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W M Smith

Publications and source records attributed to W M Smith.

At least 73 records · Page 4Linked to original sources
PubMed1997

Prevention of heart failure by antihypertensive drug treatment in older persons with isolated systolic hypertension. SHEP Cooperative Research Group.

CONTEXT: Heart failure is often preceded by isolated systolic hypertension, but the effectiveness of antihypertensive treatment in preventing heart failure is not known. OBJECTIVE: To assess the effect of diuretic-based antihypertensive stepped-care treatment on the occurrence of heart failure in older persons with isolated systolic hypertension. DESIGN: Analysis of data from a multicenter, randomized, double-blind, placebo-controlled clinical trial. PARTICIPANTS: A total of 4736 persons aged 60 years and older with systolic blood pressure between 160 and 219 mm Hg and diastolic blood pressure below 90 mm Hg who participated in the Systolic Hypertension in the Elderly Program (SHEP). INTERVENTION: Stepped-care antihypertensive drug therapy, in which the step 1 drug is chlorthalidone (12.5-25 mg) or matching placebo, and the step 2 drug is atenolol (25-50 mg) or matching placebo. MAIN OUTCOME MEASURES: Fatal and nonfatal heart failure. RESULTS: During an average of 4.5 years of follow-up, fatal or nonfatal heart failure occurred in 55 of 2365 patients randomized to active therapy and 105 of the 2371 patients randomized to placebo (relative risk [RR], 0.51; 95% confidence interval [CI], 0.37-0.71; P<.001; number needed to treat to prevent 1 event [NNT], 48). Among patients with a history of or electrocardiographic evidence of prior myocardial infarction (MI), the RR was 0.19 (95% CI, 0.06-0.53; P=.002; NNT, 15). Older patients, men, and those with higher systolic blood pressure or a history of or electrocardiographic evidence of MI at baseline had higher risk of developing heart failure. CONCLUSION: In older persons with isolated systolic hypertension, stepped-care treatment based on low-dose chlorthalidone exerted a strong protective effect in preventing heart failure. Among patients with prior MI, an 80% risk reduction was observed.

Aged↗
PubMed1997

Effect of a passive endocardial electrode on defibrillation efficacy of a nonthoracotomy lead system.

OBJECTIVES: We investigated the impact of an inactive endocardial lead on the 50% effective dose (ED50%) for successful ventricular defibrillation. BACKGROUND: The presence of abandoned epicardial mesh patch electrodes detrimentally affects the defibrillation efficacy of an endocardial lead system. It is not known whether abandoned endocardial electrodes produce a similar effect. METHODS: An endocardial lead system (ENDOTAK, model 0062, Cardiac Pacemakers, Inc.) was implanted in eight dogs (mean +/- SD weight 23.7 +/- 1.0 kg). The ED50% for each of seven lead configurations was determined by a three-reversal point protocol in a balanced-randomized order with and without a second electrically passive endocardial lead system in the right ventricle (power 0.97 to detect a 50-V difference). Biphasic shocks with 80% tilt were delivered 10 s after the induction of ventricular fibrillation. In one configuration the active electrode made contact with the passive electrode in the right ventricular (RV) apex. In another configuration the active electrode was placed in a more proximal position to avoid contact. Additionally, the ED50% was determined for the endocardial lead system with a passive pacing lead positioned in the RV apex. RESULTS: ED50% values for peak voltage, peak current and delivered energy were not significantly different with or without a passive RV electrode, and this was true whether or not the active electrode touched the passive electrode. However, ED50% values were significantly higher when the active electrode was slightly proximal than when it was positioned at the apex. CONCLUSIONS: Physical contact between active and passive endocardial electrodes does not significantly alter defibrillation efficacy in this dog model. An increase in ED50% energy was caused by a slightly proximal position. Therefore, a good electrode position within the right ventricle is a more important determinant of defibrillation efficacy than is avoidance of the electrode touching a passive electrode.

Animals↗
PubMed1997

Coronary revascularisation in young adults.

