Clinical predictors of the defibrillation threshold with the unipolar implantable defibrillation system.

OBJECTIVES: The purpose of this study was to determine the relation between clinical variables and the defibrillation threshold by using a standardized testing protocol and a uniform implantable defibrillator system. BACKGROUND: Past studied have not revealed useful correlations between clinical variables and the energy required to terminate ventricular fibrillation. Most of these studies did not use a uniform implantable defibrillator system or a standardized protocol to measure the defibrillation threshold and, thus, did not control for the influence of these technical influences. We postulated that defibrillator and defibrillation threshold measurement-based sources of variability overshadowed important clinical predictors. METHODS: The defibrillation threshold was measured by using a standardized protocol in 101 consecutive patients. We used a transvenous unipolar pectoral defibrillation system that employed a single endocardial right ventricular defibrillation coil as the anode and the shell of an 80-cm3 pulse generator as the cathode to deliver a 65% tilt biphasic pulse. RESULTS: Several clinical variables were found to be significantly associated with the defibrillation threshold: patient gender, height, weight, body surface area, heart rate at rest, QRS and corrected QT (QTc) intervals, left ventricular mass and several measures of heart and chest size by chest roentgenogram. None of these variables had a correlation coefficient > 0.45 with the defibrillation threshold. On multivariate analysis, left ventricular mass and heart rate at rest were the only independent predictors of the defibrillation threshold and explained only 25% of the observed variability. CONCLUSIONS: Despite the use of a uniform transvenous defibrillation system and a standardized protocol to measure the defibrillation threshold, no clinically relevant correlation was found between clinical variables and the defibrillation threshold. The defibrillation threshold is probably a function of a complex interaction of anatomic, physiologic and cellular variables that are not adequately represented by easily obtainable clinical information. It is probably not possible to predict defibrillation outcome from standard clinical variables.

Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy.

OBJECTIVES: The purpose of this study was to determine the time course of the appearance of abnormal Q waves on the electrocardiogram (ECG) over the first 6 h of symptoms of myocardial infarction and to determine what implications, if any, such Q waves have for the efficacy of thrombolytic therapy. BACKGROUND: Severe myocardial ischemia can produce early QRS changes in the absence of infarction. Abnormal Q waves on the baseline ECG may not be an accurate marker of irreversibly injured myocardium. METHODS: Data from 695 patients who had no past history of myocardial infarction and whose admission ECG allowed prediction of myocardial infarct size in the absence of thrombolytic therapy (Aldrich score) were pooled from four prospective trials of thrombolytic therapy. The presence and number of abnormal Q waves on each patient's initial ECG were recorded. Four hundred thirty-six patients had left ventricular infarct size measured using quantitative thallium-201 tomography a mean (+/- SD) of 52 +/- 43 days after admission. RESULTS: Of patients admitted within 1 h of symptoms, 53% had abnormal Q waves on the initial ECG. Both predicted and final infarct size were larger in patients with abnormal Q waves on the initial ECG independent of the duration of symptoms before therapy (p < 0.001). Despite this finding, the presence of abnormal Q waves on the admission ECG did not eliminate the effect of thrombolytic therapy on reducing final infarct size (p < 0.0001). CONCLUSIONS: Abnormal Q waves are a common finding early in the course of acute myocardial infarction. However, there is no evidence that abnormal Q waves are associated with less benefit in terms of reduction of infarct size after thrombolytic therapy.

Patients at lower risk of arrhythmia recurrence: a subgroup in whom implantable defibrillators may not offer benefit. Antiarrhythmics Versus Implantable Defibrillator (AVID) Trial Investigators.

