Electrophysiologic testing in the management of survivors of out-of-hospital cardiac arrest

ARRHYTHMIAS AND CONDUCTION DISTURBANCES

Electrophysiologic Testing in the Management of Survivors Of Out-of-Hospital Cardiac Arrest FRED MORADY, MD, MELVIN M. SCHEINMAN, MD, DAVID S. HESS, MD, RUEY J. SUNG, MD, EDWARD SHEN, MD, and WILLIAM SHAPIRO, MD

Forty-five patients survived a cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation (VF). Programmed ventricular stimulation was performed with the patients taking no antiarrhythmic medications. Sustained VT was induced in 26 patients ( 5 8 % ) and nonsustained VT in 8 (18%). With treatment aimed at the underlying heart disease (plus empiric antiarrhythmic therapy in 2 patients), the 11 patients who had no inducible VT have had no recurrence of symptomatic VT or cardiac arrest over a follow-up period of 19 :E 9 months (mean 4standard deviation). Conventional antiarrhythmic drugs suppressed the induction of VT and were used for chronic treatment in 9 of 34 patients (26 % ) with inducible VT. Three of these 9 patients had recurrent VT or sudden death, whereas 6 have had no recurrence over follow-up of 20 -t- 7 months. In the 25 of 34 patients in whom the induction of VT was not

suppressed by conventional antiarrhythmic drugs, 23 were treated with amiodarone (daily dose 550 4- 120 mg), and 2 underwent coronary artery bypass grafting with either aneurysmectomy or map-directed endocardial resection. One of the latter 2 patients died suddenly 12 months after surgery. Among the 23 patients treated with amiodarone, 2 had fatal VT or sudden death and 21 ( 9 1 % ) did not, over 18 -I- 14 months of follow-up. In survivors of a cardiac arrest, the chief value of electrophysiologic testing is in identifying patients without inducible VT, who appear to have a low risk of recurrent sudden death with treatment directed at the underlying heart disease. Serial electropharmacologic testing with conventional antiarrhythmic drugs is disappointing, with a low incidence of arrhythmia suppression.

Of patients who have survived an episode of out-ofhospital cardiac arrest, 29 to 74% have been reported to have inducible VT with programmed ventricular stimulation. 1-3 Only 1 study has reported long-term follow-up events in patients who had aborted cardiac arrest and in whom chronic antiarrhythmic therapy was based on the results of electropharmacologic testing. Ruskin et al 2 reported no recurrence of cardiac arrest over a mean follow-up of 15 months in 19 patients treated with drugs that suppressed the induction of VT. We performed electrophysiologic testing in 45 survivors of out-of-hospital cardiac arrest; the results of therapy guided by electropharmacologic drug testing are reported herein.

Methods Forty-five patients (Table I) survived an out-of-hospital episode of cardiac arrest. The earliest rhythm documented before direct-current cardioversion was VF in 30 and VT in 12; in 3 patients the rhythm before direct-current cardioversion was not documented. At the time of the cardiac arrest, '31 of 45 patients had been taking 1 of the following antiarrhythmic drugs orally: quinidine, 0.8 to 1.2 g/day; procainamide, 2 to 3 g/day; disopyramide, 0.6 g/day; or phenytoin, 300 mg/day. In addition, 14 patients were taking propranolol, 80 to 240 mg/day. Coronary angiography was performed within 3 weeks of the episode of aborted cardiac arrest in 31 of 45 patients, including 26 of 36 patients who had ischemic heart disease. Left ventricular (LV) ejection fraction was determined either by contrast or radionuclide angiography in 41 of 45 patients. Patients with evidence of a new myocardial infarction in association with the episode of aborted cardiac arrest were excluded from the study. In addition, patients with the congenital long Q-T syndrome were excluded because of the previous finding that programmed ventricular stimulation seldom results in VT induction in these patients.4

From the Department of Medicine and the Cardiovascular Research Institute, University of California, San Francisco. Manuscript received June8, 1982; revised manuscript received August 27, 1982, accepted August27, 1982. Address for reprints: Fred Morady, MD, Room 573, Moffitt Hospital, San Francisco, California 94143.

