ICD
Predictors of VT/VF-occurrence in ICD patients: results from the PROFIT-Study
1 Department of Cardiovascular Medicine, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany; 2 Department of Thoracic and Cardiovascular Surgery, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany; 3 Department of Clinical Chemistry, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany; 4 Department of Biometrics, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany
Manuscript submitted 28 March 2006. Accepted after revision 19 May 2006.
* Corresponding author. Tel: +49 511 5325948; fax: +49 511 5328475. E-mail address: gunnarklein{at}yahoo.de
 |
Abstract |
|---|
 Top Abstract IntroductionMaterials and methodsResultsDiscussionConclusionsReferences |
|---|
Aims Identification of risk factors for ventricular tachycardia/ventricular fibrillation (VT/VF) occurrence in patients with implantable cardioverter-defibrillators (ICD) is reasonable, because ICD patients with multiple risk factors might benefit from more aggressive anti-arrhythmic therapy for the prevention of arrhythmic events. Furthermore, in the era of prophylactic ICD therapy and limited healthcare resources, additional markers are needed for improved patient selection.
Methods and results Thus, in Prospective Analysis of Risk Factor for Appropriate ICD Therapy (PROFIT), we prospectively analyzed the role of ejection fraction (EF), N-terminal probrain natriuretic peptide (NT-proBNP), New York Heart Association (NYHA) class, atrial fibrillation, and QRS-duration as independent predictors for VT/VF occurrence in 250 ICD patients. Kaplan–Meier analysis showed that EF<40% (log-rank P=0.001), NT-proBNP levels higher than median (
405 ng/L; log-rank P=0.04), QRS-duration 150 ms (log-rank P=0.016), permanent atrial fibrillation (log-rank P=0.008), and higher NYHA class (log-rank P=0.029) were associated with VT/VF occurrence. By multivariate Cox regression analysis EF, QRS-duration and atrial fibrillation remained significantly associated with appropriate VT/VF therapy, whereas there was no relationship among NT-proBNP, NYHA class, and VT/VF occurrence. Stratifying patients according to the number of their independent risk factors (EF<40%, AF, QRS-width150 ms) showed that patients with greater than or equal to two risk factors had a 100% 2-year risk of VT/VF occurrence, whereas patients with no or one risk factor had a 19.3 and 25% 2-year risk, respectively.
Conclusions EF<40%, permanent atrial fibrillation, and QRS150 ms are independent predictors for VT/VF occurrence in predominantly secondary prophylactic ICD patients. Combining all independent predictors, we developed a risk score for VT/VF occurrence identifying a subgroup of patients with two or more risk factors who had a 100% 2-year risk. Future studies will reveal if this risk score helps to identify ICD patients suitable for empirical anti-arrhythmic therapy and to improve patient selection for prophylactic ICD therapy.
Key Words: Implantable cardioverter-defibrillator, Risk factors for VT/VF occurrence, Ventricular tachyarrhythmias
|
Introduction |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionConclusionsReferences |
|---|
Recent trials have confirmed the superiority of the implantable cardioverter-defibrillator (ICD) compared with anti-arrhythmic therapy for primary or secondary prevention of sudden cardiac death and mortality.1
–7 MUSTT7 and MADIT-I2 revealed that patients with reduced ejection fraction (EF) due to ischaemic cardiomyopathy, non-sustained ventricular tachycardias, and inducibility on electrophysiological (EP) study are suitable candidates for primary prophylactic ICD therapy.
The aim of the present study was prospectively to assess predictors of ventricular tachycardia/ventricular fibrillation (VT/VF) occurrence in ICD patients. Identification of risk factors for VT/VF occurrence in ICD patients might be of benefit: First, patients with multiple risk factors might benefit from more aggressive anti-arrhythmic therapy for the prevention of arrhythmic events. Secondly, as in AVID,1 32% of patients had not experienced spontaneous sustained VT or VF at 2 years, patient selection for ICD therapy still has to be improved. Recent primary prophylactic device studies (MADIT-II3 and SCD-HeFT5) emphasize this need, because ICD implant rates are expected to rise dramatically and healthcare resources are limited. Identification of VT/VF risk will facilitate allocation of this life-saving therapy to those patients who will benefit the most.