OBJECTIVE: To evaluate the long-term outcome of coronary artery bypass surgery (CABG) in patients < 40 years old and to determine factors predictive of adverse outcomes. METHODS: Retrospective review of data on 220 patients who underwent isolated CABG at Green Lane Hospital, New Zealand from 1970 to 1992. RESULTS: The actuarial survival after surgery was 91, 74 and 50% at 5, 10 and 15 years, respectively. Recurrence of ischaemic symptoms occurred at a median time of 72 months, and only 20% of patients remained asymptomatic 10 years after CABG. Univariate analysis of potentially adverse surgical factors showed that patients who had prolonged bypass time (> or = 100 min, P < 0.007) had increased late mortality. There were two distinct operative eras with respect to the use of IMA conduits (4% pre 1985, 87% post 1984) The relationship between IMA conduits use and survival was significant on time independent analysis (P < 0.02), but was not using the log-rank test. Preoperative clinical characteristics associated with increased late mortality were impaired left ventricular function (end-systolic volume (ESV) > or = 80 ml, P = 0.008; ejection fraction < 40%, P = 0.0005), and lack of aspirin use either pre- or post-operatively (P < 0.0001). Multivariate analysis indicated that reduced ejection fraction (P = 0.04) and prolonged bypass time (P = 0.05) was associated with an increased risk of late death. Aspirin therapy (P = 0.001) was associated with decreased late mortality. Cumulative events rate of reintervention and mortality was reduced in female patients (P = 0.0009). At review, 45% of patients had total cholesterol > 6.5 mmol/l. CONCLUSION: To avoid the early recurrence of symptoms, the need for reintervention and late mortality, young patients should receive IMA conduits, cardioplegia as myocardial protection, aspirin and therapy to modify/ameliorate their risk factors including dyslipidaemia, diabetes and left ventricular dysfunction.

Actuarial Analysis↗
PubMed1997

Defibrillation efficacy with endocardial electrodes is influenced by reductions in cardiac preload.

Little is known about the effects of cardiac preload and cardiac geometry on defibrillation efficacy with endocardial electrodes. We studied nine pigs implanted with an endocardial lead system in the normal and reduced preload state. In the reduced preload state, a balloon catheter was inflated in the inferior vena cava (IVC) for 20 seconds prior to the induction of ventricular fibrillation (VF). Complete occlusion of the IVC and reductions in preload were confirmed by observing deformation of the contrast-filled balloon, a reduction in cardiac size by fluoroscopy, and reductions in ventricular pressures. Biphasic shocks were delivered after 10 seconds of VF using a recursive up-down protocol. VF was induced 20 times for each preload state, and the 50% effective doses (ED50) for energy, current, and voltage were estimated by averaging all shocks for that state. At reduced preloads, energy decreased from 12.1 +/- 3.0 J (+/- SD) to 10.5 +/- 2.9 J (p < 0.01), voltage decreased from 415 +/- 51 V to 390 +/- 51 V (p < 0.05), and current decreased from 8.6 +/- 1.5 A to 7.6 +/- 1.5 A (p < 0.01), while impedance rose from 49.2 +/- 3.8 omega to 52.8 +/- 4.4 omega (p < 0.001). We conclude that reducing cardiac preload and cardiac size significantly lowers ED50 defibrillation energy, current, and voltage. This outcome may be caused directly by the decrease in blood volume as evidenced by increased impedance and/or may be due to changes in heart geometry and stretch.

Animals↗
PubMed1997

Effect of electrode polarity on internal defibrillation with monophasic and biphasic waveforms using an endocardial lead system.

