© 2003 by European Society of Cardiology
Unexplained syncope in patients with structural heart disease and no documented ventricular arrhythmias: value of electrophysiologically guided implantablecardioverter defibrillator therapy
Department of Cardiology, University of Vienna Vienna, Austria
Manuscript submitted 14 August 2002. Accepted after revision 12 April 2003.
Correspondence: Thomas Pezawas, Department of Cardiology, University of Vienna, Innere Medizin II, Kardiologie, Waehringer Guertel 18-20, 1090 Vienna, Austria. Fax: (43) 1404004614; E-mail: thomas.pezawas{at}univie.ac.at
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Abstract |
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AIMS: To evaluate electrophysiologically guided implantable cardioverter defibrillator (ICD) therapy in patients with syncope, structural heart disease and no documented sustained ventricular tachycardia (sVT).
METHODS AND RESULTS: Programmed ventricular stimulation (PVS) was performed in 52 patients (age 62±10 years): 40 patients had ischaemic and 12 patients had idiopathic dilated cardiomyopathy. On PVS sVT and ventricular fibrillation were induced in seven and four patients, respectively, and two patients spontaneously experienced symptomatic sVT. These patients received an ICD (ICD group, n=13). Non-inducible patients were left on conventional therapy (non-ICD group, n=39). During 5±2.8 years five ICD patients received therapies, all appropriate. There were seven non-sudden deaths and overall survival analysis revealed no significant difference. Recurrent syncope occurred in five ICD and four non-ICD patients and did not correlate well with sVT. The positive and negative predictive values of PVS for tachyarrhythmias or sudden death were 36 and 98%, respectively.
CONCLUSION: Syncope per se does not necessarily herald a bad prognosis. PVS identifies high-risk patients. Induction of ventricular fibrillation with double or triple extrastimuli is of limited value. Patients with poor left ventricular function and bad clinical condition benefit most from an ICD. Syncope and sVT are not necessarily correlated during follow-up, which may merit consideration.
Key Words: Implantable cardioverter defibrillator, unexplained syncope, electrophysiological testing
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Introduction |
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The management of patients with unexplained syncope, no documented ventricular arrhythmias and structural heart disease with ventricular dysfunction is not well established. This is reflected by the American Heart/American College of Cardiology guidelines for implantation of antiarrhythmia devices in which the indication for implantable cardioverter defibrillator (ICD) implantation is graded II b and the level of evidence is ranked C[1]
. Level C emphasizes that consensus of expert opinion and not data from multiple randomized clinical trials or even from non-randomized studies or observational data registries is the primary source of recommendation. In patients with structural heart disease the occurrence of syncope heralds an increased risk for sudden arrhythmic death[2]. The value of programmed stimulation for risk stratification is well established in patients with coronary artery disease[3–5]. In patients with non-ischaemic cardiomyopathy, however, both positive and negative predictive values of this technique are by far less reliable[6–8]. This, in particular, appears true the more the left ventricular function is compromised[9].
After initial clinical assessment in half of the patients with syncope the underlying cause remains unexplained[10]. Although the true value of electrophysiological testing in patients with unexplained syncope, no documented ventricular arrhythmias and structural heart disease, is not precisely defined this technique is commonly used for further risk stratification and guided antiarrhythmia management. It is the purpose of this retrospective study to analyse this approach with special emphasis on electrophysiologically guided ICD therapy.
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Methods |
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Study population
We evaluated 52 consecutive patients with unexplained syncope and structural heart disease who underwent electrophysiological testing between June 1992 and December 2000. Inclusion criteria were: (1) one or more episodes of unexplained syncope, (2) no documented ventricular tachyarrhythmias on surface electrocardiograms (ECG) or Holter recordings, (3) presence of structural heart disease and (4) electrophysiological testing. Exclusion criteria were: (1) history of any episode of tachycardia, (2) history of cardiac arrest, (3) history of inducible supraventricular and ventricular tachyarrhythmias, (4) diagnosis of long QT syndrome (5) presence of aortic valve stenosis and (6) susceptibility to neurally mediated syncope which was not found in any of the study patients using head-up tilt testing.
