Three-dimensional mapping of earliest activation after near-threshold ventricular defibrillation shocks

INTRODUCTION: Following shocks with a 50% defibrillation success (DFT50) delivered from electrodes at the right ventricular (RV) apex and superior vena cava (SVC), the earliest epicardial postshock activation always appears focally in the left ventricular (LV) apex for both successful and failed shocks. Because the heart is a three-dimensional (3D) structure, questions remain whether this activation truly arises from a focus or the focal pattern represents epicardial breakthrough resulting from intramural reentry. To answer these questions, 3D electrical mapping was performed. METHODS AND RESULTS: In six pigs, 60 to 84 epoxy fiberglass needles (0.7-mm-diameter), each containing six electrodes 2 mm apart, were inserted into the LV with 3- to 5-mm spacing around the apex and 5- to 10-mm spacing near the base. Ten DFT50 shocks (RV-->SVC, biphasic, 6/4 msec) were delivered after 10 seconds of fibrillation in each animal. The first five activations after each shock were mapped. Of 60 DFT50 shocks, 31 were successful, of which the first postshock cycle was a sinus beat in 13. In the other 18 successful shock episodes, the first postshock activation was detected 63 +/- 16 msec after the shock, which was not significantly different from the 58 +/- 23 msec postshock interval for the 29 failed shock episodes. In these 47 successful and failed shock episodes, the earliest postshock activation always arose focally from the LV apex. Its origin was in the subepicardium in 76% +/- 17%, midmyocardium in 16% +/- 12%, and subendocardium in 8% +/- 6% of cases. CONCLUSION: Following near-DFT50 shocks, the first postshock cycles did not arise by macroreentry. Instead, they originated from a true focus or microreentry, most commonly near the epicardium.     

Pacing following shocks stronger than the defibrillation threshold: impact on defibrillation outcome

INTRODUCTION: A recent study of shocks near defibrillation threshold (DFT) strength demonstrated that at least three rapid cycles always occur after failed shocks but not after successful shocks, suggesting that the number and rapidity of postshock cycles are important in determining defibrillation success. To test this hypothesis, rapid pacing was performed following a shock stronger than the DFT that by itself did not induce rapid cycles and ventricular fibrillation (VF). METHODS AND RESULTS: Epicardial activation was mapped in six pigs using a 504-electrode sock. The DFT was determined by an up/down protocol with S1 shocks (right ventricle-superior vena cava, biphasic). Ten shocks that were 100 to 200 V above the DFT (aDFT) were delivered after 10 seconds of VF to confirm they always defibrillated. Then, S2, S3, etc., pacing at 5 to 10 times diastolic threshold was performed from the left ventricular apex after aDFT shocks during VF. First, the postshock interval after aDFT shocks was scanned with an S2 stimulus to find the shortest S1-S2 coupling interval (CI) that captured. This was repeated for S3, S4, etc., until VF was induced. To induce VF after aDFT shocks, three pacing stimuli (S2, S3, S4) with progressively shorter CIs were always required; S2 or S2,S3 never induced VF. For the S2-S4 cycles, the intercycle interval was shorter (P < 0.01), and the wavefront conduction time was longer (P < 0.01) for episodes in which VF was induced (n = 57) than for episodes in which it was not (n = 60). Following the S4 cycle that induced VF, two types of spontaneous activation patterns appeared: focal (88%) and reentrant (12%). CONCLUSION: VF induction after aDFT shocks always required at least three rapid successive paced-induced cycles. Thus, the number and rapidity of the first several postshock cycles rather than just the first postshock cycle may be determining factors for defibrillation outcome.     

