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Circulation. 1996;94:151-157

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(Circulation. 1996;94:151-157.)
© 1996 American Heart Association, Inc.

Articles

Comparison of d,l-Sotalol and Implantable Defibrillators for Treatment of Sustained Ventricular Tachycardia or Fibrillation in Patients With Coronary Artery Disease

Dirk Bocker, MD; Wilhelm Haverkamp, MD; Michael Block, MD; Martin Borggrefe, MD; Dieter Hammel, MD; Gunter Breithardt, MD

Westfalische Wilhelms-University, Department of Cardiology, Cardiothoracic Surgery (D.H.), and the Institute for Research in Arteriosclerosis, Munster, Germany.

Correspondence to Dr Dirk Bocker, Universitatsklinik Munster, Innere Medizin C, D-48129 Munster, Germany.


*    Abstract
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 *Abstract
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Background Implantable cardioverter-defibrillators (ICDs) and d,l-sotalol are widely used to treat ventricular tachyarrhythmia and ventricular fibrillation (VT/VF). The purpose of this study was to compare the long-term efficacy of d,l-sotalol and ICDs in patients with coronary artery disease.

Methods and Results In a case-control study, 50 patients treated with oral d,l-sotalol were matched to 50 patients treated with ICDs. Both groups were matched for sex (82 men), age (58±10 years), ejection fraction (40±12%), extent of coronary artery disease, presenting arrhythmia, and year that treatment began. In all patients in the sotalol group, VT/VF was inducible in the drug-free electrophysiological study. Induction of sustained VT/VF was suppressed by d,l-sotalol (438±95 mg/d). In the ICD group, either VT/VF was not inducible (n=5) or inducible sustained VT/VF was refractory to antiarrhythmic drug treatment (n=45). Sotalol treatment led to a marked reduction in arrhythmic events. Whereas 83% of the patients in the sotalol group were free of sudden death and nonfatal VT at 3 years, only 33% of the ICD patients did not receive appropriate ICD therapies (P<.005). Actuarial rates for absence of sudden death at 3 years were 85% in the sotalol group and 100% in the ICD group (P<.005). Actuarial rates for overall survival at 3 years were 75% in the sotalol group and 85% in the ICD group (P=.02).

Conclusions In this case-control study, ICD therapy was more effective than electrophysiologically guided antiarrhythmic treatment with d,l-sotalol in prevention of sudden death and reduction of total mortality in patients with coronary artery disease. Prospective studies are needed to confirm these results.


Key Words: tachyarrhythmias • sotalol • defibrillation


*    Introduction
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Antiarrhythmic drugs and ICDs have been widely used in patients with sustained VT or VF. Although class I antiarrhythmic drugs have been the most commonly used therapy, emphasis is now shifting from class I to class III agents because of good clinical experience with sotalol1 2 3 and amiodarone.4 5 6 7 Recently, the ESVEM study8 9 suggested in a post hoc analysis the superiority of d,l-sotalol to other antiarrhythmic drugs, especially class I antiarrhythmic drugs, for the treatment of VT/VF. These results support previous data that showed that sotalol was effective when other antiarrhythmics failed.10 11 12 13 With the possible exception of amiodarone, which was not tested in the ESVEM trial but was demonstrated to be superior to class I antiarrhythmic drugs in CASCADE,7 d,l-sotalol seems to be the most potent antiarrhythmic drug currently available.

ICD therapy, first proposed by Mirowski et al14 15 in the 1970s and first implanted in humans in 1980,16 has been shown to be extremely effective in preventing sudden death.17 18 19 20 21 22 However, the benefit of this therapy in the prolongation of life is still controversial.23 24 25 26 27 In the absence of published controlled studies, various outcome analyses have been used to estimate the benefit of ICD therapy, including hypothetical expected mortality based on first appropriate shocks17 18 20 21 or the recurrence of documented rapid tachyarrhythmia terminated by the defibrillators.28 29 Although these analyses might suggest a superiority of ICD therapy to no therapy at all, they do not prove the superiority of ICD therapy to the best possible antiarrhythmic therapy.

Therefore, the purpose of this study was to compare the long-term efficacy of oral d,l-sotalol to ICDs for the treatment of VT or VF in patients with coronary artery disease.


