VF Episodes Research Articles

Abstract 2769: Bradycardia-Dependent Augmentation of J-wave Elevation in Patients with Idiopathic Ventricular Fibrillation

Although J-wave elevation (JWE) in the inferior or lateral leads is characteristic of subtype of idiopathic ventricular fibrillation (IVF), difference between malignant and benign JWE remains to be elucidated. So, we assessed the hypothesis that the rate dependent changes in JWE could be different between patients with IVF and control subjects. Six male patients with IVF and 18 age matched male controls with JWE (>2 mm) in the lateral leads were studied. CM-5 lead digital Holter ECG was recorded and J wave amplitude was automatically measured. J/RR relationships were evaluated by means of J/RR linear regression lines for 24 hours, and according to four 6-hour periods. From J-RR linear regression lines, J-RR slope (mm/sec), J wave amplitude (mm) at RR intervals of both 0.6 sec and 1.2 sec (J (0.6) and J (1.2) ) were determined. In all 6 patients with IVF, the time of spontaneous episodes of VF were investigated from the implantable cardioverter defibrillator (ICD) stored data. For 24 hours, J-RR slope was greater in IVF patients than in controls (3.5±0.7 vs 2.4±0.8, p<0.01). (J (0.6) ) wasn’t different between 2 groups; however, J (1.2) was greater in IVF patients than in controls (2.8±0.9 vs 2.0±0.6, p<0.05). In IVF patients, ST/RR slope was highest during 18:00–24:00; however, these circadian changes were blunted in controls. J(1.2) was greater during 18:00 – 6:00 in IVF patients than in controls. Seven (59%) of total 9 episodes of spontaneous VF of IVF patients occurred during 18:00 – 6:00. In patients with subtype of IVF, JWE augmented during bradycardia especially at night. This could relate to nighttime occurrence of IVF.

Abstract 4666: Anatomic Substrate as Determinant of Dominant Frequency Dynamics During Human Ventricular Fibrillation

Background: Dominant frequency (DF) analysis is a common way of quantitatively studying the spatio-temporal variation of frequency during VF. Areas of high frequencies (e.g. rotors) and low frequencies (e.g. blocks) have been associated with the occurrence and maintenance of VF. However, the relation of these high or low frequency areas to anatomical or physiological substrate remains unclear. Objective: We tested the hypothesis that the Max-Min DF locations in the epicardium during VF are due to anatomical substrate. Methods and Results: We analyzed 33, 4 seconds VF episodes acquired from 6 isolated human hearts using a Langendorff setup. The hearts were received from the heart-transplanted patients with informed consent. Electrode array consisting 112 bipolar electrodes was used to acquire the surface unipolar and bipolar electrograms from the epicardium. DF was computed as the peak frequency of the VF segment from each of electrodes using Welch’s modified periodogram method. From the DF distribution, the regions of max and min frequencies were identified for LV and RV regions. Scar maps were computed for each of the 6 hearts using a previously published method by mapping the amplitude of bipolar electrograms (<0.5mv = scar) during the pacing protocol. The areas of max-min DF frequencies in each of the VF episode were compared to the corresponding spatial locations in the scar map. Table 1 shows the match between the max-min DF frequency locations and the scar locations. 50% of max-min DF frequencies locations match the scar locations and in 97% of the matched locations the max-min DF occur at the vicinity of the scar. Conclusion: During human VF, DF dynamics are only partially explained by the anatomical substrate. This suggests that ion channel heterogeneity and dynamic physiological factors may play an important role in determining fibrillation dynamics. Match Between Max-Min DF locations and Scar Locations

Abstract 5892: Therapy For Device-determined Ventricular Arrhythmias Decrease As Biventricular Pacing Percentage Increases In Heart Failure Patients

