgically treated patients in whom sustained ventricular arrhythmias were not induced postopera-

in i

’

15

j/

FIGURE 2. Outcome in 47 patients with no inducible sustained ventricular arrhythmias during the control study. MED/SURG Rx = medically or surgically treated patients; No Rx = patients discharged with no antiarrhythmic therapy.

tively. One patient died suddenly 4 months after undergoing left ventricular endocardial resection during exercise and associated with chest pain, and the second patient died of VF 15 days after coronary bypass grafting. There have been 4 sudden deaths (22%) among the 18 medically treated patients in whom suppression of inducible sustained ventricular arrhythmias was not achieved. Nine of the 18 patients were receiving amiodarone therapy, only 1 of whom died suddenly (after 13 months). The surgically treated patient with persistence of inducible sustained ventricular arrhythmias is alive without recurrent sudden death at 17 months of follow-up. There has been 1 sudden death (at 3 months of follow-up) among the 8 medically treated patients who did not undergo a predischarge electrophysiologic study. The other 7 patients are alive without recurrent sudden death. Three of these patients are treated with amiodarone. Thus, 6 of 41 patients (15%) discharged on antiarrhythmic drug or surgical therapy that prevented the induction of sustained ventricular arrhythmias died suddenly after a mean follow-up of 18 months (range 15 days to 58 months). In comparison, 5 of 27 patients (19%) discharged on an unsuccessful antiarrhythmic regimen or without a predischarge electrophysiologic study died suddenly at a mean follow-up of 16 months (range 1 to 57). Management and follow-up of patients with no inducible sustained ventricular arrhythmias (Fig. 2): Twenty-two of the 47 patients with noninducible sustained ventricular arrhythmias were discharged on antiarrhythmic drug therapy chosen by the referring physician. Nine of these patients died suddenly, 1 patient died of congestive heart failure and 12 patients are alive after a mean follow-up of 18 months (range 1 to 54). Seven patients underwent surgical treatment. Unguided left ventricular endocardial resection was performed in 3 patients (2 of whom also had coronary artery bypass grafting) with left ventricular aneurysm

November 1, 1983

and recurrent cardiac arrest. Coronary bypass grafting alone was done in 2 patients with severe multivessel disease. One patient underwent left ventricular aneurysmectomy and 1 patient had septal myotomy. This last patient, who had idiopathic hypertrophic cardiomyopathy, died suddenly 9 months after surgery. Three patients died of congestive failure and 3 are alive after a mean follow-up of 26 months (range 15 days to 60 months). Eighteen patients were discharged without antiarrhythmic therapy. Twelve of these patients had ischemic heart disease and were discharged on beta-blocking agents alone. Ant&rhythmic therapy was discontinued in 6 patients in whom the cardiac arrest was thought to be drug-induced. In this group of patients, 5 died suddenly, 2 died of congestive heart failure, 1 died of cancer and 10 are alive after a mean follow-up of 20 months (range 1 to 42). None of the 5 sudden deaths occurred in patients who had nonsustained VT induced. Thus, 10 of 29 patients (34%) who received antiarrhythmic medical or surgical therapy and 5 of 18 patients (28%) who received no therapy died suddenly (difference not significant). Among these 15 patients, a maximum of 3 repetitive ventricular responses was initiated in 10 patients and nonsustained VT was induced in 5 patients. Overall, there have been 15 (32%) sudden deaths and 7 (15%) nonarrhythmic deaths, and 25 patients (53%) are alive after a mean follow-up of 20 months (range 15 days to 60 months). Discussion Comparison with previous studies: This study shows that rapid and poorly tolerated sustained ventricular arrhythmias can be initiated by programmed ventricular stimulation in 61% of survivors of cardiac arrest not associated with an acute myocardial infarction. Ruskin et al6 reported that ventricular arrhythmias could be induced by programmed stimulation in 25 of 31 survivors (81%) of cardiac arrest. If our nonsustained tachycardias were included, our incidence would be similar (70%). However, sustained ventricular arrhythmias were initiated in only 13 (42%) of the patients studied by Ruskin et al. This difference in the frequency of induction of sustained ventricular arrhythmias can be explained by the different stimulation protocols used. Left ventricular stimulation, the delivery of 3 ventricular extrastimuli and isoproterenol were not used in any of the patients studied by Ruskin et al. Excluding these techniques from our stimulation protocol, sustained ventricular arrhythmias would have been initiated in only 47 of our patients (39%). In our study, the arrhythmia responsible for the cardiac arrest was considered noninducible only after this more rigorous stimulation protocol failed to initiate a sustained ventricular arrhythmia. We believe that the induction of brief and spontaneously terminating ventricular arrhythmias cannot necessarily be considered a reproduction of the patient’s lethal arrhythmias, particularly with such vigorous stimulation. The specificity and sensitivity of short polymorphic runs of VT is unknown. Therefore, the suppression of these arrhythmias was not considered a therapeutic endpoint for this study.