INTRODUCTION: To test the hypothesis that the effect of shock polarity on defibrillation depends on waveform duration, this study determined strength-duration defibrillation curves of monophasic and biphasic truncated exponential waveforms for both polarities. METHODS AND RESULTS: Defibrillation thresholds (DFTs) were obtained in 32 pigs for catheter electrodes in the right ventricle (RV) and superior vena cava (SVC) using a modified Purdue technique. Both electrode polarities were tested in five different protocols. In part 1, DFTs were determined with 1- to 14-msec monophasic waveforms. In parts 2, 3, and 4, DFTs were determined with two different sizes of SVC electrodes for biphasic waveforms with a phase 1 of 4 or 6 msec and a phase 2 ranging from 1 to 10 msec. In part 5, DFTs were tested for monophasic waveforms ranging from 2 to 11 msec and for biphasic waveforms with a phase 1 duration corresponding to each monophasic waveform and a phase 2 held constant at 1 msec. Mean DFTs for monophasic waveforms were significantly lower when the RV electrode was an anode than when it was a cathode for waveform durations > or = 3 msec. For biphasic waveforms in which phase 2 was < or = phase 1 in duration, no significant difference in mean DFT was observed when polarity was reversed. Even a phase 2 as short as 1 msec could eliminate the DFT difference between polarities observed with monophasic shocks. When phase 2 was > or = 2 msec longer than phase 1, polarity did affect the DFT of biphasic waveforms; it affected the DFT similarly to a monophasic waveform of the same polarity as phase 2. Phase 1 duration and electrode size also affected the difference in DFT produced by changing the electrode polarity. CONCLUSIONS: For phase durations most commonly used clinically because of their low DFTs, reversing polarity changed defibrillation efficacy for monophasic but not biphasic shocks. For inefficient biphasic waveforms with phase 2 > or = 2 msec longer than phase 1, the DFT was lower when the RV electrode was an anode during phase 2, similar to the polarity difference for monophasic waveforms, suggesting that a long second phase of biphasic waveforms defibrillates in a similar fashion to monophasic waveforms.

Animals↗
PubMed1997

Prevention of action potentials during extracellular electrical stimulation of long duration.

INTRODUCTION: This study investigated if action potentials can be prevented by electrical field stimuli of long duration. METHODS AND RESULTS: The transmembrane potential was recorded by a double-barrel micro-electrode during field stimulation given across a papillary muscle from 10 guinea pigs. After 10 stimuli (S) with a 200-msec S-S interval, a 400-msec square wave shock was given just before or after the end of the effective refractory period following the 10th stimulus through electrodes 1 cm on either side of the papillary muscles. Another two stimuli (S' and S") having the same 200-msec S-S interval were given during the shock pulse to test if the action potentials induced by these two stimuli could be prevented by the shock. The shock strength was increased until the shock field prevented the action potentials induced by the S' and S" stimuli. The resting membrane potential was -85.5 +/- 2.9 mV. For shocks causing depolarization at the recording site, the field strength required to prevent S'- and S"-induced action potentials was 1.5 +/- 0.4 V/cm, which depolarized the transmembrane potential to -55.3 +/- 8.9 mV and -58.1 +/- 7.2 mV from the resting membrane potential at the time of the S' and S" stimuli, respectively. The strength of shocks causing hyperpolarization required to prevent S'- and S" -induced action potentials was 5.0 +/- 0.8 V/cm, which hyperpolarized the transmembrane potential to -105 +/- 6.5 mV and -115.6 +/- 6.9 mV from the resting membrane potential at the time of the S' and S" stimuli, respectively. CONCLUSION: Both depolarization and hyperpolarization caused by an electrical field can prevent action potentials.

Action Potentials↗
PubMed1997

The effects of ventricular fibrillation duration and a preceding unsuccessful shock on the probability of defibrillation success using biphasic waveforms in pigs.

