Author + information
- Received September 13, 1996
- Revision received March 5, 1997
- Accepted March 12, 1997
- Published online July 1, 1997.
- Michael R Gold, MD, PhD, FACCA,* (, )
- Neal G Kavesh, MDA,
- Robert W Peters, MDA and
- Stephen R Shorofsky, MD, PhD, FACCA
- ↵*Dr. Michael R. Gold, Division of Cardiology, N3W77, University of Maryland Medical System, 22 S. Greene Street, Baltimore, Maryland 21201.
Objectives. The purpose of this study was to compare chronic changes in monophasic and biphasic defibrillation thresholds using a uniform transvenous lead system and testing protocol.
Background. Defibrillation thresholds increase over time in patients with nonthoracotomy lead systems. This increase can result in an inadequate chronic defibrillation safety margin and could limit the safety of smaller pulse generators, which have a reduced maximal output. However, previous studies of the temporal changes of defibrillation thresholds evaluated complex lead systems or monophasic shock waveforms, neither of which are used with current technology.
Methods. This study was a prospective, randomized assessment of the effects of shock waveforms on the changes of transvenous defibrillation thresholds over time. Paired monophasic and biphasic thresholds were measured both at implantation and at follow-up (250 ± 105 days) in 24 consecutive patients who were not receiving antiarrhythmic drugs. The lead system was a dual-coil Endotak C lead, and reverse polarity shocks (distal coil = anode) were delivered.
Results. Monophasic defibrillation thresholds increased from (mean ± SD) 13.7 ± 6.0 J to 16.8 ± 6.7 J (p = 0.02), whereas biphasic thresholds were unchanged (10.4 ± 4.3 J to 10.2 ± 4.8 J, p = 0.86) in the same patients. Shock impedance chronically increased (47.0 Ω to 50.5 Ω, p = 0.02) and was unaffected by waveform.
Conclusions. These results indicate that biphasic shocks prevent the chronic increase in defibrillation thresholds with a transvenous lead system.
(J Am Coll Cardiol 1997;30:233-6)
Nonthoracotomy lead systems are preferred for initial implantable cardioverter-defibrillator (ICD) placement owing to lower perioperative morbidity, mortality and costs compared with epicardial lead systems ([1–4]). However, defibrillation thresholds at implantation are higher with the use of nonthoracotomy leads ([1, 5, 6]) and they rise over time ([7–12]). This can result in an inadequate defibrillation safety margin later on ([11–13]) and could limit the safety of smaller pulse generators, which have a reduced maximal output.
With further improvements in lead systems and shock waveforms, simple transvenous defibrillation lead systems have become routine ([14, 15]). Previous studies of the temporal changes of defibrillation efficacy evaluated monophasic shocks or complex nonthoracotomy lead systems, or both ([7–12]), and shock polarity was not standardized. Accordingly, the present study is a prospective, randomized comparison of changes of monophasic and biphasic defibrillation thresholds using a uniform transvenous lead and shock polarity.
1.1 Patient Group.
This prospective study included 24 consecutive patients undergoing initial ICD placement for standard clinical indications, who completed the chronic testing protocol. Specifically excluded by the study protocol were two patients who required a subcutaneous patch or array. In addition, patients were excluded for worsening congestive heart failure requiring intravenous inotropic therapy (n = 1), infection requiring device explantation (n = 1) or the use of class I or III antiarrhythmic drugs during the follow-up period (n = 2). Written, informed consent was obtained from each patient, and this study was approved by the Institutional Review Board of the University of Maryland.
1.2 Defibrillation Testing.
The transvenous defibrillation lead (Endotak C model 0074, Cardiac Pacemakers Inc.) used in this study was placed under fluoroscopic guidance at the right ventricular apex. Defibrillation testing was performed at implantation under general anesthesia with nitrous oxide, isoflurane and vecuronium using an external cardioverter-defibrillator (CPI model 2815). Late measurements were performed through the pulse generator (Ventak 1625 or 1715, CPI) ≥6 months after implantation using conscious sedation with midazolam and fentanyl. In each patient both monophasic and biphasic defibrillation thresholds were measured at implantation and at follow-up evaluation.