Measurement of left ventricular function
Left ventricular ejection fraction was calculated from radionuclide angiography (VERTEX® MCD/AC-PET®, ADAC Laboratories, California, U.S.A.), echocardiography (ACUSON Sequia C256®, Acuson, Mountain View, CA, U.S.A.) or from cardiac catheterization data (Quantcor.QCA®, V4.0, Pie Medical Imaging, Maastricht, The Netherlands and ELK CAP 35E® Cine Angio System, Medis, The Netherlands).
Electrophysiological study
After written consent was obtained studies were performed in the postabsorptive and non-sedated state. Prior to the study all antiarrhythmic drugs were discontinued for 
5 half lives. No patient had been treated with amiodarone. Two or three multipolar electrode catheters were used. They were percutaneously inserted under local anaesthesia through the femoral vein and positioned under fluoroscopic guidance in the high right atrium, His bundle area and right ventricle. Programmed ventricular stimulation (PVS) was performed with a Biotronik® UHS 20 Universal heart stimulator (Biotronik, Berlin, Germany) with pulse duration of 2 ms at twice diastolic threshold. The programmed ventricular stimulation protocol utilized up to three extrastimuli delivered during sinus rhythm and after eight paced ventricular cycle lengths at 500, 430, 375 and 333 ms. First the right ventricular apex, then the right ventricular outflow tract was tested in case no sustained ventricular arrhythmia was induced before. Recordings were made at paper speed of 100 mm s–1 (MICOR®, Siemens Elema AB, Solna, Sweden).
Definitions
Syncope: sudden transient loss of consciousness and postural tone with spontaneous recovery.
Structural heart disease: coronary artery disease (with or without prior myocardial infarction) or dilated cardiomyopathy (left ventricular ejection fraction <50% on echocardiography or radionuclide angiography).
Monomorphic ventricular tachycardia: ventricular tachycardia (VT) manifesting a beat-to-beat uniform surface ECG QRS configuration.
Polymorphic ventricular tachycardia: VT that has no constant morphology for more than five complexes, has no clear isoelectric baseline or has QRS complexes that are asynchronous in multiple simultaneously recorded leads.
Sustained ventricular tachycardia: VT that lasts 30 s or that is haemodynamically intolerable and needs termination.
Non-sustained ventricular tachycardia: run of 3 ventricular beats terminating within 30 s.
Ventricular fibrillation: presence of irregular undulations of varying contour and amplitude and absence of distinct QRS complexes, ST segments and T waves.
The positive end-point of programmed ventricular stimulation was defined as induction of a sustained monomorphic/polymorphic VT or as induction of ventricular fibrillation.
Cardiac death: a witnessed death of cardiac nature as result of progressive heart failure and/or myocardial infarction under observation in a medical facility at the time of death.
Sudden cardiac death: a death cardiac in nature that occurs instantaneously or within 1 h after the onset of symptoms. Unwitnessed death: a death, which is unexpected and without other apparent cause including death during sleep is considered sudden cardiac death. Non-sudden cardiac death: a death cardiac in nature that occurs >1 h after the onset of symptoms.
Non-cardiac death: all deaths that are not classified as cardiac death.
Data collection
July 1, 2002 was determined as the last day of data collection for this study. The duration of follow-up was calculated from the time of electrophysiological study. Telephone interviews were performed if patients had not been seen in the outpatient department within the previous 3 months. In case of death, physicians and family members as well as witnesses were interviewed for detailed circumstances. The ‘real’ follow-up end-point for the ICD treated group was the last time, when their device was interrogated, and this date was used for survival analysis. Stored ECGs with RR intervals and device settings for each patient's ICD were used for data analysis. Only appropriately delivered therapy was permitted for analysis.
Statistics
All continuous variables are given as mean±standard deviation and were compared using the Student's t test or Wilcoxon's non-parametric test, as appropriate. Nominal variables were compared using the chi-square or Fisher's exact test, as appropriate. Statistical significance was assumed if the null hypothesis could be rejected at the 0.05 probability level. To assess predictors of recurrent arrhythmias, recurrent syncope, clinical condition and total mortality Kaplan–Meier analysis was performed. Comparisons between survival curves were made using the logrank test to determine statistically significant (P<0.05) differences. Comparisons between induced and spontaneous detected VT cycle lengths were made using the Pearson correlation coefficient with a 95% mean predictive regression interval. Software: Statistical Analysis System, SAS® Version 8.2, Cary, NC, U.S.A.
