Early out-of-hospital experience with an impedance-compensating low-energy biphasic waveform automatic external defibrillator

Impedance-compensating low-energy biphasic truncated exponential (BTE) waveforms are effective in transthoracic defibrillation of short-duration ventricular fibrillation (VF). However, the BTE waveform has not been examined in out-of-hospital cardiac arrest (OHCA) with patients in prolonged VF often associated with myocardial ischemia. The objective of this study was to evaluate the BTE waveform automatic external defibrillator (AED) in the out-of-hospital setting with long-duration VF. AEDs incorporating a 150-J BTE waveform were placed in 12 police squad cars and 4 paramedic-staffed advanced life support ambulances. AEDs were applied to arrested patients by first-arriving personnel, whether police or paramedics. Data were obtained from PC Data Cards within the AED. Defibrillation was defined as at least transient termination of VF. Ten patients, 64 +/- 14 years, were treated for VF with BTE shocks. Another 8 patients were in nonshockable rhythms and the AEDs, appropriately, did not advise a shock. Five of the 10 VF arrests were witnessed with a 911 call-to-shock time of 6.6 +/- 1.7 minutes. VF detection and defibrillation occurred in all 10 patients. Spontaneous circulation was restored in 3 of 5 witnessed arrest patients and 1 survived to discharge home. Fifty-one VF episodes were converted with 62 shocks. Presenting VF amplitude and rate were 0.43 +/- 0.22 (0.13-0.86) mV and 232 +/- 62 (122-353) beats/min, respectively, and defibrillation was achieved with the first shock in 7 of 10 patients. Including transient conversions, defibrillation occurred in 42 of 51 VF episodes (82%) with one BTE shock. Shock impedance was 85 +/- 10 (39-138) ohms. Delivered energy and peak voltage were 152 +/- 2 J and 1754 +/- 4 V, respectively. The average number of shocks per VF episode was 1.2 +/- 0.5 (1-3). More than one shock was needed in only 9 episodes; none required > 3 shocks to defibrillate. Impedance-compensating low-energy BTE waveforms terminated VF in OHCA patients with a conversion rate exceeding that of higher energy monophasic waveforms. VF was terminated in all patients, including those with high impedance.     

The effects of lidocaine on the vulnerable period during ventricular fibrillation

INTRODUCTION: It was postulated that a subthreshold defibrillation shock failed to halt ventricular fibrillation because the shock itself reinitiated ventricular fibrillation by falling into the vulnerable period of the wavefronts. Whether or not the timing of the vulnerable period is determined by the ventricular fibrillation cycle length is unknown. METHODS AND RESULTS: We determined the patterns of epicardial activation in ten dogs by computerized mapping techniques during unsuccessful defibrillation. Lidocaine was then given to prolong the ventricular fibrillation cycle length, and the computerized mapping studies were repeated. The results showed that lidocaine increased the ventricular fibrillation cycle length from 110 +/- 13 msec to 156 +/- 5 msec (P < 0.001). Among 55 episodes of unsuccessful defibrillation, the site of the earliest postshock activation occurred in the center of the mapped tissue 12 times at baseline and 14 times during lidocaine infusion. At electrodes that registered as postshock early sites, the preshock intervals clustered within a narrow range both before (58 +/- 14 msec) and during (101 +/- 18 msec, P < 0.001) lidocaine infusion. The correlation between the preshock intervals and the ventricular fibrillation cycle length was significant for these 26 sites (r = 0.87, P < 0.001). CONCLUSION: We conclude that a vulnerable period is present during ventricular fibrillation, and the timing of the vulnerable period is determined by the ventricular fibrillation cycle length.     

