Ventricular Fibrillation Cycle Length Research Articles

Effects of combination of sotalol and verapamil on initiation, maintenance, and termination of ventricular fibrillation in swine hearts.

Sotalol and verapamil alone reduce reentry incidence during ventricular fibrillation (VF). We tested whether the combination of these two drugs had a synergistic effect on initiation, maintenance, and termination of VF. Six open-chest pigs received intravenous sotalol (1.5mg/kg) followed by verapamil (0.136mg/kg). VF threshold (VFT) was determined by a burst pacing protocol. Two 20seconds episodes of VF were recorded from a 21×24 unipolar electrode plaque on the lateral posterior left ventricular epicardium before and after each drug. VF activation patterns were quantified. The duration of long duration VF (LDVF) maintenance was compared to our previously published data. Sotalol alone and combined with verapamil significantly increased the VFT from 12.3±4.1 to 20.3±7.1 and 26.7±8.6mA compared with baseline (P<.05). Sotalol decreased the number of wavefronts by 20%, VF activation rate by 17% and conduction velocity 11%, while the addition of verapamil neutralized these effects. Addition of verapamil to sotalol further decreased the fractionation incidence from 14% to 29% and multiplicity from 24% to 31% compared with baseline. The combination of the two drugs increased the VF cycle length, decreased synchronicity, increased regularity index and shortened the duration of LDVF maintenance compared with our previous data of verapamil alone or no drug. Synchronicity index was lower and regularity index was higher in animals in which VF spontaneously terminated earlier than 10minutes than in animals in which VF terminated longer than 10minutes. The combination of sotalol and verapamil increased VFT but accelerated LDVF termination.

Dominant frequency of ventricular fibrillation can be one of predictive values to discriminate high risk patients with Brugada syndrome

Purpose: Recent European and Japanese studies showed the induction of ventricular fibrillation (VF) during electrophysiological stimulation test (EPS) could not predict the sudden cardiac death in patients with Brugada syndrome (BrS). However, some recent studies indicated that the shortness of effective refractory period (ERP) or the mode of induction of VF might be good predictive value. Those indicated the exist of inherent electrical substrates in high risk patients with BrS. We accessed VF cycle length as the dominant frequency (DF) obtained by a fast Fourier transformation (FFT) analysis. Methods: The induced VF recorded from RV apex (RVA) and RV outflow tract (RVOT) was performed with a 4096 point-FFT analysis in 28 patients (all male, 51±14 years old) with BrS. DF was obtained by Fast Fourier transform from 4-s data (phase) and sequentially every 2 s before cardioversion. The average of DF from intracardiac electrograms were compared between the symptomatic group (n=15) and the asymptomatic group (n=13). EPS was performed during isoproterenol (ISP) and after propranolol (PRO) in selected patients. Results: The DF had a weak negative correlation to ERP. The relationship of DF between RVA and RVOT had a very good correlation in all phases. The DF significantly increased from phase 1 to 6 (p<0.003; 5.72±0.36 Hz to 6.19±0.49 Hz). The DFs were significantly higher in symptomatic group than in asymptomatic group (p=0.012). ISP significantly (p<0.05) shorten ERP of RV and prevented induction of VF in 20 of 25 patients (80%). During ISP, 5 patients experienced induction of VF. ISP significantly influenced DF transition compared with the control state. DF gradually increased but was unchanged after the middle phase. PRO induced VF in 5 (83.3%) of 6 patients who tested negative during ISP. DF after PRO was higher than that in the corresponding phase in the control state. ISP suppressed the induction of VF and the increase of DF with time. PRO aggravated VF and accelerated DF. Those pharmacological results were not inconsistent with the previous reports. Conclusions: Those data suggested that the DF of VF in patients with BrS was related to the ERP of RV and/or the maintenance of VF as an electrophysiological substrate of high risk patients. Higher DF of VF can be one of predictive values to discriminate the high risk Brugada patients.