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Electrophysiologic study protocol: After informed consent had been obtained, an electrophysiologic study was performed 5 days to 6 weeks after the episode of cardiac arrest. All antiarrhythmic medications were discontinued for at least 4 half-lives before electrophysiologic study. Studies were performed in the fasting, unsedated state. Two quadripolar electrode catheters were inserted percutaneously into a femoral vein; i was positioned across the tricuspid valve for recording the His bundle electrogram, and the other was positioned against the apex of the right ventricle. In patients undergoing left ventricular stimulation, a bipolar electrode catheter was inserted percutaneously into a femoral artery and positioned against the apex of the left ventricle. Electrocardiographic leads V1, I, and III and intracardiac electrograms were recorded using a VR-12 Electronics for Medicine recorder. Ventricular stimulation was performed with 2 ms pulses, delivered by a programmable stimulator (Bloom) at a constant current of 5 mA. The following stimulation protocol was used. Right vantricular drive was instituted at a cycle length of 500 ms and diastole was scanned with 1, 2, and then 3 extrastimuli. Short bursts of right ventricular overdrive pacing were then performed at cycle lengths of 600 to 300 ms. If VT was not induced with right ventricular stimulation, left ventricular stimulation was performed, except in 1 patient who had a prosthetic aortic valve and 3 patients we studied early in our experience. In patients who did not have ischemic heart disease, if VT was not induced with this protocol, ventricular stimulation was repeated during continuous infusion of i to 5/~g/min of isoproterenol, titrated to maintain a heart rate of 120 beats/min. In patients who did not have inducible VT, a standard atrial pacing protocol was used to rule out rapid supraventricular tachycardia as a cause of cardiac arrest. Sustained VT was defined as VT at least 30 seconds in duration or requiring direct-current cardioversion or overdrive pacing for termination. Nonsustained VT was defined as VT of 6 beats to 30 seconds in duration. Eleetropharmacologic testing: Drugs were tested based on each patient's history of drug intolerance and previous clinical response. The following drugs were tested acutely in the electrophysiology laboratory after intravenous administration: procainamide, 750 to 1,500 mg; propranolol, 0.2 mg/kg; lidocaine, loading dose of 225 mg over 20 minutes, concomitant with a 2 mg/min continuous infusion; propafenone, loading dose of 2 mg/kg, concomitant with a I t ° 2 mg/min continuous infusion. The following oral agents were tested during the last 1 to 2 hours of the dosing interval, after administration of a sufficient number of doses to attain a steady-state serum drug level: procainamide, 3 to 8 g/day; quinidine, 1.2 to 1.6 g/day; disopyramide, 400 to 600 mg/day; propranolol, 160 to 480 mg/day; tocainide, 0.8 to 1.2 g/day; nadolol, 240 to 300 mg/ day. Electropharmacologic testing was usually performed until VT could no longer be induced by both right and left ventricular stimulation, even when VT had been induced by right ventricular stimulation in the baseline study; however, in 4 patients studied early in our experience and in whom VT was induced by right ventricular stimulation, left ventricular stimulation was not performed during electropharmacologic testing. If high-dose procainamide was not successful in suppressing VT induction, quinidine and disopyramide were generally not tested. When the induction of VT could not be suppressed by I or more of the aforementioned drugs, treatment was begun with amiodarone, 800 mg/day orally, except in 2 patients who underwent a surgical procedure. Because of the observation by