Anatomic heterogeneity of vascular aging: role of nitric oxide and endothelin

OBJECTIVES: This study investigated the effects of acute global ischemia on the vulnerable window, the upper limit of vulnerability and the defibrillation threshold. BACKGROUND: Myocardial ischemia, an important factor for arrhythmogenesis and sudden death, may affect the inducibility of ventricular fibrillation by T wave shocks as well as the defibrillation threshold. However, studies of the effect of ischemia on the defibrillation threshold remain inconclusive, and the effect of ischemia on recently established variables of ventricular fibrillation vulnerability is still unknown. METHODS: Ten isolated, perfused rabbit hearts were immersed in a tissue bath between two shock plate electrodes. Truncated 5-ms biphasic shocks were used to determine the vulnerable window, the upper limit of vulnerability and the defibrillation threshold. Measurements were performed during baseline and at 10 to 15 min of acute ischemia induced by an 80% reduction of coronary flow. The effects of ischemia were monitored by measuring the dispersion of ventricular activation and repolarization using multiple monophasic action potential recordings. RESULTS: Acute ischemia caused an increase in dispersion of activation (baseline vs. ischemia [mean +/- SD]: 22 +/- 6 vs. 34 +/- 10 ms, p < 0.001) and dispersion of repolarization (37 +/- 16 vs. 69 +/- 29 ms, p < 0.01). The width of the vulnerable window increased from 25 +/- 22 ms during baseline to 75 +/- 26 ms during ischemia (p = 0.001). The upper limit of vulnerability (baseline vs. ischemia: 294 +/- 44 vs. 274 +/- 53 V, p = 0.21) and the defibrillation threshold (271 +/- 33 vs. 268 +/- 42 V, p = 0.74) remained unchanged during ischemia. CONCLUSIONS: Acute global ischemia caused a threefold increase in the width of the vulnerable window. This increase was associated with increased heterogeneity of ventricular activation and repolarization. Despite these marked changes, the upper limit of vulnerability and the defibrillation threshold were not affected by acute myocardial ischemia. Thus, the previously reported similarity between both measures was maintained under these adverse conditions.     

Clinical shock tolerability and effect of different right atrial electrode locations on efficacy of low energy human transvenous atrial defibrillation using an implantable lead system

OBJECTIVES: The objectives of this study were 1) to evaluate the effect of different right atrial electrode locations on the efficacy of low energy transvenous defibrillation with an implantable lead system; and 2) to qualitate and quantify the discomfort from atrial defibrillation shocks delivered by a clinically relevant method. BACKGROUND: Biatrial shocks result in the lowest thresholds for transvenous atrial defibrillation, but the optimal right atrial and coronary sinus electrode locations for defibrillation efficacy in humans have not been defined. METHODS: Twenty-eight patients (17 men, 11 women) with chronic atrial fibrillation (AF) (lasting > or = 1 month) were studied. Transvenous atrial defibrillation was performed by delivering R wave-synchronized biphasic shocks with incremental shock levels (from 180 to 400 V in steps of 40 V). Different electrode location combinations were used and tested randomly: the anterolateral, inferomedial right atrium or high right atrial appendage to the distal coronary sinus. Defibrillation thresholds were defined in duplicate by using the step-up protocol. Pain perception of shock delivery was assessed by using a purpose-designed questionnaire; sedation was given when the shock level was unacceptable (tolerability threshold). RESULTS: Sinus rhythm was restored in 26 of 28 patients by using at least one of the right atrial electrode locations tested. The conversion rate with the anterolateral right atrial location (21 [81%] of 26) was higher than that with the inferomedial right atrial location (8 [50%] of 16, p < 0.05) but similar to that with the high right atrial appendage location (16 [89%] of 18, p > 0.05). The mean defibrillation thresholds for the high right atrial appendage, anterolateral right atrium and inferomedial right atrium were all significantly different with respect to energy (3.9 +/- 1.8 J vs. 4.6 +/- 1.8 J vs. 6.0 +/- 1.7 J, respectively, p < 0.05) and voltage (317 +/- 77 V vs. 348 +/- 70 V vs. 396 +/- 66 V, respectively, p < 0.05). Patients tolerated a mean of 3.4 +/- 2 shocks with a tolerability threshold of 255 +/- 60 V, 2.5 +/- 1.3 J. CONCLUSIONS: Low energy transvenous defibrillation with an implantable defibrillation lead system is an effective treatment for AF. Most patients can tolerate two to three shocks, and, when the starting shock level (180 V) is close to the defibrillation threshold, they can tolerate on average a shock level of 260 V without sedation. Electrodes should be positioned in the distal coronary sinus and in the high right atrial appendage to achieve the lowest defibrillation threshold, although other locations may be suitable for certain patients.     

Electromagnetic compatibility aspects of active robotic systems for surgery: the robotic prostatectomy experience

This case describes ventricular proarrhythmia as a result of a synchronized internal atrial defibrillation shock in a 29-year-old man with Ebstein's anomaly referred for radiofrequency ablation of a right posterior accessory pathway. During the electrophysiologic study, atrial fibrillation was induced and 3/3 msec shocks of various strengths were delivered between two decapolar defibrillation catheters in the coronary sinus and right atrial appendage. A 2.0-J biphasic shock synchronized to an R wave after a short-long-short ventricular cycle length pattern with a preshock coupling interval of 245 msec induced ventricular fibrillation, which was externally defibrillated with 200 J. This observation has implications for the development of implantable atrial defibrillators.     