Antitachycardia Pacing for Very Fast Ventricular Tachycardia and Low-Energy Shock for Ventricular Arrhythmias in Patients With Implantable Defibrillators

Implantable cardioverter-defibrillator therapy in the form of high-energy shock (HES) is associated with adverse effects. This study evaluated an alternative therapy to HES, including antitachycardia pacing (ATP) for very fast ventricular tachycardia (VFVT) and low-energy shock (LES) ≤5 J for ventricular tachycardia (VT) of any cycle length (CL). This multicenter study recruited 602 patients with standard indications for an implantable cardioverter-defibrillator. Programming was standardized into 3 zones: (1) ventricular fibrillation (VF) CL of <200 ms treated with HES; (2) VFVT defined within the VF zone (CL, 200 to 250 ms) treated with 2 ATP bursts, LES, and HES; and (3) fast ventricular tachycardia (CL, 251 to 320 ms) and slow VT (CL, >320 ms) treated with 3 ATP bursts, LES, and HES. The primary end point was ATP and LES efficacy and safety. After a mean follow-up of 19 ± 8 months, 2,815 device activations were recorded in 152 patients. Of 67 VFVT episodes, 34 reverted with combined ATP and LES (success rate 50.7%) with first and second ATPs successful in 36% and 13.8%, respectively. LES was used in 39 fast ventricular tachycardia and 60 slow VT episodes with success rates of 53.8% and 73.3%, respectively. Syncope occurred in 19.4%, 16.2%, and 1% of episodes because of VFVT, VF, and VT CL >250 ms, respectively. In conclusion, tiered ATP and LES therapy terminates >50% of VFVT episodes (CL, 200 to 250 ms), which otherwise would fall within the VF zone and be treated exclusively with HES. LES is efficacious and safe in patients with VTCL >250 ms with extremely low syncope rates. Limitation of ATP to a single burst in VFVT is recommended to minimize syncope.

Terminating ventricular tachyarrhythmias using far-field low-voltage stimuli: Mechanisms and delivery protocols

Low-voltage termination of ventricular tachycardia (VT) and atrial fibrillation has shown promising results; however, the mechanisms and full range of applications remain unexplored. To elucidate the mechanisms for low-voltage cardioversion and defibrillation and to develop an optimal low-voltage defibrillation protocol. We developed a detailed magnetic resonance imaging-based computational model of the rabbit right ventricular wall. We applied multiple low-voltage far-field stimuli of various strengths (≤1 V/cm) and stimulation rates in VT and ventricular fibrillation (VF). Of the 5 stimulation rates tested, stimuli applied at 16% or 88% of the VT cycle length (CL) were most effective in cardioverting VT, the mechanism being consecutive excitable gap decreases. Stimuli given at 88% of the VF CL defibrillated successfully, whereas a faster stimulation rate (16%) often failed because the fast stimuli did not capture enough tissue. In this model, defibrillation threshold energy for multiple low-voltage stimuli at 88% of VF CL was 0.58% of the defibrillation threshold energy for a single strong biphasic shock. Based on the simulation results, a novel 2-stage defibrillation protocol was proposed. The first stage converted VF into VT by applying low-voltage stimuli at times of maximal excitable gap, capturing large tissue volume and synchronizing depolarization; the second stage terminated VT. The energy required for successful defibrillation using this protocol was 57.42% of the energy for low-voltage defibrillation when stimulating at 88% of VF CL. A novel 2-stage low-voltage defibrillation protocol using the excitable gap extent to time multiple stimuli defibrillated VF with the least energy by first converting VF into VT and then terminating VT.

Cycle length characteristics differentiating non-sustained from self-terminating ventricular fibrillation in Brugada syndrome

Limited information is available on self-terminating (ST) ventricular fibrillation (VF). Understanding spontaneous fluctuations in VF cycle length (CL) is required to identify arrhythmia that will stop before shock. Using Brugada syndrome (BS) as a model, the purpose of the study was to compare ST-VF and VF terminated by electrical shock and to look for spontaneous fluctuations in ventricular CL. Occurrence of ST-VF and VF was studied in 53 patients with 46 VF episodes: (i) spontaneously, (ii) during defibrillation threshold testing, (iii) during programmed ventricular stimulation (PVS). Fifteen presented ST-VF (average duration 25 s): 11 during PVS, 1 during defibrillation threshold testing, and 3 spontaneously (at device interrogation). Self-terminating ventricular fibrillation was compared with 31 VFs terminated by electrical shock. Mean ventricular CL was longer (192.5 ± 22 vs. 149 ± 19 ms) (P < 0.0001) and CL became longer or did not change in ST-VF (187 ± 28 vs. 200 ± 25 ms) (first vs. last CL)(NS) in contrast with progressively shorter CL in electrical shock-terminated VF (177 ± 14.5 vs. 139 ± 12 ms) (first vs. last CL before electrical shock) (P < 0.0001). Ventricular fibrillation had more CL variability (average 16.4 ± 6.5 ms) for the first 50 beats than ST-VF (average 4.08 ± 2) (P < 0.0001). Cycle length range for the first 50 beats was 9.6 ± 1 ms for ST-VF and 44 ± 15 for VF (P < 0.002). Self-terminating ventricular fibrillation in BS was not rare (28%). Ventricular CL was longer and progressively increased or did not change in ST-VF compared with electrical shock-terminating VF. Cycle length variability and CL range could differentiate VF and ST-VF within the first 50 beats. These parameters should be considered in the algorithms for VF detection and termination.