Thus, PROFIT (Prospective Analysis of Risk Factors for appropriate ICD Therapy) is a prospective single-centre study, investigating the role of EF, N-terminal probrain natriuretic peptide (NT-proBNP), New York Heart Association (NYHA) class, atrial fibrillation, and QRS-duration as independent predictors for VT/VF occurrence in 250 ICD patients.
|
Materials and methods |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionConclusionsReferences |
|---|
Inclusion criteria
The PROFIT study is a single-centre prospective cohort study of consecutive ICD patients designed to identify pre-specified risk factors, i.e. EF, NT-proBNP, NYHA class, atrial fibrillation, and QRS-duration as predictors for VT/VF events. For inclusion in the study, patients had to meet the 2002 American College of Cardiology/American Heart Association guidelines for ICD implantation (Class I–IIb).8
Enrolment began in March 2003 and ended in March 2004. At entry into the study, clinical characteristics were collected through medical record review and interrogation of the patients. Congestive heart failure (CHF) severity was categorized according to NYHA class at baseline interview. EF was determined either by echocardiography or LV-angiography. For analysis of NT-proBNP blood was collected at baseline interview. NT-pro-BNP was measured using an electrochemiluminescence immunoassay ‘ECLIA’ (Roche Diagnostics, Mannheim, Germany)9.
Follow-up
Patients were monitored for ICD therapies (only sustained VT/VF episodes either treated by anti-tachycardia pacing or shock were included) and clinical endpoints (death, hospitalization due to heart failure, or myocardial infarction) during routine follow-up visits every 6 months. Hospitalization due to heart failure was defined as NYHA class IV (pulmonary oedema) or ankle oedema, making intravenous diuretic treatment necessary. Myocardial infarction (STEMI and NSTEMI) were defined as previously described.10,11 Appropriate device therapy for sustained VT/VF was confirmed by two electrophysiologists (GK/TK) by analysis of stored electrograms as previously described.12,13 The electrophysiologists were unaware of the patients' EF, NT-proBNP levels, NYHA-class, and QRS-duration.
Statistical analysis
Sample size was calculated by nQuery Advisor Release 6.0 based on previous results showing a 2.4-fold increased risk for appropriate shocks in patients with heart failure NYHAIII when compared with NYHA
II.14 Assuming an equal distribution of patients NYHAIII and NYHAII, we estimated a sample size of 125 patients per group to reach a statistical power >90%. Fisher's exact test was used to compare categorical variables, and Student's t-test was used to compare continuous variables. Cumulative event proportions were calculated by the Kaplan–Meier method, and outcome differences of patients were assessed by log-rank test. Cox regression analysis was performed to evaluate associations between risk factors at enrolment and appropriate ICD therapy. As prospectively defined, patients were stratified for EF<or 40% (median), NT-proBNP<or 405 ng/L (median), no CHF/NYHA I or NYHA II/III, and QRS-duration<or150 ms. QRS-duration was only measured in spontaneous beats in sinus rhythm or atrial fibrillation. P<0.05 was considered statistically significant. Values are means±SD. All statistical analysis was performed using SPSS for Windows 12.0 (SPSS Inc., Chicago, USA).
|
Results |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionConclusionsReferences |
|---|
Baseline characteristics
PROFIT study enrolled 250 ICD patients. At inclusion, patients were predominantly male, on average 63±13 years old (Table 1). Underlying heart disease was coronary artery disease in 62%, non-ischaemic dilated cardiomyopathy in 21%, arrhythmogenic right ventricular cardiomyopathy (ARVC), or suspected ARVC in 7% and valvular heart disease, hypertensive cardiomyopathy, long-QT-syndrome, and hypertrophic cardiomyopathy in the remaining patients (10%). Patients had a mean EF of 40±16% and a mean NYHA class of 2.1±0.8. A total of 17% had permanent atrial fibrillation, baseline QRS-duration was 144±41 ms. Indication for ICD therapy was primary prophylactic in 7.6% (non-sustained VT, EF
35% due to ischaemic cardiomyopathy, and inducibility in EP study) and secondary prophylactic in 92.4% (successful resuscitation of VT/VF or recurrent sustained VT with or without syncope). Single-chamber devices were seen in 69%; 27% had dual-chamber devices; and 4% had biventricular ICDs for primary prophylactic reasons. Lowest VT-detection zone was 174±18 bpm. In the VT-zone, three bursts and three ramps were programmed for anti-tachycardia pacing, whereas in VF-zone shocks of 30–40 J were programmed. Patients had a mean NT-proBNP serum level of 1663 ng/L at inclusion. Patients had a mean follow-up of 549±118 days (18.3 months).