TABLE I

Clinical Characteristics of 45 Survivors of Cardiac Arrest*

Age (yr) Males/females Heart disease Ischemic Single-vessel CAD Double-vessel CAD ple-vessel CAD A disease Coronary spasm Catheterization not done Previous myocardial infarction Previous CABG Congestive cardiomyopathy Valvular Mitral valve prolapse Hypertrophic cardiomyopathy No heart disease Ejection fraction Congestive heart failure NYHA I or II NYHA Ill or IV Previous episode of cardiac arrest

56 -t- 16 t 39/6 36 (78) 3 3 16 3 1 10 30 5 3 (7) 3 (7) 2 (4) 1 (2) 1 (2) 0.42 4- 0.15'

:~

14 (31) 11 (24) 6 (13)

* Numbers in parentheses represent percentages. 1 Mean :E standard deviation. CABG = coronary artery bypass grafting; CAD = coronary artery disease; LMCA = left main coronary artery; NYHA -- New York Heart Association functional class.

TABLE II Patients (n)

Surgical Procedures Performed in 45 Survivors of Cardiac Arrest Heart Disease

Operative Procedure

Before Electrophysiologic Testing 1 2

Aortic stenosis Stenosis of LMCA

Aortic valve replacement CABG

After Electrophysiologic Testing 1 1

Stenosis of LMCA Triple-vessel CAD

1

Triple-vessel CAD

CABG and aneurysmectomy CABG and map-directed endocardial resection CABG

CABG = coronary artery bypass grafting; CAD = coronary artery disease; LMCA = left main coronary artery.

ourselves and others that ventricular stimulation studies are not predictive of clinical response in patients treated with amiodarone, patients treated with this drug did not undergo repeat studies. 5-7 Surgical therapy: After their episodes of cardiac arrest, 3 patients underwent a surgical procedure before electrophysiologic testing and 3 afterwards (Table II). Chronic drug therapy and follow-up: Patients were followed on a regular basis by either 1 of the investigators or by the patient's referring physician. Drug therapy was adjusted to yield serum drug levels that matched drug levels found to be successful in suppressing VT induction in the laboratory. In patients treated with amiodarone, the dose was tapered to 600 mg/day after 6 weeks of therapy; subsequent adjustments in the dose depended on the clinical response and development of adverse effects. Twenty-four-hour ambulatory electrocardiographic recordings were obtained every 3 to 4 months. Sudden death waS defined as unexpected natural death occurring during sleep or within 1 hour of the patient's collapse.

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45

ResponSeto PVS

EPtesting with conventional drug(s)

Treatment

VT 34

No VT 11

No VT 9

VT 25

Conventional drug(s) 9

Amiodarone 23

M drugs 7

Op 2

Op 4

.wv A A A oAoA

Non-fatal VT/VF

2

0

0

0

0

FIGURE 1. Results of electrophysiologic testing and clinical follow-up in 45 survivors of cardiac arrest. EP = electropharmacologic; Misc. = miscellaneous (see text for details); Op = operation (as listed in Table II); PVS = programmed ventricular stimulation.

Statistical analysis: Values are expressed as mean + 1 standard deviation. Patients in whom VT induction was suppressed by conventional agents were compared with those in whom VT induction was not suppressed using Fischer's exact test and Student's t test. Results

During the baseline electrophysiologic study, sustained VT was induced in 26 of 45 patients (58%). Mean cycle length of VT was 273 ± 77 ms. The VT morphology was that of right bundle branch block in 18, left bundle branch block in 5, and polymorphic in 3. VT was induced with right ventricular stimulation in all but 3 patients who required left ventricular stimulation. VT was induced with burst pacing in 3 patients, with 1 extrastimulus in 1 patient, with 2 extrastimuli in 9 patients, with 3 extrastimuli in 12 patients, and with 3 extrastimuli during isoproterenol infusion in 1 patient. Direct-current cardioversion was required to terminate VT in 15 of 26 patients; in the remaining 11 patients, VT was terminated with overdrive pacing. Nonsustained VT was induced in 8 of 45 patients (18%). The mean duration of VT was 29 ± 18 beats (range 8 to 65); the mean cycle length was 224 ± 19 ms. The VT morphology was that of right bundle branch block in 4 patients, left bundle branch block in 1, and P:lym~rPwhith i n 2 h : n e ~ ~ c:s~: r nonsustained VT was r stimulation; 2 extrastirauli were necessary in 2 patients, and 3 extrastimuli m 6. Overall, VT was induced with programmed ventricular stimulation in 34 of 45 patients (76%). Of the 30 patients who had VF at the time of resuscitation, VT Wasinduced in 23 (77%); of the 12 patients who had VT at the time of resuscitation, VT was induced in 10 (83%). VT could not be induced with programmed ventricular stimulation in 11 patients (24%). Two of these pa-