Studying semblances of a true killer: experimental model of human ventricular fibrillation

It is unknown whether ventricular fibrillation (VF) studied in experimental models represents in vivo human VF. First, we examined closed chest in vivo VF induced at defibrillation threshold testing (DFT) in four patients with ischemic cardiomyopathy pretransplantation. We examined VF in these same four hearts in an ex vivo human Langendorff posttransplantation. VF from DFT was compared with VF from the electrodes from a similar region in the right ventricular endocardium in the Langendorff using two parameters: the scale distribution width (extracted from continuous wavelet transform) and VF mean cycle length (CL). In a second substudy group where multielectrode phase mapping could be performed, we examined early VF intraoperatively (in vivo open chest condition) in three patients with left ventricular cardiomyopathy. We investigated early VF in the hearts of three patients in an ex vivo Langendorff and compared findings with intraoperative VF using two metrics: dominant frequency (DF) assessed by the Welch periodogram and the number of phase singularities (lasting >480 ms). Wavelet analysis (P = 0.9) and VF CL were similar between the Langendorff and the DFT groups (225 ± 13, 218 ± 24 ms; P = 0.9), indicating that wave characteristics and activation rate of VF was comparable between the two models. Intraoperative DF was slower but comparable with the Langendorff DF over the endocardium (4.6 ± 0.1, 5.0 ± 0.4 Hz; P = 0.9) and the epicardium (4.5 ± 0.2, 5.2 ± 0.4 Hz; P = 0.9). Endocardial phase singularity number (9.6 ± 5, 12.1 ± 1; P = 0.6) was lesser in number but comparable between in vivo and ex vivo VF. VF dynamics in the limited experimental human studies approximates human in vivo VF.

Characteristics of Induced Ventricular Fibrillation Cycle Length in Symptomatic Brugada Syndrome Patients

Limited information is available on the ventricular fibrillation (VF) spectrum in Brugada syndrome (BS) patients. We clarified differences in the VF cycle length (CL) using fast-Fourier transformation (FFT) analysis in symptomatic and asymptomatic BS patients. VF was induced by pacing from the right ventricular (RV) apex and/or RV outflow tract (RVOT) for >8s. A 4096-point FFT analysis of results from 28 male BS patients (51.1 ± 13.7 years old) was performed. Dominant frequency (DF) from phases 1 (4s) to 6 was obtained at 2-s intervals. The average DF from surface and intracardiac electrograms (ECG: DF(ECG); ICE: DF(ICE,), respectively) was compared between symptomatic and asymptomatic patients. Symptomatic patients had a significantly shorter effective refractory period at a CL of 600 ms at the RVOT than asymptomatic patients. DF(ECG) significantly increased with phase (5.64 ± 0.32 Hz in phase 1 to 6.16 ± 0.52 Hz in phase 6) and was significantly higher in symptomatic patients than in asymptomatic patients. DF(ICE) had the same characteristics as DF(ECG). Induced VF in BS patients can be characterized using FFT analysis. Our data support the hypothesis that symptomatic patients have a significantly shorter VF CL than asymptomatic patients.