Introduction: CRT-D improves cardiac function and quality of life, and decreases HF hospitalization and death for many patients. However, impact on therapy delivered for ventricular arrhythmias is less clear. Methods: Device-determined VT and VF episodes with therapy (n = 1835) from CRT-D patients in two trials (CRT RENEWAL & REFLEX; n = 1698) were analyzed in a post hoc fashion. Patients were divided into lifetime biventricular (BiV) pacing percentage quartiles. Zero-inflated Poisson regression models were used to evaluate impact of pacing on VT/VF incidence and frequency, adjusting for baseline covariates including lifetime ATR mode switch percentage. Results: Patient characteristics: 69 ± 11 years, 73% male, 68% CAD. Dividing patients in quartiles resulted in the following pacing breakdown: 0–92% (n = 445), 93–97% (n = 445), 98–99% (n = 482), and 100% (n = 326). There were no differences in gender, NYHA, or history of diabetes, MI, CAD or hypertension among the groups. Patients paced 0–92% and 93–97% had similar VT/VF therapy incidence (24.72% vs. 24.27%) and frequency (17.05% vs. 16.00%). Patients paced 98–99% had lower VT/VF therapy incidence (15.15%) than patients paced ≤ 97% (p < 0.001) but similar frequency after adjusting for incidence. Patients paced 100% had similar VT/VF therapy incidence (13.80%) and frequency (6.45%) to patients paced 98–99%. The figure shows the time to first therapy for VT/VF. Conclusions: For CRT-D patients in this analysis, incidence and frequency of therapy delivered for VT/VF is significantly decreased when lifetime BiV pacing percentage is above 97%.

Abstract 98: Spontaneous Refibrillation Following External Defibrillation of Long Duration Ventricular Fibrillation in Swine

Background: Following successful defibrillation of the long duration ventricular fibrillation (LDVF) associated with sudden cardiac arrest (SCA), refibrillation occurs in over half of resuscitation attempts. In experimental animals with normal hearts, refibrillation almost never occurs following short duration VF lasting < 1 min (SDVF). It is not known if refibrillation following LDVF is due to the cardiac disease that caused the initial LDVF of SCA or if the LDVF itself causes abnormalities that can initiate VF. Further, the mechanism of refibrillation initiation is unknown. We tested the hypothesis that refibrillation occurs frequently following LDVF in previously normal hearts and propagates from a common area within the heart. Methods : In 6 pigs, 115–120 plunge needles containing 3– 6 electrodes each were inserted throughout the heart. With the chest closed, external defibrillation pads were placed in a left lateral to right lateral configuration. Following successful defibrillation of 20 s of SDVF, the animal was observed for spontaneous VF for at least 4 min. After termination of 7 min of LDVF, the animal was placed on cardiopulmonary bypass and observed for 15 min for spontaneous VF. Results: Following LDVF, 1.33 ±0.8 episodes of spontaneous VF occurred in each animal. The mean time to VF was 71 s (range 5 – 139 s) following defibrillation of LDVF. Three animals had a second episode of VF within 3 min of termination of LDVF. Earliest sites of origin of spontaneous VF occurred equally in the LV (3), RV (3), and septum (2) and arose equally from the endocardium (3), epicardium (2), and myocardium (3). Refibrillation originated in the posterior half of the ventricles 75% of the time. The first refibrillation cycle appeared focal in 75% of cases and reentrant in 25%. Premature ventricular beats arising out of the posterior RV base immediately preceded 75% of VF episodes. Conclusions: Spontaneous VF is common after defibrillation of LDVF but not SDVF in previously health swine, indicating that refibrillation does not require preexisting cardiac disease but can be caused by the detrimental effects of LDVF. Most episodes of refibrillation begin as focal activity within the posterior half of the ventricles.

Abstract 1355: Determining Wavefront Size during Ventricular Fibrillation: Optical Mapping Study from Human Langendorff Hearts

Background: We had recently established a model for the study of VF in humans using an optical mapping technique in Langendorff perfused human hearts. The optical mapping technique allows for the unequivocal evaluation of wavefront identification, the origin of wavefronts and their directional spread. Objective: The objective of this study was to measure wavefront sizes from different regions during human VF to determine the minimal spatial resolution required to study human VF in-vitro. Methods: The hearts were explanted from seven cardiomyopathic patients who underwent transplantation. The hearts were Langendorff perfused with Tyrode’s solution (95%O 2 +5%CO 2 ) and the potentiometric dye (0.2 mg Di-4-ANEPPS dissolved in 20mg of perfusate) was injected as a bolus into the coronary circulation. The imaged region was physically immobilized to minimize motion. The fluorescence was excited at 530 nm with a HL 150 W halogen lamp, the emission signal was longpass filtered at 610 nm and recorded with a CCD and CMOS camera (MiCAM02, Ultima, BrainVision Inc., Japan). The spatial resolution depending on the mapping window was 0.65–0.85 mm and the temporal resolution was 1 kHz. The heart was paced at a cycle length of 600 ms and the VF was induced by briefly touching the heart with the two poles of a 9V battery. The changes in dye signal were recorded over 1887 ms and analyzed using BV-analyzer software (BrainVision Inc, Japan). Wavefronts were identified using high-pass filter (0.01 Hz) on the fluorescence data. Recordings were performed at 4 sites: LV Septum (LVS), Right Ventricle Endocardium (RV), Left Ventricle Endocardium (LVendo) and Left Ventricle Epicardium (LVepi). Results: 16 episodes of VF were recorded and a total of 54 wavefronts were identified. Average wavefront size was 23.6 mm. By region, the average wavefront sizes were: LVS = 26.3 mm; RV = 22.4 mm; LVendo = 29.7 mm; LVepi = 19.3 mm. Conclusion: These results show that different regions on the human ventricle during VF show different wavefront size suggesting that propensity for wavebreak maybe spatially differentially distributed. To study human VF with multi-electrode mapping tools using inter-electrode spacing of less than 1–2 cm should provide sufficient resolution.

