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The benefits and use of shock advisory defibrillators in hospitals.

Survival to discharge following a cardiac arrest is dependent on rapid and effective basic and advanced life support. Paramount to a rapid response is access to sufficiently trained health care providers, who have a duty to perform basic life support and initiate early defibrillation. In hospitals, defibrillation remains the domain of specially prepared staff and the type of defibrillator used might be crucial to rapid and effective defibrillation. The advent of automatic external defibrillators has increased the range of people who can use a defibrillator successfully. For nurses, arguably a lack of familiarity about the benefits of and the use of automatic external defibrillators are the greatest barriers to nurse-initiated defibrillation programmes. This paper explores the use of automatic external defibrillators, their relationship to the associated defibrillator waveforms and the benefits of their use by registered nurses within the hospital setting.

Clinical Competence↗

Internal cardiac defibrillation threshold: effects of acute ischemia.

The influence of myocardial ischemia on defibrillation success was studied using two different lead orientations in halothane-anesthetized pigs. Ischemia was induced by ligating the left anterior descending artery in its distal third. Controls had loosely tied ligatures placed around the artery at the same site. Ventricular fibrillation was induced by electrical stimulation 30 minutes after coronary artery ligation. Defibrillation used a single truncated pulse of approximately 6 ms duration passed to either: a transvenous electrode catheter (Medtronic, 6880) with the cathode in the apex of the right ventricle and the anode in the superior vena cava-atrial junction region, or the cathode in the apex of the right ventricle and a mesh plaque on the epicardium of the basal lateral left ventricle as anode. Ten seconds after the onset of ventricular fibrillation, defibrillation was attempted with increasing incremental energies until defibrillation was achieved. Fibrillation episodes were repeated at 15-minute intervals until the minimum first shock was successful in defibrillating the animal (i.e., defibrillation threshold). The number of animals successfully defibrillated with a minimum energy above or below 30 J was not different between normal and ischemic animals for either electrode configuration (i.e., 3 out of 20 vs 1 out of 13 for the catheter and 5 out of 6 vs 6 out of 7 for the epicardial plaque, respectively). Also, the cumulative percent success as a function of defibrillation energy was similar in both the normal and ischemic groups. There was a significant reduction in the minimum energy necessary for defibrillation when passing current between the right ventricular apex and the left ventricular epicardial plaque. The present results indicate that, despite differences in lead orientations, acute ischemia in the anesthetized pig does not appear to influence defibrillation success.

Animals↗

Defibrillation using a high-frequency series of monophasic rectangular pulses: observations and model predictions.

INTRODUCTION: Capacitor-discharge type waveforms are practical for defibrillation devices but may not be optimum. Discharging a capacitor as a series of high-frequency (HF) pulses may allow effective waveform shaping by modulating the pulses. This approach could lead to improved defibrillation by allowing waveforms that would otherwise be unachievable with a capacitor-discharge approach. However, little is known about defibrillation with HF. METHODS AND RESULTS: In open chest pentobarbital anesthetized dogs, we measured defibrillation thresholds for continuous rectangular waveforms with 5-, 10-, and 20-msec durations and for 10- and 20-msec long series of HF rectangular pulses. HF series had a 50% "on-time" duty cycle at 100 Hz to 20 kHz. At 1 kHz and above, defibrillation with HF required the same time-averaged current but approximately twice the peak current and energy as defibrillation with continuous waveforms having the same envelope duration. At lower frequencies, defibrillation peak current and energy approached values required for the continuous waveforms. While waveforms were not actually filtered, the heart responded as though the HF series were low-pass filtered. A filtered effective waveform model with a 3.7-msec time constant predicts these HF data and makes reasonable predictions for various continuous waveform shapes. CONCLUSION: Defibrillation is possible using HF pulses up to 20 kHz and has a frequency response similar to a low-pass filter. A filtered effective waveform model predicts these HF results and may help explain how waveforms influence defibrillation efficacy. While the unmodulated HF pulsing used in this study increased defibrillation requirements, these findings support the concept that HF pulse modulation can be used to change the effective shape of a waveform, which could permit more efficacious waveform shapes and a net reduction of thresholds.