Role of K ATP Channels in the Maintenance of Ventricular Fibrillation in Cardiomyopathic Human Hearts

Ventricular fibrillation (VF) leads to global ischemia. The modulation of ischemia-dependent pathways may alter the electrophysiological evolution of VF. We addressed the hypotheses that there is regional disease-related expression of K(ATP) channels in human cardiomyopathic hearts and that K(ATP) channel blockade promotes spontaneous VF termination by attenuating spatiotemporal dispersion of refractoriness. In a human Langendorff model, electric mapping of 6 control and 9 treatment (10 μmol/L glibenclamide) isolated cardiomyopathic hearts was performed. Spontaneous defibrillation was studied and mean VF cycle length was compared regionally at VF onset and after 180 seconds between control and treatment groups. K(ATP) subunit gene expression was compared between LV endocardium versus epicardium in myopathic hearts. Spontaneous VF termination occurred in 1 of 6 control hearts and 7 of 8 glibenclamide-treated hearts (P=0.026). After 180 seconds of ischemia, a transmural dispersion in VF cycle length was observed between epicardium and endocardium (P=0.001), which was attenuated by glibenclamide. There was greater gene expression of all K(ATP) subunit on the endocardium compared with the epicardium (P<0.02). In an ischemic rat heart model, transmural dispersion of refractoriness (ΔERP(Transmural)=ERP(Epicardium)-ERP(Endocardium)) was verified with pacing protocols. ΔERP(Transmural) in control was 5 ± 2 ms and increased to 36 ± 5 ms with ischemia. This effect was greatly attenuated by glibenclamide (ΔERP(Transmural) for glibenclamide+ischemia=4.9 ± 4 ms, P=0.019 versus control ischemia). K(ATP) channel subunit gene expression is heterogeneously altered in the cardiomyopathic human heart. Blockade of K(ATP) channels promotes spontaneous defibrillation in cardiomyopathic human hearts by attenuating the ischemia-dependent spatiotemporal heterogeneity of refractoriness during early VF.

Temporal and spectral analysis of ventricular fibrillation in humans

Analysing ventricular fibrillation (VF) rate and regularity at different sites and at different times may help understanding some of the mechanisms underlying VF in humans. Twelve episodes of VF (19.4 ± 5.6s) were induced during electrophysiological study in eight men (63 ± 14years old). Calculation of dominant frequency (DF) by fast Fourier transform, short-time Fourier transform, and analysis of the pitch frequency [VF cycle length duration (CL)] were performed. For each episode, we analysed the 12 lead-surface ECG, three unipolar, 10 near-field, and three far-field bipolar recordings by means of three quadripolar catheters positioned at the right ventricular apex (RV apex), right ventricular outflow tract, and at the coronary sinus (exploring the lateral left ventricular epicardium) (LV). Fast and regular discrete activation covered the whole duration of every intracardiac recording, whereas surface ECG consistently displayed chaotic and fibrillatory pattern. DF (5.25 ± 0.64Hz) was very similar on surface ECG recordings and in various intracardiac recordings. Intracardiac activation was rather regular during VF despite the fibrillatory process with very low SD of the CL. There were some significant inverse correlations between VF rate and VF regularity. Intracardiac sites displaying the fastest and most regular activations were those including the RV apex. VF rate and stability slightly increased over time. Finally, the parameters exploring the VF rate were found to be well correlated together, as well as parameters of VF regularity Human VF induced during electrophysiological study has a clear DF of activation and appears quite regular in intracardiac recordings. There is some spatial heterogeneity, which needs to be more detailed in order to localize possible driving sources. Fastest VF are the most regular. Rate and stability tend to increase during the initial phases of VF.

Ventricular Fibrillation Cycle Length in Patients with Brugada Syndrome

Background: Patients with Brugada syndrome (BRS) have a shorter ventricular fibrillation cycle length (VFCL) than patients with a structural heart disease. Object: The aim of this study was to reveal the differences in the VFCL between patients with asymptomatic BRS and those with symptomatic BRS. Method: This study included 21 patients (21 men; age 53.4±3.4 years) who received implantable cardioverter defibrillators (ICDs) between April 2005 and December 2010. Among these patients, 16 patients did not have ventricular arrhythmia (asymptomatic group), while 5 had ventricular arrhythmia (symptomatic group). We examined the cycle length of the ventricular fibrillation that was induced by extra-stimulation from right ventricular and T wave shock. Results: Patients with symptomatic BRS had a significantly shorter VFCL than those with asymptomatic BRS; the ventricular fibrillation had been induced by extra-stimulation form the right ventricular apex (147.2±15.4 ms vs 178.5±3.2 ms, P=0.0062) and the right ventricular outflow tract (153.6±8.9 ms vs 180.7±3.9 ms, P=0.0106), and by T wave shock from the ICDs (162±8.6 msec vs 193.9±2.9 ms, P=0.0003). Conclusion: The estimation of VFCL may be useful for the risk stratification of patients with BRS.