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Results |
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Of 423 patients with syncope, who had undergone electrophysiological testing, 52 patients (12.3%), 34 males and 18 females with a mean age of 62±10 years, met the required inclusion criteria. The underlying heart disease was coronary artery disease in 40 patients (77%) and dilated cardiomyopathy in 12 patients (23%). Based on the result of the electrophysiological study 11 patients with inducible sustained ventricular tachyarrhythmias were treated with an ICD and non-inducible patients were left on best conventional therapy (non-ICD group, 39 patients). Two non-inducible patients (only non-sustained VT) spontaneously experienced symptomatic ventricular tachyarrhythmias minutes after PVS (one patient with sustained VT and one patient with ventricular fibrillation). Subsequently, both were referred for ICD implantation and enrolled in the ICD group (ICD group, 13 patients). Overall, two patients received epicardial ICD devices (Medtronic 7217B, Medtronic, Inc., Minneapolis, MN, U.S.A.), the remaining 11 patients received transvenous subpectoral ICD devices (Medtronic 7218, 7219, 7227 and 7250, Medtronic, Inc., Minneapolis, MN, U.S.A., CPI 1753, 1793 and 1851, Cardiac Pacemakers, Inc., St. Paul, MN, U.S.A.). Three patients underwent elective generator replacement during follow-up. The clinical characteristics of the two study groups are detailed in Table 1.
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Electrophysiological study results and spontaneous arrhythmias
ICD group. Sustained monomorphic VT was induced in six patients (five patients with coronary artery disease, one patient with dilated cardiomyopathy), sustained polymorphic VT in one patient with dilated cardiomyopathy and ventricular fibrillation was induced in four patients (three patients with coronary artery disease, one patient with dilated cardiomyopathy). During a mean follow-up period of 5±2.8 years none of the patients with inducible polymorphic VT or inducible ventricular fibrillation experienced spontaneous ventricular arrhythmias. In contrast, four of six patients (three patients with coronary artery disease, one patient with dilated cardiomyopathy) with inducible monomorphic VT experienced arrhythmic events. (Table 2) To the best of our knowledge, all arrythmias and/or syncopal events during follow-up were not related to an acute coronary syndrome. Among ICD patients who received appropriate shocks the mean time from defibrillator implantation to the first appropriate shock was 2.2±3.3 years. Comparison of the cycle lengths of spontaneous ICD detected tachyarrhythmias and induced VTs in patients with appropriate ICD discharge revealed no relationship (negative correlation coefficient, R=–0.224, P=ns).
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Five of 13 ICD patients (39%) had one or more recurrent syncopal event without device discharge during follow-up.
Non-ICD group. None of the patients without inducible arrhythmias experienced documented sustained ventricular arrhythmias during follow-up. During Holter monitoring four of 39 patients (10%) experienced one or more recurrent syncopal event not associated with ventricular arrhythmias during follow-up. Calculated from these data the positive and negative predicted values of programmed ventricular stimulation for tachyarrhythmias and sudden cardiac death were 36 and 98%, respectively (sensitivity, 80%; specificity, 85%).
Survival analysis
ICD group. One patient died from stroke. This death was classified non-cardiac.
Non-ICD group. Six patients died: there were two non-sudden cardiac deaths (one death was caused by pulmonary embolization and one patient died intra-operatively during coronary bypass surgery). The remaining four deaths were classified non-cardiac: one patient died from stroke, two patients died from pneumonia and the fourth patient died from Hepatitis C induced liver failure.
Kaplan–Meier analysis for overall survival between the two groups is shown in Fig. 1. After a follow-up period of 2, 5 and 7 years 90% of ICD patients and 97, 90 and 75% of non-ICD patients were still alive. The difference in survival did not reach statistical significance.
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Figure 2 shows a hypothetical survival curve of ICD patients in comparison with the overall survival of non-ICD patients. ICD terminated episodes of ventricular tachyarrhythmias at a heart rate of more than 240 beats per minute (bpm) serve as surrogate for sudden death. The hypothetical survival curve immediately diverges in the early follow-up period to reach a statistically significant difference (P=0.047) after 4 years of follow-up. Thereafter, the two survival curves converge again.