Ventricular fibrillation-induced intracellular Ca2+ overload causes failed electrical defibrillation and post-shock reinitiation of fibrillation

Despite high efficacy, electrical defibrillation shocks can fail or ventricular fibrillation (VF) is reinitiated after the application of the initial shock. The goal of this study was to determine whether [Ca2+]i overload, induced by VF itself, can cause failed electrical defibrillation and post-shock reinitiation of VF. For this purpose, we simultaneously measured [Ca2+]i transients (assessed by indo-1 fluorescence) and defibrillation energies (assessed by a modified implantable cardioverter defibrillator) in intact perfused rat hearts during pacing-induced sustained VF (10 min) in the absence of ischemia. We found that increasing [Ca2+]i during VF (by increasing [Ca2+]o from 3 to 6 mM) increased the defibrillation threshold (DFT) from 1.9 +/- 0.6 to 3.5 +/- 0.5 J/g (P<0.05) and also increased the total defibrillation energy (TDE) required for stabilization of sinus rhythm from 15.6 +/- 7.7 to 48.6 +/- 7.42 J/g (P<0.05). In addition, both DFT and TDE correlated linearly with [Ca2+]i (r=0.69 and 0.83, P<0.05). Furthermore, shortening the duration of VF from 10 to 1.5 min tended to limit [Ca2+]i overload and decreased TDE. Finally, all successful defibrillation shocks led to a sudden reduction of VF-induced [Ca2+]i overload (-115 +/- 3%). In contrast, failed shocks did not alter [Ca2+]i. Incomplete reduction of [Ca2+]i overload after initially successful shocks were often followed by synchronized spontaneous [Ca2+]i oscillations and subsequent reinitiation of VF. In conclusion, the present study showed for the first time that VF-induced [Ca2+]i overload can cause failed electrical defibrillation and post-shock reinitiation of VF. Because VF inevitably causes [Ca2+]i overload, this finding might be a crucial mechanism of failed defibrillation and spontaneous reinitiation of VF.     

Effect of the addition of an abdominal hot can cardioverter/defibrillator pulse generator on the defibrillation energy requirements in a single-lead endocardial defibrillation system

AIMS: The effects of a cardioverter/defibrillator system with an electrically active generator can, applied without recourse to thoracotomy, have not been investigated in the abdominal position in humans. The purpose of this acute clinical study was to evaluate the defibrillation efficacy of an abdominally positioned hot can electrode in connection with a single lead endocardial defibrillation system. PATIENTS AND METHODS: Thirty consecutive patients undergoing implantation of a cardioverter/defibrillator or pulse generator replacement were enrolled in this study Each patient received an integrated, tripolar single-lead system. This was tested using an asymmetrical biphasic defibrillation waveform with constant energy delivery. Defibrillation energy, peak voltage, peak current and impedance were compared between two electrode configurations: (A) in this configuration the distal right ventricular coil was negative and the proximal coil positive; (B) in this configuration the distal right ventricular coil was negative and the proximal coil and the abdominal hot can (65 ccm), as common anode, were positive. Defibrillation threshold testing started at 15 J with stepwise energy reduction (10 J, 8 J, 5 J and 3 J) until defibrillation was ineffective. RESULTS: Compared to the single-lead configuration, the abdominal hot can configuration revealed at 17.5% reduction in defibrillation energy requirements (8.6 J +/- 4.3 J vs 10.43 J +/- 3.9 J; P = 0.041), a 15.7% reduction in peak voltage (308.6 V +/- 63 V vs 365.3 V +/- 68 V; P = 0.003), and a 21.6% reduction in impedance (41.1 omega +/- 6.3 omega vs 52.4 omega +/- 6.6 omega; P < 0.001). Peak current showed a significant increase during hot can testing of 8.2% (7.2 A +/- 1.8 A vs 7.8 A +/- 2.2 A; P = 0.16). CONCLUSION: An abdominally placed hot can pulse generator lowered defibrillation energy requirements in patients with an endocardial defibrillation lead system.     