Induction by direct current pulse versus 50-Hz pacing on ventricular fibrillation and defibrillation

Ventricular fibrillation (VF) induced by different modes of induction may have different characteristics and defibrillation thresholds. This study compares the cycle lengths and defibrillation of VF induced by direct current (DC) pulses vs 50Hz. We compared induction by DC pulses and 50-Hz pacing in this single-centre observational study of 259 consecutive patients with implantable cardioverter defibrillators in 2007-2008. Patients with inadequate defibrillation safety margin (DSM), defined as unsuccessful defibrillation at 25J, were identified. Of the 259 patients, 132 underwent induction with DC pulses and 127 with 50-Hz pacing. DC pulses induced VF of shorter cycle lengths (207 ± 16 vs 231 ± 24ms, p < 0.001) compared to 50-Hz pacing. There were 17 patients (6.6%) with inadequate DSM-13/132 (9.8%) with DC pulse vs 4/127 (3.1%) with 50-Hz pacing (p < 0.001). The induced VF cycle lengths were shorter in patients with inadequate DSM (186 ± 25 vs 221 ± 21ms, p < 0.001). On multivariate analysis, only the induced VF cycle length (p = 0.002) was independently associated with inadequate DSM. VF of shorter cycle lengths is independently associated with inadequate DSM. DC pulses are associated with greater proportion of patients with inadequate DSM as it induces VF of shorter cycle lengths compared to 50-Hz pacing.

Increased cycle length during long-duration ventricular fibrillation is caused by decreased upstroke velocity as well as prolonged refractoriness

Cycle length (CL) increases as ventricular fibrillation (VF) progresses. The purpose of this study was to test the hypotheses that increased CL is due to increased diastolic interval (DI), not increased action potential duration (APD), and that the DI increase is not solely due to increased postrepolarization refractoriness. In 10 swine, VF was recorded for 20 minutes using a floating microelectrode through a hole in a 504-electrode epicardial plaque. Mean APD, DI, action potential amplitude (APA), maximum change in voltage during the AP upstroke (V(max)), and CL were calculated from the floating microelectrode recordings each minute of VF. The refractory period was estimated from the minimum DI (DI(min)). In two animals, rapid pacing was performed to gauge refractoriness. As VF progressed, CL, DI, and DI(min) increased (P <.05), whereas APD, V(max), and APA decreased (P <.05). At 20 minutes, DI(min) was not different from mean DI at VF onset. Pacing captured, but 53% of paced wavefronts blocked within the plaque. Increasing CL in VF is due to increased DI and not APD, which shortens. The increase in DI(min) over time is much less than the increase in mean DI, indicating that the myocardium is excitable during much of the DI. This finding, along with the ability to pace at a CL shorter than the native VF CL and the poor paced wavefront propagation, suggests that the increase in DI is due not only to increased postrepolarization refractoriness but also to poor wavefront propagation because of decreased APA and V(max) secondary to global ischemia caused by VF.

The Impact of Acute Myocardial Ischemia on the Ventricular Defibrillation Threshold During Chronic Oral Azimilide Therapy

The effects of chronic oral azimilide therapy on the ventricular defibrillation threshold (DFT) during ischemia are unknown. The effects of azimilide on defibrillation efficacy under ischemic condition were investigated in a closed-chest animal model. Azimilide (20 mg/kg/d) was administered orally for 7 days to 10 pigs (20 to 25 kg). The control group (no treatment) comprised 15 pigs. A 2-lead defibrillation system was used. Each shock was delivered after 8 seconds of ventricular fibrillation. A step-up and step-down protocol was used to calculate mean DFT before and 10 minutes after coronary artery occlusion using an angioplasty balloon in the left descending artery. The basal DFT of the azimilide group did not differ from controls (20.8 +/- 4.8 versus 18.8 +/- 2.8; P = 0.33). After ischemia, the mean DFT of the azimilide-treated animals was similar to controls (21.8 +/- 5.2 versus 23.2 +/- 3.8 J; P = 0.54), despite significant lengthening of ventricular repolarisation (428.2 +/- 51.8 versus 494.1 +/- 46.6 msec; P = 0.005) and significant prolongation of the ventricular fibrillation cycle length (85.1 +/- 13 versus 104.7 +/- 24 msec; P < 0.04). Chronic oral azimilide treatment does not affect the DFT at baseline or during acute myocardial ischemia.

