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Notes: Abstract: Rat medullary brain segments containing primarily nucleus tractus solitarius (NTS) were used for superfusion studies of evoked transmitter release and for isotherm receptor binding assays. Isotherm binding assays with [3H]CGS-21680 on membranes prepared from NTS tissue blocks indicated a single high-affinity binding site with a KD of 5.1 ± 1.4 nM and a Bmax of 20.6 ± 2.4 fmol/mg of protein. The binding density for [3H]CGS-21680 on NTS membranes was 23 times less than comparable binding on membranes from striatal tissue. Electrically stimulated (1 min at 25 mA, 2 ms, 3 Hz) release of [3H]norepinephrine ([3H]NE) from 400-µm-thick NTS tissue slices resulted in an S2/S1 ratio of 0.96 ± 0.02. Superfusion of single tissue slices with 0.1–100 nM CGS-21680, a selective adenosine A2a receptor agonist, for 5 min before the S2 stimulus produced a significant concentration-dependent increase in the S2/S1 fractional release ratio that was maximal (31.3% increase) at 1.0 nM. However, superfusion of tissue slices with CGS-21680 over the same concentration range for 20 min before the S2 stimulus did not alter the S2/S1 ratio significantly from control release ratios. The augmented release of [3H]NE mediated by 1.0 nM CGS-21680 with a 5-min tissue exposure was abolished by 1.0 and 10 nM CGS-15943 as well as by 100 nM 8-(3-chlorostyryl)caffeine, both A2a receptor antagonists, but not by 1.0 nM 8-cyclopentyl-1,3-dipropylxanthine, the A1 receptor antagonist. Taken together, these results suggest that CGS-21680 augmented the evoked release of [3H]NE in the NTS via activation of presynaptic A2a receptors within the same concentration range as the binding affinity observed for [3H]CGS-21680. It was also apparent that this population of presynaptic adenosine A2a receptors in the NTS desensitized within 20 min because the augmenting action of CGS-21680 on evoked transmitter release was not evident at the longer interval.

Notes: This article describes a suite of 250, 280, and 350 eV copper-doped Be [Be(Cu)] capsule designs for the National Ignition Facility [Paisner et al., Laser Focus World 30, 75 (1994)] and compare these to previous Be(Cu) and bromine-doped CH plastic [CH(Br)] capsule designs for 300 and 330 eV drives. These capsule designs are constrained to have the same deuterium-tritium (DT) fuel mass as the 300 and 330 eV designs so that differences in yield are due to differences in capsule compression before ignition. The one-dimensional (1-D) calculations show that the fuel ρr reaches a maximum value when about 20–30 μm of ablator material is left behind, and this amount of ablator material provides the best trade-off between maximizing the fuel ρr, the implosion velocity, and the calculated clean yield. The results of this paper add optimized 1-D capsule designs that operate at drive temperatures of 250, 280, and 350 eV and they complement the established 300 eV CH(Br) ablator and the 330 eV Be(Cu) ablator designs.

Notes: Ventricular Defibrillation and Cardiac Function. Introduction: The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics. Methods and Results: The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27- to 34-, 15-, 10-, 5-, 3-, or 1-J shocks. The cardiac Index was also measured at the same time points after 27- to 34-, and 1-J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 ± 0.40 L/min per m2 before a 27- to 34-J shock during defibrillation energy requirement testing to 2.14 ± 0.45 L/min per m2 immediately afterwards (P= 0.001). This effect persisted for 〉4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P= 0.003) and 10-J shocks (P= 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P= 0.03). The cardiac index decreased 14% after a 27- to 34-J shock during the baseline rhythm (P 〈 0.0001). This effect persisted for 〈4 minutes. A 1- J shock during the baseline rhythm did not effect the cardiac index. Conclusion: Defibrillator shocks 〉9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for This effect. Therefore, the detrimental hemodynamic effects of high-energy shocks may be avoided when low-energy defibrillation is used.