OBJECTIVES: The goal of this study was to identify subgroups of arrhythmia patients who do not benefit from use of the implantable cardiac defibrillator (ICD). BACKGROUND: Treatment of serious ventricular arrhythmias has evolved toward more common use of the ICD. Since estimates of the cost per year of life saved by ICD therapy vary from $25,000 to perhaps $125,000, it is important to identify patient subgroups that do not benefit from the ICD. METHODS: Data for 491 ICD patients enrolled in the Antiarrhythmics Versus Implantable Defibrillators Study were used to create a hazards model relating baseline factors to time to first recurrent arrhythmia. The model was used to predict the hazard for recurrent arrhythmia among all trial patients. A priori cut points provided lower and higher recurrent arrhythmia risk strata. For each stratum the incremental years of life due to ICD versus antiarrhythmic drug therapy were calculated. RESULTS: Factors that predicted recurrent arrhythmia were: ventricular tachycardia as the index arrhythmia, history of cerebrovascular disease, lower left ventricular ejection fraction, a history of any tachyarrhythmia before the index event and the absence of revascularization after the index event. Survival times (over a follow-up of three years) were identical in each arm of the lowest risk sextile (survival advantage 0.03 +/- 0.12 [se] years), while the survival advantage for patients above the first sextile was 0.27 +/- 0.07 (se) years (two-sided p = 0.05). CONCLUSIONS: Patients presenting with an isolated episode of ventricular fibrillation in the absence of cerebrovascular disease or history of prior arrhythmia who have undergone revascularization or who have moderately preserved left ventricular function (left ventricular ejection fraction > 0.27) are not likely to benefit from ICD therapy compared with amiodarone therapy.

Life-threatening ventricular arrhythmias due to transient or correctable causes: high risk for death in follow-up.

OBJECTIVES: This study evaluated the prognosis of patients resuscitated from ventricular tachycardia (VT) or ventricular fibrillation (VF) with a transient or correctable cause suspected as the cause of the VT/VF. BACKGROUND: Patients resuscitated from VT/VF in whom a transient or correctable cause has been identified are thought to be at low risk for recurrence and often receive no primary treatment for their arrhythmias. METHODS: In the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial, patients with a potentially transient or correctable cause of VT/VF were not eligible for randomization. The mortality of these patients was compared with the mortality of patients with a known high risk of recurrence of VT/VF in the AVID registry. RESULTS: Compared with patients having high risk VT/VF, those with a transient or correctable cause for their presenting VT/VF were younger and had a higher left ventricular ejection fraction. These patients were more often treated with revascularization as the primary therapy, more commonly received a beta-blocker, less often required therapy for congestive heart failure and less commonly received either an antiarrhythmic drug or an implantable cardioverter defibrillator. Nevertheless, subsequent mortality of patients with a transient or correctable cause of VT/VF was no different or perhaps even worse than that of the primary VT/VF population. CONCLUSIONS: Patients identified with a transient or correctable cause for their VT/VF remain at high risk for death. Further research is needed to define truly reversible causes of VT/VF. Meanwhile, these patients may require more aggressive evaluation, treatment and follow-up than is currently practiced.

Combined historical and electrocardiographic timing of acute anterior and inferior myocardial infarcts for prediction of reperfusion achievable size limitation.

The historical time of acute symptom onset is not always an accurate indication of the timing of onset of an acute myocardial infarction (AMI). Consideration of electrocardiographic (ECG) timing parameters could supplement historical timing alone as a clinical guide for decisions regarding the use of reperfusion therapy. Three hundred ninety-five patients from 4 trials of thrombolytic therapy conducted in the northwestern United States and western Canada are included in the present study. A total of 316 patients received either streptokinase or tissue plasminogen activator, and 79 received no reperfusion therapy. Historical time of symptom onset was acquired by emergency or cardiology department personnel and recorded on patient report forms. An ECG method for estimating the timing of the AMI, the Anderson-Wilkins (AW) acuteness score, was calculated from the initial standard 12-lead recording by investigators blinded to the knowledge of symptom duration or any other study variables. Tomographic thallium-201 imaging 7 weeks after hospital admission was used to measure final AMI size. The ECG timing method achieved a relation with final AMI size similar to that previously reported for historical timing. The AW acuteness score proved most useful for anterior AMI location when there was a > or = 2 hour delay following symptom onset, but was most useful for the inferior AMI location when there was a < 2 hour delay. Despite a longer delay, patients with high AW acuteness scores had 50% lower final anterior AMI size than those with low scores; and despite a shorter delay, those with low ECG acuteness scores had 50% greater final inferior AMI size than those with high scores. The AW acuteness score combined with the historical estimation of symptom duration should provide a more accurate basis for predicting the potential for limitation of final AMI size than either method alone. These results could potentially provide the basis for developing a new method for noninvasive guidance of clinical decisions regarding administration of reperfusion therapy in the initial evaluation of patients with AMI.