*    Methods
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Study Patients
In a case-control study, patients with coronary artery disease and VT/VF treated with oral d,l-sotalol were compared with patients receiving ICD therapy (the TableDown).


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  		Table 1. Clinical Characteristics

The sotalol group consisted of 50 consecutive responders to oral d,l-sotalol as predicted by electrophysiological testing. They were matched for age, sex, ejection fraction, extent of coronary artery disease, presenting arrhythmia, and year of treatment to 50 patients who were treated with ICDs because of drug-refractory VT/VF (ICD group). For matching, identity in the following variables was mandatory: sex, single-vessel versus multivessel coronary artery disease, and history of VF versus history of VT only. The initiation of treatment had to be within 365 days of the control patient. Patients were then selected so that differences in age, ejection fraction, and number of vessels with a stenosis >50% were minimized.

Sotalol Group
The sotalol group consisted of 50 patients (41 men, 9 women; mean age, 56±10 years) with coronary artery disease (single-vessel disease in 23 patients; multivessel disease in 27). These patients were selected from a database containing 396 patients that had been treated with oral d,l-sotalol for various indications. All patients with coronary artery disease and a history of VT or VF who became noninducible at programmed ventricular stimulation under oral d,l-sotalol were included in the study. Mean left ventricular ejection fraction was 41±13%. The Table gives the clinical characteristics.

Programmed ventricular stimulation was performed with one or two extrastimuli during sinus rhythm and four paced drive cycle lengths (120, 140, 160, and 180 bpm) at two right ventricular sites (right ventricular apex and outflow tract). If no VT was induced, a third extrastimulus was induced during a paced cycle length of 500 ms. The stimulation protocol was described in detail previously.30 31 In all patients in the sotalol group, sustained ventricular tachyarrhythmias (monomorphic VT in 42, polymorphic VT in 3, ventricular flutter in 1, and VF in 4) could be induced reproducibly (at least twice) in a drug-free electrophysiological study. VT/VF was inducible with two extrastimuli during sinus rhythm in 2 patients; with one or two extrastimuli at paced drive cycle length of 500, 430, 370, and 330 ms, respectively, in 19, 10, 6, and 7 patients, respectively; and with three extrastimuli at a paced drive cycle length of 500 ms in 6 patients. Mean cycle length of the induced VT was 269±68 ms.

All patients received d,l-sotalol in a dosage that was gradually increased to 480 mg or the maximum tolerated dosage. The control study was performed 4 or 5 days after oral d,l-sotalol was begun with a mean sotalol dosage of 438±95 mg/d. With d,l-sotalol, the cycle length during sinus rhythm increased from 782±156 ms by 280±163 ms, the corrected QT interval increased from 0.43±0.05 by 0.03±0.07, and the effective refractory period at a drive cycle length of 500 ms increased from 230±19 ms by 50±20 ms. In the programmed ventricular stimulation on oral d,l-sotalol, no sustained VT was induced until full completion of the stimulation protocol. No signs of proarrhythmia were detected in exercise ECGs and Holter recordings performed before hospital discharge.

ICD Group
These patients were drawn from a database accumulated at the same institution consisting of 487 patients presenting with sustained VT or aborted sudden death who were treated with implantable defibrillators. Of these patients, 41 were men and 9 were women. Mean age was 59±11 years. All patients had coronary artery disease: 23 had single-vessel disease and 27 had multivessel disease. Mean left ventricular ejection fraction was 39±12%. A drug-free electrophysiological study was performed in all patients. In 5 patients (10%), no sustained VT was inducible during the baseline electrophysiological study; thus, serial drug testing could not be performed. In 45 of the patients (90%), the induction of VT could not be suppressed by antiarrhythmic drugs during serial electrophysiological studies. All patients received an ICD system for treatment of their tachyarrhythmias. The devices included a Medtronic PCD 7216A in 2 patients, a Medtronic PCD 7217B in 17, a Medtronic PCD 7219D in 10, a CPI Ventak P in 1, a CPI Ventak P2 in 2, a CPI Ventak PRx in 11, and a CPI Ventak PRX2 in 7. All but one device stored either cycle lengths (n=30) or electrograms (n=19) from treated episodes. Two cardiologists classified episodes as appropriate (ie, caused by VT) or inappropriate (ie, caused by supraventricular tachycardias or oversensing) on the basis of clinical symptoms (ie, syncope or near syncope), stored electrograms, and/or cycle lengths. It should be noted, however, that this classification might be inaccurate in some cases because of limited available information. Nonthoracotomy lead systems were used in all but 1 patient.