Compatibility of a nonthoracotomy lead system with a biphasic implantable cardioverter-defibrillator. Cadence-Endotak 60-Series IDE investigators

This prospective multicenter study was conducted under the Food and Drug Administration Investigational Device Exemption to evaluate the safety and efficacy of the combination of the Cadence implantable defibrillator (Ventritex, Inc.) and 60-series Endotak C leads (Cardiac Pacemakers, Inc.). Implantation was attempted in 148 patients with hemodynamically compromising ventricular tachycardia or fibrillation (VF), or with pace-terminable ventricular tachycardia. The system was successfully implanted in 97% of patients, with 96% of implants in a transvenous-lead-alone configuration. At implantation, the defibrillation threshold was 455 +/- 94 V (14 +/- 6 J) for lead-alone patients and 532 +/- 40 V (19 +/- 3 J) for those requiring a subcutaneous patch. VF conversion efficacy was reconfirmed in patients who underwent a 3-month chronic induction study. The system successfully detected all 763 induced arrhythmias and terminated 99.5% of them; after system modification, successful conversion was demonstrated in the 2 patients who initially had induced episodes requiring external defibrillation (1 lead revision; 1 reprogramming). All spontaneous episodes were terminated with an implantable-cardioverter defibrillator. Postshock VF redetection times were significantly shorter than initial detection times (4.5 +/- 1.8 seconds detection, 2.1 +/- 0.7 seconds redetection; p<0.0001). During an 8-month mean follow-up (range 1 to 31 months), 2 unwitnessed deaths were classified as sudden cardiac deaths, and 11 patients experienced a total of 12 complications, none of which was associated with the Cadence-Endotak combination.     

Anti-verotoxin-neutralizing antibody in intravenous gammaglobulin preparations

BACKGROUND: A previous retrospective study by our group suggested that shocks timed to the upslope of the shocking lead electrogram improved defibrillation efficacy. The goal of this study was to prospectively determine whether defibrillation threshold could be reduced by use of an algorithm that timed shocks to the upslope of coarse ventricular fibrillation (test treatment) compared with shocks delivered asynchronously after 10 seconds of fibrillation (control treatment). METHODS AND RESULTS: Ten pigs were instrumented with a 3-lead system for internal defibrillation. Initial estimates of the energy required to achieve defibrillation E50 for both treatments were made by an up/down method. Subsequently, additional shocks at V50+/-10% and V50-20% were given for each treatment to obtain data points at higher and lower intensities. Probability-of-success curves were estimated for both treatments by the best-fit method. Energies required were significantly lower for the timed shocks than for the asynchronous shocks (P<0.00 1). E80 was reduced 15.5%, from 27.1+/-2.5 to 22.9+/-1.8 J (P<0.002). The width of the probability-of-success curve (E80-E20) for the test treatment was also significantly narrower than that for the control treatment (7.1+/-0.9 versus 10.8+/-1.7, P<0.01). Normalized curve width (E80-E20)/E50 was decreased from 51+/-5% of E50 for control shocks to 37+/-4% of E50 for synchronous shocks (P<0.02). CONCLUSIONS: In this model, defibrillation threshold is lower and more deterministic when shocks are timed to the upslope of the shocking lead electrogram. If a similar reduction is observed in humans, shock timing may lower defibrillation threshold and simplify programming of shock intensity.     

Transthoracic defibrillation of swine with monophasic and biphasic waveforms

BACKGROUND: Biphasic waveforms have had a favorable impact on internal defibrillation but have seen minimal use in transthoracic defibrillation systems. The purpose of this study was to compare monophasic and biphasic waveforms for transthoracic defibrillation in swine. METHODS AND RESULTS: Three interrelated studies were performed in 19 swine to establish the relative transthoracic defibrillation efficacy of biphasic shock waveforms. In study 1, we measured voltage (V50) and energy (E50) strength-duration curves for monophasic and biphasic truncated exponential waveforms. We then independently examined the effects of phase duration and tilt on biphasic waveform defibrillation with a total waveform duration from study 1 that provided the minimum V50 (study 2) and the minimum E50 (study 3). At each pulse duration tested in study 1, biphasic waveforms defibrillated with significantly less voltage and energy than monophasic waveforms. At a duration of 12 ms, there was a voltage minimum for biphasic waveform defibrillation. At this duration, V50 was 1378 +/- 505 V for the biphasic waveform compared with 2185 +/- 361 V for the monophasic waveform, P = .01. For both monophasic and biphasic waveforms, E50 increased with pulse duration. With a total pulse duration of 12 ms, E50 was 169 +/- 101 J for the biphasic waveform compared with 414 +/- 114 J for the monophasic waveform, P = .003. In study 2, optimization of phase duration and total tilt reduced the defibrillation requirements of the 12-ms "minimum voltage" biphasic waveform to 1284 +/- 187 V and 129 +/- 36 J. In study 3, the 8-ms "minimum energy" biphasic waveform had an E50 of 115 +/- 35 J that was 11% less than the 12-ms biphasic waveform, P = .11; however, voltage requirements of 1476 +/- 239 V were 15% higher, P = .005. CONCLUSIONS: This study demonstrates the superiority of truncated biphasic waveforms over truncated monophasic waveforms for transthoracic defibrillation of swine. Biphasic waveforms should prove as advantageous at reducing voltage and energy requirements for transthoracic defibrillation as they have for internal defibrillation.     