Abstract 2645: Longer Ventricular Fibrillation Detection Duration Does Not Increase Rate of Undersensing: Results from the PREPARE Study

Background: The PREPARE study was designed to evaluate ICD detection and therapy parameters strategically selected to safely reduce all-cause shocks in patients with primary prevention indications by treating only truly sustained fast VT/VF. Electrophysiologic properties have been shown to deteriorate during long-duration VF episodes. There was concern that electrogram deterioration might result in increased undersensing (US) and delayed detection of VF. In this analysis we compared the rate of US between episodes detected with shorter (number of intervals to detect (NID) =12/16) and longer (NID=30/40) detection settings to assess whether delayed detection times for VF increased the rate of US. Methods: All induced VT/VF episodes from PREPARE patients programmed to NID 12/16 or 30/40 and sensitivity 1.2 mV were included in the analysis. US was determined automatically from the stored episode record. The numbers of US and the times from onset through initial detection and from detection to shock were computed. The rates of US over time were compared between the shorter and longer NIDs using a GEE analysis with time as the offset. Results: Seven hundred fifty six VF inductions in 432 patients from the PREPARE study were included in the analysis. There were 319 VF inductions (180 pts) with NID 12/16 and 437 VF inductions (261 pts) with NID 30/40. The average time from VF onset to shock increased from 6.0 to 9.5 seconds with the longer VFNID with no evidence of an increase in the rate of US over time. Conclusion: The longer NID delayed shock delivery by an average of 3.5 seconds but did not result in an increased rate of undersensing.

Electrical storms in Brugada syndrome successfully treated with isoproterenol infusion and quinidine orally

Brugada syndrome is an inherited cardiac disease and is associated with a peculiar pattern on the electrocardiogram and an increased risk of sudden death. Electrical storm is a malignant but rare phenomenon in symptomatic patients with Brugada syndrome. We describe a patient who presented with repetitive ICD discharges during two episodes of recurrent VF. After the initiation of isoproterenol infusion and oral quinidine, the ventricular tachyarrhythmias were successfully suppressed. (Neth Heart J 2007;15:151-4.).

Implantable cardioverter defibrillator shock reduction using new antitachycardia pacing therapies

The main purpose of ICDs is to abort sudden death by delivering therapy at the moment of tachycardia. Shocks accomplish this goal but are painful. Alternatively antitachycardia pacing is painless and if deemed safe may be reasonable substitute. Multiple trials show a high efficacy rate by ATP (78-94%) for treating VTs below 200 bpm. ATP has had less efficacy for faster VTs (41-79%) and have higher probability of accelerating tachycardia (5-55%). The PainFREE trials address these issues. The first pilot study PainFREE Rx applied standardized VT detection and ATP regimen to 220 patients with 1100 spontaneous episodes of VT. ATP success for slow VT success was 92% and fast VT > 188 bpm raw success rate was 89%. None of these trials randomize shock versus ATP so comparative safety data was missing. Thus, the PainFREE Rx II trial was designed to make direct safety comparison between shock and ATP therapies for fast VT > 188 bpm. It included 634 patients with either ischemic or nonischemic cardiomyopathy followed for 1 year yielding 1760 episodes of slow VT, fast VT plus VF. The results of the PainFREE Rx II trial showed that a single regimen of ATP, burst pace 8 pulses at 88% VT cycle length could safely terminate 77% of fast VT and 90% of slow VT. Consequently, shocks were reduced by 70% compared to the shock group. Furthermore, ATP was proven safe because there was no increase in sudden death, syncope or even arrhythmia acceleration compared to shock. The quality of life of the ATP group was found to be superior to the shock group validating ATP's intent. Secondary yet important findings also included the fact that by programming the ICD to wait for 18 beats in PainFREE Rx II before treating an episode reduced markedly the number of episodes treated when compared to 12 beat detection as done in PainFREE Rx I. Since syncope occurred in only 1% of episodes, the authors suggested that a longer wait for ICD detection needs to be evaluated.