Analysis of Variance↗

Potential impact of public access defibrillators on survival after out of hospital cardiopulmonary arrest: retrospective cohort study.

OBJECTIVE: To estimate the potential impact of public access defibrillators on overall survival after out of hospital cardiac arrest. DESIGN: Retrospective cohort study using data from an electronic register. A statistical model was used to estimate the effect on survival of placing public access defibrillators at suitable or possibly suitable sites. SETTING: Scottish Ambulance Service. SUBJECTS: Records of all out of hospital cardiac arrests due to heart disease in Scotland in 1991-8. MAIN OUTCOME MEASURES: Observed and predicted survival to discharge from hospital. RESULTS: Of 15 189 arrests, 12 004 (79.0%) occurred in sites not suitable for the location of public access defibrillators, 453 (3.0%) in sites where they may be suitable, and 2732 (18.0%) in suitable sites. Defibrillation was given in 67.9% of arrests that occurred in possibly suitable sites for locating defibrillators and in 72.9% of arrests that occurred in suitable sites. Compared with an actual overall survival of 744 (5.0%), the predicted survival with public access defibrillators ranged from 942 (6.3%) to 959 (6.5%), depending on the assumptions made regarding defibrillator coverage. CONCLUSIONS: The predicted increase in survival from targeted provision of public access defibrillators is less than the increase achievable through expansion of first responder defibrillation to non-ambulance personnel, such as police or firefighters, or of bystander cardiopulmonary resuscitation. Additional resources for wide scale coverage of public access defibrillators are probably not justified by the marginal improvement in survival.

Cardiopulmonary Resuscitation↗

Advance prediction of transthoracic impedance in human defibrillation and cardioversion: importance of impedance in determining the success of low-energy shocks.

The purposes of this study were to evaluate a method that predicts transthoracic impedance in advance of defibrillating shocks in humans and to assess the importance of transthoracic impedance in low-energy defibrillation. Via defibrillator electrodes we applied 31 kHz current to the chest during the defibrillator charge cycle, before the defibrillating shock was actually delivered. The current flow was limited by transthoracic impedance; a microprocessor monitored the predischarge current flow and determined the predischarge impedance by calibration against known resistance values. Actual impedance to the defibrillating shock was also determined and compared with the predicted impedance. With this approach we predicted impedance in 19 patients who received 66 shocks for ventricular and atrial arrhythmias. Predicted impedance (y) correlated very well with actual impedance (x):y = .90x + 11.3; r = .97. To determine the importance of impedance in defibrillation and cardioversion, we prospectively gathered data from 96 patients who received shocks of various energies for ventricular or atrial arrhythmias. In patients with high transthoracic impedance (greater than 97 omega), low-energy shocks (less than or equal to 100 J) for ventricular defibrillation had only a 20% success rate as opposed to a 70% success rate for low-energy shocks in patients with low or average impedance (p less than .05). We conclude that transthoracic impedance can be accurately predicted in advance of defibrillation and cardioversion. This method permits the preshock identification of patients with high impedance in whom attempts to defibrillate with low-energy shocks are inappropriate.

Arrhythmias, Cardiac↗

The potential gradient field created by epicardial defibrillation electrodes in dogs.

Knowledge of the potential gradient field created by defibrillation electrodes is important for the understanding and improvement of defibrillation. To obtain this knowledge by direct measurements, potentials were recorded from 60 epicardial, eight septal, and 36 right ventricular transmural electrodes in six open-chest dogs while 1 to 2 V shocks were given through defibrillation electrodes on the right atrium and left ventricular apex (RA. V) and on the right and left ventricles (RV .LV). The potential gradient field across the ventricles was calculated for these low voltages. Ventricular fibrillation was electrically induced, and ventricular activation patterns were recorded after delivering high-voltage shocks just below the defibrillation threshold. With the low-voltage shocks, the potential gradient field was very uneven, with the highest gradient near the epicardial defibrillation electrodes and the weakest gradient distant from the defibrillation electrodes for both RA. V and RV .LV combinations. The mean ratio of the highest to the lowest measured gradient over the entire ventricular epicardium was 19.4 +/- 8.1 SD for the RA. V combination and 14.4 +/- 3.4 for the RV .LV combination. For both defibrillation electrode combinations, the earliest sites of activation after unsuccessful shocks just below the defibrillation threshold were located in areas where the potential gradient was weak for the low-voltage shocks. We conclude that there is a markedly uneven distribution of potential gradients for epicardial defibrillation electrodes with most of the voltage drop occurring near the electrodes, the potential gradient field is significant because it determines where shocks fail to halt fibrillation, and determination of the potential gradient field should lead to the development of improved electrode locations for defibrillation.

