Optimizing the clinical use of implantable defibrillators in patients with Brugada syndrome
1 Heart Rhythm Management Institute, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090-B Brussels, Belgium
2 Cardiology Department, Thorax Institute, University of Barcelona, Barcelona, Spain
* Corresponding author. Tel: +32 2477 6010; fax: +32 2477 6840. E-mail address: andreasarkozy{at}yahoo.ca
 |
Abstract |
|---|
 Top Abstract IntroductionConclusionsAcknowledgementsReferences |
|---|
Our review highlights the difficulties we face when treating patients with Brugada syndrome (BS) by an implantable cardioverter defibrillator (ICD). Higher defibrillation thresholds, high inappropriate shock rates because of sinus tachycardia and supraventricular tachycardias, T wave oversensing, and high lead failure rates should be expected. Psychosocial adjustment problems also occur frequently in this patient population. These high complications rates are because of specific characteristics of the BS patient population, consisting of young, active patients with a primary electrical disease. The management strategies include prevention and early recognition of the expected complications. Additionally, individualized careful programming of the ICD is essential to ensure maximal safety and minimal complication rates in patients with BS.
Key Words: Brugada syndrome • Implantable cardioverter defibrillator • Ventricular tachyarrhythmias
|
Introduction |
|---|
|
TopAbstractIntroductionConclusionsAcknowledgementsReferences |
|---|
The first human internal defibrillator was implanted in 1980, and 5 years later the artificial implantable defibrillator was approved for general use in the USA.1,2 Later devices included lower energy shocks and were called implantable cardioverter defibrillators (ICD). These early devices consisted of a large pulse generator placed in the abdominal wall, epicardially implanted patch electrodes for defibrillation and epicardial screw in electrodes for rate sensing. Each device was ordered individually from the manufacturer with a prespecified detection rate. The implant procedures required thoracotomy with general anaesthesia and significant perioperative mortality rates. Following the implantation the detection rate or any other parameter of the device was no longer programmable. These early defibrillators were able to deliver only monophasic shocks as therapy and their storage capacities of episodes for review were minimal.2
In the last 20 years enormous advances in lead, pulse generator systems, and defibrillation waveforms opened a new era of cardioverter defibrillator therapy. The current devices are implanted pectorally and transvenously without general anaesthesia and with minimal perioperative complication rates. These sophisticated devices can be programmed to several tachycardia zones with programmable antitachycardia pacing or mono or biphasic shock as therapies. The analysis of the stored electrograms (EGM) allows a unique opportunity to study spontaneous arrhythmias. Furthermore, carefully designed rhythm algorithms are incorporated in the devices to differentiate between supraventricular and ventricular arrhythmias. Ten years ago, dual-chamber devices with additional atrial sensing and pacing possibilities were introduced allowing even more sophisticated rhythm algorithms.3
Since its introduction, the clinical efficacy of the ICD in preventing sudden death has been extensively studied in patients with structural heart disease. The prototype patient in these studies was a 60- to 65-year-old male following myocardial infarction with decreased left ventricular function. It has been proven that in this patient population the ICD is able significantly to prolong life.4 Although similar randomized trials are not available, the benefit of the ICD therapy is even more impressive in patients with primary electrical diseases, the so-called ‘channelopathies’. This patient population differs significantly from the patients with structural heart disease. Patients with primary electrical disease are younger have a structurally normal heart with a normal left ventricular ejection fraction, and therefore do not have any competing risk factors for death. Their life expectancy is normal, provided that their potentially lethal ventricular arrhythmias are effectively treated.