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The influence of left ventricular ejection fraction and clinical condition on arrhythmic events in the ICD group is shown in Fig. 3. After 3 years of follow-up about half the patients in clinical class NYHA II and two-thirds of the patients in clinical class NYHA III have received at least one appropriate ICD discharge. After 5.2 years of follow-up virtually all patients in clinical class NYHA III had received ICD therapies. Actually the same was true when patients were stratified according to the degree of left ventricular dysfunction.
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ICD patients had more syncopal events than non-ICD patients. This reached statistical significance during follow-up (P=0.016). Figure 4 shows the syncope free time in both groups. After a follow-up period of 2 and 5 years, 71 and 60% of ICD patients and 92 and 89% of non-ICD patients, respectively, were free of recurrent syncope.
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Discussion |
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The results of this study provide further evidence that in patients with unexplained syncope, underlying structural heart disease and no documented arrhythmias electrophysiological testing with induction of sustained ventricular tachyarrhythmias is of diagnostic value. Using this technique in 21% of our patients potentially life-threatening tachyarrhythmias could be induced and were considered potentially causative of syncopal episodes. Similar results are reported in the literature with induction of sustained ventricular tachyarrhythmias in 21–50% of patients with unexplained syncope and structural heart disease[11
–15]. Considering patients with positive test results at high risk for sudden arrhythmic death[16–20] all patients inducible into sustained ventricular tachyarrhythmias received implantable devices whereas non-inducible patients received no antiarrhythmia therapy at all.
Overall, mortality in the two study groups was virtually identical. In good accordance with published data[3,12] patients with negative results from electrophysiological testing had no documented arrhythmic events and none of the patients died suddenly during a follow-up period of 4.6±2.7 years. In contrast, 39% of the ICD patients received appropriate ICD therapies due to recurrent ventricular tachyarrhythmias. To the best of our knowledge, there are only limited data available on spontaneous arrhythmic events in patients with unexplained syncope, no documented arrhythmias and positive results from electrophysiological testing[21–26]. In good accordance with our findings Link et al.[25] reported similar appropriate ICD discharge rates of 50% at 3 years of follow-up. Not all VT necessarily result in sudden cardiac death, although in patients with severely reduced LV function VT events easily may degenerate into VF. There is general agreement on the fact that VT with a heart rate of 240 bpm reflects a life-threatening condition serving as a surrogate for sudden arrhythmic death[27]. In our study two out of 13 patients experienced device defined VF and sudden death was immediately aborted by the implanted device. Comparison of the survival curves of the two study groups reveals that the hypothetical survival curve of the ICD group immediately diverges from the survival curve of the control group indicating the worse prognosis of high-risk patients.
A strong correlation between arrhythmic events, the degree of left ventricular dysfunction and the clinical condition of the patients was found. Overall, the worse the clinical condition of the patients and the more left ventricular function was compromised the earlier the implanted device was needed for arrhythmia intervention. After 4.5 years of follow-up virtually all patients in NYHA III class and all patients with an ejection fraction below 25% needed the implanted device.
ICDs store endocardial electrograms before and after energy discharge allowing at least discrimination between monomorphic and polymorphic VT and ventricular fibrillation.
The majority of VT detected and treated by the devices had monomorphic QRS complexes and only one patient who was inducible into monomorphic VT on programmed stimulation spontaneously developed polymorphic VT requiring device discharge.
Of note, patients with ventricular fibrillation and polymorphic VT induced on EP-testing who were considered at high risk and therefore were referred for ICD implantation, have not yet experienced any arrhythmic event during follow-up. This is in accordance with Mittal et al.[28], who recently showed that the long-term follow-up of patients with and without inducible VF demonstrates no difference in survival between the two groups.
In contrast to others[21,22] no strong relationship between induced and spontaneous VT cycle length was detected in our series. This could be due to the use of an aggressive stimulation protocol which included triple extrastimuli.
In our study, electrophysiological testing had a sensitivity and specificity of 80 and 85%, respectively, resulting in a positive predictive value of 36% and a negative predictive value of 98%.
These data support the hypothesis that only monomorphic VT induced on programmed stimulation are of predictive value. The results of our study justify aggressive prophylactic arrhythmia management in high-risk patients even in the absence of available randomized studies. In randomized prospective studies in different clinical settings[29–32] the superiority of ICD therapy in comparison with conventional antiarrhythmic treatment has been well established and it is only reasonable to infer comparable results in the given patient population.