|
NT-proBNP and EF are independent predictors for death, myocardial infarction, and hospitalization for heart failure in ICD patients
Kaplan–Meier analysis showed that patients with EF<40% or NT-proBNP levels higher than the median (
405 ng/L) had a significantly higher probability of experiencing any of the clinical endpoints (Figure 1A and B). By univariate analysis, NT-proBNP and EF, but not atrial fibrillation or QRS-duration 150 ms were significant predictors for the combined clinical endpoint (Table 1). Multivariate Cox regression analysis including EF, atrial fibrillation, QRS-duration, and NT-proBNP revealed that NT-proBNP was an independent predictive factor for the occurrence of any clinical event (Table 2).
|
|
EF, permanent atrial fibrillation, and QRS-duration are independent predictors for occurrence of VT/VF
Among the 250 patients enrolled in PROFIT, 427 sustained VT/VF episodes treated by the ICD were recorded. A total of 46 patients suffered from sustained VT/VF. Mean time to first episode was 529±128 days and mean cycle length of VT/VF was 289±55 ms.
Kaplan–Meier analysis showed that NT-proBNP levels higher than median (405 ng/L) were associated with a significantly higher probability of VT/VF occurrence (Figure 2A, log-rank P=0.004). Furthermore, Kaplan–Meier analysis showed that EF<40% (log-rank P=0.001), QRS-duration 150 ms (log-rank P=0.016), permanent atrial fibrillation (log-rank P=0.008), and higher NYHA class (log-rank P=0.029) were associated with VT/VF occurrence (Figure 2B–E). Of those patients with wide QRS (101 patients), 81% had left bundle branch block pattern, 8% had right bundle branch block pattern, and another 8% had intraventricular conduction delay. Kaplan–Meier analysis showed a higher incidence of VT/VF occurrence in patients with left than with right bundle branch block pattern (log-rank P=0.09, non-significant). Even after multivariate analysis adjusted for underlying heart disease, baseline medication (beta-blocker, sotalol, amiodarone), ICD indication, and CRT-treatment, QRS-duration 150 ms remained an independent predictor of VT/VF occurrence [P=0.042; Exp(B) 0.499; SE 0.341].
|
By multivariate Cox regression analysis, EF, QRS-duration, and atrial fibrillation remained significantly associated with appropriate VT/VF therapy, whereas there was no relationship among NT-proBNP, NYHA-class, and VT/VF occurrence (Table 3).
|
Risk score for prediction of VT/VF occurrence in ICD patients
According to the number of independent risk factors for VT/VF occurrence (EF<40%, QRS-duration
150 ms, and atrial fibrillation), we stratified patients in two groups: patients with no or one risk factor and patients with two or more risk factors. Patients with greater than or equal to two risk factors had a 100% 2-year risk of VT/VF occurrence, whereas patients with no or one risk factor had a 19.3% and 25% 2-year risk of experiencing VT/VF, respectively (Figure 3).
|
|
Discussion |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionConclusionsReferences |
|---|
Major findings
The present study shows that EF, permanent atrial fibrillation, and QRS-duration are independent predictors for VT/VF therapy in predominantly secondary prophylactic ICD patients. Furthermore, NT-proBNP and EF were both independent predictors for the combined clinical endpoint of death, myocardial infarction, and hospitalization for heart failure. By stratifying patients according to their independent risk factors for appropriate VT/VF therapy, we developed a risk score identifying patients with a 100% 2-year risk for VT/VF occurrence.
NT-proBNP for risk stratification
BNP is mainly synthesized and released from ventricular myocytes as a 76 aminoacid N-terminal fragment (N-terminal BNP) and a 32-aminoacid active hormone (BNP) in response to myocyte stretch and transmural pressure load.15 Our data show that NT-proBNP is an independent predictor for clinical events such as death, myocardial infarction, or hospitalization due to heart failure in ICD patients. This is in accordance with various previous studies in heart failure and acute coronary syndrome.16–18
Regarding ventricular arrhythmia burden, our study shows that patients with elevated NT-proBNP are at higher risk for VT/VF. This appears to be reasonable, as BNP is released as a response of the heart to intraventricular pressure or stretch, which in turn causes EP abnormalities like slowing of intraventricular conduction, triggering after depolarizations, and ventricular ectopic beats.14,15,19–21 Moreover, recent studies in mild-to-moderate and severe heart failure identified BNP as an independent risk factor for sudden death.22,23 However, neither study specified arrhythmic death as an outcome. Non-arrhythmic causes of sudden death such as pulmonary emboli, ruptured aneurysms, myocardial infarctions, hyperkalaemia, and electromechanical dissociation could have been underestimated in these studies. In our study, NT-proBNP was not an independent predictor for VT/VF occurrence, possibly because EF was the most reliable predictor for appropriate ICD therapy. The higher incidence of VT/VF episodes in the group with higher NT-proBNP-levels might, therefore, simply reflect the higher risk of ventricular arrhythmias in patients with LV-dysfunction.