The Brugada syndrome (BS), described in 1992, is one of the primary electrical diseases, characterized by coved type ST elevation in the right precordial leads (V1–3) (Figure 1) and increased risk of sudden death in the absence of structural heart disease.5 Currently, in high-risk BS, ICD therapy is the only effective treatment for the prevention of sudden death.6 Initially, the prototype patient was a 40- to 45-year-old male with normal left ventricular function presenting after aborted sudden death because of ventricular fibrillation (VF). Currently, because of the increased awareness worldwide, the majority of patients diagnosed as having BS presents with syncope or is identified accidentally on routine ECG examination. Given the fact that BS is a potentially lethal, rare, and only a recently described disease, randomized studies are not available (and are not expected for ethical reasons) to guide our management of patients with ICDs and BS. The best available evidence comes from one large European multicentre registry of 220 patients, but in this registry implantation and device programming differed from centre to centre,7 and in our single-centre retrospective study of only 47 patients.8 Both of these recently available studies indicate that the ICD patient population with BS has features which are unique to the disease. This review will focus on these specific features.
|
Defibrillation thresholds
The accepted method for ICD implantation for the last two decades included defibrillation threshold (DFT) testing, namely the induction of ventricular fibrillation to ensure that the ICD will properly detect and terminate spontaneous ventricular arrhythmias. The recently raised questions and doubts over DFT testing in the general ICD patient population have been reviewed.9 It is believed that defibrillation does not have a threshold but a probabilistic nature.9 Furthermore, many factors influence the actual DFT, including sympathetic tone, circadian variations, antiarrhythmic drugs, and baseline heart disease.9 For these reasons, the widely adopted standard practice to achieve an acceptable DFT is a 10 J safety margin between the lowest successful defibrillation energy and the maximal device output.9 The evident risk of unacceptable high DFT is sudden death because of the failure of the ICD to terminate spontaneous ventricular fibrillation (VF). Recent studies indicate that in the general ICD population 4.6–6.2% of patients has unacceptably high DFTs at implantation testing, requiring corrective measures.9,10 The patient population with BS was expected to have normal DFTs, given the absence of any underlying structural heart disease.
However, Watanabe et al.11 recently studied 22 patients with BS undergoing ICD implantation with single-coil shock leads. They observed an elevated DFT (>25 J) in 18% of their study population. Compared with patients with structural heart disease, the mean effective refractory period and the VF cycle lengths were significantly shorter in patients with BS. However, VF cycle length was not different between patients with and without defibrillation failure in BS, suggesting that short refractoriness and consequent reinitiation of VF is not sufficient to explain the observed high DFTs.11 The suggested alternative explanation, which also lacks any solid evidence, was the absence of sufficient current densities in the epicardium of the right ventricular outflow tract (thought to be responsible for the typical ECG pattern and initiation of lethal ventricular arrhythmias) to achieve uniform prolongation of refractoriness. Sacher et al.7 in the above-mentioned large multicentre study of 220 patients, with BS following ICD implantation, found that 12% of the patients had a DFT >21 J. Similarly, our single-centre experience of 62 patients with BS with primary or secondary indication for ICD implantation showed that 13% of the patients had a DFT >21 J (unpublished data).
The reasons for the higher than expected DFTs in BS are unknown. Factors to predict which patient will have elevated DFTs are not identified. The treatment options for high DFTs during ICD implantation have recently been reviewed and are not different in BS from the general ICD population.10 For prevention, as in BS, left-sided pectoral implantation should be favoured. In current standard clinical practice a triangular configuration is used including an active can and a dual-coil single lead with proximal coil in the superior vena cava (SVC) right atrial junction and the distal coil in the apex. The distal shock coil should be positioned apically in the right ventricle (RV). Adequate sensing should be ensured at the time of implantation to prevent T wave oversensing, which is also a characteristic in this syndrome. The most straightforward solution for high DFT is the implantation of a high-output pulse generator (Table 1). However, besides the stored shock energy reported by the manufactures, attention should also be paid to the delivered energy at different loads.12 More importantly, it should be kept in mind that the voltage and the waveform duration influence defibrillation efficacy more directly than the stored energy.13 Another option for the treatment of high DFT includes the programming of the biphasic shock waveform depending on its availability (Table 1). One manufacturer offers the opportunity to programme both the tilt (the percentage difference between leading and trailing edge voltages at which the phase shifts) and the pulse durations of the biphasic waveform.14 This allows individual patient optimization at implant based on protocols taking into account the lead impedance and device capacitance.14 Further management options in all current devices include the programming option of the shock polarity. Recent evidence suggests that the distal RV coil functioning as anode results in lower DFT in the majority of patients.15 Another possibility is to change the lead configuration.10 In patients with dual-coil leads, one manufacturer allows programming of the SVC coil out of circuit, in other devices the SVC coil can be manually disconnected. In contrast, in patients with a single-coil lead the addition of an SVC coil might be helpful. In some patients, a RV outflow tract lead position may be attempted to achieve a lower DFT.10 Finally, implantation of a subcutaneous array electrode is an efficient way to lower DFT in the majority of the patients.10
|
Inappropriate shocks
Our recent single-centre study of 47 patients demonstrated that during a follow-up of 54 ± 33 months after primary prophylactic ICD implantation 36% of the patients received inappropriate shocks (IS).8 Patients with IS tended to be younger than those without; mean age: 39.2 ± 11 vs. 47.5 ± 16 years (P = 0.06).8 Similarly, Sacher et al.7 observed after primary or secondary prophylactic ICD implantation in 220 patients, an IS rate of 20% during a mean follow-up of 38 ± 27 months. Also in this study, patients with IS tended to be younger (43 ± 13 vs. 47 ± 12, P = 0.07). In both studies the same causes were found to account for the high IS rates.