INTRODUCTION: While the defibrillation threshold has been reported to increase with ventricular fibrillation (VF) duration for monophasic waveforms, the effect of VF duration for biphasic waveforms is unknown. METHODS AND RESULTS: The ED 50 requirements (the 50% probability of defibrillation success) for an endocardial lead system, which included a subcutaneous array, were determined by logistic regression using a recursive up-down algorithm for a biphasic waveform (6/6 msec). The study was performed in two parts, each with eight pigs. In part 1, ED 50 was compared for shocks delivered after 10 seconds of VF and for shocks delivered after 20 seconds of VF following a failed first shock at 10 seconds. Energy at ED 50 decreased from 6.5 +/- 0.9 J for shocks delivered after 10 seconds of VF to 4.9 +/- 0.8 J (P < 0.01) for shocks delivered after 20 seconds. To determine if improved second shock efficacy was a result of preconditioning by the failed first shock or a function of VF duration, part 2 of the study compared defibrillation efficacy between shocks delivered after 10 seconds of VF with shocks delivered after 20 seconds of VF with and without a failed first shock at 10 seconds. Mean energy at ED 50 decreased from 10.1 +/- 2.4 J for shocks delivered after 10 seconds of VF to 7.9 +/- 2.4 J (P < 0.01) and 7.5 +/- 3.2 J (P < 0.01) for shocks delivered after 20 seconds of VF with and without a failed first shock, respectively. The mean energy at ED 50 for shocks delivered after 20 seconds of VF with and without a failed first shock was not significantly different (P = 0.53). A strong linear correlation for energy at ED 50 was found between shocks delivered after 10 seconds of VF and shocks delivered after 20 seconds of VF following a failed first shock (r = 0.95, P < 0.01). CONCLUSION: (1) As opposed to monophasic shocks, ED 50 is significantly lower for biphasic shocks delivered after 20 seconds of VF compared with shocks delivered after 10 seconds of VF in pigs. (2) An unsuccessful biphasic shock in pigs does not affect the defibrillation efficacy for a subsequent shock. (3) ED 50 for a biphasic shock delivered after 20 seconds of VF is linearly related to ED 50 for a shock delivered after 10 seconds of VF.

Animals↗
PubMed1996

Effect of changing capacitors between phases of a biphasic defibrillation shock.

BACKGROUND: In this study, we examined the effect of changing capacitor values between phases of a biphasic waveform with the goal of lowering leading edge voltage (LEV), total delivered energy (TDE), and total stored energy (TSE). METHODS: Defibrillation thresholds were determined in 18 open-chest swine using epicardial patch electrodes. In part I, three combinations of capacitors were tested: 150:150 microF; 150:300 microF; and 300:150 microF. Waveform durations were 6/0, 6/2, 6/4, 6/6, and 6/8 ms. In part II, phase 1 capacitance was 150 microF. Three phase 2 capacitance values were used: 150 microF; 75 microF; and 37.5 microF. Phase 2 LEV was a multiple of phase 1 trailing edge voltage: x 0.5; x 0.75; x 1; x 2; x 3; and x 4. A 3.5/2.0 ms biphasic waveform was used. In part III, thresholds were determined for two sets of capacitor values, which can be created by switching a pair of capacitors from in parallel to in series, 150:37.5 microF and 300:75 microF, and nine waveform durations, 4/0, 4/2, 4/4, 6/0, 6/3, 6/6, 8/0, 8/4 and 8/8 ms. RESULTS: In part I, the 300:150 microF system defibrillated with the lowest LEV, TDE and TSE were not different for any of the biphasic waveforms tested except for the 6/8 ms, which was higher. In part II, there was no difference in LEV among any of the three phase 2 capacitor values. LEV was lowest for the x 2, x 3, x 4 multipliers. Peak voltage was lowest for the x 1 and x 2 multipliers. TDE was lowest for the x 0.5, x 0.75, x 1, and x 2 multipliers. In part III, the 300:75 microF system defibrillated at a lower LEV than did the 150:37.5 microF system. The 150:37.5 microF system defibrillated at a lower total delivered energy than did the 300:75 microF. CONCLUSION: These results suggest that defibrillation can be accomplished with lower LEV, TDE, and TSE if two capacitors are switched from a parallel configuration to a series configuration between phases of the biphasic waveform.

Animals↗
PubMed1996

Effects of polarity for monophasic and biphasic shocks on defibrillation efficacy with an endocardial system.

Electrode polarity has been reported to be one of the factors that affect defibrillation efficacy. We studied the influence of polarity on defibrillation efficacy when monophasic and biphasic waveforms were used with an endocardial lead system. In six anesthetized pigs, defibrillation catheters were placed in the right ventricular (RV) apex and at the junction of the superior vena cava (SVC) and right atrium. Monophasic shocks were 6 ms in duration, while for biphasic shocks the first phase was 6 ms and the second was 4 ms in duration. Four electrode configurations were tested: R:S, M (the RV electrode, cathode; the SVC electrode, anode, with a monophasic shock); S:R: S, B(the RV electrode, first phase cathode; the SVC electrode, first phase anode, with a biphasic shock); S:R, B. Defibrillation probability of success curves were determined using an up/down protocol requiring 15 shocks for each configuration. For monophasic shocks, total delivered energy at the 50% probability of success point was significantly lower when the RV electrode was an anode than when it was a cathode (R: S, M: 24.4 +/- 7.4 J [mean +/- SD] vs S:R, M: 16.4 +/- 5.5 J; P < 0.05). For biphasic shocks, total energy was not affected by polarity reversal of the electrodes (R:S, B: 8.7 +/- 1.4 J vs S:R, B: 8.4 +/- 2.5 J; P = NS). The endocardial electrode configuration with the RV electrode as an anode requires less energy for defibrillation with a monophasic but not a biphasic waveform.