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tients had undergone coronary artery bypass grafting because of stenosis of the left main coronary artery, and 1 had undergone aortic valve replacement for aortic stenosis. A fourth patient had had a cardiac arrest 2 weeks after initiation of quinidine for prevention of atrial fibrillation; an electrocardiogram obtained several days before the cardiac arrest showed a Q-T interval of 0.52 seconds (Q-To = 0.58 second). A fifth patient who had coronary artery disease (CAD) had no inducible VT despite frequent episodes of spontaneous VT before and after electrophysiologic study. Of the other 6 patients, 5 had CAD and 1 had coronary artery spasm. Three of these patients were engaged in strenuous exertion at the time of the cardiac arrest. One patient had no underlying heart disease. Clinical follow-up in patients with no inducible VT during baseline study (Fig. 1): Eleven patients with no inducible VT have had no recurrence of symptomatic VT or VF over a mean follow-up period of 19 + 9 months (range 9 to 34). Four patients underwent coronary artery bypass grafting or aortic valve replacement (before the electrophysiologic study in 3 patients and afterwards in 1). The patient who had coronary artery spasm was treated with nitrates. Three patients who had CAD but who either refused or were not suitable candidates for coronary artery bypass grafting were treated with nitrates and beta-adrenergic blocking agents aimed at preventing myocardial ischemia; i of these patients was also treated with encainide for suppression of asymptomatic premature ventricular beats. The patient who had been treated with quinidine and had Q-T interval prolongation before a cardiac arrest was treated with procainamide (for paroxysmal atrial fibrillation); no VT could be induced while taking procainamide. The patient who had no inducible VT but who had frequent spontaneous episodes of VT was treated with amiodarone. The patient without underlying heart disease was initially treated empirically with nadolol for 6 months and has subsequently taken no medication over an additional 7 months of follow-up. Results of electropharmacologic drug testing and clinical follow-up (Fig. 1): VT could no longer be induced after administration of a conventional antiarrhythmic drug in 9 of 34 patients (26%) who had inducible VT during the baseline electrophysiologic study. Induction of VT was suppressed by procainamide in 4 patients (mean serum level 10.3 ± 5.9 #g/ml), quinidine in 1 (serum level 3.2 ~g/ml), nadolol or propranolol in 2, and a combination of procainamide (serum level 6.4 ± 0.9 #g/ml) and propranolol in 2. These patients were treated chronically with the drug(s) that suppressed the induction of VT. One patient died suddenly after 1 month of treatment. Another patient (who did not undergo left ventricular stimulation during electropharmacologic testing) had an episode of symptomatic VT after 1 week of treatment, underwent coronary bypass grafting, and has had no recurrence of VT or cardiac arrest over 21 months of follow-up. A third patient had recurrence of aborted cardiac arrest after 17 months of treatment, and subsequently underwent insertion of an