Activation sequences following failed atrial defibrillation

OBJECTIVES: The purposes of this study were to examine the first activations following atrial defibrillation shocks to help understand how and where atrial fibrillation (AF) relapsed following failed shocks and to assess the difference in postshock activation between failed and successful shocks. BACKGROUND: While many studies have investigated the mechanism of ventricular defibrillation, much less is known about the mechanisms of AF. METHODS: Sustained AF was induced electrically after pericardial infusion of methylcholine in 10 sheep. Biphasic subthreshold shocks were delivered to three configurations: right atrium to distal coronary sinus (RA-CS), sequential shocks with RA-CS as the first pathway followed by proximal CS to superior vena cava as the second pathway (Sequential), and right ventricle to superior vena cava plus can (V-triad). In eight sheep, global atrial mapping was performed with 504 electrodes spaced 3 to 4 mm apart. RESULTS: Earliest postshock activations mostly arose from the left atrium for V-triad but arose from either atrium for RA-CS and Sequential. Preshock AF cycle lengths were significantly shorter at the earliest activation sites than at seven of eight other sites globally distributed over both atria. In all type B successful episodes in which one or more rapid activations occurred after the shock and in 50 of the 72 failed episodes analyzed, activation fronts spread away from the earliest site in a focal pattern, and discrete nonfragmented activation complexes were present in the first derivatives of the electrograms. In the other 22 failed episodes, earliest activation fronts spread in a nonfocal pattern, and earliest postshock electrogram derivatives were fractionated. To better interpret the activation pattern in the fragmented regions, a 504 electrode plaque with 1.5-mm electrode spacing was placed on the right atrial appendage in two additional sheep. In 11 of 108 failed episodes, earliest postshock activation appeared inside the plaque and spread in a focal pattern with nonfragmented electrogram derivatives in 10 episodes and in a reentrant pattern with fragmented electrogram derivatives in the other. CONCLUSIONS: (1) The electrode configuration influenced the location of earliest postshock activation. (2) Earliest postshock activation occurred where the preshock AF cycle length was short. (3) Earliest activations following all type B successful and most failed episodes were not fragmented and spread in a focal pattern. (4) The region of earliest postshock activation in the failed episodes without a focal postshock activation pattern exhibited regions of fragmented electrogram derivatives that may represent conduction block and possibly reentry.     

Delayed afterdepolarization inhibitor: a potential pharmacologic intervention to improve defibrillation efficacy

INTRODUCTION: Electrical and optical mapping studies of defibrillation have demonstrated that following shocks of strength near the defibrillation threshold (DFT), the first several postshock cycles always arise focally. No immediate postshock reentry was observed. Delayed afterdepolarizations (DADs) have been suggested as a possible cause of this rapid repetitive postshock activity. The aim of this study was to test the hypothesis that DFT is decreased by application of a DAD inhibitor. METHODS AND RESULTS: Six pigs (30-35 kg) were studied. First, control DFT was determined using a three-reversal up/down protocol. Each shock (RV-SVC, biphasic, 6/4 msec) was delivered after 10 seconds of ventricular fibrillation (VF). Then, flunarizine (a DAD inhibitor) was injected intravenously (2 mg/kg bolus and 4 mg/kg/hour maintenance) and the DFT was again determined. A third DFT was determined 50 minutes after drug infusion was terminated to allow the drug to wash out. DFT after flunarizine application (520 +/- 90 V, 14 +/- 3 J) was significantly lower than control DFT (663 +/- 133 V, 23 +/- 4 J). After the drug washed out, DFT (653 +/- 107 V, 22 +/- 4 J) returned to the control DFT value (P = 0.6). Flunarizine reduced the DFT approximately 22% by leading-edge voltage and approximately 40% by energy. CONCLUSION: Flunarizine, a DAD inhibitor, significantly improved defibrillation efficacy. This finding suggests that DADs could be the source of the rapid repetitive focal activation cycles arising after failed near-DFT shocks before degeneration back into VF. Future studies are needed to investigate the cause of the earliest postshock activation and to determine if the DADs are responsible.     