Follow-up
All patients were followed in the outpatient clinic at intervals between 3 and 6 months. No patient was lost to follow-up. If a patient died, every effort was made to clarify the circumstances of death.

Recorded study end points were the following: sudden death (defined as either death within 1 hour after the onset of symptoms or unwitnessed and unexpected death), cardiac death (defined as sudden death plus death from any other arrhythmic or nonarrhythmic cardiac cause), and total mortality.

Statistical Methods
Mean, SD, and range were used as indexes of dispersion of the values observed. The log-rank test for overall comparison of the two groups was used to compare survival variables. Statistical analysis was done with SPSS for Windows (version 5.01; SPSS Inc) software package. A value of P<.05 was considered statistically significant.


*    Results
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Patient Characteristics
As a result of the matching procedure, both groups were comparable in terms of age, underlying cardiac disease, extent of coronary artery disease, left ventricular ejection fraction, and type of presenting arrhythmia (see the Table). No statistically significant differences could be observed in either of these parameters. Differences existed in the inducibility during drug-free electrophysiological study and the ability of antiarrhythmic drugs to suppress the induced arrhythmias because these differences were the rationale for the different treatment strategies.

In-Hospital Course
All patients in the sotalol group were discharged 1 or 2 days after the last electrophysiological study. The d,l-sotalol dosage at discharge was identical to that found to be effective at the electrophysiological testing in all patients. No VT recurrences or deaths occurred during this short period of time. Exercise ECG and 24-hour Holter recordings did not demonstrate any nonsustained or sustained VT or torsade de pointes before discharge.

Patients in the ICD group were discharged 6±3 days after implantation of the ICD. There were no perioperative deaths. Of the patients in the ICD group, 6 (12%) received antiarrhythmic drug therapy (all d,l-sotalol). The reasons for sotalol administration included prevention of frequent ICD discharges in 5 patients and slowing of the tachycardia rate to allow antitachycardia pacing in 1 patient. In addition, 10 patients (20%) were treated with ß-blockers to prevent inappropriate discharges because of atrial fibrillation or sinus tachycardia.

Long-term Follow-up
During follow-up (24±19 months in the sotalol group versus 31±13 months in the ICD group, P=NS), there were 8 sudden deaths in the sotalol group compared with none in the ICD group. The first sudden death in the sotalol group occurred after 1.2 months. Actuarial rates for absence of sudden death at 1 and 3 years were significantly lower in the ICD group compared with the sotalol group (Fig 1Down). In the ICD group, all patients were free of sudden death versus 91% and 85% in the sotalol group after 1 and 3 years, respectively (P<.005). Two patients in the sotalol group had recurrences of nonfatal but symptomatic VT. Both were treated with ICDs after these recurrences. Actuarial rates for absence of sudden death and nonfatal symptomatic VT were 89% and 83% at 1 and 3 years, respectively, in the sotalol group (Fig 2Down). In the ICD group, only 52% and 33%, respectively, of the patients did not receive appropriate ICD therapies. Because of frequent episodes of VT, antiarrhythmics had to be added in 5 ICD patients (amiodarone in 1 patient, d,l-sotalol in 2, dofetilide in 1, and propafenone in 1). Three patients had to undergo ablation therapy because of incessant VT.



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  		Figure 1. Actuarial curves for the absence of sudden death in patients treated with oral d,l-sotalol (91%, 84%, and 84% at 1, 2, and 3 years, respectively) vs ICDs (100%, 100%, and 100%, respectively).



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  		Figure 2. Actuarial curves for the absence of sudden death and symptomatic VT in the patients treated with oral d,l-sotalol (89%, 83%, and 83% at 1, 2, and 3 years, respectively) and absence of "appropriate" ICD therapies in the patients treated with an ICD system (52%, 36%, and 33%, respectively).