Runaway pacemaker during high-energy neutron radiation therapy.

Runaway pacemaker occurred in a patient undergoing high-energy neutron radiation therapy despite adherence to published safety guidelines. The very low estimated dose of 0.9 Gy received by the pacemaker demonstrates the extreme sensitivity of integrated circuits to this new modality of radiation therapy.

Beta-adrenergic receptor downregulation and recovery in heart and lung in the Fischer 344 rat: effects of aging and correlation with mRNA levels.

Using indirect methods to downregulate beta-adrenergic receptor (BAR) density, several investigators have observed an aging-related delay in the recovery of BAR density after downregulation and suggested this finding may in part explain the decreased beta-adrenergic responsiveness associated with aging. We downregulated BAR density in male Fischer 344 rats ages 3, 12, and 24 months using the direct BAR agonist, metaproterenol. Lung and heart BAR density and BAR mRNA levels were measured daily for 5 days during recovery. Heart BAR density was downregulated significantly more in the 24-month compared to the 3-month-old animals (ANOVA p < .05). The rate of recovery of heart BAR density was greater in the 24-month compared to the 3-month-old animals (ANOVA, p = .05). Lung BAR density showed no significant age-related differences at baseline, after downregulation, or during recovery. There was no significant change in lung or heart BAR mRNA levels observed in association with downregulation of BAR density. The previously documented decrease in myocardial beta-adrenergic responsiveness with aging in this animal appears to not be related to delayed or incomplete recovery of BAR density after agonist-induced downregulation, but may be associated with greater initial downregulation of heart BAR density.

Atrial fibrillation: a risk factor for increased mortality--an AVID registry analysis.

Emerging evidence suggests that atrial fibrillation is not a benign arrhythmia. It is associated with increased risk of death. The magnitude of association is controversial and potential causes remain unknown. Patients in the registry of the Antiarrhythmics Versus Implantable Defibrillators (AVID) Trial form the basis for this report. Baseline variables, in particular the presence or absence of a history of atrial fibrillation/flutter, were examined in relation to survival. Multivariate Cox regression was used to adjust for differences in important baseline co-variables using 27 pre-selected variables. There were 3762 subjects who were followed for an average of 773+/-420 days; 1459 (39 %) qualified with ventricular fibrillation and 2303 (61 %) with ventricular tachycardia. A history of atrial fibrillation/flutter was present in 24.4 percent. There were many differences in baseline variables between those with and those without a history of atrial fibrillation/flutter. After adjustment for baseline differences, a history of atrial fibrillation/flutter remained a significant independent predictor of mortality, (relative risk=1.20; 95 % confidence intervals=1.03-1.40; p=0.020). Antiarrhythmic drug use, other than amiodarone or sotalol, was also a significant independent predictor of mortality (relative risk 1.34; 95 % confidence intervals 1.07-1.69, p=0.011. Atrial fibrillation/flutter is a significant independent risk factor for increased mortality in patients presenting with ventricular tachyarrhythmias. This risk may have been overestimated in previous studies that could not adjust for the proarrhythmic effects of antiarrhythmic drugs other than amiodarone or sotalol.

Advances in implantable cardioverter-defibrillator therapy.

The use of implantable defibrillation systems in patients with cardiac arrest has resulted in lower mortality than expected from studies of similar patients not receiving defibrillators. Nonthoracotomy lead systems have led to a decrease in operative mortality and lowered the cost of defibrillator implantation, but these systems have a higher energy requirement for defibrillation than do epicardial ones. The recent introduction of single-lead systems and bipolar defibrillation pulses has simplified nonthoracotomy defibrillator implantation and improved defibrillation efficiency. A prototype unipolar, single-lead pectoral implant defibrillation system is described that may significantly improve the reliability, safety, and cost effectiveness of nonthoracotomy defibrillators. This and other improved nonthoracotomy systems may expand the indications for defibrillator implantation to prophylactic use in high-risk patients who have not yet experienced life-threatening ventricular arrhythmias.