Preshock phase singularity and the outcome of ventricular defibrillation

BACKGROUND: Phase singularity (PS) is a topological defect that serves as a source of ventricular fibrillation (VF). Whether or not the quantity of preshock PS determines defibrillation outcome is unclear. OBJECTIVE: The purpose of this study was to test the hypothesis that the number of PSs at the time of shock is an important factor that determines the shock outcome. METHODS: Isolated, perfused rabbit hearts (n = 7) were optically mapped with a potentiometric dye (di-4-ANNEPS). Shocks were delivered during short (10 seconds) and long (1 minute) VF, and the outcome was classified as successful type A (immediate termination), type B (postshock repetitive responses before termination), and unsuccessful. RESULTS: When shock strengths of 50% probability of successful defibrillation (DFT50) +/- 50 V were given in short VF, the types A and B and unsuccessful shocks were associated with a preshock PS number of 0.3 +/- 0.4, 1.4 +/- 0.3, and 1.5 +/- 0.4 (P <.01 by analysis of variance) and shock strengths of 205 +/- 77, 207 +/- 65, and 173 +/- 74 V (P <.01), respectively. When the same shocks were applied during long VF, the PS numbers were 1.7 +/- 0.5, 3.0 +/- 0.5, and 3.5 +/- 0.6, respectively (P <.01), and the shock strengths were 282 +/- 100, 283 +/- 135, and 256 +/- 126 V, respectively (P <.01). If we only analyze shocks with strength at DFT(50), the preshock PS number was still significantly different for short VF (0.6 +/- 0.5, 1.6 +/- 0.9, and 1.5 +/- 0.8; P <.05) and for long VF (1.4 +/- 0.5, 2.7 +/- 0.6, and 2.7+/-1.3; P <.05), respectively. All preshock PSs were eliminated by shocks. However, rapid repetitive activity was then reinitiated in unsuccessful and type B successful shocks but not in type A successful shocks. CONCLUSIONS: A low number or an absence of preshock PS was associated with type A successful defibrillation. There was no difference in preshock PS numbers between unsuccessful and type B successful defibrillation.     

Evidence that activation following failed defibrillation is not caused by triggered activity

BACKGROUND: Earliest postshock activation following failed defibrillation shocks slightly lower than the defibrillation threshold (DFT) in large animals appears to arise from a focus. We tested the hypothesis that these foci are caused by early or delayed afterdepolarizations (EADs or DADs) by performing epicardial electrical mapping and giving the EAD inhibitor pinacidil or the DAD inhibitor flunarizine to see if the foci were extinguished or altered in timing or location. METHODS AND RESULTS: A sock containing 504 electrodes was placed over the entire ventricular epicardium of 12 open-chested pigs. After the DFT was determined and additional shocks given, pinacidil was administered to 6 pigs and flunarizine to 6 pigs. Then, the DFT was again determined and additional shocks were given. Pinacidil significantly shortened the effective refractory period (ERP) (162 +/- 16 vs 130 +/- 28 msec) and action potential duration (APD(90)) (179 +/- 6 vs 149 +/- 19 msec) and significantly increased the peak frequency of the power spectrum of a left ventricle (LV) electrode during ventricular fibrillation (VF) (9.3 +/- 0.6 vs 10.5 +/- 1.0 Hz), while flunarizine did not significantly alter the ERP (162 +/- 8 vs 167 +/- 18 msec) or APD(90) (187 +/- 12 vs 191 +/- 20) but significantly reduced the peak frequency (9.2 +/- 0.5 vs 7.5 +/- 1.0 Hz). These findings suggest the drugs had their expected electrophysiological effects. However, the DFT was not significantly changed by either drug. Following the same strength shock 10% below the predrug DFT, earliest postshock activation arose in a focal epicardial pattern from the anterior-apical LV both before and after the drugs. The time from the shock until the appearance of this activation was not significantly different before and after either drug. CONCLUSION: The lack of change in DFT as well as the lack of change in the incidence, location, and timing of the postshock focus with sub-DFT strength shocks before and after pinacidil and flunarizine provide evidence that these foci are not caused by triggered activity.     

Comparison of activation during ventricular fibrillation and following unsuccessful defibrillation shocks in open-chest dogs