Whereas 10 patients in the sotalol group died from cardiac causes, only 5 of the patients in the ICD group died from cardiac causes. Again, a significant benefit for the ICD group could be demonstrated: Actuarial rates for absence of cardiac death at 1 and 3 years were 100% and 87% in the ICD group versus 89% and 79% in the sotalol group, respectively (P=.019). Of 10 cardiac deaths, 8 (80%) in the sotalol group were sudden, whereas all cardiac deaths in the ICD group were not sudden and were due to end-stage heart failure.

In addition, there were 4 noncardiac deaths in the sotalol group (2 cerebral strokes, 1 lung cancer, 1 colon cancer) compared with 1 noncardiac death (cerebral stroke) in the ICD group. Actuarial rates for overall survival at 1 and 3 years were 98% and 85% in the ICD group versus 89% and 75% in the sotalol group, respectively (Fig 3Down). Again, the difference between the two forms of treatment was significant (P=.02).



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  		Figure 3. Actuarial curves for the total mortality in patients treated with oral d,l-sotalol (88%, 74%, and 74% at 1, 2, and 3 years, respectively) vs ICDs (98%, 89%, and 84%, respectively).

Patients who died suddenly were not different from the surviving patients in either of the baseline variables, whereas patients who died nonsuddenly had significantly lower ejection fractions (32±11% in the patients who died versus 42±12% in the survivors; P=.02).

Complications During Long-term Follow-up
In the sotalol group, no patient experienced adverse drug reactions during the follow-up. Late-onset ventricular proarrhythmia was not observed. No patient stopped taking the drug or reduced the dosage prescribed at discharge. In the ICD group, several complications related to the ICD system required intervention: 3 patients experienced spurious shocks during sinus rhythm owing to oversensing of noise at 17, 21, and 28 months, respectively, after implantation (fracture of the sensing electrode in 1 and isolation defect of an adapter in 2). All had to undergo revision of the lead system. One patient required revision of the lead system because of a pacing exit block 19 months after implantation. Infection of the device pocket made the temporary removal of the ICD system necessary in 1 patient 2 months after implantation. In addition, 5 patients suffered from delivery of inappropriate shocks because of sinus tachycardia (n=4) or atrial fibrillation (n=1).


*    Discussion
up arrowTop
 up arrowAbstract
 up arrowIntroduction
 up arrowMethods
 up arrowResults
 *Discussion
down arrowReferences
 
The present study is a case-control study to define the potential role of ICD therapy compared with the antiarrhythmic drug therapy found most effective in the ESVEM8 9 trial for treatment of patients with a history of VT or VF. While there has been no serious discussion that ICDs are extremely effective in the prevention of sudden death, there has been considerable uncertainty as to how this reduction translates into a reduction of overall mortality.23 24 25 26 27 Several methods have been used to quantify the possible effect of ICD therapy on mortality. Many groups used the occurrence of presumably appropriate shocks for calculation of hypothetical mortality rates, thus grossly overestimating the beneficial effect of ICD therapy.18 21 In previous studies,28 29 we used the recurrences of documented rapid VT (>240 bpm) or VF for calculation of hypothetical mortality rates. However, both calculations do not compare ICD therapy with medical antiarrhythmic drug therapy but with no antiarrhythmic therapy. Several studies that compared ICD therapy with medical therapy have used historical controls, reported in studies from the 1970s32 33 when left ventricular dysfunction and ischemic heart disease were treated much less aggressively and with other types of antiarrhythmic drugs than those currently available. In a study that included 331 patients treated between 1978 and 1990, Powell et al34 examined the influence of the implantable defibrillator on long-term outcome in survivors of out-of-hospital cardiac arrest who underwent electrophysiologically guided therapy. In their multivariate survival analysis, the independent predictors of total cardiac mortality were left ventricular ejection fraction of <40%, absence of an ICD, and persistence of inducible sustained VT. In patients with an ejection fraction of <40% whose arrhythmias were suppressed with drugs, total mortality was higher at 1 and 5 years and comparable at 3 years to that observed in patients treated with defibrillators. In patients with left ventricular ejection fraction of >=40%, total mortality for patients without ICDs whose arrhythmias had been rendered noninducible with pharmacological or surgical therapy was similar to that of patients with ICDs at 1 and 3 years and poorer than that of defibrillator patients at 5 years. However, left ventricular ejection fraction, the most powerful predictor of mortality in this study, was significantly different between both groups (35.2% and 45.3% in the ICD and non-ICD group, respectively), as was the duration of follow-up (24 and 46 months in the ICD and non-ICD groups, respectively). A recent Dutch study by Wever et al35 demonstrated a benefit of ICD implantation as first-choice therapy (early ICD group) against the conventional therapeutic strategy of starting with antiarrhythmic drugs (conventional strategy group). In the conventional strategy group, only 8 of 31 patients were discharged on antiarrhythmics as sole therapy, 3 of whom died suddenly during the follow-up. Of the 31 patients in this group, 16 ended up with an ICD. Total mortality in the conventional strategy group was 11 of 31 patients. In contrast, only 4 of the 29 patients in the early ICD group died during the follow-up of 24 months. However, most of the patients in the conventional strategy group had been treated with class I antiarrhythmic drugs that already had been shown to be less effective than sotalol in the ESVEM trial. Another limitation of this small randomized trial is that 69% of the patients in the early ICD group versus 81% in the conventional strategy group had multivessel disease. In addition, because the transthoracic approach was used for ICD implantation, revascularization was performed in 8 patients in the early ICD group although severe angina was an exclusion criterion from the study.