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The frequency of induction of sustained ventricular arrhythmias was highest among patients with VT as the initiating mechanism for the cardiac arrest. Furthermore, patients with inducible sustained ventricular arrhythmias had greater left ventricular dysfunction and a higher incidence of intraventricular conduction defects than patients without inducible ventricular arrhythmias. These findings confirm earlier observations from this laboratory and reemphasize the association between a fixed anatomic substrate and the induction of sustained ventricular arrhythmias by electrophysiologic stimulation.5 Relation of inducibility or noninducibility to outcome: Recent studies have suggested that survivors of cardiac arrest in whom VT or VF cannot be induced at control electrophysiologic testing are unlikely to experience recurrent sudden death. Ruskin et al7 reported that 14 survivors of cardiac arrest without inducible ventricular arrhythmias were discharged without antiarrhythmic therapy and have not had recurrent sudden death at 15 months of follow-up. Kehoe et al8 described 16 similar patients who remain free of recurrent sudden death at 14 months of follow-up. Our findings differ from these observations. Fifteen of our 47 patients (32%) without inducible sustained ventricular arrhythmias have died suddenly at a mean follow-up of 20 months. This incidence of recurrent sudden death among noninducible patients is similar to the 30 to 40% incidence reported in earlier clinical studies1,314 of survivors of cardiac arrest. The high incidence of sudden death was not changed by treatment in our noninducible patients and was observed in both treated (34%) and untreated (28%) patients. The incidence of recurrent sudden death was not significantly higher in patients with nonsustained VT (5 of 11 patients) compared with patients without inducible ventricular arrhythmias (10 of 36 patients). Although a complete stimulation protocol was not performed in all patients, patients without inducible sustained ventricular arrhythmias actually underwent a more aggressive stimulation protocol than those with inducible sustained arrhythmias (Table III). Therefore, it is unlikely that our results are due to inadequate stimulation techniques in the noninducible group. The protocol used by Ruskin et al7 only included the use of 2 extrastimuli and bursts of pacing, which were performed in all our patients. Thus, discrepancies in stimulation protocol cannot explain differences in our study and theirs. Tommaso et all” subsequently reported that acute ischemia probably precipitated the cardiac arrest in their 16 patients, all of whom underwent coronary bypass surgery. Thus, their patient population is not comparable to ours. Recently, Benson et al9 also reported recurrent sudden death in 2 young survivors of cardiac arrest who had no inducible ventricular arrhythmias. We believe that the inability to initiate ventricular arrhythmias and to test the effect of therapy contributes to the high incidence of recurrent sudden death in these patients. In our series, the lowest incidence of recurrent sudden death was observed in patients in whom medical or surgical therapy prevented the induction of sustained ventricular arrhythmias. In this group of 41 patients,

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ELECTROPHYSlOLOGlC

STUDIES

OF CARDIAC

ARREST

SURVIVORS

6 (15%) died suddenly and 35 (85%) had no recurrences at a mean follow-up of 18 months. This finding is similar to the incidence of predicted success that has been reported in medically and surgically treated patients with recurrent, sustained VT.i4 However, the incidence of recurrent sudden death was only slightly higher in the group of patients discharged with persistence of inducible ventricular arrhythmias or without a predischarge electrophysiologic study. In this group, 5 of 27 patients (19%) died suddenly at a mean follow-up of 16 months. Twelve of these 27 patients were receiving amiodarone treatment, only 1 of whom died suddenly. Recent studies have shown that the clinical response to amiodarone cannot be accurately predicted from the laboratory response.15Js Therefore, if we exclude the amiodarone-treated patients, 4 of 15 patients (27%) discharged with persistence of inducible ventricular arrhythmias or without electrophysiologic reevaluation had recurrent sudden death. These observations suggest that amiodarone can be effective in preventing recurrent sudden death and probably contributes to the relatively low incidence of recurrent sudden death among patients discharged with persistence of inducible ventricular arrhythmias. Conclusions: Sustained VT or VF could be initiated by programmed ventricular stimulation in 61% of survivors of cardiac arrest. Medical or surgical treatment that prevented the induction of sustained ventricular arrhythmias predicted a successful outcome in 85% of patients. We believe that electrophysiologic studies can be useful in identifying and treating this subset of survivors of cardiac arrest. Patients with persistence of inducible sustained ventricular arrhythmias despite conventional drug therapy and patients without inducible ventricular arrhythmias in whom therapy cannot be guided by electrophysiologic testing are more likely to experience recurrent sudden death. Further