Limitations of the study
A combination of a prospective evaluation with a partially retrospective investigation such as this study is subject to well-known limitations. All ‘missing data’ had to be retrieved by intensive search in several patient files or by additional calls for patients to come to the outpatient department. LV ejection fraction data could not be calculated appropriately in about 10% of the non-ICD group.
Conclusions
Syncope per se does not necessarily herald a bad prognosis in patients with structural heart disease and no documented ventricular arrhythmias. Moreover, syncope does not correlate well with potentially life-threatening arrhythmias.
PVS reliably stratifies high-risk patients from low-risk patients irrespective of syncopal events. Patients with severely depressed left ventricular function and bad clinical condition benefit most from an ICD.
Even after the exclusion of all possible non-arrhythmogenic diseases and the induction of sustained VT, syncope and ventricular arrhythmias do not necessarily correlate. This finding should be taken into consideration when dealing with this clinical setting.
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[1] Gregoratos G, Cheitlin MD, Conill A, et al. ACC/AHA guidelines for implantation of cardiac pacemakers and antiarrhythmia devices: executive summary. Circulation 1998; 97: 1325–1335.[Medline]
[2] Kapoor WN, Karpf M, Wieand S, et al. A prospective evaluation and follow-up of patients with syncope. N Engl J Med 1983; 309: 197–204.[Abstract]
[3] Kushner JA, Kou WH, Kadish AH, et al. Natural history of patients with unexplained syncope and a nondiagnostic electrophysiologic study. J Am Coll Cardiol 1989; 14: 391–396.[Abstract]
[4] Klein GJ, Gersh BJ, Yee R. Electrophysiological testing: the final court of appeal for diagnosis of syncope? Circulation 1995; 92: 1332–1335.
[5] Brugada P, Green M, Abdollah H, et al. Significance of ventricular arrhythmias initiated by programmed ventricular stimulation: the importance of the type of ventricular arrhythmia induced and the number of premature stimuli required. Circulation 1984; 69: 87–92.
[6] Stevenson WG, Stevenson LW, Weiss J, et al. Inducible ventricular arrhythmias and sudden death during vasodilator therapy of severe heart failure. Am Heart J 1988; 116: 1447–1454.[CrossRef][Web of Science][Medline]
[7] Hammill SC, Trusty JM, Wood DL, et al. Influence of ventricular function and presence or absence of coronary artery disease on results of electrophysiologic testing for asymptomatic nonsustained ventricular tachycardia. Am J Cardiol 1990; 65: 722–728.[Medline]
[8] Lindsay BD, Osborn JL, Schechtman KB, et al. Prospective detection of vulnerability to sustained ventricular tachycardia in patients awaiting cardiac transplantation. Am J Cardiol 1992; 69: 619–624.[CrossRef][Medline]
[9] Powell AC, Fuchs T, Finkelstein DM, et al. Influence of implantable cardioverter defibrillators on the long-term prognosis of survivors of out-of-hospital cardiac arrest. Circulation 1993; 88: 1083–1092.
[10] Manolis AS, Linzer M, Salem D, et al. Syncope: current diagnostic evaluation and management. Ann Intern Med 1990; 112: 850–863.
[11] Krol RB, Morady F, Flaker GC, et al. Electrophysiologic testing in patients with unexplained syncope: clinical and noninvasive predictors of outcome. J Am Coll Cardiol 1987; 10: 358–363.[Abstract]
[12] Bachinsky WB, Linzer M, Weld L, et al. Usefulness of clinical characteristics in predicting the outcome of electrophysiologic studies in unexplained syncope. Am J Cardiol 1992; 69: 1044–1049.[CrossRef][Web of Science][Medline]
[13] Morady F, Shen E, Schwartz A, et al. Long-term follow-up of patients with recurrent unexplained syncope evaluated by electrophysiologic testing. J Am Coll Cardiol 1983; 2: 1053–1059.[Abstract]
[14] Sra JS, Anderson AJ, Sheikh SH, et al. Unexplained syncope evaluated by electrophysiologic studies and head-up tilt testing. Ann Intern Med 1991; 114: 1013–1019.[Web of Science][Medline]
[15] Akhtar M, Shenasa M, Denker S, et al. Role of cardiac electrophysiologic studies in patients with unexplained recurrent syncope. Pacing Clin Electrophysiol 1983; 6: 192–201.[CrossRef][Medline]
[16] Bass EB, Elson JJ, Fogoros RN, et al. Long-term prognosis of patients undergoing electrophysiologic studies for syncope of unknown origin. Am J Cardiol 1988; 62: 1186–1191.[CrossRef][Web of Science][Medline]
[17] Doherty JU, Pembrook-Rogers D, Grogan EW, et al. Electrophysiologic evaluation and follow-up characteristics of patients with recurrent unexplained syncope and presyncope. Am J Cardiol 1985; 55: 703–708.[CrossRef][Web of Science][Medline]
[18] Denes P, Uretz E, Ezri MD, et al. Clinical predictors of electrophystologic findings in patients with syncope of unknown origin. Arch Intern Med 1988; 148: 1922–1928.