Ventricular fibrillation was induced with high output ramp pacing through the defibrillation lead. Shocks were delivered through a 125-μF capacitance with either a 65% tilt (monophasic) or a 60% first-phase tilt and 50% second-phase tilt (biphasic). The right ventricular coil was the anode (i.e., reverse polarity) for the monophasic and first phase of the biphasic waveform in all patients ().
The initial monophasic-delivered shock energy for testing was 20 J. If successful, the energy was decreased to 15, 10, 8, 5, 3 and 1 J on successive trials until defibrillation failed. If the initial 20-J shock failed, the energy was increased in 5-J steps on subsequent trials until defibrillation was successful. For biphasic shocks, the same protocol was used, except that the initial energy was 15 J. The defibrillation threshold for one waveform was measured, followed by testing of the other waveform, with the order of testing at each session determined randomly. The defibrillation threshold was defined as the lowest initial shock energy that successfully terminated ventricular fibrillation. The same protocol and initiating energies were used regardless of preceding measurements of defibrillation thresholds.
1.3 Statistical Analysis.
A two-tailed, paired ttest was used to compare temporal changes and the effects of shock waveform on defibrillation thresholds. All results are expressed as mean value ± SD, and p < 0.05 was considered significant.
2.1 Patient Group.
There were 18 men (75%) and six women (25%) in the study. Their mean age was 57 ± 12 years, and the mean left ventricular ejection fraction was 0.36 ± 0.15. Coronary artery disease with ischemic cardiomyopathy was the primary structural heart disease in 16 patients. Three patients had idiopathic dilated cardiomyopathy, one had mitral valve prolapse and three had primary electric disease with no known structural heart disease.
2.2 Defibrillation Testing.
All 24 patients underwent successful defibrillator implantation without perioperative morbidity or mortality. Chronic follow-up assessment occurred 250 ± 105 days after implantation. The initial waveform tested was monophasic in 12 patients at implantation and 13 patients at follow-up. The monophasic defibrillation thresholds at implantation and at late testing for each patient are shown in Fig. 1. There was a significant rise of defibrillation thresholds, from 13.7 ± 6.0 J to 16.8 ± 6.7 J (p = 0.02). Defibrillation thresholds increased chronically in 15 patients; they were unchanged in four patients; and they decreased in five patients. In addition, a high defibrillation threshold (>20 J) was observed in one patient (4%) at implantation and five patients (21%) at follow-up.
The biphasic defibrillation thresholds measured for each patient are shown in Fig. 2. In contrast to the results noted earlier, there was no increase of biphasic thresholds over time. In fact, there was a small, nonsignificant decrease of threshold energy at the follow-up evaluation, from 10.4 ± 4.3 J to 10.2 ± 4.8 J (p = 0.86). Defibrillation thresholds increased in eight patients, were unchanged in seven patients and decreased chronically in nine patients. No patient had a defibrillation threshold >20 J at either measurement. Subgroup analysis of the eight patients with an increased threshold at late follow-up revealed no distinguishing characteristics compared with the rest of the cohort. Specifically, there were no differences in age, gender, ejection fraction, implantation defibrillation threshold or change of shock impedance. Moreover, the distribution of changes of thresholds was normally distributed around 0 (Fig. 3B), consistent with the observed changes being due to measurement variability in a homogeneous population of patients ([12, 17]). This finding is in contrast to the change of thresholds with monophasic shocks, where the distribution is skewed toward positive values (Fig. 3A).
The disparity of the change of defibrillation efficacy over time with the two waveforms resulted in a much greater benefit of biphasic shocks during late follow-up. Thus, at implantation mean delivered energy at threshold was 32% greater with monophasic shocks, whereas at the late evaluation energy requirements were 61% greater (p = 0.05). There was a small rise in shock impedance (47.0 Ω to 50.5 Ω, p = 0.02) between evaluations, which was independent of shock waveform.