Notes: Adenosine and Retrograde Fast Pathway Conduction. Introduction: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. Methods and Results: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 ± 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P 〈 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 ± 78 vs 333 ± 74 msec, P 〈 0.01), a shorter VA block cycle length (383 ± 121 vs 307 ± 49 msec, P 〈 0.001), and a shorter VA interval during tachycardia (53 ± 23 vs 41 ± 17 msec, P 〈 0.01). Conclusion: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.

Notes: Impedance Versus Temperature Monitoring. Introduction: The purpose of this study was to prospectively compare the value of impedance and temperature monitoring during accessory pathway ablation. Temperature and impedance monitoring can be used during radiofrequency ablation of accessory pathways to titrate power to achieve adequate but not excessive tissue beating. Methods and Results: One hundred thirty-two patients with a single accessory pathway were randomly assigned to undergo ablation using either impedance monitoring or temperature monitoring. During impedance monitoring, the endpoint for titration of power was a 5-to 10-Ω decrease in the measured impedance while for temperature monitoring the endpoint was to achieve a temperature of 58° to 62°C. Two protocols were used. In protocol 1 (90 patients), impedance monitoring was performed with a nonthermistor catheter and temperature monitoring was performed with a thermistor catheter. In protocol 2 (42 patients), a thermistor catheter was used in all patients. In protocol 1, the success rate (93% vs 93%; P = 1.0), ablation procedure duration (57 ± 56 vs 41 ± 41 min), fluoroscopy time (48 ± 29 vs 41 ± 23 min; P = 0.3), number of applications (6.2 ± 4.7 vs 5.7 ± 4.6; P = 0.8), and the number of applications associated with coagulum formation (0.1 ± 0.3 vs 0.3 ± 0.6; P = 0.1) were similar in the two groups. In protocol 2, as in protocol 1, there were no differences in the success rate (91% vs 95%; P = 1.0), ablation procedure duration (49 ± 37 vs 62 ± 55 min; P = 0.4), fluoroscopy time (46 ± 24 vs 49 ± 36 min; P = 0.8), number of applications (6.8 ± 7.0 vs 7.8 ± 12.1; P = 0.7), or number of applications associated witb coagulum formation (0.3 ± 0.6 vs 0.2 ± 0.7; P = 0.6) between the impedance and temperature monitoring groups. Conclusion: Temperature and impedance monitoring are equally effective in optimizing the results of accessory pathway ablation.

Notes: Cardiac Memory. Introduction: “Cardiac memory” (primary T wave change) is thought to occur after 15 minutes to several hours of right ventricular (RV) pacing. The two components of the temporal change in repolarization are memory and accumulation. The purpose of this study was to examine quantitatively the effect of short periods of ventricular pacing on the human cardiac action potential, using monophasic action potential (MAP) recordings. Methods and Results: Thirty-one patients (ages 43 ± 14 years) with structurally normal hearts undergoing a clinically indicated electrophysiologic procedure were enrolled. Catheters were placed in the right atrium (RA) and RV, and a MAP catheter was positioned at the RV septum. APD90 was calculated from digitized MAP recordings. MAP morphology comparisons were performed using the root mean square (RMS) of the difference between complexes. All pacing was at 500-msec cycle length. There were four pacing protocols: (1) RA pacing was performed for approximately 15 minutes to evaluate temporal stability of the MAP recordings (5 pts); (2) to evaluate the memory phenomenon, four successive 1-minute episodes of RV pacing were interspersed with 2 minutes of RA pacing (5 pts); (3) the accumulation phenomenon was evaluated by assessing the effects of 1, 5, 10, and 15 minutes of RV pacing on the MAP during RA pacing (16 pts); and (4) 20 minutes of RV pacing was followed by 10 minutes of RA pacing to correlate visually apparent T wave changes with changes in MAP recordings (5 pts). In the control patients, no changes in APD90 or RMS analysis were noted during 14.9 ± 1.4 minutes of RA pacing. In the second protocol, RMS of the difference between the baseline MAP complexes and the signal average of the first 50 beats following each of four 1-minute RV pacing trains demonstrated progressively greater differences in morphology after successive episodes of RV pacing. In protocol 3, RMS analysis identified a progressively greater difference between the baseline MAP recording and the average of the first 50 beats after 1,5, 10, and 15 minutes of RV pacing. In protocol 4, visually apparent changes in T waves occurred in parallel with the RMS of the difference between the baseline MAP recordings and the average of the first 50 beats after 20 minutes of RV pacing. Similar changes also were demonstrated by APD90 analysis. Conclusion: This study is the first to demonstrate that episodes of abnormal ventricular activation as short as 1 minute in duration may exert lingering effects on the repolarization process once normal ventricular activation resumes.