The purpose of this study was to map in detail the spread of activation away from sites of early postshock excitation following unsuccessful defibrillation to determine whether these activation fronts are the unaltered continuation of activation fronts present just before the shock. We recorded simultaneously from 120 bipolar electrodes on 40 plunge needles in a 20 x 35 x 5-mm volume of tissue of the right ventricular outflow tract immediately before and after shocks of 190-350 V were given via electrodes on the right atrium and left ventricular apex to six open-chest dogs with electrically induced ventricular fibrillation. For 20 shocks approximately 100 V below the defibrillation threshold, the site of earliest recorded activation following the shock was near the center of the mapped region. At the earliest recorded activation sites, there was an isoelectric window in the immediate postshock period lasting 42 +/- 15 msec after which activation fronts either spread away from a site in all directions in a focal pattern (12 episodes) or else spread away in only one direction (eight episodes). Comparison of activation patterns immediately before and after the shock revealed that in 18 of the 20 episodes, the location and pathway of activation fronts after the shock were markedly different from those before the shock. The preshock intervals at the sites of earliest activation following the shock, that is, the interval between the last activation at the site and the time of the shock, were not randomly distributed but were similar, averaging 64 +/- 11 msec, and were negatively correlated with the isoelectric postshock window (r = -0.70, p = 0.0001). These findings indicate that the presence and the site of origin of activation fronts after the shock are influenced by at least two factors: the shock itself and the electrophysiological state of the myocardium at the time of the shock. Thus, epicardial shocks approximately 100 V below the defibrillation threshold markedly alter the activation sequences of fibrillation but are unsuccessful because the activation fronts following the shock reinitiate fibrillation.     

Post-shock synchronized pacing in isolated rabbit left ventricle: evaluation of a novel defibrillation strategy

Introduction: A failed near-threshold defibrillation shock is followed by an isoelectric window (IEW) and rapid repetitive responses that reinitiate ventricular fibrillation (VF). We hypothesized that properly timed (synchronized) postshock pacing stimuli (SyncP) may capture the recovered tissues during the repetitive responses and prevent postshock reinitiation of VF, resulting in improved defibrillation efficacy.
Methods and Results: We explored the effect of postshock SyncP on defibrillation efficacy in isolated rabbit hearts (n = 12). Optical recording-guided real-time detection and electrical stimulation (5 mA) of recovered tissues in anterior/posterior left ventricle (LV) were performed following IEW. The IEW duration was found to be 69 ± 13 ms. With the same shock strength, successful and failed defibrillation episodes were associated with 50% and 15% of the myocardium, respectively, captured by the SyncP (P < 0.001). Electrical stimulation from the posterior LV resulted in 75% of episodes capturing myocardium, as compared with anterior LV stimulation (55%; P < 0.01) and higher successful defibrillation rate (14%, posterior vs. 3%, anterior LV). The overall success in terminating VF by postshock SyncP was approximately 10%. The causes for failed myocardium capture by postshock SyncP included lack of IEW after low-strength shock (42.9%), incorrect locations of reference site (25.7%) and pacing electrodes (17.9%), and others, such as wave breakthroughs (13.5%).
Conclusion: Postshock SyncP was feasible and the larger the myocardium captured area, the more likely was the successful defibrillation. Postshock SyncP delivered to the posterior LV was more effective than anterior LV to terminate VF.     

Transmural and endocardial Purkinje activation in pigs before local myocardial activation after defibrillation shocks.

BACKGROUND: Earliest recorded postshock myocardial activations in pigs originate in the subepicardium of the apex and lateral free wall of the left ventricle (LV) 30-90 ms after the shock. OBJECTIVE: The purpose of this study was to determine whether the Purkinje system is a candidate for the source of postshock activations by performing endocardial and transmural postshock activation mapping. METHODS: In five pigs, 32 plunge needles with 12 electrodes (1-mm spacing) were inserted into the LV apex and lateral free wall. Up to 70 plunge needles with six electrodes (2-mm spacing) were spread throughout the remainder of the LV, while 9-12 plunge needles with four electrodes (2-mm spacing) were inserted into the right ventricle. A basket catheter with 32 bipolar recording sites was inserted into the LV. Defibrillation-threshold (DFT)-level shocks were delivered during 10 episodes of electrically induced ventricular fibrillation. Electrograms of postshock activation cycles were analyzed for Purkinje and myocardial activations. RESULTS: Purkinje activations were recorded before local myocardial activation in 9% of basket electrograms and in 15% of plunge needles during the first postshock activation cycle. Purkinje activations were identified during the first and subsequent several postshock activation cycles in at least one basket and one needle electrogram in 96% and 98% of defibrillation episodes, respectively. CONCLUSIONS: The Purkinje system is active during the early postshock activation cycles after DFT-level shocks. Further studies are required to determine whether activation initiates in the Purkinje system or whether it is activated by the myocardium or by Purkinje-myocardial junctional cells.     