Only one case-control study has compared ICD therapy with medical antiarrhythmic therapy. Newman et al36 matched 60 ICD recipients to 120 patients treated with antiarrhythmic drugs for prevention of VT recurrences. A benefit of ICD therapy was demonstrated: At 3 years, actuarial survival was 65% for ICD recipients versus 49% for control subjects. However, this study has several limitations. Both groups were heterogeneous concerning the underlying disease (78% had ischemic heart disease; 22% had nonischemic disease). In addition, 68% of the patients in the ICD group were treated with amiodarone in addition to their ICDs.

To avoid these problems, the groups in this study are defined more clearly in terms of the underlying heart disease and antiarrhythmic drug treatment (only coronary artery disease; all patients in the sotalol group responded to oral d,l-sotalol as predicted by electrophysiological testing). The comparison to d,l-sotalol was chosen because sotalol therapy was demonstrated to be superior to class I antiarrhythmic drugs8 9 and was associated with reduced overall mortality. Response to sotalol in an electrophysiological study was a prerequisite for inclusion in the sotalol group because this type of testing is still routine for the evaluation of antiarrhythmic drug treatment in many centers and because the majority of patients with a history of VT or VF do not have enough spontaneous ventricular ectopy to be candidates for evaluation of drug efficacy by ambulatory ECG. With regard to the inclusion criteria for this study, the groups were even more homogeneous than the patients to be included in prospective studies undertaken to define the role of ICD therapy more clearly. Although both amiodarone and sotalol were used in the AVID trial,37 a differentiation between both drugs will not be possible because of the study design. In CASH,38 only propafenone (the arm that was discontinued), metoprolol, and amiodarone were used; thus, the drug that was the best in the ESVEM trial was omitted. The same is true for CIDS39 in which patients were randomized to receive an ICD or empirical amiodarone. Although the choice of amiodarone over class I antiarrhythmics seems reasonable, the evidence for a beneficial effect of sotalol is at least equivalent to amiodarone, especially because there was no difference in mortality between the amiodarone group and the class I antiarrhythmics group in the CASCADE trial.7

In-Hospital Course
There was no perioperative mortality in our ICD group. This finding is in accordance with the very low perioperative mortality (<1%) found in studies with transvenous (or transvenous subcutaneous) defibrillation lead systems40 41 42 43 and is significantly below the perioperative mortality in studies that included patients who underwent thoracotomy.

Long-term Follow-up
ICD Group
The sudden death rate observed in the ICD group was comparable to findings in the literature. Most studies reported a sudden death rate of {approx}1.5% per year in patients treated with ICDs.19 40 41 42 43 44 45 46 The total mortality rates of 2% at 1 year and 15% at 3 years also were comparable to data from the literature, demonstrating that the ICD recipients selected for this study are representative of ICD patients. Winkle et al19 published a total mortality rate of 18% at 3 years; Akhtar et al,44 a rate of 19%; and Edel et al,46 a rate of 24% at 3 years in patients treated with ICDs and epicardial lead systems. For patients treated with endocardial lead systems, Block et al43 reported a total mortality of 8% at 2 years, and Saksena42 reported a mortality rate of 12% at 2 years. Longer follow-up data for endocardial lead systems have not been published. However, because all but 1 of the ICD patients included in this study were treated with endocardial leads, the mortality rate of 15% at 3 years is well in the expected range.