Effect of ventricular dilatation on defibrillation threshold in the isolated perfused rabbit heart

INTRODUCTION: Ventricular dilatation has important electrophysiologic effects, but its effect on ventricular defibrillation threshold (DFT) is unknown. METHODS AND RESULTS: A fluid-filled, latex balloon was placed in the left ventricular cavity of 19 isolated rabbit hearts. In each experiment, an undilated volume (equivalent to a left ventricular end-diastolic pressure of approximately 0 mmHg) was compared to a dilated volume achieved by adding 1.0 mL of saline (n = 10) or 5% dextrose (n = 9) to the intracavitary balloon. Left ventricular effective refractory period (ERP) and DFT were determined at each volume. Defibrillation was attempted with a monophasic shock delivered between a patch electrode positioned over the posterior left ventricle (cathode) and a metallic aortic cannula (anode). DFT was determined using a modified "down/up" protocol with 10 V steps. Ventricular dilatation increased the left ventricular end-diastolic pressure from 0 +/- 0.5 mmHg to 35 +/- 3 mmHg (P < 0.001), decreased the average left ventricular ERP 15% (from 116 +/- 3 msec to 99 +/- 3 msec; P < 0.001), and increased the average DFT 30% (from 96 +/- 4 V to 125 +/- 7 V; P < 0.001). In one third of experiments, the dilated DFT was > or = 150% of the DFT at zero volume. The mechanism of the observed increase in DFT is unknown but may be related to the decrease in refractoriness observed with ventricular dilatation. CONCLUSION: Acute ventricular dilatation in this model increased DFT an average of 30%, an effect not previously described. This observation may have implications for patients with implantable cardioverter defibrillators.     

Postshock potential gradients and dispersion of repolarization in cells stimulated with monophasic and biphasic waveforms

INTRODUCTION: Even though the clinical advantage of biphasic defibrillation waveforms is well documented, the mechanisms that underlie this greater efficacy remain incompletely understood. It is established, though, that the response of relatively refractory cells to the shock is important in determining defibrillation success or failure. We used two computer models of an isolated ventricular cell to test the hypothesis that biphasic stimuli cause a more uniform response than the equivalent monophasic shocks, decreasing the likelihood that fibrillation will be reinduced. METHODS AND RESULTS: Models of reciprocally polarized and uniformly polarized cells were used. Rapid pacing and elevated [K]o were simulated, and either 10-msec rectangular monophasic or 5-msec/5-msec symmetric biphasic stimuli were delivered in the relative refractory period. The effects of stimulus intensity and coupling interval on response duration and postshock transmembrane potential (Vm) were quantified for each waveform. With reciprocal polarization, biphasic stimuli caused a more uniform response than monophasic stimuli, resulting in fewer large gradients of Vm (only for shock strengths < or = 1.25x threshold vs < or = 2.125x threshold) and a smaller dispersion of repolarization (1611 msec2 vs 1835 msec2). The reverse was observed with uniform polarization: monophasic pulses caused a more uniform response than did biphasic stimuli. CONCLUSION: These results show that the response of relatively refractory cardiac cells to biphasic stimuli is less dependent on the coupling interval and stimulus strength than the response to monophasic stimuli under conditions of reciprocal polarization. Because this may lead to fewer and smaller spatial gradients in Vm, these data support the hypothesis that biphasic defibrillation waveforms will be less likely to reinduce fibrillation. Further, published experimental results correlate to a greater degree with conditions of reciprocal polarization than of uniform polarization, providing indirect evidence that interactions between depolarized and hyperpolarized regions play a role in determining the effects of defibrillation shocks on cardiac tissue.     

