Notizen: ULV-DFT Waveform. Introduction: The upper limit of vulnerability (ULV) correlates with the defibrillation threshold (DFT). The ULV can he determined with a single episode of ventricular fibrillation and is more reproducible than the single-point DFT. The critical-point hypothesis of defibrillation predicts that the relation between the ULV and the DFT is independent of shock waveform. The principal goal of this study was to test this prediction. Methods and Results: We studied 45 patients at implants of pectoral cardioverter defibrillators. In the monophasic-biphasic group (n = 15), DFT and ULV were determined for monophasic and biphasic pulses from a 120-μF capacitor. In the 60- to 110-μF group (n = 30), DFT and ULV were compared for a clinically used 110-μF waveform and a novel 60-μF waveform with 70% phase 1 tilt and 7-msec phase 2 duration. In the monophasic-biphasic group, all measures of ULV and DFT were greater for monophasic than biphasic waveforms (P 〈 0.0001). In the 60- to 110-/tF group, the current and voltage at the ULV and DFT were higher for the 60-μF waveform (P 〈 0.0001), hut stored energy was lower (ULV 17%, P 〈 0.0001; DFT 19%, P = 0.03). There was a close correlation between ULV and DFT for both the monophasic-biphasic group (monophasic r2= 0.75, P 〈 0.001; hiphasic r2= 0.82, P 〈 0.001) and the 60- to 110-μF group (60 μF r2= 0.81 P 〈 0.001; 110 μF r2= 0.75, P 〈 0.001). The ratio of ULV to DFT was not significantly different for monophasic versus biphasic pulses (1.17 ± 0.12 vs 1.14 ± 0.19, P = 0.19) or 60-μF versus 110-μF pulses (1.15 ± 0.16 vs 1.11 ± 0.14, P = 0.82). The slopes of the ULV versus DFT regression lines also were not significantly different (monophasic vs biphasic pulses, P = 0.46; 60-μF vs UO-μF pulses, P = 0.99). The sample sizes required to detect the observed differences between experimental conditions (P 〈 0.05) were 4 for ULV versus 6 for DFT in the monophasic-biphasic group (95% power) and 11 for ULV versus 31 for DFT in the 60- to 110-μF group (75% power). Conclusion: The relation between ULV and DFT is independent of shock waveform. Fewer patients are required to detect a moderate difference in efficacy of defibrillation waveforms by ULV than by DFT. A small-capacitor biphasic waveform with a long second phase defibrillates with lower stored energy than a clinically used waveform.

Notizen: Activations in Permanent Atrial Fibrillation. Introduction: Activation patterns during permanent atrial fibrillation (AF) in patients with organic heart diseases are unclear. Methods and Results: We studied six patients with permanent AF and organic heart diseases undergoing surgery. The duration of AF averaged 4.9 ± 7.6 years. Computerized epicardial mappings of the right atrial (RA) free wall and the left atrial (LA) posterior wall were simultaneously performed with 224 bipolar electrodes at 3-mm spatial resolution. In the RA, large wavefronts and conduction blocks were frequently observed. The lines of block correlated with the crista terminalis and large pectinate muscles. In contrast, the LA had rapid repetitive activities originated from corners of the electrode plaque, near the four pulmonary veins (PVs). On average, 2.8 ± 1.2 sites of rapid repetitive activities were identified per patient. They activated continuously, intermittently, or alternately during AF. The mean activation cycle length in the RA (196 ± 22 msec) was significantly longer than that in the LA (179 ± 26 msec; P = 0.004). The maximum dominant frequency in the LA was higher than that in the RA (6.41 ± 1.18 Hz vs 5.66 ± 0.55 Hz; P = 0.049). The maximum dominant frequency was consistently located in areas with rapid repetitive activations near the PVs. Conclusion: During human permanent AF associated with organic heart diseases, the activation cycle length was shorter in the LA posterior wall than in the RA free wall. Rapid repetitive activities are consistently observed in the LA posterior wall, at or near the PVs.

Notizen: Critical Mass for Human Ventricular Fibrillation. Introduction: The critical mass for human ventricular fibrillation (VF) and its electrical determinants are unclear. The goal of this study was to evaluate the relationship between repolarization characteristics and critical mass for VF in diseased human cardiac tissues. Methods and Results: Fight native hearts from transplant recipients were studied. The right ventricle was immediately excised, then perfused (n = 6) or superfused (n = 2) with Tyrode's solution at 36° C. The action potential duration (APD) restitution curve was determined by an S1-S2 method. Programmed stimulation and burst pacing were used to induce VF. In 3 of 8 tissues, 10 μM cromakalim, au ATP-sensitive potassium channel opener, was added to the perfusate and the stimulation protocol repeated. Results show that, at baseline, VF did not occur either spontaneously or during rewarming, and it could not he induced by aggressive electrical stimulation in any tissue. The mean APD at 90% depolarization (APD90) at a cycle length of 600 msec was 227 ± 49 msec, and the mean slope of the APD restitution curve was 0.22 ± 0.08. Among the six tissues perfused, five were not treated with any antiarrhythmic agent. The weight of these five heart samples averaged 111 ± 23 g (range 85 to 138). However, after cromakalim infusion, sustained VF (〉 30 min in duration) was consistently induced. As compared with baseline in the same tissues, cromakalim shortened the APD90 from 243 ± 32 msec to 55 ± 18 msec (P 〈 0.001) and increased the maximum slope of the APD restitution curve from 0.24 ± 0.11 to 1.43 ± 0.10 (P 〈 0.01). Conclusion: At baseline, the critical mass for VF in diseased human hearts in vitro is 〉 111 g. However, the critical mass for VF can vary, as it can he reduced by shortening APD and increasing the slope of the APD restitution curve.