[19] Click RL, Gersh BJ, Sugrue DD, et al. Role of invasive electrophysiologic testing in patients with symptomatic bundle branch block. Am J Cardiol 1987; 59: 817–823.[CrossRef][Web of Science][Medline]
[20] Lacroix D, Dubuc M, Kus T, et al. Evaluation of arrhythmic causes of syncope: correlation between Holter monitoring, electrophysiologic testing and body surface potential mapping. Am Heart J 1991; 122: 1346–1354.[CrossRef][Web of Science][Medline]
[21] Andrews NP, Fogel RI, Pelargonio G, et al. Implantable defibrillator event rates in patients with unexplained syncope and inducible sustained ventricular tachyarrhythmias. J Am Coll Cardiol 1999; 34: 2023–2030.
[22] Menon V, Steinberg JS, Akiyama T, et al. Implantable cardioverter defibrillator discharge rates in patients with unexplained syncope, structural heart disease, and inducible ventricular tachycardia at electrophysiologic study. Clin Cardiol 2000; 23: 195–200.[Web of Science][Medline]
[23] Militianu A, Salacata A, Seibert K, et al. Implantable cardioverter defibrillator utilization among device recipients presenting exclusively with syncope or near-syncope. J Cardiovasc Electrophysiol 1997; 8: 1087–1097.[Web of Science][Medline]
[24] Knight BP, Goyal R, Pelosi F, et al. Outcome of patients with nonischemic dilated cardiomyopathy and unexplained syncope treated with an implantable defibrillator. J Am Coll Cardiol 1999; 33: 1964–1970.
[25] Link MS, Costeas XF, Griffith JL, et al. High incidence of appropriate implantable cardioverter-defibrillator therapy in patients with syncope of unknown etiology and inducible ventricular arrhythmias. J Am Coll Cardiol 1997; 29: 370–375.[Abstract]
[26] Mittal S, Iwai S, Stein KM, et al. Long-term outcome of patients with unexplained syncope treated with an electrophysiologic-guided approach in the implantable cardioverter-defibrillator era. J Am Coll Cardiol 1999; 34: 1082–1089.
[27] Bocker D, Block M, Isbruch F, et al. Do patients with an implantable defibrillator live longer? J Am Coll Cardiol 1993; 21: 1638–1644.[Abstract]
[28] Mittal S, Hao SC, Iwai S, et al. Significance of inducible ventricular fibrillation in patients with coronary artery disease and unexplained syncope. J Am Coll Cardiol 2001; 38: 371–376.
[29] Prystowsky EN and Nisam S. Prophylactic implantable cardioverter defibrillator trials: MUSTT, MADIT, and beyond. Multicenter unsustained tachycardia trial. Multicenter automatic defibrillator implantation trial. Am J Cardiol 2000; 86: 1214–1215.[CrossRef][Web of Science][Medline]
[30] The antiarrhythmics versus implantable defibrillators (AVID) investigators: a comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med 1997; 337: 1576–1583.
[31] Siebels J and Kuck KH. Implantable cardioverter defibrillator compared with antiarrhythmic drug treatment in cardiac arrest survivors (the Cardiac Arrest Study Hamburg). Am Heart J 1994; 127: 1139–1144.[CrossRef][Web of Science][Medline]
[32] Connolly SJ, Gent M, Roberts RS, et al. Canadian Implantable Defibrillator Study (CIDS): a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation 2000; 101: 1297–1302.
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