Sinus tachycardia
In our study, we used a conservative lower VF detection rate of 180 b.p.m., and 17% of the patients received ISs for sinus tachycardia at a mean rate of 184 ± 11 b.p.m. during a mean follow-up of about 4.5 years. Patients with IS because of sinus tachycardia tended to be younger than the rest of the population; mean age 36.4 ± 8 vs. 46.2 ± 15 years (P = 0.08). In most cases of IS for sinus tachycardia, reprogramming of higher lower detection rates (
200 b.p.m.) was safe and prevented recurrent shocks.8
Sacher et al.7 observed in their multicentre study, likely because of their choice of higher VF detection rates selected at baseline, only 5% of patients had ISs for sinus tachycardia during a mean follow-up of approximately 3.2 years.
Given the young age and active lifestyle of our patients, many of them engaging in regular sports activities, it is not surprising that one of the leading causes of IS in BS is sinus tachycardia at rates >180 b.p.m. Additionally, patients with BS, in contrast to the long QT and hypertrophic cardiomyopathy ICD populations, are less likely to receive beta-blockers, because of the previously described worsening effect of these drugs on the ST elevation pattern.6
Supraventricular tachycardias
In our study, the second most frequent cause of IS was supraventricular tachycardia (SVT) with fast ventricular rates (197 ± 28 b.p.m.) falling into the VF zone, where neither the dual- nor the single-chamber algorithms are able to differentiate VF from SVT. During a mean follow-up of 4.5 years, 13% of our patients had IS most frequently for atrial flutter-fibrillation. All of these patients developed the atrial arrhythmia for the first time following the ICD implantation, and therefore were not on any medication at the time of the IS.8 The combination of reprogramming to higher VF detection rates or incorporating the SVT enhancement criteria and initiation of antiarrhythmic treatment prevented the recurrence of IS in most cases.8
Sacher et al.7 also observed in 4% of their patient population ISs for SVT during a mean follow-up of 3.2 years. They found that a history of SVT was predictive of ISs, but the antiarrhythmic medication at the time of IS was not mentioned in this study.
It is also not surprising that atrial arrhythmias were a frequent cause of IS. It is well documented that patients with BS have a higher risk of atrial arrhythmias.16 Additionally, the absence of rate-slowing medications, especially in the case of new onset arrhythmias explains the extremely fast ventricular rates, high enough to fall into the VF zone.