Animals↗

Evaluation of antiarrhythmic drugs on defibrillation energy requirements in dogs. Sodium channel block and action potential prolongation.

Antiarrhythmic drugs have been reported to produce variable effects on defibrillation energy requirements. However, the relation between the in vitro electrophysiologic effects of these agents and the changes in defibrillation energy requirements have not been systematically examined. Therefore, we evaluated the effects of the sodium channel blocking drugs lidocaine and procainamide, the action potential prolonging drugs N-acetyl procainamide and clofilium, and the potassium current blocker cesium in acute canine models with the same internal spring and epicardial patch electrodes used in humans for ventricular defibrillation testing. Ten series of experiments were performed in 78 dogs. Nonlinear regression was used to derive curves of energy dose versus percent successful defibrillation attempts and the 50% and 90% effective energy dose for each experimental condition. Saline control experiments indicated that the preparation was stable throughout the 6-hour duration of the experiments. Lidocaine doubled the defibrillation energy requirement (p less than 0.001) at a mean plasma concentration of 8.2 micrograms/ml. The effect of lidocaine on defibrillation energy was reversible, present at therapeutic plasma concentrations, linearly related to plasma concentration (r = 0.69, p less than 0.002), and present even after only 5-second episodes of ventricular fibrillation. In contrast, procainamide had no effect on defibrillation energy at mean plasma concentrations of 8.5 and 13 micrograms/ml, even after prolonged (30-second) episodes of ventricular fibrillation, whereas N-acetyl procainamide, clofilium, and cesium all decreased the energy requirement for defibrillation by 13-27%. Moreover, with the addition of N-acetyl procainamide, there was a trend toward diminishing the increase in defibrillation energy requirement caused by lidocaine. All agents prolonged the mean ventricular fibrillation cycle length. Lidocaine shortened the QT interval, whereas all other agents increased the QT (p less than 0.05). The major electrophysiologic effect of lidocaine is of sodium channel blockade, whereas, N-acetyl procainamide, clofilium, and cesium predominantly increase the action potential duration, and procainamide exerts both effects. Thus, these data indicate that sodium channel block and action potential prolongation exert significant and antagonistic modulating effects on defibrillation energy requirements.

Acecainide↗

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

To test the hypothesis that a defibrillation shock is unsuccessful because it fails to annihilate activation fronts within a critical mass of myocardium, we recorded epicardial and transmural activation in 11 open-chest dogs during electrically induced ventricular fibrillation (VF). Shocks of 1-30 J were delivered through defibrillation electrodes on the left ventricular apex and right atrium. Simultaneous recordings were made from septal, intramural, and epicardial electrodes in various combinations. Immediately after all 104 unsuccessful and 116 successful defibrillation shocks, an isoelectric interval much longer than that observed during preshock VF occurred. During this time no epicardial, septal, or intramural activations were observed. This isoelectric window averaged 64 +/- 22 ms after unsuccessful defibrillation and 339 +/- 292 ms after successful defibrillation (P less than 0.02). After the isoelectric window of unsuccessful shocks, earliest activation was recorded from the base of the ventricles, which was the area farthest from the apical defibrillation electrode. Activation was synchronized for one or two cycles following unsuccessful shocks, after which VF regenerated. Thus, after both successful and unsuccessful defibrillation with epicardial shocks of greater than or equal to 1 J, an isoelectric window occurs during which no activation fronts are present; the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; unsuccessful shocks transiently synchronize activation before fibrillation regenerates; activation leading to the regeneration of VF after the isoelectric window for unsuccessful shocks originates in areas away from the defibrillation electrodes. The isoelectric window does not support the hypothesis that defibrillation fails solely because activation fronts are not halted within a critical mass of myocardium. Rather, unsuccessful epicardial shocks of greater than or equal to 1 J halt all activation fronts after which VF regenerates.