studies are needed to determine if amiodarone therapy is effective in preventing recurrent sudden death in these patients. References 1. Liberthson RR? Nagel EL, HIrschman JC, Nussenfeld SR. Prehospital ventricular defibrillation. Prognosis and follow-up course. N Engl J t&d 1974;291:317-321. 2. Baum RS, Alvarez H Ill, Cobb LA. Survival after resuscitation from outof-hospital ventricular fibrillation. Circulation 1974;50:1231-1235. 3. Cobb LA, Baum RS, Alvarez H Ill, Schaffer WA. Resuscitation from outof-hospital ventricular fibrillation: 4-year follow-up. Circulation 197552:suppl lll:lll-223-111-228 4. Schaffer WA, Cobb LA. Recurrent ventricular fibrillation and modes of death in survivors of out-of-hospital ventricular fibrillation. N Engl J Med 1975; 293:259-282. 5. Josephson ME, Horowitz LN, Splelman SR, Greenspan AM. Electrophysrologic and hemodynamic studies in patients resuscitated from cardiac arrest. Am J Cardiol 1980;48:948-955. 8. Ruskln JN, DlMarco JP, Garan H. Out-of-hospital cardiac arrest: electrophysiologic cbswvatfcns and selection of long-term antiarrhythmic therapy. N Engl J Med 1980;303:807-613. 7. Ruskln JN, Garan H, DlYarco JP, Kelly E. Electrophysiologic testing in survivors of prehospital cardiac arrest: therapy and long term follow-up (abstr). Am J Cardiol 1982;49:958. 8. Kehoe RF, Moran JM, Zheallln T, Tommaso C, Lesch M. Electrophysiologic study to direct therapy in survivors of prehospital ventricular fibrillation (abstr). Am J Cardiol 1982;49:928. 9. Benson DW Jr, Hessfort WT, Zavoral JH, Bendftt DG. Sudden cardiac arrest in young adults: clinical and electrophysiological findings (abstr). Am J Cardiol 1982:49:928. 10. Horowfiz LN; Josephson ME, Farrhldl A, Splelman SR, Michelson EL, GreensPan AM. Recurrent sustained ventricular tachycardra. 3. Role of the electrophysiologic sttxfy in selection of antianhythmic regimens. Circulation 1978;58:988-997. 11. Josephson ME, Harken AH, Horowltr LN. Endocardial excision: a new surgical technique for tie treatment of recurrent ventricular tachycardia. Circulation 1979:80:1430-1439. 12. Hceowftz LN, Ha&en AH, Kasfor JA, Josephson ME. Ventricular resection guided by epicardial and endocardial mapping for treatment of recurrent ventricular tachycardia. N Engl J Med 1980;302:589-593. 13. Tommase D, Kehoe R, Eheutlin T. Survivors of ischemic mediated sudden death-clinrcal angiographic and electrophysiologic features and response to therapy (abstr). Circulation 1982;88:suppl ll:ll-25. 14. Waxman HL, Sadowskl LM, Horownz LN, Harken AH, Josephson ME. Electrophysiologic study to guide medical and surgical therapy of sustained ventricular tachycardia: long term predictive values (abstr). Circulation 1981;84:suppl IV:IV-240. 15. He r JJ, Prystowsky EN, Jackman WM, Naccarelll GV, Warfel KA, RlnP enberger RL, Zl~es DP. Amiodarone. Clinical efficacv and electrophysiology-during longterm therapy for recurrent ventricular tachycardia or ventricular fibrillation. N Engl J Med 1981;305:539-545. 18. Waxman HL, Groh WC, Marchlkwkl FE, Buxton AE, Badowskl LM, Horowitz LN, Josephson ME, Kaslor JA. Amiodarone for control of sustained ventricular tachyarrhythmias: clinical and electrophysiologic effects in 51 patients. Am J Cardiol 1982;50:1088-1074.