There are several management options for prevention of the very high IS rates because of SVT and sinus tachycardia. We do not advocate routine use of dual-chamber devices in patients with BS to avoid IS for several reasons. First, in our study the occurrence of IS was not different in single- vs. dual-chamber devices. This is likely because of the fact that the ventricular rates are usually very fast falling into the VF zone where the therapy is not influenced by the atrial information. Secondly, given the young age of our patient population, similar to the paediatric and adolescent population, multiple lifetime pulse generator and lead replacement are expected.17 The addition of an atrial lead not only limits future access for new leads, but recent evidence suggests that it also increases lead failure rates, already high in patients with BS.18 Therefore, our approach favours the use of individualized programming options in single-chamber devices before upgrading to dual chamber. Currently, in patients younger than 50 years, we recommend programming a single VF zone with the lower detection rate 200 b.p.m. We are careful with the routine programming of a single VF zone with a lower detection rate >220 b.p.m., since during our follow up of 62 patients after primary or secondary ICD implantation we have lost one patient in whom ventricular fibrillation at rates of 180–200 b.p.m. occurred during redetection within 30 s of episode initiation (Figure 2). In the presence of documented or expected fast atrial arrhythmias, or antiarrhythmic therapy known to decrease VF cycle lengths (for example quinidine or amiodarone therapy given for atrial fibrillation) or documented spontaneous or induced monomorphic ventricular tachycardia (VT), programming a fast VT zone at 180 up to 220 b.p.m. with SVT enhancement criteria is a reasonable option. In current devices the programmable SVT criteria, which withhold therapy, are the onset, stability, morphology, and their combination (Table 1). The ‘sudden onset’ criterion will diagnose ventricular origin of the tachycardia in the VT rate zone if the first two R–R intervals of tachycardia decrease (reflecting heart rate increase) with more than a preprogrammed value (for example 20%). This criterion is designed to prevent inappropriate therapy for sinus tachycardia, when the heart rate is expected to increase gradually into the VT zone. The limitation of this feature is the potential failure to detect VTs that arise during exercise or a VT, which is initiated during a SVT with fast ventricular rates that we have observed in several of our patients (Figure 2). The ‘stability’ criterion refers to the variability of the R–R intervals during tachycardia and was designed to differentiate stable monomorphic VT from atrial fibrillation. However, in patients with BS this criterion is not very useful and might even be dangerous leading to the withholding of therapy for VT/VF, since most of the ventricular arrhythmias are polymorphic. Theoretically, the most promising feature to avoid recurrent ISs for SVT/sinus tachycardia in BS is the ‘morphology’ feature. This algorithm compares (depending on the manufacturer) different characteristics of the electrogram (EGM) QRS complex morphology during tachycardia and sinus rhythm.19–21 The QRS complex morphology is expected to be different during VT and similar during SVT. Two manufacturers express the similarity as a morphology % match between the tachycardia and the stored sinus QRS complex template.19,20 The threshold match value above which the QRS complex is diagnosed as supraventricular is programmable in these devices (nominal: 60 or 70%). A third manufacturer, collecting a sinus QRS EGM template from two channels, depending on the automatically calculated similarity score, labels the complexes automatically as normal, if they are similar enough to the template saved and abnormal if not.21 In all three algorithms a certain number of beats must qualify as match or normal (programmable by one manufacturer and three out of eight tachycardia beats by the others) for the tachycardia to be diagnosed as SVT resulting in no therapy. The reported sensitivities and specificities with these algorithms vary.19–21 However, all these studies were performed in the general ICD population, where the majority of arrhythmias are monomorphic VTs.19–21 Theoretically in BS where the ventricular arrhythmias are more likely polymorphic, the morphology discriminators should even perform better. However, recent data indicate that the variability of the surface ECG pattern in BS is even more than previously thought.8,22 Evidence suggests that surface ECG alterations are coupled with right ventricular endocardial EGM changes.23 Although in all three algorithms an automatic template update system has recently been incorporated, allowing the automatic collection of a new template if change is detected and is compared with the previous one. Given the large variability, further studies are necessary to test the safety of these algorithms in BS. The danger of all of these SVT enhancement criteria is undersensing and withholding therapy for ventricular arrhythmia. Theoretically, withholding therapy might be more dangerous in BS where ventricular arrhythmias occur much less frequently but are likely to be more fatal compared with the general ICD population. In this latter population slower monomorphic VTs occur more frequently, and they are probably less dangerous. These speculations need further investigations. Although ISs impair quality of life24,25 and can be proarrhythmic, until further evidence is available the patients' safety should be the primary concern.
|
T wave oversensing
In our study only 2% of the patients have received IS because of T wave oversensing.8 Sacher et al.7 reported IS because of T wave oversensing in 5% of their patient population. Additionally, they observed that patients with T wave oversensing at follow-up were more likely to have low (<5 mV) R wave amplitude at implant (P = 0.02).