Animals↗

Influence of acute coronary artery occlusion on direct ventricular defibrillation in dogs.

Automatic defibrillators have been successfully tested in normal animals. However, human candidates for implantation of such devices are likely to have ischemic heart disease. This study examined the optimal site of defibrillation and the influence of acute myocardial ischemia upon the defibrillation threshold in anesthetized dogs. The defibrillation threshold was determined from a transvenous right ventricular intracavitary electrode and from right and left ventricular epicardial electrodes. Shocks were delivered before and after occlusion of the left anterior descending coronary artery. Before occlusion, the rate of successful shocks was low from the right ventricular epicardium, moderate from the right ventricular cavity, and high from the left ventricular epicardium. Furthermore, the defibrillation threshold was significantly lower at the left ventricular epicardium than at the right ventricular sites. During coronary artery occlusion, the rate of successful defibrillation remained high from the left ventricular epicardium, and there was no significant change in the defibrillation threshold. It was concluded that the left ventricular epicardium is the optimal site for defibrillation in the anesthetized dog. Acute coronary artery occlusion did not modify the success rate of defibrillation or the energy required for defibrillation.

Animals↗

Cardioverter-defibrillator implantation in the catheterization laboratory: initial experiences in 48 patients.

The exponential increase in cardioverter-defibrillator implantations has resulted in a need for safe implantations that do not require long waiting periods. We report intraoperative and follow-up results in 48 patients with ventricular tachyarrhythmias who underwent cardioverter-defibrillator implantation in the catheterization laboratory. Twenty-six (54%) patients had their first cardioverter-defibrillator implant (group 1), and 22 (46%) patients underwent pulse-generator replacement (group 2). In all patients, cardioverter-defibrillator implant or pulse-generator replacement was performed with the patient under general anesthesia. In 25 (96%) of 26 patients in group 1, cardioverter-defibrillator implantation was possible with a mean defibrillation threshold of 13 +/- 8 J. One patient had a defibrillation threshold of > 25 J, and therefore cardioverter-defibrillator implant was not achieved. This patient underwent epicardial device implantation 1 day later. Another patient in group 1 had vessel rupture (vena subclavia) intraoperatively. During a mean follow-up of 2 +/- 1 months, two patients died from congestive heart failure 2 and 4 months after device implantation. An infection occurred in one patient in group 2, 3 months after generator replacement. In conclusion, these data show that in the majority of patients cardioverter-defibrillator implantation in the catheterization laboratory is safe and has a low complication rate and therefore can generally be recommended.

Adolescent↗

Effect of shock polarity on ventricular defibrillation threshold using a transvenous lead system.

OBJECTIVES: The purpose of this study was to determine whether the polarity of a monophasic shock used with a transvenous lead system affects the defibrillation threshold. BACKGROUND: The ability to implant an automatic defibrillator depends on achieving an adequate defibrillation threshold. METHODS: A transvenous defibrillation lead with distal and proximal shocking electrodes was used in this study. In 29 consecutive patients, the defibrillation threshold, using a stepdown protocol was determined twice in random order: 1) with the distal coil as the anode, and 2) with the polarity reversed. Only the 20 patients in whom an adequate defibrillation threshold could be obtained with the transvenous lead alone were included in this study. These patients were 61 +/- 14 years old (mean +/- SD) and had a mean ejection fraction of 28 +/- 12%. RESULTS: The mean defibrillation threshold was 11.5 +/- 5.0 J with the distal coil as the anode versus 16.9 +/- 7.7 J with the distal coil as the cathode (p = 0.04). The defibrillation threshold was lower by a mean of 9 +/- 7 J with the former configuration in 14 patients and was lower by a mean of 7 +/- 6 J with the latter configuration in 3 patients; in 3 patients it was the same with both configurations. Use of a subcutaneous patch was avoided in five patients by utilizing the distal electrode as the anode. CONCLUSIONS: Defibrillation thresholds with monophasic shocks are approximately 30% lower with the distal electrode as the anode. The use of anodal shocks may obviate the need for a subcutaneous patch and allow more frequent implantation of a transvenous lead system.