Abstract 192: Defibrillation Strategy with Postshock Synchronized Pacing in Excitable Gaps

Introduction: It was previously demonstrated that ventricular fibrillation (VF) can be synchronized with a novel spatiotemporal excitable gap pacing (SyncP) technique using low-energy pacing pulses that causes pace termination of VF. Therefore, we hypothesize that a spatiotemporally controlled (STCD) defibrillation strategy using defibrillation shocks followed by SyncP may be effective in defibrillation efficacy improvement. Methods and Results: We explored the STCD effects in 10 isolated rabbit hearts (n=10) with optical mapping of the anterior wall in LV. Optical recording guided real-time detection and stimulation of spatiotemporal excitable gaps was performed. SyncP was shown to cause wavefront synchronization as indicated by a decreased number of phase singularity points (p&lt;0.0001) and reduced spatial dispersion of VF cycle length (p&lt;0.01). After a defibrillation shock delivery, an isoelectrical window (IW) was present and the duration of the IW was a function of the shock strength. When the reference site detected the earliest activation (early site) of the reinitiated VF during IW, a 5-mA electric stimulus was delivered from the pacing electrode to depolarize the excitable gap, creating a functional block to stop VF propagation or change the propagation timing/pattern for VF termination. The location of the early site varied, however, about 80% arose from the right side of LV anterior wall close to apex, with the arrangement of the defibrillation anode electrode in the RV and cathode against the posterior wall. For 90% of the episodes where the reference site accurately detected the early site location, the SyncP pacing electrode successfully administered pacing in the excitable gap after low-energy shock delivery. VF was demonstrated to be successfully terminated by the STCD defibrillation with low-energy shock and pacing in the excitable gaps to cause functional block for reinitiated VF propagation in heart tissues. Conclusion: We implemented the concept of post-shock synchronized pacing in excitable gaps by a real-time feedback mechanism. Further optimization of this technique may prove effective in improving the defibrillation efficacy by synchronized VF activation.

Influence of Drive Cycle Length on Initiation of Ventricular Fibrillation During Implantable Cardioverter Defibrillator Threshold Testing

Programmed electrical stimulation of the heart as a method to induce tachyarrhythmias has been described since the 1960s. To date, no study has examined optimal drive cycle length in the induction of ventricular fibrillation (VF) during defibrillation threshold testing after implantable cardioverter-defibrillator placement. We hypothesized that longer drive cycle length, by means of the longer action potential duration, would promote intramyocardial phase 2 reentry and facilitate induction of VF. Fifty consecutive implants were randomized in a prospective crossover format for this study. The group consisted of 40 men and 10 women, with each patient receiving either a 400 or 600 ms initial drive train prior to 1.2 J internal shock on the T wave with a goal to induce ventricular fibrillation. The timing of the T wave shock was determined by measuring the interval from the beginning of the QRS to the apex of the T wave in lead II. Successful inductions were defibrillated via the cardioverter defibrillator. Patients were then crossed over and the protocol repeated. Twenty of 23 (87%) patients were successfully induced into VF in the initial 400 ms drive train arm whereas 22 of 27 (81%) were successfully induced in the 600 ms arm. Thus, a total of 44 (88%) patients were successfully induced at 400 ms, 41 (82%) patients were successfully induced at 600 ms, and 2 (4%) patients were not inducible at either cycle length, but were inducible with 50 Hz ventricular stimulation. However, no significant difference was noted between the two groups. No investigation to date has questioned whether a relationship exists between drive cycle length and initiation of ventricular fibrillation. Our study addresses this question, though negative for difference between 400 and 600 ms drive trains. Further research into optimal strategies for inducing ventricular fibrillation will minimize patient sedation time and discomfort while undergoing defibrillator threshold testing.