Several cases of T wave oversensing in BS have been reported previously.23 In one report, dynamic surface ECG changes, which are characteristic of the syndrome were accompanied by right endocardial EGM changes leading to R wave amplitude decrease and T wave increase. Interestingly, these changes were not observed on the left epicardial endocardial signal, but were reproducible with ajmaline administration.23
Management options of T wave oversensing in all devices include decreasing the sensitivity. However, if this treatment option is chosen, DFT testing should be repeated to ensure appropriate sensing of ventricular fibrillation. In certain devices two more parameters of sensitivity are programmable to avoid T wave oversensing. One of them is the starting threshold (in percentages) of the R wave amplitude, where, at the end of the QRS complex, sensing begins. Increasing this value leads to decrease in sensitivity. Secondly, the start of the subsequent automatic decay in sensitivity could be delayed. If the programming options are exhausted without success, a new lead should be implanted. Some authors advocate a left-sided epicardial sense and pace lead implantation to avoid recurrence.23 Another recent report described two interesting cases of T wave oversensing solved by pulse generator replacement without new lead implantation. The authors concluded that the T wave oversensing was because of inadequate signal processing by the ICD generators.26
Lead-related issues
In our study another important reason for IS was the oversensing of noise. During our follow-up, altogether 13% of our patients required a new lead implantation because of sensing or pacing malfunction of the lead. The patients with lead-related problems were significantly younger at the time of first implantation than those without; mean age, 32 ± 6 vs. 46.4 ± 14 years (P = 0.02), suggesting that the age and the active lifestyle of patients were the important aetiological factors.8 Similarly, Sacher et al.7 reported 9% lead failure rate in their study with approximately 1 year shorter mean follow-up.
In a recent large study in a general ICD population similar high annual lead failure rates were observed during long-term follow-up; the lead survival rates 5 and 8 years after implantation were 85 and 60%, respectively. In this study similar to our results the patients with lead defects were younger than those without.18 Additionally, patients with single chamber devices tended to have lead defects less frequently.18
The management options for lead failures besides replacement include prevention and early recognition. As a possibly useful preventive measure, the shock lead should be introduced through the cephalic vein. Additionally, patients should be advised to avoid regular practice of some sports activities, such as rowing and weight lifting. Regarding early recognition, home monitoring is an excellent method for the detection of lead defects prior to the occurrence of ISs.27
Psychosocial issues
Studies of young ICD recipients revealed that these patients have frequent psychosocial adjustment problems following the implantation. These lifestyle adjustment problems are significant and are different from those of older ICD recipients. Their level of anxiety is higher and they frequently fear physical exertion and shocks.24 This evidence suggests that special attention should be paid to assessing and addressing the psychological aspects. The routine assessment following the implantation of an ICD in a young patient and, if necessary, follow-up consultations by a psychologist might help to prevent and treat these psychosocial adjustment problems.24
|
Conclusions |
|---|
|
TopAbstractIntroductionConclusionsAcknowledgementsReferences |
|---|
Our review highlights the difficulties we face when treating patients with BS by ICD therapy, or in other words, the clinical problems of saving many healthy patient years in young active patients. Higher DFTs, high IS rates because of sinus tachycardia, SVTs, T wave oversensing, and high lead failure rates must be expected. Psychosocial adjustment problems also occur frequently in this patient population. These high complications rates are because of specific characteristics of the BS patients who are young and active with structurally normal hearts. The management strategies include prevention and early recognition of expected complications. Additionally, careful individualized programming of the ICD is essential to ensure maximal safety and minimal IS and other complication rates.
|
Acknowledgements |
|---|
|
TopAbstractIntroductionConclusionsAcknowledgementsReferences |
|---|
The authors would like to thank to Michel Janssens (St Jude Medical), Manuel Sabbe (Biotronik GMBH), Jos Backers (ELA Medical Sorin), Alex Mestdag (Medtronic Inc.), and Peter Goemaere (Guidant Inc.) for their support.