EF, atrial fibrillation, and QRS-duration for risk stratification
In accordance with our data, reduced EF has been shown to be a strong risk factor for VT/VF occurrence in various published studies including ICD patients.14,24–27 In our study, patients with EF<40% had a 2.1-fold increase in 2-year risk for experiencing appropriate ICD therapy. The TOVA study has recently shown that patients with EF<20% and NYHA class III have a 3.6-fold 1-year risk for appropriate ICD shock when compared with patients with EF20% and NYHA class I and II.14 However, in TOVA only ICD shocks but not ATP-therapies were included and neither NT-proBNP nor other risk factors, i.e. atrial fibrillation and QRS-duration were studied as predictors for VT/VF occurrence. In our study, multivariate analysis also revealed QRS-duration as an independent predictor for arrhythmia burden. Notably, Kaplan–Meier analysis showed a higher incidence of VT/VF occurrence in patients with left than with right bundle branch block pattern (log-rank P=0.09), although this did not reach significance because of the low number of patients with right bundle branch block pattern. This is in accordance with data showing that heart failure patients with prolonged QRS-duration have higher mortality, show a significant benefit from ICD therapy, and have more recurrences of fast VTs.4,28,29 Our study does not permit the drawing of any conclusions on the role of CRT–ICDs on the incidence of VT/VF occurrence in patients with wide QRS-complexes, but our data suggest that a wide QRS-complex is an independent risk factor for VT/VF occurrence. Controlled, randomized, prospective, and adequately powered studies to assess any beneficial effect of CRT on episode occurrence in ICD patients are still lacking. However, a retrospective ad hoc analysis of the MIRACLE ICD population did not find a beneficial effect of CRT on VT/VF occurrence, neither in patients with primary nor secondary prophylactic ICD indication.30
Another independent predictor of VT/VF by multivariate analysis in our study was permanent atrial fibrillation. Patients with atrial fibrillation had a 1.8-fold increase in 2-year risk of VT/VF. Many hypotheses have been put forward to explain this pathophysiological phenomenon such as tachycardia-induced changes in ventricular refractoriness or indirectly haemodynamic alteration, ischaemia, or neuroendocrine activation because of atrial fibrillation.31,32 In accordance with our data, Gronefeld et al.32 have recently shown that patients with persistent atrial fibrillation at ICD implant had a higher incidence of appropriate ICD therapy than patients in sinus rhythm. Furthermore, the ‘Jewel-AF-study’ showed that atrial tachyarrhythmias increase the risk of ventricular tachyarrhythmias in ICD patients.31
Risk score for VT/VF occurrence and clinical impact
Combining all three independent risk factors (EF<40%, atrial fibrillation, and QRS-duration 150 ms) and stratifying patients according to the number of their individual risk factors showed that patients with two or more risk factors had a 100% 2-year risk of suffering from VT/VF. In the era of primary prophylactic ICD implantation more patients receive ICD therapy. However, after SCD-HeFT, a further risk stratification of heart failure patients beyond EF will be necessary especially on economic grounds. A risk score as described in our study identifies patients at high risk for VT/VF occurrence, who might profit most from ICD therapy. Since in our study most of the patients had a secondary prophylactic ICD indication, further prospective and randomized studies are needed to confirm the value of this easily obtainable risk factor score for patients with primary prophylactic ICD indications.
Apart from patient selection in prophylactic ICD therapy a risk score for appropriate ICD interventions might also be helpful in allocating patients to an empirical anti-arrhythmic medication to prevent ICD shocks and thus improve quality of life. It has recently been shown, that sotalol, azimilide, and amiodarone are effective in reducing appropriate and inappropriate ICD interventions.33–36 Patients with a higher risk score could be good candidates for such therapy.
A potential limitation of our study is the lack of standardized device programming. However, rate-detection settings in patients with and without ICD therapy were identical, arguing against programming differences accounting for the results in the present study.