Animals↗
PubMed1996

Epicardial sock mapping following monophasic and biphasic shocks of equal voltage with an endocardial lead system.

INTRODUCTION: The reason for the increased defibrillation efficacy of biphasic shocks over monophasic shock is not definitely known. METHODS AND RESULTS: In six anesthetized pigs, we mapped the epicardium after transvenous defibrillation shocks to compare the activation patterns following successful biphasic shocks with unsuccessful monophasic shocks of the same voltage. The heart was exposed and a 510-electrode sock with approximately 4-mm interelectrode spacing was pulled over the entire ventricular epicardium and sutured to the pericardium. Defibrillation catheters were placed in the right ventricular apex and in the superior vena cava. Paired monophasic 12 msec and biphasic 6/6 msec defibrillation shocks were given using an up-down protocol to keep shock strength between the defibrillation thresholds for the two waveforms so that the biphasic shock was successful while the monophasic shock was not. Activation fronts immediately following 60 paired shocks were recorded and analyzed by animated maps of the first derivative of the electrograms. The ventricles were divided into apical (I), middle (II), and basal (III) thirds, and early sites, i.e., the sites from which activation fronts first appeared on the epicardium following the shock, were grouped according to their location. Postshock intervals, i.e., the time from the shock until earliest epicardial activation occurred, were also determined. No ectopic activation fronts followed the shock in 20 biphasic episodes. In the other 40 paired episodes, the number of early sites was smaller after biphasic shocks than after monophasic shocks [monophasic: 198 (total), 3.3 +/- 0.9 (mean +/- SD) per shock episode; biphasic: 67, 1.1 +/- 1.0, P < 0.05]. For biphasic but not monophasic shocks, early sites were less likely to arise from the middle (II) and basal (III) thirds than from the apical third (I) [monophasic: I: 84 (42%), II: 68 (34%), III: 46 (23%); biphasic: I: 49 (73%), II: 10 (15%), III: 8 (12%), P < 0.05]. Postshock intervals were significantly shorter for monophasic shocks (54 +/- 14 msec) than for biphasic shocks (75 +/- 23 msec, P < 0.05). CONCLUSION: The decreased number of activation fronts and the longer delay following the shock for the earliest epicardial appearance of those activation fronts that do occur may be responsible for the increased defibrillation efficacy for biphasic shocks.

Animals↗
PubMed1996

Transmembrane potential changes caused by shocks in guinea pig papillary muscle.