Notizen: Vulnerability to VF in Humans. Introduction: Shocks during the vulnerable period of the cardiac cycle induce ventricular fibrillation (VF) if their strength is above the VF threshold (VFT) and less than the upper limit of vulnerability (ULV). However, the range of shock strengths that constitutes the vulnerable zone and the corresponding range of coupling intervals have not been defined in humans. The ULV has been proposed as a measure of defibrillation because it correlates with the defibrillation threshold (DFT), but the optimal coupling interval for identifying it is unknown. Methods and Results: We studied 14 patients at implants of transvenous cardioverter defibrillators. The DFT was defined as the weakest shock that defibrillated after 10 seconds of VF. The ULV was defined as the weakest shock that did not induce VF when given at 0, 20, and 40 msec before the peak of the T wave or 20 msec after the peak in ventricular paced rhythm at a cycle length of 500 msec. The VFT was defined as the weakest shock that induced VF at any of the same four intervals. To identify the upper and lower boundaries of the vulnerable zone, we determined the shock strengths required to induce VF at all four intervals for weak shocks near the VFT and strong shocks near the ULV. The VFT was 72 ± 42 V, and the ULV was 411 ± 88 V. In all patients, a shock strength of 200 V exceeded the VFT and was less than the ULV. The coupling interval at the ULV was 19 ± 11 msec shorter than the coupling interval at the VFT (P 〈 0.001). The vulnerable zone showed a sharp peak at the ULV and a less distinct nadir at the VFT. A 20-msec error in the interval at which the ULV was measured could have resulted in underestimating it by a maximum of 95 ± 31 V. The weakest shock that did not induce VF was greater for the shortest interval tested than for the longest interval at both the upper boundary (356 ± 108 V vs 280 ± 78 V; P 〈 0.01) and lower boundary (136 ± 68 msec vs 100 ± 65 msec; P 〈 0.05). Conclusions: The human vulnerable zone is not symmetric with respect to a single coupling interval, but slants from the upper left to lower right. Small differences in the coupling interval at which the ULV is determined or use of the coupling interval at the VFT to determine the ULV may result in significant variations in its measured value. An efficient strategy for inducing VF would begin by delivering a 200-V shock at a coupling interval 10 msec before the peak of the T wave.

Notizen: Abstract Background: The upper limit of vulnerability (ULV) is the stimulus strength above which ventricular fibrillation cannot be induced, even when the stimulus occurs during the vulnerable period of the cardiac cycle. Determination of ULV using T-wave shocks during ventricular pacing has been shown to closely correlate with the defibrillation threshold (DFT) at ICD implantation. However, there are no data correlating ULV determined in sinus rhythm at ICD implantation, with DFT determined at implantation or during long-term follow-up. This is of clinical importance since ULV may be used to estimate DFT during ICD implantation, both during ventricular pacing or sinus rhythm. Methods and Results: Twenty-one patients receiving a transvenous ICD system were studied prospectively. There were 16 males and 5 females, mean age 68 ± 15 years, with mean ejection fraction 37.4 ± 17.4%. All had structural heart disease. The ULV was defined as the lowest energy that did not induce ventricular fibrillation with shocks at 0, 20 and 40ms before the peak of the T-wave, using a step-down protocol. The initial energy tested was 15J and the lowest energy 2J. DFT was determined following a similar step-down protocol. The DFT was defined as the lowest energy that successfully defibrillated the ventricles. The linear correlation coefficient between ULV and DFT was r = 0.73 (p 〈 0.001). At implant, mean ULV was 9.2 ± 5J, not statistically different from mean DFT 9.4 ± 4J. ULV plus 5J successfully defibrillated 19 of 21 patients. During long-term follow-up of 10.1 ± 1.8 months in eight patients, DFT was 8.8 ± 5.8J, not significantly different than the DFT of 7.5 ± 4.1J or ULV of 8.0 ± 5.3 at implant. Conclusion: 1) When determined during normal sinus rhythm the ULV significantly correlates with DFT. 2) ULV testing might be used in lieu of standard DFT testing to confirm adequate lead placement thus minimizing or eliminating VF inductions, particularly in hemodynamically unstable patients. 3) Since ULV + 5J has a high probability of successful defibrillation in most patients, programming ICD first shock energy for VF at ULV + 5J may result in lower first shock energies compared to the standard methods of programming first shock energy at twice DFT. Condensed Abstract. The purpose of this study was to determine if the upper limit of vulnerability (ULV) determined during normal sinus rhythm correlates with the defibrillation threshold (DFT), as has been previously shown when determined during ventricular pacing. The linear correlation coefficient between the ULV and DFT was r = 0.73 (p 〈 0.001). Mean ULV at implant was 9.2 ± 5J, not statistically different from mean DFT of 0.4 ± 4J. During long-term follow-up of 10.1 ± 1.8 months in 8 patients, DFT was 8.75 ± 8J, not significantly different than the DFT of 7.5 ± 4.1J or ULV of 8.0 ± 5.3 at implant. Shocks energies of ULV + 5J successfully defibrillated 19 of 21 patients at implant and 8 of 8 at follow-up. This study indicates that the ULV determined in normal sinus rhythm closely correlates with the DFT, and that ULV + 5J defibrillated most patients. ULV testing could be used to predict DFT and reduce or eliminate the need for DFT testing and VF induction. Programming ICD first shock energy for VF to ULV + 5J will result in lower energy than that used with standard DFT testing.