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automatic internal defibrillator. The remaining 6 of 9 patients had no recurrence of cardiac arrest or symptomatic VT over a mean follow-up period of 20 ± 7 months. During electropharmacologic testing with conventional antiarrhythmic drugs, VT remained inducible in 25 of 34 (74%)patients who had inducible VT during the baseline electrophysiologic study. These patients underwent an average of 1.8 drug trials each. Twenty-one of these 25 patients failed testing with intravenous procainamide (mean serum level 12.9 ± 6.8 #g/ml). There was no significant difference in the proportion of patients with ischemic heart disease (20 of 25 versus 5 of 9) or mean ejection fraction (0.38 ± 0.10 versus 0.46 + 0.15) in these 25 patients and the 9 in whom VT induction was suppressed by a conventional antiarrhythmic drug. One of these 25 patients underwent coronary artery bypass grafting and aneurysmectomy and died suddenly 12 months after surgery. Another patient underwent coronary artery bypass grafting and map-directed endocardial resection and has remained well for 39 months. The remaining 23 of 25 patients were treated with amiodarone (mean dose 550 ± 120 mg) either alone (17 patients) or in combination with procainamide (in 6 patients procainamide slowed the rate of induced VT). One patient died suddenly after 1 month of treatment, and another patient died from refractory VT after 3 months of treatment. The remaining 21 of 23 patients (91%) who were treated with amiodarone have had no recurrence of cardiac arrest or symptomatic VT over a mean follow-up period of 18 ± 14 months (range 7 to 65). Overall, in the 45 patients who survived a cardiac arrest and underwent electrophysiologic testing, 4 of 45 patients (9%) died due to VT or VF at 4.2 :t: 5 months of follow-up, 2 of 45 (4%) had a nonfatal recurrence of VT at I week and 17 months of follow-up, and 39 of 45 (87%) have had no recurrence of symptomatic VT or VF over a follow-up period of 18 + 12 months. Discussion Previous studies have shown that patients who survive an episode of cardiac arrest in the absence of a transmural myocardial infarction and who are treated with conventional antiarrhythmic drugs in a nonstandardized fashion have a mortality of 34 to 36% at 1 year of follow-up, s-l° In comparison, in the present series of 45 patients in whom therapy was guided by the results of electrophysiologic testing and in whom amiodarone was used in 50% of patients, the mortality from VT or VF was only 9% at 1.5 years of follow-up. The lower mortality in the present series suggests that electrophysiologic testing and/or the use of amiodarone may p l a y a role in improving survival in a group of patients at high risk of sudden death. The finding of inducible VT in 76% of patients who survived a cardiac arrest is similar to the findings of Josephson, 3 Ruskin, 2 and their co-workers, who reported inducible VT in 60 and 74% of such patients, respectively. In contrast, Myerburg et al 1 found that only 29% of patients who had survived a cardiac arrest

had inducible VT. However, in the last series, only 1 extrastimulus was used in the ventricular stimulation protocol, compared with 2 extrastimuli in the series of Josephson and Ruskin and 3 extrastimuli in our series. Thus, programmed ventricular stimulation should be performed with at least 2 extrastimuli to avoid falsenegative results. The relative sensitivity and specificity of 2 versus 3 extrastimuli remain to be determined. Left ventricular stimulation was required to induce VT in approximately 10% of patients who had inducible VT. However, we performed right ventricular stimulation at only 1 site, the apex. It is possible that right ventricular stimulation at more than i site may at times eliminate the need for left ventricular stimulation. In any case, to maximize the yield of VT induction studies, ventricular stimulation should be performed at more than 1 site. In the patients in this series who did not have inducible VT with programmed ventricular stimulation, possible reasons for its lack include the following: (1) The spontaneous arrhythmia may have been due to abnormal automaticity rather than reentry and thus may not be provocable with programmed stimulation. This is the most likely explanation in the patient who had no inducible VT despite having frequent spontaneous episodes of VT before and after the electrophysiologic study. (2) The onset of spontaneous VT or VF may have been related to transient myocardial ischemia that was not present at the time of the ventricular stimulation study. This is a likely explanation in the patient who had coronary spasm, in the 2 patients who had stenosis of the left main coronary artery and underwent coronary artery bypass grafting before the ventricular stimulation study, and in the 3 patients with CAD who experienced a cardiac arrest during strenuous exertion. (3) The spontaneous episode of VT or VF was related to an abnormality that was corrected by the time of the electrophysiologic study (for example, hypokalemia, quinidine-induced Q-T prolongation, or aortic stenosis). Thus, in 2 of our patients the lack of inducible VT can be attributed to discontinuation of quinidine in 1 and aortic valve replacement in the other. In patients who survive a cardiac arrest and do not have inducible VT, another possible explanation for the lack of inducible VT may be that the patient has the congenital long Q-T syndrome; VT can be induced with programmed stimulation in only a minority of these patients. 4 In the series by Ruskin et al, 2 6 patients who had survived a cardiac arrest did not have inducible VT; these patients were not treated with antiarrhythmic drugs and had no recurrence of cardiac arrest over a mean follow-up of 15 months. However, no details of their treatment, such as surgery or antianginal drugs, were given. The 11 patients in our series who did not have inducible VT also have had no recurrence of symptomatic VT or VF. Only 2 of 11 patients were treated with antiarrhythmic drugs specifically aimed at suppressing ventricular arrhythmias. Thus, in patients who have survived a cardiac arrest, electrophysiologic testing may be helpful in identifying those with