To study transmembrane potential (Vm) changes (delta Vm) caused by extracellular field stimulation, Vm was recorded in 10 guinea pig papillary muscles by a double-barrel microelectrode. A 10-ms shock was delivered during the action potential plateau or during diastole. Six shock strengths (1.8 +/- 0.4, 3.8 +/- 0.7, 5.6 +/- 0.9, 7.2 +/- 1.1, 11.1 +/- 1.9, and 17.8 +/- 1.5 V/cm) were given with both polarities. The tissue was then treated with either 30 microM tetrodotoxin (TTX; n = 5) or 30 microM TTX plus Ca(2+)-free (n = 5) perfusion. For shocks during the action potential plateau, delta Vm caused by the six potential gradients was 22.4 +/- 9.6, 43.6 +/- 17.4, 54.7 +/- 17.9, 60.4 +/- 18.1, 65.4 +/- 13.7, and 66.4 +/- 12.2 mV for shocks causing depolarization and 41.1 +/- 16.5, 68.3 +/- 22, 80.5 +/- 20.4, 84.0 +/- 19.5, 93.6 +/- 16.3, and 98.9 +/- 15.4 mV for shocks causing hyperpolarization. The relationship between delta Vm and shock potential gradient was not linear. During diastole, hyperpolarizing shocks induced initial hyperpolarization, then depolarization followed again by hyperpolarization. A new depolarization upstroke occurred immediately after the shock. After TTX or TTX plus Ca(2+)-free perfusion, point stimuli 10 times diastolic threshold could not induce an action potential, but a shock field of 1.8 +/- 0.2 V/cm still induced action potentials. The peak value of depolarization measured with respect to resting potential (-87 +/- 5 mV) during the hyperpolarizing shock decreased from +14 +/- 22 before to -66 +/- 30 mV with TTX perfusion (P < 0.01). The fast upstroke rate of depolarization both during and immediately after the end of hyperpolarizing shocks was inhibited by TTX perfusion. Thus 1) the relationship between delta Vm and shock potential gradient is not linear; 2) field but not point stimulation can induce an action potential when Na+ channels are inactivated; and 3) during diastole Na+ channels are activated twice by a 10-ms hyperpolarizing shock, once during shock-induced hyperpolarization and again immediately after the end of the shock.

Action Potentials↗
PubMed1995

Late outcome after coronary artery bypass graft surgery in patients < 40 years old.

BACKGROUND: Randomized trials confirm the long-term efficacy of coronary artery bypass graft surgery (CABG), although there are no randomized data in patients < 40 years old. Because these patients have been reported to have an early recurrence of symptoms, the long-term postoperative outcome was examined. METHODS AND RESULTS: The long-term outcome of patients (n = 221) < 40 years old undergoing CABG at Green Lane Hospital, New Zealand, from 1970 to 1992 was determined. The 30-day mortality rate was 1.8% for initial and 9.5% for redo CABG. The median times to angina or myocardial infarction (recurrent ischemic event), further intervention, and death were 6.0, 9.6, and 14.2 years, respectively. Factors associated with increased late mortality on univariate analysis included end-systolic volume (ESV) > or = 80 mL (P = .004; 10-year mortality 19% versus 39% ESV > or = 80 mL), no internal mammary conduit (P = .01), no lipid-modifying therapy (P = .005), and no postoperative aspirin use (P = .0002); the latter was also associated with increased recurrent ischemic events (P = .04) or increased reintervention (P = .02). On stepwise logistic regression analysis, factors associated with increased late mortality were increasing ESV (P = .004), no internal mammary artery conduit (P = .009), diabetes (P = .04), and no postoperative aspirin (P = .02); the latter was also associated with increased recurrent ischemic events (P = .02). Hypercholesterolemia (> or = 6.5 mmol/L) was present in 65% of patients at presentation and 45% at follow-up. CONCLUSIONS: To attempt to prevent recurrent ischemia or late death, patients < 40 years old who require CABG should receive internal mammary conduits, aspirin, lipid-modifying therapy, therapy to inhibit ventricular dilatation, and strict diabetes management.

Actuarial Analysis↗
PubMed1995

Endocardial carbon-braid electrodes. A new concept for lower defibrillation thresholds.