Improved defibrillation thresholds with large contoured epicardial electrodes and biphasic waveforms

A reduction in the shock strength required for defibrillation would allow use of a smaller automatic implantable cardioverter-defibrillator and would reduce the possibility of myocardial damage by the shock. Most internal defibrillation electrodes require 5 to 25 J for successful defibrillation in human beings and in dogs. In an attempt to lower the shock strength needed for defibrillation, we designed two large titanium defibrillation patch electrodes that were contoured to fit over the right and left ventricles of the dog heart, covering areas of approximately 33 and 39 cm2, respectively. In six anesthetized open-chest dogs, the electrodes were secured directly to the epicardium and ventricular fibrillation was induced by 60 Hz alternating current. Truncated exponential monophasic and biphasic shocks were given 10 sec later and defibrillation thresholds (DFTs) were determined. The DFT was 159 +/- 48 V, 3.2 +/- 1.9 J (mean +/- SD) for 10 msec monophasic shocks and 106 +/- 22 V, 1.3 +/- 0.4 J, for biphasic shocks with both phase durations equal to 5 msec (5-5 msec). The experiment was repeated in another six dogs in which the electrodes were secured to the pericardium. The mean DFT was not significantly higher than that for the electrodes on the epicardium: 165 +/- 27 V, 3.1 +/- 1.2 J for 10 msec monophasic shocks and 116 +/- 19 V, 1.6 +/- 0.5 J for 5-5 msec biphasic shocks. Low DFTs were also obtained with biphasic shocks in which the duration of the first phase was longer than that of the second.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic deterioration after one-minute fibrillation increases relative biphasic defibrillation efficacy

INTRODUCTION: The probability of survival decreases to 70% after 2 minutes of ventricular fibrillation. Biphasic shocks are more effective than monophasic shocks in terminating short-duration (<30 sec) ventricular fibrillation. We tested the hypotheses that developing ischemia changes the electrophysiologic characteristics of fibrillation and that the relative efficacy of biphasic shocks increases as electrophysiologic characteristics deteriorate. METHODS AND RESULTS: Monophasic (12 msec) and biphasic (6/6 msec) shocks (1 to 4 A) were tested in random order in isolated rabbit hearts after 1-minute ischemic fibrillation. Monophasic action potentials showed only a sporadic occurrence of electrical diastole after 5 seconds of fibrillation (24% of action potentials in the right ventricle and 18% in the left ventricle). After 60 seconds of fibrillation, diastole (17.83+/-1.14 msec in the right ventricle and 21.52+/-1.16 msec in the left ventricle) appeared after almost every action potential (P < 0.0001 compared with 5 sec), despite a lack of change in fibrillation cycle length and dominant frequency. Monophasic I50 was 2.89 A, and biphasic I50 was 1.4 A (77% reduction in energy). Normalized curve width decreased 28%. Retrospective analysis showed that shocks delivered early in the fibrillation action potential had a greater probability of succeeding (89%) than shocks delivered late (30%; P < 0.001). CONCLUSION: After 1-minute ischemic fibrillation, diastolic intervals occur during fibrillation. Therefore, defibrillation shocks have an approximately 29% probability of interacting with the fibrillation action potential during diastole. At this time, biphasic shocks produced a more deterministic defibrillation threshold and became even more efficacious (I50 B/M = 0.48) than at short fibrillation durations (I50 B/M = 0.7).     