Sotalol Group
In the sotalol group, we found a sudden death rate of 15% at 3 years despite the fact that all patients responded to sotalol in the electrophysiological study. In addition, 2 patients had recurrences of nonfatal VT, leading to an arrhythmia recurrence rate of 17% at 3 years. These results are different from those reported by Steinbeck et al3 and Gonzalez et al,11 who found an excellent long-term prognosis for patients who were rendered noninducible after they took sotalol. However, both study groups are very small (12 and 8 sotalol responders, respectively). In contrast to these findings, Rankin et al47 reported 5 sudden deaths and 10 nonfatal sustained VTs in 77 patients discharged on sotalol during a mean follow-up of 18 months. The arrhythmia recurrence rate in a study of 286 patients reported by Kehoe et al10 was 34% at 27 months for all patients discharged on sotalol and 24% at 24 months for 86 responders to sotalol during programmed electric stimulation. However, while only a quarter of the recurrences manifested as sudden death in the study by Kehoe et al,10 sudden death was the most common manifestation of arrhythmia recurrence in our study, leading to the relatively high sudden and total death rates. This finding is in accordance with data reported by Lee et al,48 who also found a sudden death rate twice as high as the recurrence rate for symptomatic VT in 52 patients under sotalol. They concluded that although VT recurrence is well controlled with sotalol, the "incidence of sudden death continues to be worrisome." The arrhythmic death rate of 16% at 3 years of the sotalol-treated patients in the ESVEM trial8 (event rates taken from Fig 1 of that study8 ) almost exactly matches the sudden death rate in our patients. In addition, the total mortality rate of the sotalol-treated patients in the ESVEM trial (22% at 3 years8 ) is almost identical to that observed in our patients.

Study Limitations
Several aspects of the study require further comments. Because this study was retrospective, a bias against one form of therapy cannot be fully excluded. However, all patients were matched very carefully, and no significant differences were found in those baseline variables attributed to a high mortality risk. The only variable found to be different was inducibility of VT during programmed ventricular stimulation under sotalol because this was the rationale for the different forms of treatment. However, if suppression of VT induction by antiarrhythmics were a marker of a low-risk group, a better outcome of the patients in the sotalol group compared with the ICD group would be expected.

It is noteworthy that the patients discussed here have a mean ejection fraction of 40%, a value higher than that expected for a group of patients in whom sustained VT predominated as the presenting arrhythmia. This may be due to the fact that sotalol-treated patients may have been biased toward having reasonably good left ventricular function to minimize the risk of causing drug-induced ventricular proarrhythmia and heart failure.

As has already been pointed out, most of the devices stored only the cycle length from treated episodes, and only 36% were able to store intracardiac electrograms. Therefore, classification of treated episodes might have been inaccurate in some cases. However, it has been demonstrated that spurious shocks caused by oversensing of noise can be diagnosed not only by electrograms but also by stored cycle lengths.49 Accessory pathways as a source for supraventricular tachycardias were excluded in all patients during the baseline electrophysiological study. However, atrial flutter with 2:1 AV conduction might, in particular, be misdiagnosed as VT by use of stored cycle lengths. Therefore, an overestimation of the incidence of VT in the ICD group cannot be excluded.

The stimulation protocol used during baseline and follow-up testing used only delivery of a third extrastimulus after a paced drive cycle length of 500 ms. This protocol has been used in Germany for more than a decade and has yielded the same rate of inducibility as protocols that use 1, 2, and 3 extrastimuli at paced drive cycle lengths of 600 and 400 ms, possibly because induction with 2 extrastimuli is attempted more extensively (at sinus rhythm and 4 different drive cycle lengths). However, we cannot exclude the possibility that the use of 3 extrastimuli only at a drive cycle length of 500 ms might have resulted in overestimation of the clinical response rate of d,l-sotalol.