BACKGROUND: In the treatment of patients with life-threatening ventricular arrhythmia, transvenous implantable cardioverter/defibrillators provide significant advantages over devices requiring a thoracotomy. This study tested the hypothesis that a new carbon-fiber electrode, designed at the Technische Universität in Munich, Germany, has a lower defibrillation threshold (DFT) than standard transvenous defibrillation electrodes. METHODS AND RESULTS: In 8 mongrel dogs (weight, 25.2 +/- 0.8 kg; heart weight, 192 +/- 19 g), we examined the efficacy and electrical characteristics of a right ventricular endocardial carbon prototype defibrillation electrode (9.5F, 4.4-cm2 surface) compared with a standard CPI 0062 Endotak electrode and a Medtronic 6966 Transvene endocardial right ventricular defibrillation electrode. The new electrode consists of 24 braided, tubular carbon filaments, each containing 1000 highly isotropic carbon fibers of 7-microns diameter, yielding a theoretical electrical surface of 480 cm2. The DFTs were determined in random order between each of the three right ventricular electrodes and a subcutaneous wire array anode placed on the left thorax. A standard step-down/up DFT protocol of 20-V shock steps was applied. Two different biphasic waveforms with a 1-ms delay between phases were tested: 3.2-ms first phase/2.0-ms second phase, and 6.0-ms first phase/6.0-ms second phase. For the 3.2/2.0-ms waveform, we found a significantly lower DFT for the carbon lead (4.96 +/- 1.58 J) compared with the CPI 0062 (6.93 +/- 1.67 J) and the Medtronic 6966 (7.49 +/- 0.99 J) leads. For the 6.0/6.0-ms waveform, the DFT for the carbon electrode (5.97 +/- 2.09 J) was significantly lower than for the Medtronic 6966 lead (8.55 +/- 1.93 J) but not for the CPI 0062 lead (6.30 +/- 1.41 J). The impedance with carbon was lower than with the other two leads for the 6.0/6.0-ms waveform but not for the 3.2/2.0-ms waveform. For the carbon electrode, the 3.2/2.0-ms waveform had a lower DFT than the 6.0/6.0-ms waveform. CONCLUSIONS: The present canine study found a lower DFT for a new carbon electrode compared with DFTs for endocardial defibrillation electrodes made of standard metal. Further long-term animal studies and clinical studies are needed to determine whether carbon materials and braided-lead technology are practical and beneficial in patients.

Animals↗
PubMed1995

Improved defibrillation threshold with a new epicardial carbon electrode compared with a standard epicardial titanium patch.

BACKGROUND: Recent studies show that depending on the type of shock morphology used, 5% to 15% of patients requiring implantable defibrillators cannot be treated with a nonthoracotomy system. In these cases, an epicardial patch-based system becomes necessary. In this study, we investigated a newly developed epicardial carbon electrode as an alternative to a standard epicardial titanium patch. METHODS AND RESULTS: A tubular epicardial braided carbon electrode of 7F diameter and 14-cm length applied in a U-shape to the epicardium was compared with a standard left ventricular epicardial 15-cm2 titanium mesh patch (CPI Inc). As cathode, a CPI endocardial lead, a Medtronic lead, or a carbon-platinum-iridium prototype electrode was used. Ventricular fibrillation was induced with a 60-Hz generator and allowed to continue for 10 seconds before a shock was given. Two different biphasic shock waveforms (3.2/2- and 6/6-millisecond) were delivered by the six electrode configurations. Eight dogs (weight, 24.5 +/- 1.3 kg) underwent an up-down defibrillation protocol. The order of testing the epicardial electrodes, the endocardial cathodes, and the waveform was randomized. With the epicardial carbon electrode, the mean defibrillation threshold (DFT) energy decreased 39% to 56% and the voltage decreased 24% to 35% compared with the titanium patch: from 8.3 +/- 2.5 to 4.9 +/- 3.6 J with the CPI lead and the 3.2/2-millisecond waveform, from 6.2 +/- 2.5 to 2.9 +/- 2.1 J with the carbon-platinum-iridium prototype, and from 6.4 +/- 3.4 J to 3.5 +/- 2.6 J with the Medtronic lead (P < or = .05). The DFT determinations with the 6/6-millisecond biphasic waveform showed a similar trend with slightly higher values. CONCLUSIONS: Compared with a titanium patch, the new braided epicardial electrode significantly decreases the defibrillation energy requirements. This effect can be maximized by using an endocardial carbon-platinum-iridium prototype as cathode and a short duration biphasic waveform.

Animals↗
PubMed1995

Comparison of defibrillation probability of success curves for an endocardial lead configuration with and without an inactive epicardial patch.