长时间心室颤动除颤成功后早期复发的电生理作用机制

目的通过整体左室心内膜电生理标测研究长时间心室颤动(简称室颤)除颤成功后室颤早期复发的电生理作用机制。方法将64极伞状电极经颈动脉逆行植入6只正常比格犬的左室行电生理标测。通过快速电刺激,分别诱发20 s短时间室颤和7 min长时间室颤,随后给予体内双相波除颤。比较不同时间室颤除颤成功后最早激动时间和室颤复发率。利用电生理激动图分析室颤复发时的激动特征。结果 6只动物累计短时间室颤除颤成功24次,无1次室颤复发。7 min长时间室颤除颤成功6次,每次成功除颤后至少1次室颤早期复发,观察时间内累计复发14次,平均每只动物发作2.3±1.9次,与短时间室颤相比,室颤复发率显著升高(P<0.01)。与短时间室颤相比,长时间室颤除颤后最早激动时间显著延长(5 125±3 373 ms vs 322±166 ms,P<0.01)。14次复发室颤前,均有室性早搏。电生理标测提示,10次复发源自间隔部附近的局灶活动。结论无器质性心脏疾病的长时间室颤除颤成功后室颤早期复发十分常见,但未见于短时间室颤,提示长时间室颤本身可致室颤复发,其复发的起始电生理机制可能与局灶兴奋相关。     

Reentry site during fibrillation induction in relation to defibrillation efficacy for different shock waveforms

INTRODUCTION: Unsuccessful defibrillation shocks may reinitiate fibrillation by causing postshock reentry. METHODS AND RESULTS: To better understand why some waveforms are more efficacious for defibrillation, reentry was induced in six dogs with 1-, 2-, 4-, 8-, and 16-msec monophasic and 1/1- (both phases 1 msec) 2/2-, 4/4-, and 8/8-msec biphasic shocks. Reentry was initiated by 141+/-15 V shocks delivered from a defibrillator with a 150-microF capacitance during the vulnerable period of paced rhythm (183+/-12 msec after the last pacing stimulus). The shock potential gradient field was orthogonal to the dispersion of refractoriness. Activation was mapped with 121 electrodes covering 4 x 4 cm of the right ventricular epicardium, and potential gradient and degree of recovery of excitability were estimated at the sites of reentry. Defibrillation thresholds (DFTs) were estimated by an up-down protocol for the same nine waveforms in eight dogs internally and in nine other dogs externally. DFT voltages for the different waveforms were positively correlated with the magnitude of shock potential gradient and negatively correlated with the recovery interval at the site at which reentry was induced by the waveform during paced rhythm for both internal (DFT = 1719 + 64.5VV - 11.1RI; R2 = 0.93) and external defibrillation (DFT = 3445 + 150VV - 22RI; R2 = 0.93). CONCLUSION: The defibrillation waveforms with the lowest DFTs were those that induced reentry at sites of low shock potential gradient, indicating efficacious stimulation of myocardium. Additionally, the site of reentry induced by waveforms with the lowest DFTs was in myocardium that was more highly recovered just before the shock, perhaps because this high degree of recovery seldom occurs during defibrillation due to the rapid activation rate during fibrillation.     

Relationship between shock energy and postdefibrillation ventricular arrhythmias in patients with implantable defibrillators

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. Postdefibrillation ventricular arrhythmias were noted. Postdefibrillation ventricular arrhythmias with a cycle length < or = 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 < or = 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 postdefibrillation 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 < or = 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: Postdefibrillation ventricular arrhythmias with a cycle length < or = 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.     

Effects of pacing rate and timing of defibrillation shock on the relation between the defibrillation threshold and the upper limit of vulnerability in open chest dogs

To test the relation between the defibrillation threshold and the upper limit of vulnerability, the shock strength associated with 50% probability of successful defibrillation (DFT50) and that associated with 50% probability of reaching the upper limit of vulnerability (ULV50) were determined in 20 open chest dogs with use of the delayed up-down method, with pacing drive cycle lengths of 150 to 500 ms and either single 6-ms shocks (10 dogs) or 12-ms biphasic shocks (10 dogs) given at the mid-upslope, peak and mid-downslope of the T wave of electrocardiographic lead II. The shocks were given by means of a patch-patch configuration on the anterior and posterior surfaces of the heart, which was paced from a stimulating electrode attached to the left ventricular apex. Analysis of variance showed no statistically significant differences in ULV50 as determined with different pacing cycle lengths. For monophasic shocks, DFT50 (331 +/- 66 V or 5.8 +/- 2.7 J) was not significantly different from ULV50 determined at the mid-upslope of the T wave (318 +/- 64 V or 5 +/- 2 J). The correlation coefficients between the two values were 0.74 (p = 0.014) for voltage and 0.67 (p = 0.034) for energy. In contrast, DFT50 was significantly higher than ULV50 as determined at the peak of the T wave (219 +/- 43 V or 2.3 +/- 1 J) and mid-downslope of the T wave (200 +/- 38 V or 1.9 +/- 0.9 J). In three dogs, ventricular fibrillation could not be induced at the mid-downslope of the T wave with any baseline pacing (Si) cycle length.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transesophageal low-energy cardioversion in an animal model of life-threatening tachyarrhythmias