Another limitation of our study refers to the patient population, which is a predominantly secondary prophylactic ICD population. Thus, our results do not reflect the situation in primary prophylactic ICD patients. Further prospective studies are needed to show if the risk score holds true also for primary prophylactic ICD patients.
|
Conclusions |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionConclusionsReferences |
|---|
EF <40%, permanent atrial fibrillation, and QRS
150 ms are independent predictors for VT/VF occurrence in predominantly secondary prophylactic ICD patients. Combining all independent predictors, we developed a risk score for VT/VF occurrence identifying a subgroup of patients with two or more risk factors who had a 100% 2-year risk. Future studies will reveal if this risk score helps to identify ICD patients suitable for empirical anti-arrhythmic therapy and improve patient selection in prophylactic ICD therapy. |
References |
|---|
|
TopAbstractIntroductionMaterials and methodsResultsDiscussionConclusionsReferences |
|---|
[1] 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: 1576–83.
[2] Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med 1996; 335: 1933–40.
[3] Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med 2002; 346: 877–83.
[4] Bristow MR, Saxon LA, Boehmer J, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med 2004; 350: 2140–50.
[5] Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005; 352: 225–37.
[6] Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med 2004; 350: 2151–8.
[7] Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med 1999; 341: 1882–90.
[8] Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). J Cardiovasc Electrophysiol 2002; 13: 1183–99.[CrossRef][ISI][Medline]
[9] Bettencourt P, Azevedo A, Pimenta J, Frioes F, Ferreira S, Ferreira A. N-terminal-pro-brain natriuretic peptide predicts outcome after hospital discharge in heart failure patients. Circulation 2004; 110: 2168–74.
[10] Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—summary article: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol 2002; 40: 1366–74.
[11] Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction–executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol 2004; 44: 671–719.
[12] Korte T, Koditz H, Niehaus M, Paul T, Tebbenjohanns J. High incidence of appropriate and inappropriate ICD therapies in children and adolescents with implantable cardioverter defibrillator. Pacing Clin Electrophysiol 2004; 27: 924–32.[CrossRef][Medline]
[13] Korte T, Jung W, Ostermann G, et al. Hospital readmission after transvenous cardioverter/defibrillator implantation; a single centre study. Eur Heart J 2000; 21: 1186–91.
[14] Whang W, Mittleman MA, Rich DQ, et al. Heart failure and the risk of shocks in patients with implantable cardioverter defibrillators: results from the Triggers Of Ventricular Arrhythmias (TOVA) study. Circulation 2004; 109: 1386–91.
[15] de Lemos JA, McGuire DK, Drazner MH. B-type natriuretic peptide in cardiovascular disease. Lancet 2003; 362: 316–22.[CrossRef][ISI][Medline]
[16] Anand IS, Fisher LD, Chiang YT, et al. Changes in brain natriuretic peptide and norepinephrine over time and mortality and morbidity in the Valsartan Heart Failure Trial (Val-HeFT). Circulation 2003; 107: 1278–83.
[17] Kragelund C, Gronning B, Kober L, Hildebrandt P, Steffensen R. N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med 2005; 352: 666–75.
[18] Doust JA, Pietrzak E, Dobson A, Glasziou P. How well does B-type natriuretic peptide predict death and cardiac events in patients with heart failure: systematic review. BMJ 2005; 330: 625.
[19] Hansen DE, Craig CS, Hondeghem LM. Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback. Circulation 1990; 81: 1094–105.
[20] Franz MR, Cima R, Wang D, Profitt D, Kurz R. Electrophysiological effects of myocardial stretch and mechanical determinants of stretch-activated arrhythmias. Circulation 1992; 86: 968–78.
[21] Reiter MJ. Effects of mechano-electrical feedback: potential arrhythmogenic influence in patients with congestive heart failure. Cardiovasc Res 1996; 32: 44–51.[CrossRef][ISI][Medline]
[22] Berger R, Huelsman M, Strecker K, et al. B-type natriuretic peptide predicts sudden death in patients with chronic heart failure. Circulation 2002; 105: 2392–7.
[23] Isnard R, Pousset F, Chafirovskaia O, et al. Combination of B-type natriuretic peptide and peak oxygen consumption improves risk stratification in outpatients with chronic heart failure. Am Heart J 2003; 146: 729–35.[CrossRef][ISI][Medline]
[24] Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs. Implantable Defibrillator study. Cardiac Arrest Study Hamburg. Canadian Implantable Defibrillator Study. Eur Heart J 2000; 21: 2071–8.