Signal-averaged P wave duration predicts early recurrence of atrial fibrillation after cardioversion.

Thirty-two patients had signal-averaged P wave duration measured after electrical cardioversion of AF, and were followed for 1 year or until there was a recurrence. The use of antiarrhythmic medications was left to the discretion of the attending physician. Among 20 patients not taking antiarrhythmic medication, the 11 patients who had a recurrence of AF within 3 months of cardioversion had a significantly longer signal-averaged P wave duration compared to the 9 patients who did not (148 +/- 17 vs 135 +/- 20 ms, P = 0.005). There was no difference in clinical parameters or left atrial diameter. A signal-averaged P wave duration cutoff anywhere between 130 and 135 ms correctly classified 85% of patients with a sensitivity of 81% and a specificity of 89%. In patients taking antiarrhythmic medications, signal-averaged P wave duration did not correlate with the risk of recurrence. In patients not taking antiarrhythmic medications, signal-averaged P wave duration can be used to predict the risk of an early recurrence of AF after cardioversion. The poor predictive value in patients taking antiarrhythmics may be due to changes in the atrial refractory period, which are not reflected in P wave duration.

ECG findings in acute myocardial infarction. Are there sex-related differences?

Women with acute myocardial infarction are less likely than men to receive thrombolytic therapy. It is not known whether sex-related differences in the presenting 12-lead electrocardiogram (ECG) account for this relative underutilization of acute reperfusion therapy in women. The authors examined the initial ECGs of 188 men and 185 women matched for age and history of previous acute myocardial infarction randomly selected from the Myocardial Infarction Triage and Intervention registry who presented with 4 hours of confirmed acute myocardial infarction. There were no sex-related differences in the number of leads with ST elevation, the presence of diagnostic ST elevation, or the overall magnitude of ST elevation. In addition, there was no sex-related difference in associated ECG findings that might effect physicians' utilization of acute reperfusion therapy, including the location of ST elevation (anterior vs inferior), the presence of abnormal Q waves in leads with ST elevation, the association of ST depression with ST elevation (reciprocal changes), or the presence of confounding factors, such as bundle branch block or hypertrophy. Differences in the presenting ECG do not explain the underutilization of acute reperfusion therapy in women.

Subacute ventricular free wall rupture complicating myocardial infarction.

Myocardial free wall rupture accounts for between 8% and 17% of mortality after myocardial infarction. In up to 40% of cases death occurs subacutely over a matter of hours, not minutes. Illustrative clinical cases and data suggest that a high degree of clinical suspicion, along with the early use of echocardiography, could significantly reduce mortality resulting from myocardial free wall rupture complicating myocardial infarction. Myocardial free wall rupture should be suspected in patients with recent myocardial infarction who have recurrent or persistent chest pain, hemodynamic instability, syncope, pericardial tamponade, or transient electromechanical dissociation. In this clinical situation, emergent echocardiography showing a pericardial effusion or pericardial thrombus is highly suggestive of free wall rupture. Surgical exploration and rupture repair is the definitive diagnostic and therapeutic procedure.

Relation between symptom duration before thrombolytic therapy and final myocardial infarct size.