Conflict of Interest: none declared.
|
References |
|---|
|
TopAbstractIntroductionConclusionsAcknowledgementsReferences |
|---|
- Mirowski M, Mower MM, Reid RR. The automatic implantable defibrillator. Am Heart J (1980) 100:1089–1092.[CrossRef][Web of Science][Medline]
- Gollob MH, Seger JJ. Current status of the implantable cardioverter defibrillators. Chest (2001) 119:1210–1221.[CrossRef][Web of Science][Medline]
- Lavergne T, Daubert JC, Chauvin M, Dolla E, Kacet S, Leenhardt A, Mabo P, Ritter P, Sadoul N, Saoudi N, Henry C, Nitzsche R, Ripart A, Murgatroyd F. Preliminary clinical experience with the first dual chamber pacemaker defibrillator. Pacing Clin Electrophysiol (1997) 20:182–188.[CrossRef][Medline]
- Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, Domanski M, Troutman C, Anderson J, Johnson G, McNulty SE, Clapp-Channing N, Davidson-Ray LD, Fraulo ES, Fishbein DP, Luceri RM, Ip JH. Sudden Cardiac Death in Heart Failure (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Eng J Med (2005) 352:225–237.
[Abstract/Free Full Text] - Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol (1992) 20:1391–1396.[Abstract]
- Antzelevitch C, Brugada P, Borggrefe M, Brugada J, Brugada R, Corrado D, Gussak I, LeMarec H, Nademanee K, Perez Riera AR, Shimizu W, Schulze-Bahr E, Tan H, Wilde A, Brugada syndrome. Report of the second consensus conference. Circulation (2005) 111:659–670.
[Abstract/Free Full Text] - Sacher F, Probst V, Iesaka Y, Jacon P, Laborderie J, Mizon-Gerard F, Mabo P, Reuter S, Lamaison D, Takahashi Y, O'Neill MD, Garrigue S, Pierre B, Jais P, Pasquie J, Hocini M, Salvador-Mazenq M, Nogami A, Amiel A, Defaye P, Bordachar P, Boveda S, Maury P, Klug D, Babuty D, Haissaguerre M, Mansourati J, Clementy J, Le Marec H. Outcome after implantation of a cardioverter-defibrillator in patients with Brugada syndrome: a multicenter study. Circulation (2006) 114:2317–2324.
[Abstract/Free Full Text] - Sarkozy A, Boussy T, Kourgiannides G, Chierchia GB, Richter S, De Potter T, Geelen P, Wellens F, Spreeuwenberg, Brugada P. Long term follow up of primary prophylactic implantable cardioverter-defibrillator therapy in Brugada syndrome. Eur Heart J (2007) 28:334–344.
[Abstract/Free Full Text] - Swerdlow CD, Russo AM, Degroot PJ. The dilemma of ICD implant testing. Pacing Clin Electrophysiol (2007) 30:675–700.[CrossRef][Medline]
- Mainigi SK, Callans DJ. How to manage the patient with a high defibrillation threshold. Heart Rhythm (2006) 3:492–495.[CrossRef][Web of Science][Medline]
- Watanabe H, Chinushi M, Sugiura H, Washizuka T, Komura S, Hosaka Y, Furushima H, Watanabe H, Hayashi J, Aizawa YJ. Unsuccessful internal defibrillation in Brugada syndrome: focus on refractoriness and ventricular fibrillation cycle length. J Cardiovasc Electrophysiol (2005) 16:262–266.[CrossRef][Web of Science][Medline]
- Thammanomai A, Sweeney MO, Eisenberg SR. A comparison of the output characteristics of several implantable cardioverter-defibrillators. Heart rhythm (2006) 3:1053–1059.[CrossRef][Web of Science][Medline]
- Swerdlow CD. ICD waveforms: what really matters. Heart Rhythm (2006) 3:1060–1062.[CrossRef][Web of Science][Medline]
- Mouchawar G, Kroll M, Val-mejias JE, Schwartzman D, Mckenzie J, Fitzgerald D, Prater S, Katcher M, Fain E, Syed Z. ICD waveform optimization: a randomized prospective pair-sampled multicenter study. Pacing Clin Electrophysiol (2000) 23:1992–1995.[Medline]
- Kroll M, Efimov IR, Tchou PJ. Present understanding of shock polarity for internal defibrillation: The obvious and non-obvious clinical implications. Pacing Clin Electrophysiol (2006) 29:885–891.[CrossRef][Medline]
- Bordachar P, Reuter S, Garrigue S, Cai X, Hocini M, Jais P, Haissaguerre M, Clementy J. Incidence, clinical implications and prognosis of atrial arrhythmias in Brugada syndrome. Eur Heart J (2004) 25:879–884.