Notes: Defibrillation Energy Requirements. Introduction: Defibrillation energy requirements in patients with nonthoracotomy defibrillators may increase within several months after implantation. However, the stability of the defibrillation energy requirement beyond 1 year has not been reported. The purpose of this study was to characterize the defibrillation energy requirement during 2 years of clinical follow-up. Methods and Results: Thirty-one consecutive patients with a biphasic nonthoracotomy defibrillation system underwent defibrillation energy requirement testing using a step-down technique (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, and 1 J) during defibrillator implantation, and then 24 hours, 2 months, 1 year, and 2 years after implantation. The mean defibrillation energy requirement during these evaluations was 10.9 ± 5.5 J, 12.3 ± 7.3 J, 11.7 ± 5.6 J, 10.2 ± 4.0 J, and 11.7 ± 7.4 J, respectively (P= 0.4). The defibrillation energy requirement was noted to have increased by 10 J or more after 2 years of follow-up in five patients. In one of these patients, the defibrillation energy requirement was no longer associated with an adequate safety margin, necessitating revision of the defibrillation system. There were no identifiable clinical characteristics that distinguished patients who did and did not develop a 10-J or more increase in the defibrillation energy requirement. Conclusion: The mean defibrillation energy requirement does not change significantly after 2 years of biphasic nonthoracotomy defibrillator system implantation. However, approximately 15% of patients develop a 10-J or greater elevation in the defibrillation energy requirement, and 3% may require a defibrillation system revision. Therefore, a yearly evaluation of the defibrillation energy requirement may he appropriate.

Notes: Postdefibrillation Ventricular Arrhythmias. Background: The relationship between postdefibrillation ventricular arrhythmias and shock strength is poorly understood in patients with implantable defibrillators. The purpose of this study was to characterize the relationship between postdefibrillation ventricular arrhythmias and shock strength. Methods and Results: Forty-three patients with an implanted defibrillator underwent six separate inductions of ventricular fibrillation (VF) after a step-down defibrillation energy requirement (7.3 ± 4.6 J) was determined. For each of the first three inductions of VF, the first two shocks were low energy and equal to approximately 75 % of the defibrillation energy requirement (5.4 ± 3.3 J), or to the defibrillation energy requirement plus 10 J (17.5 ± 4.3 J). After the first two shocks, subsequent shocks were programmed to the maximum available energy (29.0 ± 2.5 J). The alternate technique was used for the subsequent three inductions of VF. Post defibrillation ventricular arrhythmias were noted. Post defibrillation ventricular arrhythmias with a cycle length ≤ 300 msec were more frequent after a low-energy shock (19%), than after a high-energy shock (1.5 %; P = 0.005). Postdefibrillation ventricular arrhythmias with a cycle length 〉 300 msec were more frequent after a high-energy shock (32%), than after a low-energy shock (7.1%; P = 0.002). A relationship between the cycle length of the post defibrillation ventricular arrhythmias and the absolute defibrillation energy was observed (P 〈 0.001; r = 0.6), and ventricular arrhythmias with a cycle length 〉 300 msec were uncommon after shocks ≤ 10 J (P = 0.001). The characteristics of ventricular arrhythmias after maximum-energy shocks were similar to those that occurred after high-energy shocks. Conclusions: Post defibrillation ventricular arrhythmias with a cycle length ≤ 300 msec are more common after shocks of strength associated with a low probability of successful defibrillation. Postdefibrillation ventricular arrhythmias with a cycle length of 〉 300 msec are more common after high- and maximum-energy shocks, and are directly related to the absolute defibrillation energy.