The purity of the analysis of the relative benefits of ICD systems compared with antiarrhythmic drugs is somewhat weakened by the fact that 6 (12%) of the ICD-treated patients were ultimately compelled to undergo additional treatment with d,l-sotalol to prevent frequent ICD discharges or to slow down the tachycardia rate to allow antitachycardia pacing. This rate of use of antiarrhythmic drugs in patients treated with third- and fourth-generation ICDs is comparable to the findings of Bardy et al,40 50 who used antiarrhythmic drugs in 10% to 18% of their patients.

The results of this study suggest that the outcome of patients with coronary artery disease and VT treated with ICDs is possibly better than the outcome of similar patients treated with d,l-sotalol.

Conclusions
In patients with coronary artery disease, treatment with ICD (in combination with ß-blockers or empirical d,l-sotalol in several patients) seems to be more effective than electrophysiologically guided antiarrhythmic treatment with oral sotalol in the prevention of sudden death and reduction of cardiac mortality. However, the results of ongoing randomized trials (AVID,37 CASH,38 and CIDS39 ) must be examined before recommendations concerning the use of ICDs as first-line therapy for VT or VF can be made.


*    Selected Abbreviations and Acronyms
 
AVID = Antiarrhythmics Versus Implantable Defibrillator study
CASCADE = Conventional Antiarrhythmic Versus Amiodarone in Survivors of Cardiac Arrest Drug Evaluation
CASH = Cardiac Arrest Study Hamburg
CIDS = Canadian Implantable Defibrillator Study
ESVEM = Electrophysiologic Study Versus Electrocardiographic Monitoring
ICD = implantable cardioverter-defibrillator
VF = ventricular fibrillation
VT = ventricular tachycardia

Received October 25, 1995; revision received January 3, 1996; accepted January 4, 1996.


*    References
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 *References
 

  1. Senges J, Lengfelder W, Jauernig R, Czygan E, Brachmann J, Rizos I, Cobbe S, Kubler W. Electrophysiologic testing of therapy with sotalol for sustained ventricular tachycardia. Circulation. 1984;69:577-584.[Abstract/Free Full Text]
  2. Nademanee K, Feld GK, Hendrickson J, Singh PN, Singh BN. Electrophysiologic and antiarrhythmic effects of sotalol in patients with life-threatening ventricular tachyarrhythmias. Circulation. 1985;72:555-564.[Abstract/Free Full Text]
  3. Steinbeck G, Bach P, Haberl R. Electrophysiologic and antiarrhythmic efficacy of oral sotalol for sustained ventricular tachyarrhythmias: evaluation by programmed stimulation and ambulatory electrocardiogram. J Am Coll Cardiol. 1986;8:949-958.[Abstract]
  4. Burkart F, Pfisterer M, Kiowski W, Follath F, Burckhardt D. Effect of antiarrhythmic therapy on mortality in survivors of myocardial infarction with asymptomatic complex ventricular arrhythmias: Basel Antiarrhythmic Study of Infarct Survival (BASIS). J Am Coll Cardiol. 1990;16:1711-1718.[Abstract]
  5. Ceremuzynski L, Kleczar E, Krzeminska-Pakula M, Kuch J, Nartowicz E, Smielak-Korombel J, Dyduszynski A, Maciejewicz J, Zaleska T, Lazarczyk-Kedzia E, Motyka J, Paczkowska B, Sczaniecka O, Yusuf S. Effect of amiodarone on mortality after myocardial infarction: a double-blind, placebo-controlled, pilot study. J Am Coll Cardiol. 1992;20:1056-1062.[Abstract]
  6. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction: an overview of results from 22 randomized controlled trials. JAMA. 1993;270:1589-1595.[Abstract]
  7. The CASCADE Investigators. Randomized antiarrhythmic drug therapy in survivors of cardiac arrest (the CASCADE study). Am J Cardiol. 1993;72:280-287.[Medline] [Order article via Infotrieve]
  8. Mason JW, for the ESVEM Investigators. A comparison of seven antiarrhythmic drugs in patients with ventricular tachyarrhythmias. N Engl J Med. 1993;329:452-458.[Abstract/Free Full Text]
  9. Mason JW, for the ESVEM Investigators. A comparison of electrophysiologic testing with Holter monitoring to predict antiarrhythmic-drug efficacy for ventricular tachyarrhythmias. N Engl J Med. 1993;329:445-451.[Abstract/Free Full Text]
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