Adult↗

Effect of first-phase polarity of biphasic shocks on defibrillation threshold with a single transvenous lead system.

OBJECTIVES: The purpose of this study was to determine whether the polarity of the first phase of a biphasic shock affects the defibrillation threshold. BACKGROUND: The polarity of a monophasic shock has been shown to affect the defibrillation threshold. METHODS: A transvenous defibrillation lead with distal and proximal shocking electrodes was used in this study. In 15 consecutive patients, the defibrillation threshold was determined twice using a step-down protocol, in random order: with the distal coil as the anode for the initial phase (anodal biphasic shock) and with the polarity reversed (cathodal biphasic shock). The power to detect a 5.0-J difference in this study is 0.96. These patients were 61 +/- 11 years old (mean +/- SD), and the mean left ventricular ejection fraction was 0.32 +/- 0.10. RESULTS: Mean defibrillation threshold using anodal biphasic shocks was 9.9 +/- 4.8 J, compared with 9.5 +/- 4.2 J using cathodal biphasic shocks (p = 0.8). In three patients the defibrillation threshold was lower by a mean of 6.3 +/- 2.9 J with the former configuration; in three patients the defibrillation threshold was lower by a mean of 6.7 +/- 2.5 J with the latter configuration; and in nine patients it was the same. Using the standard cathodal configuration, a defibrillation threshold < or = 10 J was obtained in approximately 70% of patients, and a subcutaneous patch was not required in any patient. CONCLUSIONS: The polarity of the first phase of a biphasic shock used with a single transvenous lead does not affect the defibrillation threshold.

Defibrillators, Implantable↗

Postoperative lead-related complications in patients with nonthoracotomy defibrillation lead systems.

OBJECTIVES: This study sought to document postoperative complications attributable to nonthoracotomy defibrillation lead systems in a large cohort. BACKGROUND: The incidence of postoperative complications specifically associated with nonthoracotomy defibrillation lead systems is unknown. METHODS: Postoperative lead-related complications were evaluated in 170 patients with a nonthoracotomy defibrillation lead system who were followed up for a mean (+/- SD) of 17 +/- 12 months. Each system incorporated one or more intravascular leads. In 117 patients (69%), the system incorporated a subcutaneous defibrillation patch. All implantations were performed in an operating room by cardiothoracic surgeons. Defibrillation thresholds were measured at implantation, before hospital discharge (mean 3 +/- 2 days) and at 4 to 18 weeks after implantation. Patients were evaluated every 2 to 3 months after implantation or as indicated by clinical exigency. RESULTS: Twenty-seven patients (15.9%) were diagnosed with a lead-related complication that either extended the initial hospital period or led to a second hospital admission. Complications included endocardial lead or subcutaneous defibrillation patch dislodgment in eight patients (4.7%), which was diagnosed between 2 and 345 days after implantation; endocardial or subcutaneous patch lead fracture in six (3.5%), which was diagnosed between 53 and 600 days after implantation; subcutaneous patch mesh fracture in one, which was diagnosed at 150 days after implantation; subclavian vein thrombosis in three (1.8%), which was diagnosed at 2 to 50 days after implantation; and unacceptably elevated defibrillation threshold (within 5 J of maximal device output) in nine (5.3%), which was documented at one of the two postimplantation evaluations in eight patients or at the time of failure to terminate a spontaneous ventricular tachycardia in one. Seventeen of the 27 patients required reoperation for correction of their complication. In addition, system infection requiring complete explantation occurred in seven other patients (4.1%) at an interval from implantation ranging from 14 to 120 days. CONCLUSIONS: Postoperative complications related to a nonthoracotomy defibrillation lead system were common and frequently required reoperation for correction. The rate of system explantation due to infection was also significant. Postoperative defibrillation testing and vigilant outpatient follow-up evaluation are necessary to ensure normal lead function.

Binomial Distribution↗

Lead system optimization for transvenous defibrillation.