The major finding of this study is that biphasic shocks prevent the chronic rise of defibrillation thresholds observed with monophasic shocks using a transvenous lead system. Randomized, paired comparisons of monophasic and biphasic defibrillation thresholds demonstrated that the shock waveform is the critical factor involved because monophasic defibrillation thresholds increased in the same patients. In addition, the use of a uniform lead system, shock polarity and testing protocol eliminated any confounding influence of changes of these variables.
3.1 Comparison with Previous Studies.
In general, epicardial lead systems have stable thresholds over time, although a small rise was reported recently (). In contrast, studies of nonthoracotomy lead systems have consistently demonstrated late increases of monophasic defibrillation thresholds. Multiple lead systems, including subcutaneous patches, have been used in these studies ([7–12]). To our knowledge, the present study is the first systematic evaluation of temporal changes of defibrillation thresholds with a single transvenous lead system. Recently, we reported a 38% rise of defibrillation thresholds at follow-up evaluation with a hybrid lead system in which the right atrial transvenous coil was the anode for defibrillation (). In the present study, the proximal right atrial coil served as the cathode. Thus, although polarity has important effects on monophasic defibrillation thresholds ([16, 18]), it does not prevent the late rise of thresholds.
Martin et al. () evaluated changes of biphasic defibrillation thresholds with an Endotak lead system and a comparable period of follow-up. In contrast to the present study, they reported a 27% increase in defibrillation thresholds 6 months after implantation. One possible explanation for the discrepancy of the results in these studies involves the use of subcutaneous patches in some of their patients. Careful inspection of their data indicates that the rise of biphasic thresholds was confined to those patients with a patch. More recently, Schwartzman et al. () retrospectively evaluated patients undergoing follow-up defibrillation testing with three different lead systems. They observed attenuation of the rise of defibrillation thresholds with biphasic shocks during the early (49 ± 22 days) follow-up period. This is consistent with our study of much longer follow-up (250 ± 105 days).
The mechanism responsible for the late rise of monophasic defibrillation thresholds is poorly understood. It is assumed that changes at the electrode–tissue interface contribute to the increased energy requirements ([7–9]). We previously showed that the rise of shock impedance was sufficient to account for the increase of defibrillation energy at threshold ([11, 19]), assuming that current is the major determinant of defibrillation ([20, 21]). However, this would not explain why the mean threshold is unchanged with biphasic shocks delivered chronically, despite similar impedance rises and local tissue reactions.
3.2 Study Limitations.
Our results must be interpreted in the face of certain methodologic limitations. The number of patients evaluated was relatively small. This sample size was chosen because it has an 80% power to show a 25% increase in defibrillation threshold, as previously reported. By performing paired testing in each patient, we demonstrated that monophasic defibrillation thresholds rose, whereas biphasic thresholds were unchanged. A second limitation is that different anesthetic techniques were used at implantation and at follow-up testing. However, in similar patients at our center undergoing implantation with general anesthesia (n = 40) or conscious sedation (n = 20) using the same agents and lead system as in this study, there were no differences in monophasic (14.3 ± 5.2 vs. 13.3 ± 6.9, p = 0.55) or biphasic (11.5 ± 4.8 vs. 11.4 ± 5.7, p = 0.97) defibrillation thresholds. Accordingly, it is unlikely that the anesthetic agent contributed to the observed findings. Finally, the defibrillation threshold protocol we used has some limitations. The relation between defibrillation success and energy is accurately described as a dose-response curve (). The use of a step-down protocol to first failure to determine defibrillation thresholds is a reasonable estimate of the 75% defibrillation success energy (), and it has been shown to be reproducible (). The step size used in testing will affect the variability of measurements. These steps are smaller at low energies to more closely keep the relative changes of energies constant.
Our results demonstrate that a biphasic waveform prevents the chronic rise of mean defibrillation thresholds observed with monophasic shocks. These findings indicate that the use of downsized pulse generators with reduced maximal outputs appears safe if an adequate transvenous defibrillation safety margin is present at implantation.
- Received September 13, 1996.
- Revision received March 5, 1997.
- Accepted March 12, 1997.
- The American College of Cardiology
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