January 1, 1983

a low risk of recurrent VT or VF when treatment is directed toward the underlying heart disease without specific antiarrhythmic therapy. In the patients in whom VT was induced with programmed ventricular stimulation, electropharmacologic testing with conventional antiarrhythmic drugs was disappointing, with suppression of VT induction in only 26%. Of the patients in whom the induction of VT could not be suppressed, 21 of 25 were tested with large doses of procainamide. A|though most of these patients were not tested with a second type I antiarrhythmic drug, it is unlikely that such testing would have been successful in suppre.ssing the induction of VT, since Waxman et a111reported that in 63 patients who had inducible VT with procainamide, only 9% of 144 additional drug trials with conventional agents were successful in suppressing VT induction. Similarly, in the series by Ruskin et al, 2 conventional antiarrhythmic drugs were successful in suppressing the induction of VT in only 34% of patients undergoing electropharmacologic testing. Electrophysiologic testing is therefore helpful in the management of patients with aborted cardiac arrest by identifying the large subgroup of patients who should be treated wtih investigational drugs or surgery. Of the 9 patients who were treated with conventional drugs that suppressed the induction of VT during electropharmacologic testing, 3 had a recurrence of VT or VF despite continued treatment with the original drug regimen, Thus, the suppression of inducible VT .during electropharmacologic testing in patients who have survived a cardiac arrest may not guarantee a successful long-term clinical response. Discordance between the results of acute drug testing and the chronic clinical response may be a result of progression of the underlying heart disease or fluctuations in other variables that may influence the propensity to develop VT or VF, such as sympathetic tone and the degree of myocardial ischemia. Of the 23 patients who were treated with amiodarone, 92% have remained free of symptomatic VT or VF over 18 months of follow-up. Previous studies have also reported an excellent response to amiodarone in patients with recurrent VT or VF. 6,12,13 We and others have demonstrated that the induction of VT during chronic oral amiodarone therapy does not preclude a good clinical response. 5-7 Therefore, in our series no further electropharmacologic testing was performed when patients were treated with amiodarone. In light of the excellent response in the subgroup of patients treated with amiodarone, an alternate approach to electropharmacologic testing in the management of patients who have survived a cardiac arrest might be simply to treat all such patients empirically with amiodarone. This approach was employed by Peter et a114in 27 patients who had survived a cardiac arrest;