Effect of selective aortic arch perfusion on median frequency and peak amplitude of ventricular fibrillation in a canine model

STUDY OBJECTIVE: To determine whether the computer-derived measures of median frequency or peak amplitude of ventricular fibrillation (VF), obtained by fast Fourier transform of the VF waveform, change during selective aortic arch perfusion in a canine model of cardiac arrest. METHODS: Eight mongrel dogs (including 4 control animals) were sedated, intubated, catheterized, and instrumented to record the electrocardiogram (digitally at 100 Hz, filtered with a finite impulse response filter at 2 Hz), right atrial pressure, and aortic pressure during resuscitation in a model of VF-induced cardiac arrest. After 10 minutes of VF-induced arrest, cardiopulmonary resuscitation (CPR) with a mechanical chest compression device was initiated. Beginning 2 minutes later, the 4 study animals received, every 2 minutes, 45 seconds of selective aortic arch perfusion (SAAP) with autologous blood infusions under high pressure. Defibrillation was attempted after 3 minutes of CPR and every minute thereafter. Both study and control groups received standard-dose epinephrine (.01 mg/kg) every 3 minutes by means of an intraaortic catheter. The median frequency, peak amplitude, and coronary perfusion pressure (CPP) during the 5-second period just before defibrillation were obtained with the use of computer algorithms. RESULTS: All SAAP animals and 1 control animal were resuscitated. Baseline measures of median frequency (8.4 +/- 1.5 versus 6.6 +/- 1.0 Hz) and peak amplitude (.18 +/- .05 versus .36 +/- .13 mV) were not different between the SAAP and control groups, respectively, at the start of CRP. SAAP infusion resulted in significant increases in the SAAP group compared with the control group: median frequency, 9.6 +/- .4 versus 7.3 +/- 1.4 Hz; peak amplitude, .74 +/- .21 versus .39 +/- .15 mV; and CPP, 40.5 +/- 7.1 versus 18.0 +/- 15.0 mm Hg, respectively. Median frequency correlated with CPP (r2 = .67). Peak amplitude did not correlate with CPP (r2 = .06). CONCLUSION: Median frequency and peak amplitude increase with SAAP during cardiac arrest in a canine model. This method of resuscitation was reliable in allowing restoration of a stable perfusing rhythm after defibrillation. Changes in measures of peak amplitude and median frequency may reflect interventions that enhance the likelihood of successful defibrillation and may thereby offer a noninvasive means of monitoring interventions during cardiac arrest.     

Spontaneous reinitiation of atrial fibrillation following transvenous atrial defibrillation

Spontaneous reinitiation of atrial fibrillation (AF) has not been systematically looked at in patients undergoing transvenous AF. This study involved 11 patients, the mean age 60 +/- 8 years, 3 male and 8 female, in whom transvenous atrial defibrillation successfully converted AF to sinus rhythm. Eight patients had paroxysmal AF and three patients had chronic persistent AF for 4 weeks or more. Four patients were taking antiarrhythmic medications at the time of testing. Multipolar transvenous catheters were positioned inside the coronary sinus, right atrium, and the right ventricle. Atrial defibrillation testing was performed using the METRIX atrial defibrillation system in nine patients and the Ventritex HVSO2 in the remaining two patients. A total of 64 therapeutic shocks (range 3-11) were delivered in the 11 patients, and 31 of these successfully converted AF to sinus rhythm. In four patients spontaneous AF was reinitiated following 12 successful transvenous atrial defibrillation episodes. The mean time to reinitiation of AF following shock delivery and restoration of sinus rhythm was 8.26 +/- 5.25 seconds, range 1.8-19.9 seconds. All 12 episodes of spontaneous AF were preceded by a spontaneous premature atrial complex. The coupling interval of the premature atrial complexes was 443 +/- 43 ms, range 390-510 ms. None of the patients taking antiarrhythmic medications or those demonstrating no premature atrial complexes had spontaneous reinitiation of AF. In conclusion, spontaneous reinitiation of AF can occur in a significant proportion of patients with AF undergoing transvenous atrial defibrillation. This phenomenon is preceded by the occurrence of atrial premature complex. Findings of this study may have significant clinical implications.     