BACKGROUND: Myocardial salvage is most likely to occur when thrombolytic therapy is administered within 4 to 6 hours of the onset of symptoms of myocardial infarction. The impact of delays within this early time period on final myocardial infarct size are unknown. The purpose of this study was to quantitate the relation between final myocardial infarct size and duration of symptoms before initiation of thrombolytic therapy in patients treated within 6 hours of symptom onset. METHODS AND RESULTS: The findings from patients in four prospective randomized trials of thrombolytic therapy were combined for analysis. The study population consisted of 432 patients presenting within 6 hours of onset of symptoms of first acute myocardial infarction who met ECG criteria that allowed estimation of myocardial area at risk before treatment with thrombolytic therapy and who had thallium-201 myocardial infarct-size measurements performed several weeks after infarction. ECG analysis revealed no difference in myocardium at risk for infarction as a function of duration of symptoms before initiation of thrombolytic therapy. In contrast, univariate and multivariate analysis showed that final infarct size was highly dependent on duration of symptoms before initiation of therapy. Each 30-minute increase in symptom duration before thrombolytic therapy was associated with an increase in infarct size of 1% of the myocardium. Final infarct size in patients treated 4 to 6 hours after symptom onset was indistinguishable from patients who did not receive thrombolytic therapy. CONCLUSIONS: These findings suggest that for patients treated within 4 to 6 hours of the onset of symptoms, there is a progressive decline in the extent of myocardium salvaged as the duration of symptoms before therapy increases. These results support efforts to minimize the time delay between symptom onset and initiation of reperfusion therapy in all eligible patients.

Ventricular arrhythmias detected after transvenous defibrillator implantation in patients with a clinical history of only ventricular fibrillation. Implications for use of implantable defibrillator.

BACKGROUND: Patients with a history of ventricular fibrillation (VF) have been shown to have a clinical profile, response to electrophysiological testing (EPS), and response to antiarrhythmic therapy that distinguishes them from patients with a history of sustained monomorphic ventricular tachycardia (MVT). Despite these differences, it is not clear whether VF in these patients is triggered by MVT or occurs de novo. The incidence of MVT and VF in such patients after their index VF event has important implications for therapeutic decisions regarding implantable defibrillator selection and programming. METHODS AND RESULTS: The records of 111 consecutive patients who had undergone transvenous cardioverter/defibrillator (ICD) implantation for malignant ventricular arrhythmias were reviewed retrospectively. For each patient, all device tachyarrhythmia detections were examined and classified as VF, MVT, rapid polymorphic VT, or other. The number of events, time to first arrhythmia detection, and cycle length of MVTs were recorded. There were 55 patients with a history of only VF and 56 with a history that included an episode of MVT. Over 14 months of follow-up, with all patients initially off of antiarrhythmic medications, MVT was detected by only 18% of patients with a history of only VF compared with 54% of those with a history that included MVT (P = .002). Among patients who did detect MVT, those with a history of only VF had fewer episodes (7 +/- 7 versus 20 +/- 31, P = .001) and a shorter mean MVT cycle length (279 versus 314 ms, P = .03) than those with a clinical history of MVT. Abrupt onset of VF not preceded by MVT was detected in 11% of patients with VF only. In addition to a history of MVT, male sex, age < 60 years, and MVT inducible on EPS were all significantly associated with an increased likelihood of MVT detection. On multivariate analysis, the inducibility of MVT was the primary independent predictor of MVT detection but was of minimal incremental predictive value in the subgroup of patients with a history of only VF. When EPS results were not considered, arrhythmia history was the primary independent predictor of MVT detection. CONCLUSIONS: Patients with a history of only VF infrequently have MVT detected by their defibrillators. When these patients do detect MVT, it is faster than that detected in patients with a clinical history of MVT before ICD surgery. A significant percentage of VF survivors detected the abrupt onset of VF not preceded by MVT, suggesting that the deterioration of rapid MVT to VF is not the only clinically important mechanism of VF induction. These findings may have important implications for the understanding of the mechanism of VF induction and for use of an implantable defibrillator.

Development of an aortic valve mass after radiofrequency catheter ablation.

A 49-year-old woman underwent a successful radiofrequency catheter ablation of a left-sided accessory pathway using a retrograde approach across the aortic valve. Routine echocardiography performed 20 hours after the procedure revealed a new aortic valve mass. Five blood cultures were negative. An echocardiogram after 2 days of heparin therapy showed complete resolution of the mass. There was no clinical evidence of embolization. Echocardiography may need to be performed routinely after catheter ablations performed retrograde across the aortic valve so that this potentially devastating complication can be diagnosed and treated early in its course.

Management of ventricular fibrillation with transvenous defibrillators without baseline electrophysiologic testing or antiarrhythmic drugs.