The Effect of Induction Method on Defibrillation Threshold and Ventricular Fibrillation Cycle Length

Since no clinical data are available on the comparison of the "shock on T-wave" and "high frequency burst" ventricular fibrillation (VF) induction modes during defibrillation threshold (DFT) testing, we aimed to compare these two methods during implantable cardioverter defibrillator implantation. The DFT was determined with a step-down protocol using biphasic, anodal polarity (100%, 40%, 20% voltage control) shocks. Patients were randomized: VF was induced by 50 Hz burst in group B (n = 45) and T-wave shock in group T (n = 41). The DFT was defined as the lowest energy level that terminated VF; confirmed DFT (DFTc) was defined as the minimal energy level that consecutively terminated VF twice. Success rate of DFTc was calculated during an intraindividual test for the alternate induction method. A total of 546 episodes of VF were induced: n = 278 (B) vs n = 268 (T). Incidence of VT during inductions was 9.9% (B) vs 2.7% (T), P < 0.05. Neither the DFT, 8.8 +/- 4.0 J (B) vs 9.7 +/- 4.2 J (T), nor the DFTc, 10.6 +/- 5.1 J (B) vs 10.8 +/- 4.2 J (T), proved to be significantly different. A significant correlation was found between VF cycle length (CL) and the concomitant DFT (r = 0.298, P < 0.05) in group T only. Subgroup analysis of patients under chronic class III antiarrhythmic treatment showed no increase of the DFT in either group and significantly lower incidence of VT induction in group T regardless of antiarrhythmic treatment. The DFT and the VFCL proved to be independent of the VF induction method. The T-wave shock was more unlikely to induce VT during DFT testing. These results suggest that both methods are reliable in DFT determination, though T-wave shock application is a more reliable method for DFT testing.

The Impact of Catecholamines in Patients with or without Beta‐Blockers on the Ventricular Fibrillation Cycle Length and Ventricular Fibrillation Cycle Length Variability

To evaluate the impact of epinephrine, norepinephrine, or placebo on the ventricular fibrillation cycle length (VFCL) and the variability of VFCL (cvVFCL) measurements in implantable cardioverter defibrillator (ICD) patients with or without beta-blockers. Forty-three patients scheduled for their 6-week post-ICD placement noninvasive electrophysiologic study were included in the study at the Arrhythmia Procedure Laboratory at Hartford Hospital, Hartford, CT. This randomized, double-blind, placebo-controlled evaluation was approved by the Hartford Hospital Institutional Review Board. After 2 seconds of continuous VF, 7 consecutive VFCLs were measured from the ICD device recording printout using a 0.5 mm scale ruler under magnification at baseline and after the infusion of catecholamines (epinephrine or norepinephrine at 2 mcg/min) or matching placebo at steady state. The average VFCL and the cvVFCL were determined for each study phase. Subgroup analysis based on chronic beta-blocker use was performed. No between-group differences were noted for epinephrine, norepinephrine, or placebo group for baseline (P=0.538) or postinfusion VFCL (P=0.749) or for baseline (P=0.561) or postinfusion cvVFCL (P=0.623) Regardless of catecholamine group randomization, longer pre- and postinfusion VFCL were noted in those receiving beta-blockers (P=0.157, P=0.019) but no differences in cvVFCL were noted (P=0.216, P=0.474) versus those without beta-blockers, respectively. Moderately dosed epinephrine or norepinephrine does not affect either VFCL or the variability of VFCL after short duration of ventricular fibrillation. Chronic cardioselective beta-blockade prolongs VFCL without any impact on coefficient of variation of VFCL.

Long‐Term Incidence of Malignant Ventricular Arrhythmia and Shock Therapy in Patients with Primary Defibrillator Implantation Does Not Differ from Event Rates in Patients Treated for Survived Cardiac Arrest