The purpose of this study was to determine the feasibility and efficacy of terminating life-threatening ventricular tachyarrhythmia by low-energy synchronous or asynchronous shocks delivered through a transesophageal catheter that had both an anode and a cathode. Forty-three episodes of ventricular fibrillation or flutter (Vf or VF) were provoked by transesophageal asynchronous random shocks occurring during the vulnerable period of the ventricular cycle in seven dogs and seven pigs that were healthy adults. The 43 episodes of Vf or VF were terminated by the transesophageal technique. The defibrillation energy thresholds were 23.11 +/- 6.28 J (range, 5-30 J). Seven episodes of ventricular tachycardia (VT) with a cycle length of 360 msec or less (330 +/- 27 msec) were provoked by ventricular pacing stimuli during acute myocardial ischemia resulting from delayed resuscitation in two dogs and three pigs. Five of the seven VTs had a duration of 31 seconds or more, and they were all terminated by transesophageal synchronous shocks, the cardioversion thresholds being 1.71 +/- 2.25 J (range, 0.25-5 J). Fourteen episodes of idioventricular tachycardia (IVT) with a cycle length of 400 msec or more (445 +/- 33.5 msec) spontaneously occurred after the use of adrenaline and after defibrillation in four dogs and five pigs. We also succeeded in terminating seven episodes of IVT with a duration of 34 seconds or more by the same means of treating VT, although IVT is not an indication for cardioversion in the clinical setting.(ABSTRACT TRUNCATED AT 250 WORDS)     

Marked reduction of ventricular defibrillation threshold by application of an auxiliary shock to a catheter electrode in the left posterior coronary vein of dogs

INTRODUCTION: For endocardial shocks near the defibrillation threshold (DFT), postshock activity originates from the lateral left ventricular apex, where the shock field is weak. This study tested the hypothesis that an auxiliary shock (AS) delivered between an electrode at this site and a superior vena cava (SVC) electrode before the primary endocardial shock (PS) would reduce the DFT. METHODS AND RESULTS: In six pentobarbital-anesthetized dogs (26 to 36 kg), catheter electrodes were placed in the right ventricular (RV) apex and the SVC. To simulate transvenous introduction, a small electrode was inserted into the posterior cardiac vein using an epicardial approach. For dual shock treatments, AS (2-msec monophasic) was applied to the coronary vein electrode at different time intervals before a biphasic PS (4 msec/3 msec) to the RV-SVC electrodes. The mean DFT energy for dual shocks treatments were significantly reduced (P < 0.05) in comparison to the control treatment (no AS, 26.5+/-8.8 J). Mean DFT energy after 10 seconds of electrically induced ventricular fibrillation for dual shocks, in which AS and PS were separated by 1, 5, 10, and 20 msec, were 10.2+/-4.1 J, 10.9+/-5.5 J, 11.3+/-6.3 J, and 15.4+/-7.2 J, respectively. These values were all significantly lower than the PS alone (26.5+/-8.8 J). CONCLUSION: Addition of an AS from the posterior cardiac vein before an endocardial PS reduces DFT energy by more than 50%. Such DFT reduction could improve therapeutic safety margin or permit reduction in volume of implantable cardioverter defibrillators.     