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these patients were treated empirically with amiodarone without undergoing an electrophysiologic study. The recurrence rate of VT or VF was only 7% at the end of 1 year of treatment. The principal disadvantage of this approach is that those patients who would have responded to conventional drugs are exposed to the risks of therapy with an experimental agent. In summary, the following conclusions can be drawn from our study of 45 patients who survived a cardiac arrest: (1) VT can be induced in 76% of patients. (2) The lack of inducible VT may identify patients who have a low risk of recurrent VT or sudden death when therapy is directed toward the underlying cardiac abnormality. (3) Electropharmacologic testing with conventional antiarrhythmic drugs is disappointing, with a minority (26%) of patients responding to these drugs. (4) In the patients who do not respond to electropharmacologic testing with conventional drugs, treatment with amiodarone is associated with a low recurrence rate of VT or sudden death. If the favorable outcome of amiodarone therapy in these patients is confirmed; empiric trials with this drug would be indicated, obviating serial electropharmacologic testing. References 1. Myerburg RJ, Conde CA, Sung RJ, Mayorga-Cortes A, Mallon SM, Sheps DS, Appel RA, Castellanos A. Clinical, electrophysiologic and hemodynamic profile of patients resuscitated from prehospital cardiac arrest. Am J Med 1980;68:568-576. 2. Ruskin JN, DIMarco JP, Garan H. Out-of-hospltal cardiac arrest. Electrophysiologic observations and selection of long-term antiarrhythmic therapy. N Engl J Med 1980;303:607-613. 3, Josephson ME, Horowitz LN, Spielman SR, Greenspan AM. Electrophysiologic and hemodynamic studies in patients resuscitated from cardiac arrest. Am J Cardio11980;,$6:948-955. 4. Morady F, Scheinman MM, Hess DS, Chen R, Stanger P. Clinical characteristics and results of electrophysiologic testing in young adults with ventficular tachycardia or ventricular fibrillation. Am Heart J, in press. 5. Morady F, Scheinman MM, Hess DS. Ami0darone in the management of patients with malignant ventricular arrhythmias (abstr). Circulation 1981; 64:Suppl IV:IV-36. 6. Heger JJ, Prystowsky EW, Jackman WM, Naccarelli GV, Warfel KA, Rinkenberger RL, Zipes DP. Amiodarone. Clinical efficacy and electrophysiology during long-term therapy for recurrent ventdcular tachycardia or ventricular fibrillation. N Engl J Med 1981;305:539-545. 7. Hamer AW, Finerman WB, Peter T, Mandel WJ. Disparity between the clinical and electrophysiologic effects of amiodarone in the treatment of recurrent ventricular tachyarrhythmias. Am Heart J 1981;102:9921000. 8. Liberthson RR, Nagel EL, Hirschman JC, Nussenfeld SR. Prehospital ventricular defibrillation. Prognosis and follow-up course. N Engl J Med 1974;291:317-321, 9, Cobb LA, Baum RS, Alvarez H Ill, Schaffer WA. Resuscitation from outof-hospital ventricular fibrillation: 4 years follow-up. Circulation 1975; 51-52:Supp1111:111-223-111-228. 10. Schaffer WA, Cobb LA. Recurrent ventricular fibrillation and modes of death in survivors of out-of-hospital ventricular fibrillation. N Engl J Med 1975; 293:259-262, 11. Waxman HL, Sadowki LM, Josephson ME. Response to procainamide during eiectrophysiologic study for sustainedventricular tachycardia predicts response to other drugs (abstr). Circulation 1981;64:Suppl W:IV-87. 12. Podrid PJ, Lown B, Amiodarone therapy in symptomatic, sustained refractory atrial and ventricular tachyarrhythmias. Am Heart J 1981; 101: 374-379. 13. Kaski JC, Girottl LA, Messuti H, Rutitzky B, Rosenbaum MB. Long-term management of sustained, recurrent, symptomatic ventricular tachycardia with amiodarone. Circulation 1981;64:273-279. 14. Peter T, Hamer A, Weiss D, Mandel W. Suddendeath survivors: experience with )eng-term empiric therapy with amiodarone (abstr). Circulation 1981;64:Suppl IV:IV-36.