[25] Grimm W, Flores BT, Marchlinski FE. Shock occurrence and survival in 241 patients with implantable cardioverter-defibrillator therapy. Circulation 1993; 87: 1880–8.
[26] Levine JH, Mellits ED, Baumgardner RA, et al. Predictors of first discharge and subsequent survival in patients with automatic implantable cardioverter-defibrillators. Circulation 1991; 84: 558–66.
[27] Freedberg NA, Hill JN, Fogel RI, Prystowsky EN. Recurrence of symptomatic ventricular arrhythmias in patients with implantable cardioverter defibrillator after the first device therapy: implications for antiarrhythmic therapy and driving restrictions. CARE Group. J Am Coll Cardiol 2001; 37: 1910–5.
[28] Cleland JG, Daubert JC, Erdmann E, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med 2005; 352: 1539–49.
[29] Bode-Schnurbus L, Bocker D, Block M, et al. QRS duration: a simple marker for predicting cardiac mortality in ICD patients with heart failure. Heart 2003; 89: 1157–62.
[30] Wilkoff BL, Hess M, Young J, Abraham WT. Differences in tachyarrhythmia detection and implantable cardioverter defibrillator therapy by primary or secondary prevention indication in cardiac resynchronization therapy patients. J Cardiovasc Electrophysiol 2004; 15: 1002–9.[CrossRef][ISI][Medline]
[31] Stein KM, Euler DE, Mehra R, et al. Do atrial tachyarrhythmias beget ventricular tachyarrhythmias in defibrillator recipients? J Am Coll Cardiol 2002; 40: 335–40.
[32] Gronefeld GC, Mauss O, Li YG, Klingenheben T, Hohnloser SH. Association between atrial fibrillation and appropriate implantable cardioverter defibrillator therapy: results from a prospective study. J Cardiovasc Electrophysiol 2000; 11: 1208–14.[CrossRef][ISI][Medline]
[33] Pacifico A, Hohnloser SH, Williams JH, et al. Prevention of implantable-defibrillator shocks by treatment with sotalol. DL-Sotalol Implantable Cardioverter-Defibrillator Study Group. N Engl J Med 1999; 340: 1855–62.
[34] Dorian P, Borggrefe M, Al-Khalidi HR, et al. Placebo-controlled, randomized clinical trial of azimilide for prevention of ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator. Circulation 2004; 110: 3646–54.
[35] Aiba T, Kurita T, Taguchi A, et al. Long-term efficacy of empirical chronic amiodarone therapy in patients with sustained ventricular tachyarrhythmia and structural heart disease. Circ J 2002; 66: 367–71.[CrossRef][ISI][Medline]
[36] Connolly SJ, Dorian P, Roberts RS, et al. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: the OPTIC Study: a randomized trial. JAMA 2006; 295: 165–71.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  M. T. Koller, B. Schaer, M. Wolbers, C. Sticherling, H. C. Bucher, and S. Osswald Death Without Prior Appropriate Implantable Cardioverter-Defibrillator Therapy: A Competing Risk Study Circulation, April 15, 2008; 117(15): 1918 - 1926. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Gardiwal, H. Yu, H. Oswald, U. Luesebrink, A. Ludwig, A. M. Pichlmaier, H. Drexler, and G. Klein Right ventricular pacing is an independent predictor for ventricular tachycardia/ventricular fibrillation occurrence and heart failure events in patients with an implantable cardioverter-defibrillator Europace, March 1, 2008; 10(3): 358 - 363. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Mittal Selecting Patients for an Implantable Cardioverter-Defibrillator: Can the Genie Be Put Back Into the Bottle? J. Am. Coll. Cardiol., January 22, 2008; 51(3): 297 - 299. [Full Text] [PDF]
|
|
|
|
|
|
R. Worck, J. Haarbo, and P. E. B. Thomsen Electrophysiological study and 'slow' ventricular tachycardia predict appropriate therapy: results from a single-centre implantable cardiac defibrillator follow-up Europace, November 1, 2007; 9(11): 1048 - 1053. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Ezekowitz, B. H. Rowe, D. M. Dryden, N. Hooton, B. Vandermeer, C. Spooner, and F. A. McAlister Systematic Review: Implantable Cardioverter Defibrillators for Adults with Left Ventricular Systolic Dysfunction Ann Intern Med, August 21, 2007; 147(4): 251 - 262. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. J. Wellens The significance of atrial fibrillation in heart failure Eur. Heart J., December 1, 2006; 27(23): 2740 - 2741. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||