Role of co-stimulation in CD8+ T cell activation

This study was undertaken to determine whether dl-sotalol can prevent ventricular tachyarrhythmia inducibility that can be predicted from electrophysiologic parameters. The effects of dl-sotalol in 16 patients (ventricular tachycardia (VT) in 11 and fibrillation (VF) in 5) were determined in electrophysiologic studies before and after dl-sotalol (320 mg/day). In 9 of 16 patients (56%) after dl-sotalol, ventricular tachyarrhythmia could not be induced by the entire stimulation protocol (responders). There were significant differences in QT interval (462 +/- 52 vs. 415 +/- 34 msec; p < 0.05) and ventricular effective refractory period (VERP) at 600, 400 and 300 msec (302 +/- 28 vs. 262 +/- 20 msec; p < 0.001, 280 +/- 23 vs. 240 +/- 21 msec; p < 0.001, 256 +/- 24 vs. 222 +/- 12 msec; p < 0.005, respectively) between responders and non-responders. The percentile increases in VERP (% VERP) at 600, 400, and 300 msec in responders were 25%, 26%, and 27%, whereas those in non-responders was 9%, 7%, and 7%, respectively. Isoproterenol administered to responders did not fully reverse the dl-sotalol-induced prolongation of VERP (delta VERP) at 600, 400, and 300 msec, which remained significantly prolonged compared to the baseline (281 +/- 18 vs. 241 +/- 16 msec; p < 0.01, 258 +/- 20 vs. 223 +/- 21 msec; p < 0.01, 247 +/- 22 vs. 202 +/- 16 msec; p < 0.01, respectively). % VERP did not exhibit significant differences at 600 (16%), 400 (15%), and 300 (20%) msec, indicating the lack of a reverse use-dependency. The results suggest that delta VERP in responders did not show reverse use-dependency, and that the phenomenon may account for the efficacy of dl-sotalol.     

Urinary excretion of arsenic species after exposure to arsenic present in drinking water

The effects of intravenous MS-551, a new class III antiarrhythmic drug, on atrium and ventricle were evaluated in 6 patients with ventricular tachyarrhythmias (4 males and 2 females; mean age 45 +/- 21 years) in an electrophysiologic study. Two patients had sustained ventricular tachycardia (VT) and 4 patients had ventricular fibrillation (VF). Electrophysiologic study was performed before and after the administration of MS-551 (loading infusion 0.3 mg/kg for 5 min + 0.01 mg/kg/min). The QT and QTc intervals were significantly prolonged by MS-551 from 359 +/- 52 to 411 +/- 63 msec (p = 0.01) and from 410 +/- 36 to 452 +/- 47 (p = 0.0172), respectively. No effect was observed on the sinus cycle length, QRS duration, or AH and HV intervals in sinus rhythm. The effective refractory periods of the right atrium (AERP) were significantly prolonged at paced cycle lengths of 600 (from 222 +/- 19 to 250 +/- 23 msec, p = 0.0009), 400 (from 207 +/- 15 to 228 +/- 15, p < 0.0001) and 300 (from 193 +/- 10 to 205 +/- 8 msec, p = 0.0127) msec. Similarly, the right ventricular ERP (VERP) were significantly prolonged at paced cycle lengths of 600 (from 240 +/- 23 to 268 +/- 23 msec, p < 0.0001), 400 (from 225 +/- 22 to 250 +/- 24 msec, p = 0.0007), and 300 msec (from 213 +/- 14 to 228 +/- 18 msec, p = 0.0071). MS-551 prolonged AERP and VERP in a "reverse" use-dependent manner without changing the conduction time in patients with ventricular tachyarrhythmias. MS-551 prevented the induction of VT in 1 patient and VF in only 1 patient in this electrophysiologic study. Further evaluation of the therapeutic potential of MS-551 using higher dosages is necessary.     

Preimplant atrial defibrillation testing with a temporary catheter in sheep

Prior to implantation of an atrial defibrillator, its effectiveness should be tested in each patient. A new catheter design for temporary use with electrodes for atrial defibrillation, electrogram sensing, and pacing was tested in this study. Atrial defibrillation thresholds defined using this temporary catheter were compared to the ones defined by catheters intended for chronic use with an implantable atrial defibrillator. Atrial defibrillation threshold was determined in six sheep using both types of catheters. Each animal was subjected to studies on 2 consecutive days. On the first day, shocks were applied between two of the temporary catheters. On the following day, permanent leads were inserted and atrial defibrillation threshold was redetermined. In both cases, defibrillation electrodes were positioned in the same heart location with one electrode in the distal coronary sinus and the second electrode in the right atrium. Atrial defibrillation threshold was obtained using 10 V increments or decrements to determine the lowest shock intensity needed to defibrillate the atria. Threshold was defined as the shock intensity at which 20 shock percent success was at or between 15% and 85%. Statistical analysis showed no significant difference (P < 0.05) between atrial defibrillation threshold energy (0.53 J vs 0.55 J), voltage (122 V vs 120 V) or current (2.2 A vs 2.6 A) measured with the temporary catheters and the permanent leads, respectively. These data indicate that temporary catheters can be used for efficacy testing prior to implant of an atrial defibrillator, and that they predict atrial defibrillation threshold adequately for chronic leads.     