[Abstract/Free Full Text] - Love BA, Barrett KS, Alexander ME, Bevilacqua LM, Epstein MR, Triedman JK, Walsh EP, Berul CI. Supraventricular arrhythmias in children and young adults with implantable cardioverter defibrillators. J Cardiovasc Electrophysiol (2001) 12:1097–1101.[CrossRef][Web of Science][Medline]
- Kleemann T, Becker T, Doenges K, Vater M, Senges J, Schneider S, Saggau W, Weisse U, Seidl K. Annual rate of transvenous defibrillation lead defects in implantable cardioverter-defibrillators over a period of 10 years. Circulation (2007) 115:2474–2480.
[Abstract/Free Full Text] - Boriani G, Occhetta E, Pistis G, Menozzi C, Jofrida M, Sermasi S, Pagani M, Gasparini G, Musso G, Dall'Acqua A, Biffi M, Branzi A. Combined use of morphology discrimination, sudden onset and stability as discriminating algorithms in single chamber cardioverter defibrillators. Pacing Clin Electrophysiol (2002) 25:1357–1366.[CrossRef][Medline]
- Klein GJ, Gillberg JM, Tang A, Inbar S, Sharma A, Unterberg-Buchwald C, Dorian P, Duru F, Rooney E, Becker D, Schaaf K, Benditt D, for the worldwide WAVE investigators. Improving SVT discrimination in single-chamber ICDs: a new electrogram morphology-based algorithm. J Cardiovasc Electrophysiol (2006) 17:1310–1319.[CrossRef][Web of Science][Medline]
- Gold MR, Shorofsky SR, Thompson JA, Kim J, Schwartz M, Bocek J, Lovett EG, Hsu W, Morris MM, Lang DJ. Advanced rhythm discrimination for implantable cardioverter defibrillators using electrogram vector timing and correlation. J Cardiovasc Electrophysiol (2002) 13:1092–1097.[CrossRef][Web of Science][Medline]
- Veltman C, Schimpf R, Echternach C, Eckardt L, Kuschyk J, Streitner F, Spehl S, Borggrefe M, Wolpert C. A prospective study on spontaneous fluctuations between diagnostic and non-diagnostic ECGs in Brugada syndrome: implications for correct phenotyping and risk stratification. Eur Heart J (2006) 27:2544–2552.
[Abstract/Free Full Text] - Stix G, Della Bella P, Carbucicchio C, Schmidinger H. Spatial and temporal heterogeneity of depolarization and repolarization may complicate implantable cardioverter defibrillator therapy in Brugada syndrome. J Cardiovasc Electrophysiol (2000) 11:516–521.[CrossRef][Web of Science][Medline]
- Sears SF, Burns JL, Handberg E, Sotile WM, Conti JB. Young at heart: understanding the unique psychosocial adjustment of young implantable cardioverter defibrillator recipients. Pacing Clin Electrophysiol (2001) 24:1113–1117.[CrossRef][Medline]
- Schron EB, Exner DV, Yao Q, Jenkins LS, Steinberg JS, Cook JR, Kutalek SP, Friedman PL, Bubien RS, Page RL, Powell J. Quality of life in the antiarrhythmics versus implantable defibrillators trial: impact of therapy and influence of adverse symptoms and defibrillator shocks. Circulation (2002) 105:589–594.
[Abstract/Free Full Text] - Gilliam FR. T-wave oversensing in implantable cardiac defibrillators is due to technical failure of device sensing. J Cardiovasc Electrophysiol (2006) 17:553–556.[CrossRef][Web of Science][Medline]
- Lazarus A. Remote wireless, ambulatory monitoring of implantable pacemakers, cardioverter defibrillators, and cardiac resynchronization therapy systems: analysis of a worldwide database. Pacing Clin Electrophysiol (2007) 30:S2–S12.[Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||