Lead systems that include an active pectoral shell reduce defibrillation thresholds and permit transvenous defibrillation in nearly all patients. A further improvement in defibrillation efficacy is desirable to allow for smaller pulse generators with a reduced maximum output. Accordingly, the purpose of this study was to compare defibrillation thresholds with multiple transvenous lead systems including those with an active pectoral shell to determine which system would optimize defibrillation energy requirements. This prospective study was performed on 21 consecutive patients. Each subject was evaluated with 3 lead configurations with the order of testing randomized. The configurations were a dual coil transvenous lead (lead), the distal right ventricular coil and pectoral pulse generator shell (unipolar), and all 3 components (triad). The right ventricular coil was the cathode for the first phase of the biphasic defibrillation waveform. Delivered energy at defibrillation threshold was 11.2 +/- 3.4 J for the lead configuration, 10.1 +/- 5.2 J for the unipolar configuration, and 7.8 +/- 3.6 J for the triad configuration (p <0.01). Leading edge voltage (p <0.01) and shock impedance (p <0.001) were also decreased for the triad configuration compared with the lead or unipolar configurations, whereas peak current was minimized with the unipolar configuration (p <0.01). We conclude that the combination of a dual coil, transvenous lead and an active pectoral shell reduces defibrillation energy requirements compared with either the lead alone or unipolar configuration. Moreover, the defibrillation thresholds were < or =15 J in all patients using the triad lead system.

Defibrillators, Implantable↗

[Electromagnetic interference between automatic defibrillators and digital and analog cellular telephones].

BACKGROUND AND OBJECTIVES: Functional pacemaker interference by mobile telephones has been described with analogical systems and with possible greater influence, digital systems, including inhibition and inadequate pacing. The influence of both system has not been extensively studied in patients with implantable cardioverter defibrillators (ICD). PATIENTS AND METHODS: We studied the influence of mobile phones, both digital and analogic network, on the performance of several models of defibrillators, in a standardised test set up designed to provide high sensitivity. The purpose of our study was to establish whether there are any influences on ICD functions, both in in vivo and in in vitro models. Several mobile phones, with different transmission powers, were moved towards the defibrillator and the electrode, under continuous documentation of defibrillator sensing and interrogation afterwards. The experimental model was performed with the aid of an arrhythmia simulator (Intersim) and demo-defibrillators. The tests were repeated both in and out of a solution of saline water with an impedance within normal human limits. RESULTS: Partial loss of telemetry was found in 14 patients, 8 with analogical phones and 6 with digital phones. Fourteen patients showed alterations only on the surface electrocardiogram channel and five on the intracavitary channel. The same results were reproduced in the in vitro model. However, the in vitro test allowed us to simulate multiple ventricular arrhythmias, and demonstrate the normal sensing and functioning of the defibrillator during a "spontaneous" arrhythmia. After testing, we demonstrate that no real oversensing/undersensing was documented in any device. There was no evidence of ICD reprogramming or pacing inhibition. In particular, no inadequate therapies were delivered. CONCLUSIONS: a) in our series, we have not demonstrated clinically significant electromagnetic interferences with mobile phones of digital or analogical networks: b) the in vitro model allowed us to conclude that even if a spontaneous arrhythmia appears, the function of the defibrillator is not altered; c) the use of mobile phones seems to be safe for defibrillator patients, and d) however, some basic rules, such as to maintain the phone at least 15 cm away from the defibrillator, are advised.

Defibrillators, Implantable↗

Pacing threshold increase in nonthoracotomy implantable defibrillator leads: implications for battery longevity and margin of safety.