INTRODUCTION: Baseline electrophysiologic study (EPS) is routinely performed in patients resuscitated from ventricular fibrillation (VF) to risk stratify and select patients for chronic antiarrhythmic drug therapy. The role of EP testing prior to insertion of a multiprogrammable implantable cardioverter defibrillator (ICD), however, is unclear. METHODS AND RESULTS: This study was a retrospective review of outcome in 66 survivors of an initial episode of out-of-hospital VF not associated with a Q wave myocardial infarction or reversible causes, treated with transvenous ICDs as first-line therapy. Patients were excluded from the study if they had a previous history of monomorphic ventricular tachycardia (VT), a clinical history suggestive of supraventricular tachycardia, or had undergone preoperative EP testing. Fifty-two of the patients (79%) were male with an average age of 58 +/- 11 years. Coronary artery disease was present in 43 patients (66%), cardiomyopathy in 15 patients (23%), and valvular heart disease in 1 patient (1.5%). Seven patients (11%) had no detectable structural heart disease. The mean left ventricular ejection fraction was 0.40 +/- 0.16. With an average follow-up of 25 +/- 12 months, survival free of death from any cause was 100%. Twenty-three patients (35%) experienced 48 episodes of recurrent rapid VT or VF (average cycle length: 236 +/- 47 msec) treated by their device. The mean time to first therapy was 223 +/- 200 days. Only one of these patients also received antitachycardia pacing for two episodes of VT. One patient (1.5%) temporarily received amiodarone after removal of an infected device that was subsequently replaced. No other patient received antiarrhythmic drug therapy. CONCLUSION: After a cardiac arrest due to primary VF, select patients treated with multiprogrammable ICDs can be managed successfully without baseline EPS or antiarrhythmic drug therapy.

Prospective randomized comparison of biphasic waveform tilt using a unipolar defibrillation system.

BACKGROUND: A unipolar defibrillation system using a single right ventricular (RV) electrode and the active shell or container of an implantable cardioverter defibrillator situated in a left infraclavicular pocket has been shown to be as efficient in defibrillation as an epicardial lead system. Additional improvements in this system would have favorable practice implications and could derive from alterations in pulse waveform shape. The specific purpose of this study is to determine whether defibrillation efficacy can be improved further in humans by lowering biphasic waveform tilt. METHODS: We prospectively and randomly compared the defibrillation efficacy of a 50% and a 65% tilt asymmetric biphasic waveform using the unipolar defibrillation system in 15 consecutive cardiac arrest survivors prior to implantation of a presently available standard transvenous defibrillation system. The RV defibrillation electrode has a 5-cm coil located on a 10.5 French lead and was used as the anode. The system cathode was the active 108 cm2 surface area shell (or "CAN") of a prototype titanium alloy pulse generator placed in the left infraclavicular pocket. The defibrillation pulse derived from a 120-microF capacitor and was delivered from RV-->CAN, with RV positive with respect to the CAN during the initial portion of the cycle. Defibrillation threshold (DFT) stored energy, delivered energy, leading edge voltage and current, pulse resistance, and pulse width were measured for both tilts examined. RESULTS: The unipolar single lead system, RV-->CAN, using a 65% tilt biphasic pulse resulted in a stored energy DFT of 8.7 +/- 5.7 J and a delivered energy DFT of 7.6 +/- 5.0 J. In all 15 patients, stored and delivered energy DFTs were < 20 J. The 50% tilt biphasic pulse resulted in a stored energy DFT of 8.2 +/- 5.4 J and a delivered energy DFT of 6.1 +/- 4.0 J; P = 0.69 and 0.17, respectively. As with the 65% tilt pulse, all 15 patients had stored and delivered energy DFTs < 20 J. CONCLUSION: The unipolar single lead transvenous defibrillation system provides defibrillation at energy levels comparable to that reported with epicardial lead systems. This system is not improved by use of a 50% tilt biphasic waveform instead of a standard 65% tilt biphasic pulse.

A prospective randomized comparison in humans of biphasic waveform 60-microF and 120-microF capacitance pulses using a unipolar defibrillation system.