The contribution of peridurography to the anatomy of the lumbosacral spinal canal

Phonocardiography and echocardiography were used to examine 20 patients with a normally functioning Beall disc mitral valve prosthesis. Phonocardiographic intervals were: Q-S1 interval 67 +/- 3 msec; A2-OC interval 118 +/- 8 msec. Maximal variation of the Q-S1 interval within one examination was 21 +/- 2 msec, for A2-OC interval it was 31 +/- 5 msec. Echocardiographic disc velocities were: opening velocity 296 +/- 30 mm/sec, closing velocity 414 +/- 44 mm/sec. Maximal variation of the opening velocity was 126 +/- 25 msec; maximal variation of the closing velocity was 334 +/- 57 msec. Abnormal poppet function was suspected in one patient with unusual prolongation and variability of A2-OC interval.     

Monetary compensation for plasma donors: a record of safety

BACKGROUND: Atrial fibrillation (AF) is the most common arrhythmia after open heart surgery. Traditional treatment with a range of antiarrhythmic drugs and electrical cardioversion is associated with considerable side effects. The aim of this study was to examine the feasibility and efficacy of low-energy atrial defibrillation with temporary epicardial defibrillation wire electrodes. METHODS AND RESULTS: Epicardial defibrillation wire electrodes were placed at the left and right atria during open heart surgery in 100 consecutive patients (age 65+/-9 years; male to female ratio 67:23). Electrophysiological studies performed postoperatively revealed a test shock (0.3 J) impedance of 96+/-12 omega (monophasic) and 97+/-13 omega (biphasic). During their hospital stay, AF occurred in 23 patients (23%) at 2.1+/-1.3 days postoperatively. Internal atrial defibrillation was performed in 20 patients. Of these patients, 80% (16/20) were successfully cardioverted with a mean energy of 5.2+/-3 J. Early recurrence of AF (< or =60 seconds after defibrillation) developed in 8 patients. Five patients had multiple episodes of AF. In total, 35 episodes of AF were treated, with an 88% success rate. Only 6 patients (30%) required sedation. No complications were observed with shock application or with lead extraction. CONCLUSIONS: Atrial defibrillation with temporary epicardial wire electrodes can be performed safely and effectively in patients after cardiac operations. The shock energy required to restore sinus rhythm is low. Thus, patients can be cardioverted without anesthesia.     

Nonthoracotomy implantation of cardioverter defibrillators: preliminary experience with a defibrillation lead placed at the right ventricular outflow tract

Although morbidity and mortality associated with defibrillator implantation using a nonthoracotomy approach have decreased as compared with a thoracotomy approach, defibrillation thresholds have been higher and fewer patients satisfied implant criteria. It may be possible to improve on the success of nonthoracotomy defibrillator implantation by the placement of a right ventricular (RV) outflow defibrillation lead. Implantable cardioverter defibrillator implantation data of 30 consecutive patients with clinical VT or VF were reviewed. Three defibrillation leads were routinely used. When either pacing threshold at the RV apex was inadequate (n = 2) or 18-J shocks were not successful in terminating VF in 3 of 4 trials (n = 8), the RV apex lead was positioned to the RV outflow tract attaching to the septum. Defibrillation testing was first performed with the RV apex lead in combination with CS, SVC, and/or subcutaneous leads. Twenty patients satisfied implant criteria with a defibrillation threshold of 13.5 +/- 3.6 J. In 7 of the 10 patients, whose RV lead was repositioned to the RV outflow tract, this lead in combination with SVC, CS, or subcutaneous leads produced successful defibrillation at < or = 18 J or in 3 of 4 trials. This approach improved the overall success of nonthoracotomy implantation of defibrillators from 69% to 90%. After a follow-up of 27 +/- 6 months, there was no dislodgment of the RV outflow tract defibrillation leads. CONCLUSIONS: This article reports the preliminary observation that placement of defibrillation leads to the RV outflow tract in humans was possible and without dislodgment. RV outflow tract offers an alternative for placement of defibrillation leads, which may improve on the success of nonthoracotomy defibrillator implantation.