OBJECTIVES: This study sought to assess the effect of passive "bystander" epicardial electrodes on defibrillation efficacy. BACKGROUND: We hypothesized that an inactive epicardial patch placed in an area of low potential gradient from an endocardial electrode shock might affect defibrillation efficacy through its effects on the shock field and the underlying potential gradient. METHODS: We studied the effects of an inactive 18-cm2 titanium mesh patch placed on the anterolateral left ventricular epicardium on the 50% probability of successful defibrillation. A biphasic shock with both phases 6 ms in duration was delivered between superior vena cava and right ventricular catheter electrodes 10 s after the electrical induction of ventricular fibrillation. Six dogs underwent an up/down defibrillation protocol randomized with or without the patch on the heart. RESULTS: Mean 50% (+/-) probability point for energy doubled with the conductive patch on the heart, from 8.0 +/- 3.2 to 16.8 +/- 7.0 J (p < 0.01), and leading-edge voltage increased from 334 +/- 64 to 477 +/- 98 V (p < 0.01). Mean 50% probability points for energy and leading-edge voltage were not significantly changed when the procedure was repeated using a nonconductive patch in another six dogs as a control group. In a saline-saturated foam model, measurements from electrodes placed around and under the patch revealed a 72% mean decrease in the potential gradient in the foam under the conductive patch. CONCLUSIONS: A passive defibrillator patch can markedly increase the energy requirements for defibrillation, probably by decreasing the potential gradient under the patch. These results suggest the use of caution when passive electrodes are present, for example, when a patient receives a nonthoracotomy defibrillator system while epicardial electrodes from a previously implanted system are left in place.

Animals↗
PubMed1995

Predicting patterns of epicardial potentials during ventricular fibrillation.

Ventricular fibrillation (VF) is a fatal cardiac arrhythmia, characterized by uncoordinated propagation of activation wavefronts in the ventricular myocardium. Short-term predictions of epicardial potential fields during VF in pigs were attempted using linear techniques, and prediction accuracy was measured at various stages during sustained episodes. VF was induced in five pigs via premature electrical stimulation. Unipolar electrograms were recorded from an epicardial array of 506 electrodes in a 22 x 23 array with 1-mm spacing. Optimal spatial basis functions (modes) and time-varying weighting coefficients were found using the Karhunen-Loeve decomposition. Linear autoregressive (AR) models incorporating the dynamics of only a few spatial modes led to predicted patterns that were qualitatively similar to observed patterns. Predictions were made 0.256 s into the future, based on 0.768 s of past data, over an area of approximately 5 cm2 on the ventricular epicardium. The mean squared error of predictions varied from as much as 1.23 to as little as 0.14, normalized to the variance of the actual data. Inconsistency in long-term forcasts is partly due to the limitations of linear AR models. Changes in predictability, however, were consistent. Predictability varied inversely with spatial complexity, as measured by the mean squared error of a five-mode approximation. Predictability also increased significantly during the first minute of VF.

Algorithms↗
PubMed1995

Influence of malpositioned transvenous leads on defibrillation efficacy with and without a subcutaneous array electrode.

Some patients cannot receive a transvenous lead system because of high defibrillation thresholds (DFTs). We hypothesized that a right ventricular (RV) catheter electrode not extending as far as possible into the RV apex could cause high DFTs. Recently, a subcutaneous array (SQA) electrode has been shown to lower DFTs substantially. We compared the influence of a malpositioned RV catheter electrode on defibrillation efficacy for endocardial lead systems with and without a SQA. In eight anesthetized pigs, defibrillation catheters were placed in the RV apex and near the junction of the superior vena cava (SVC) and right atrium. SQA, formed by three elements, each 20 cm in length, was placed in the left thorax. DFTs were determined for a biphasic waveform using an up/down protocol with the RV catheter at the apex and with it repositioned 1-cm and 2-cm proximal to the apex. The mean DFT energies for the configurations with a SQA were less than those without a SQA for every catheter position. The placement of the RV catheter away from the apex caused an increase in defibrillation energy for the configurations without a SQA (apex: 17.1 +/- 3.8 J [mean +/- SD]; 1 cm: 20.1 +/- 4.6 J; 2 cm: 27.6 +/- 9.5 J; P < 0.05), but not for the configurations with a SQA (apex: 12.2 +/- 2.2 J; 1 cm: 12.3 +/- 2.9 J; 2 cm: 12.1 +/- 0.9 J: P = NS). These results suggest that a malpositioned RV catheter electrode, at the time of implantation or by late dislodgment, significantly elevates DFTs for a total endocardial system but not for a system that includes a SQA.

Animals↗