BACKGROUND: Improving unipolar implantable cardioverter-defibrillator (ICD) effectiveness has favorable implications for ICD safety, efficacy, and size. Advances in defibrillation efficacy would accelerate ICD ease of use by decreasing device size and by minimizing morbidity and mortality related to an improved defibrillation safety margin. The specific purpose of the present study was to determine whether unipolar defibrillation efficacy could be improved further in humans by lowering biphasic waveform capacitance. METHODS AND RESULTS: We prospectively and randomly compared the defibrillation efficacy of a 60-microF and a 120-microF capacitance asymmetrical 65% tilt biphasic waveform using a unipolar defibrillation system in 38 consecutive cardiac arrest survivors before implantation of a presently available standard transvenous defibrillation system. The right ventricular defibrillation electrode had a 5-cm coil located on a 10.5F lead and was used as the anode. The system cathode was the electrically active 108-cm2 surface area shell (or "can") of a prototype titanium alloy pulse generator placed in a left infraclavicular pocket. The defibrillation pulse was derived from either a 60-microF or a 120-microF capacitance and was delivered from RV-->CAN. Defibrillation threshold (DFT) stored energy, delivered energy, leading-edge voltage and current, pulse resistance, and pulse width were measured for both capacitances examined. The 60-microF capacitance biphasic pulse resulted in a stored-energy DFT of 8.5 +/- 4.1 J and a delivered-energy DFT of 8.4 +/- 4.0 J. In 34 of 38 patients (89%), the stored-energy DFT was < 15 J. Leading-edge voltage at the DFT was 517 +/- 128 V. Mean pulse impedance for the 60-microF waveform was 60.6 +/- 7.1 omega. The 120-microF capacitance biphasic pulse resulted in a stored-energy DFT of 10.1 +/- 7.4 J and a delivered-energy DFT of 10.0 +/- 7.2 J (P = .13 and .13, respectively). In 28 of 38 patients (74%), the stored-energy DFT was < 15 J (P = .052). Leading-edge voltage at the DFT with the 120-microF capacitance pulse was 386 +/- 142 (P < .00001). Mean pulse impedance for the 120-microF waveform was 60.7 +/- 7.0 omega (P = .80). CONCLUSIONS: The results of the present study suggest that a relatively small capacitance, 60 microF, can be used for unipolar defibrillation systems without compromising defibrillation energy requirements compared with more typical ICD capacitance values, but this will require a higher circuit voltage. The use of lower capacitance also provides a modest increase in the percent of patients who have very low energy defibrillation requirements, an important issue should maximum ICD energy be decreased from the present level of 34 J. Such a move to smaller output devices could allow significant decreases in device size, a necessary feature of making cardioverter-defibrillator implantation comparable to that of standard pacemaker surgery.

"Stable" ventricular tachycardia is not a benign rhythm : insights from the antiarrhythmics versus implantable defibrillators (AVID) registry.

BACKGROUND: Sustained ventricular tachycardia (VT) can be unstable, can be associated with serious symptoms, or can be stable and relatively free of symptoms. Patients with unstable VT are at high risk for sudden death and are best treated with an implantable defibrillator. The prognosis of patients with stable VT is controversial, and it is unknown whether implantable cardioverter-defibrillator therapy is beneficial. METHODS AND RESULTS: Screening for the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial identified patients with both stable and unstable VT. Both groups were included in a registry, and their clinical characteristics and discharge treatments were recorded. Mortality data were obtained through the National Death Index. The mortality in 440 patients with stable VT tended to be greater than that observed in 1029 patients presenting with unstable VT (33.6% versus 27.6% at 3 years; relative risk [RR]=1.22; P:=0.07). After adjustment for baseline and treatment differences, the RR was little changed (RR=1.25, P:=0.06). CONCLUSIONS: Sustained VT without serious symptoms or hemodynamic compromise is associated with a high mortality rate and may be a marker for a substrate capable of producing a more malignant arrhythmia. Implantable cardioverter-defibrillator therapy may be indicated in patients presenting with stable VT.