Just as a stable defibrillation threshold is required for implantable defibrillators to maintain efficacy and a margin of safety for the conversion of life-threatening ventricular arrhythmias, a stable pacing threshold is also required to provide bradycardia support and pacing to terminate ventricular tachycardias. This article reports the temporal course of pacing thresholds in patients treated with a tripolar, tined endocardial defibrillator lead capable of bipolar sensing and pacing, and defibrillation. Seventeen patients who underwent implantation of an implantable defibrillator system using an integrated bipolar pacing/sensing system were prospectively studied over 18 months. There were 16 males and one female, with a mean age of 69 +/- 5 years (range 61-75 years). At implantation, predischarge, and every 2 months thereafter, the pacing pulse-width threshold was tested at both 2.5 and 5.0 V stimulus amplitudes. After a mean follow-up of 363 +/- 173 days (range 34-597 days), the pacing threshold increased from 0.08 +/- 0.08 ms to 0.5 +/- 0.3 ms at the 2.5 V amplitude (p < or = 0.01, CI-0.57 to -0.27) and from 0.04 +/- 0.02 ms to 0.25 +/- 0.14 ms at the 5.0 V amplitude (p < or = 0.01, CI -0.28 to -0.14). Eight of the 17 patients (47%) received spontaneous implantable defibrillator shocks for clinically detected arrhythmias, and the total number of joules delivered via the leads did not correlate with the pacing threshold changes. We conclude that the pacing threshold for the nonthoracotomy implantable defibrillator lead system studied is not stable and increases with time. This finding has implications for defibrillator battery life in patients who use implantable defibrillators for bradycardia pacing.

Aged↗

Can microvolt T-wave alternans testing reduce unnecessary defibrillator implantation?

The Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) and the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) have established that patients with a reduced ejection fraction gain an overall mortality benefit from prophylactic implantable cardioverter-defibrillator therapy. Only a small proportion of the patients in these studies, however, have received life-saving therapy from the defibrillator. Because defibrillator therapy is invasive and expensive, patients with a low ejection fraction would benefit from effective risk stratification so that defibrillator therapy was used only in those at significant risk. In this review, we analyze prospective clinical trials that have evaluated microvolt T-wave alternans (MTWA) testing as a predictor of ventricular tachyarrhythmic events in populations of patients similar to those studied in MADIT II or SCD-HeFT; that is, patients with a reduced ejection fraction who were not selected on the basis of a history of ventricular tachyarrhythmias. In these studies, the average annual rate of fatal and nonfatal ventricular tachyarrhythmic events among the patients who tested negative for MTWA was around 1%. This rate is so low that it is unlikely that such patients would benefit from implantable cardioverter-defibrillator therapy. The mortality, moreover, was lower among MTWA-negative patients who did not receive implantable defibrillators than that observed in the MADIT II and SCD-HeFT patients who received implantable cardioverter-defibrillators. In response, patients with a low ejection fraction who are being considered for implantable cardioverter-defibrillator therapy should undergo MTWA testing as part of their evaluation.

Clinical Trials as Topic↗

The effects of atrial electrical remodeling on atrial defibrillation thresholds.

Electrical remodeling of atrial fibrillation may account for the increase in atrial defibrillation thresholds over time. The aim of this study was to examine the time course of electrical remodeling and the benefit of early defibrillation on the defibrillation threshold. Twenty-six mongrel dogs weighing 27.6 +/- 3.3 kg were induced into AF by repeated high output burst atrial pacing. Eight dogs were paced for multiple time periods of 5, 20, 40, and 60 minutes. Five dogs each had burst pacingfor 4 hours and 8 hours, and eight dogs were paced at a high rate (640 beats/min) for 48 hours. Biphasic atrial defibrillation shocks with a pulse width of 3/3 ms synchronized to the left apical electrogram were delivered to coil electrode catheters positioned in the lateral left and right atria. Defibrillation voltage was increased from 50 V in 20- to 30-V steps until defibrillation was successful. As the pacing period increased, a decrease in atrial fibrillation cycle lengths and atrial effective refractory period was not observed before 8 hours. Similarly, the defibrillation threshold did not change significantly until the 8-hour pacing period was reached. The defibrillation thresholds were 69 +/- 28 V for 5 minutes, 64 +/- 20 V for 20 minutes, 99 +/- 85 V for 40 minutes, 78 +/- 51 V for 60 minutes, 78 +/- 38 V for 4 hours, 124 +/- 33 V for 8 hours, and 133 +/- 32 V for 48 hours (mean +/- SD) (P < 0.05). Atrial electrical remodeling in a rapid atrial pacing canine model is not observed until after 4 hours of burst atrial pacing. The atrial defibrillation threshold increases with increasing duration of burst atrial pacing, and follows a similar time course to other parameters of electrical remodeling.

Animals↗