Recent trials have demonstrated benefit of prophylactic defibrillator (ICD) implantation compared to conventional treatment in high-risk patients. However, many patients have rare or no sustained arrhythmias following implantation. Our study addresses the question, whether patients with prophylactic defibrillator implantation have a lower risk for life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF) compared to sudden cardiac death (SCD) survivors. Over 7 years we enrolled 245 patients. Occurrence of spontaneous sustained VT/VF resulting in adequate ICD treatment was the endpoint. Incidence, type, and treatment of sustained arrhythmia in 43 previously asymptomatic ICD recipients (group B) were compared to data of 202 survivors of imminent SCD (group A). All patients had severely impaired left ventricular ejection fraction (<45%). Group B patients had long runs (>6 cycles, <30 s) of VT during Holter monitoring and inducible sustained arrhythmia. Incidence of rapid VT and VF (cycle length <240 ms/heart rate >250 bpm) after 4 years (35% in both groups, P = ns) and adequate defibrillator therapies (57% vs 55%, P = ns) were similar in both groups after univariate and multivariate analysis. Cumulative mortality tended to be lower in group B compared to group A, but the difference was not statistically significant. During long-term follow-up, incidence of sustained rapid ventricular arrhythmia in prophylactically treated patients is as high as that of SCD survivors. Benefit from defibrillator implantation for primary prevention (group B) appears to be comparable to that for survived cardiac arrest (group A).

Unsuccessful Internal Defibrillation in Brugada Syndrome: Focus on Refractoriness and Ventricular Fibrillation Cycle Length

In patients with Brugada syndrome, implantable cardioverter defibrillator (ICD) is the only reliable treatment to prevent sudden death though, in some cases, internal defibrillation may be unsuccessful. The aim of this study was to examine the determinants of defibrillation failure, with a focus on electrophysiologic characteristics. The study included 51 patients treated with ICD: 22 with Brugada syndrome and 29 with structural heart disease (SHD). The prevalence of defibrillation energy requirement precluding the programming of a 10-J safety margin, the mean right ventricular effective refractory period (ERP), and mean induced ventricular fibrillation cycle length (VFCL) from the stored ICD electrograms, were compared between the two patient groups. High defibrillation requirements were observed in 18% of patients with Brugada syndrome versus 0% of patients with SHD. However, the patients with SHD had larger heart size than those with Brugada syndrome. Mean VFCL and mean ERP were both significantly shorter in patients with Brugada syndrome than in patients with SHD, and ERP and VFCL were significantly correlated. Patients with Brugada syndrome have a high prevalence of high defibrillation energy requirement, and short ventricular ERP and VFCL.

Is there a correlation between ventricular fibrillation cycle length and electrophysiological and anatomic properties of the canine left ventricle?

We hypothesized that myocardial infarction-related alterations in ventricular fibrillation (VF) cycle length (VFCL) would correlate with changes in local cardiac electrophysiological and anatomic properties. An electrophysiological study was performed in normal, subacute, and chronic infarction mongrel dogs. VF was induced by programmed electrical stimulation and mean and minimum early and late VFCL was determined and correlated with local electrophysiological and anatomic properties. Effective refractory period (ERP), activation recovery time (ART), ERP/ART ratio, threshold, and ERP and ART dispersion were determined at 112 sites on the anterior left ventricle. Wave front progression was analyzed over a 2-s period. The extent of local tissue necrosis and of myocardial fiber disarray was also evaluated. The early mean VFCL was significantly longer in the subacute infarction (149 +/- 35 ms) and chronic infarction dogs (129 +/- 18 ms) compared with control dogs (102 +/- 15 ms; P < 0.0001 for both comparisons) as was the early minimum VFCL with similar trends seen during late VF. Complete epicardial reentrant circuits were significantly more common in normal dogs (4.3 +/- 2.4, 22.4% of cycles) than in subacute (0.75 +/- 0.96, 5.3% of cycles, P < 0.05 vs. normal) and chronic infarction dogs (1.3 +/- 1.3, 7.5% of cycles, P < 0.05 vs. normal). There was a poor correlation between the mean and minimum early and late VFCL and local electrophysiological and anatomic properties (R(2) < 0.2 for all comparisons) with a much better correlation between average mean and minimum VFCL (over the entire plaque) and global ERP and ART dispersion during early and late VF. In conclusion, VFCL in normal and infarcted myocardium shows a poor correlation with local ventricular electrophysiological and anatomic properties measured in sinus rhythm. However, there was a much better correlation between the average VFCL with global dispersion of repolarization. The lack of correlation between local VFCL and refractoriness and the infrequent occurrence of epicardial reentry suggests that intramural reentry may be the primary mechanism of VF in this model.