Success and failure of the defibrillation shock: insights from a simulation study

INTRODUCTION: This simulation study presents a further inquiry into the mechanisms by which a strong electric shock fails to halt life-threatening cardiac arrhythmias. METHODS AND RESULTS: The research uses a model of the defibrillation process that represents a sheet of myocardium as a bidomain. The tissue consists of nonuniformly curved fibers in which spiral wave reentry is initiated. Monophasic defibrillation shocks are delivered via two line electrodes that occupy opposite tissue boundaries. In some simulation experiments, the polarity of the shock is reversed. Electrical activity in the sheet is compared for failed and successful shocks under controlled conditions. The maps of transmembrane potential and activation times calculated during and after the shock demonstrate that weak shocks fail to terminate the reentrant activity via two major mechanisms. As compared with strong shocks, weak shocks result in (1) smaller extension of refractoriness in the areas depolarized by the shock, and (2) slower or incomplete activation of the excitable gap created by deexcitation of the negatively polarized areas. In its turn, mechanism 2 is associated with one or more of the following events: (a) lack of some break excitations, (b) latency in the occurrence of the break excitations, and (c) slower propagation through deexcited areas. Reversal of shock polarity results in a change of the extent of the regions of deexcitation, and thus, in a change in defibrillation threshold. CONCLUSION: The results of this study indicate the paramount importance of shock-induced deexcitation in both defibrillation and postshock arrhythmogenesis.     

Ventricular refractory period extension caused by defibrillation shocks

In pentobarbital-anesthetized dogs, transcardiac shocks of up to 30 J or pacing stimuli were delivered to myocardial tissue at different times in the electrical cycle. When delivered midway or later into electrical systole, shocks, but not pacing stimuli, greatly extended the refractory period as determined by left ventricular pacing. There was a positive correlation between both the shock energy and timing and the amount of delay. A 30-J shock given 10 msec before the end of the refractory period extended the refractory period by 63 +/- 15 msec (p less than 0.001), whereas the same shock given 40 msec earlier produced only 25 +/- 10 msec (p less than 0.001) of extension. By comparison, a 5-J shock given at those times produced 36 +/- 18 (p less than 0.005) and 10 +/- 8 msec (p less than 0.001) of extension, respectively. When delivered early into electrical systole, both a pacing stimulus and a shock had no substantial effect on the tissue refractory period. Because the tissue that is late in electrical systole would otherwise be the first to repolarize if no shock were given, the selective refractory period extension may create a period after the shock during which no tissue is repolarized to a level sufficient for wavefront propagation. Thus, the energy- and time-dependent refractory period extension may help explain the mechanism by which ventricular defibrillation occurs during transcardiac shocks.     

Transthoracic defibrillation of short-lasting ventricular fibrillation: a randomised trial for comparison of the efficacy of low-energy biphasic rectilinear and monophasic damped sine shocks

BACKGROUND: Biphasic rectilinear shocks are more effective than monophasic shocks for transthoracic atrial defibrillation and for ventricular arrhythmias during electrophysiological testing.We undertook the present study to compare the efficacy of 100 J rectilinear biphasic waveform shocks with 150 J monophasic damped sine waveform shocks for transthoracic defibrillation of true ventricular fibrillation during defibrillation threshold testing (DFT).The second aim of the study was to analyse the influence of patch positions on the efficacy of defibrillation. METHODS: 50 episodes of 14 patients (age ranging from 37 to 82 years) who underwent DFT testing were randomised for back-up shocks with either a sequence of 100 and 200 J biphasic waveform, or a sequence of 150 and 360 J conventional monophasic shocks. A binary search protocol was used at implantation and before hospital discharge. Patients were also randomised to an anteroposterior position versus a right-anterior-apical position. A crossover was performed between implantation and pre-hospital discharge for biphasic versus monophasic sequence as well as for the 2 different positions. RESULTS: After failed internal shocks, 27 episodes were treated with biphasic, and 23 with monophasic shocks.The first attempt by the external device did not terminate II episodes (2 biphasic, 9 monophasic).The first shock efficacy was significantly greater with biphasic than with monophasic shocks (p < 0.02).The overall success rate was 93% with biphasic shocks and 64% with monophasic shocks. In multivariate regression analysis including patch position, arrhythmia duration, type of waveform, testing order and session, only waveform was associated with successful defibrillation (p < 0.02). CONCLUSION: For transthoracic defibrillation of ventricular fibrillation, low-energy rectilinear biphasic shocks are more effective than monophasic shocks.The position of the defibrillation shock pads has no influence on the biphasic shock efficacy, but anteroposterior pad position is more effective using monophasic shocks.