Diagnostic and Prognostic Value of a Type 1 Brugada Electrocardiogram at Higher (Third or Second) V 1 to V 2 Recording in Men With Brugada Syndrome

To evaluate the diagnostic and prognostic value of an electrocardiogram (ECG) recorded at a higher (third or second) intercostal space, 98 men (17 to 76 years of age, mean +/- SD 47 +/- 13; with documented ventricular fibrillation [VF] in 22 and syncope in 32) were categorized into 3 groups; 68 men had a spontaneous type 1 ECG in standard leads V(1) and V(2) (S group), 19 had a spontaneous type 1 ECG only in the higher V(1) and V(2) leads (H group), and 11 had a type 1 ECG only after receiving class Ic sodium channel blockers (Ic group). There were no significant differences in baseline clinical characteristics, including VF episodes, syncope, atrial fibrillation, family history, late potentials, and inducibility of VF during electrophysiologic study across the 3 groups. During prospective follow-up periods (779 +/- 525, 442 +/- 282, and 573 +/- 382 days, respectively), subsequent cardiac events occurred in 11 men (16%) within the S group, in 2 men (11%) in the H group, and in 0 men (0%) in the Ic group (p = NS, S vs H group). In men with previous episodes of VF, subsequent cardiac events occurred in 7 (44%) within the S group and in 2 (50%) in the H group (p = NS). In conclusion, men with a spontaneous type 1 Brugada ECG recorded only at higher leads V(1) and V(2) showed a prognosis similar to that of men with a type 1 ECG in using standard leads V(1) and V(2).

Prevention of Fatal Arrhythmias in High-Risk Subjects by Fish Oil n-3 Fatty Acid Intake

The long-chain n-3 fatty acids in fish have been demonstrated to have antiarrhythmic properties in experimental models and to prevent sudden cardiac death in a randomized trial of post-myocardial infarction patients. Therefore, we hypothesized that these n-3 fatty acids might prevent potentially fatal ventricular arrhythmias in high-risk patients. Four hundred two patients with implanted cardioverter/defibrillators (ICDs) were randomly assigned to double-blind treatment with either a fish oil or an olive oil daily supplement for 12 months. The primary end point, time to first ICD event for ventricular tachycardia or fibrillation (VT or VF) confirmed by stored electrograms or death from any cause, was analyzed by intention to treat. Secondary analyses were performed for "probable" ventricular arrhythmias, "on-treatment" analyses for all subjects who had taken any of their oil supplements, and "on-treatment" analyses only of those subjects who were on treatment for at least 11 months. Compliance with double-blind treatment was similar in the 2 groups; however, the noncompliance rate was high (35% of all enrollees). In the primary analysis, assignment to treatment with the fish oil supplement showed a trend toward a prolonged time to the first ICD event (VT or VF) or of death from any cause (risk reduction of 28%; P=0.057). When therapies for probable episodes of VT or VF were included, the risk reduction became significant at 31%; P=0.033. For those who stayed on protocol for at least 11 months, the antiarrhythmic benefit of fish oil was improved for those with confirmed events (risk reduction of 38%; P=0.034). Although significance was not achieved for the primary end point, this study provides evidence that for individuals at high risk of fatal ventricular arrhythmias, regular daily ingestion of fish oil fatty acids may significantly reduce potentially fatal ventricular arrhythmias.

Ventricular Pacing Thresholds Following High-Energy Ventricular Defibrillation Shocks

Increased ventricular pacing thresholds have been observed following monophasic waveform shocks in implantable cardioverter defibrillators (icds). This study aimed to examine such changes following high-energy biphasic shocks in icds. Ten episodes of VF were induced every 10 minutes in 10 pigs (23.1±3.0 kg). After 10 seconds of VF a 40J biphasic shock (total 10 shocks) was delivered for successful defibrillation in the true-bipolar sensing lead system of the ICD. Ventricular bipolar pacing thresholds before and after these shocks were evaluated at one-minute intervals. The mean pacing threshold before shock delivered was 0.066 ± 0.059 uj. Those of the first, second and third minutes after the first shock were 0.052 ± 0.061 uj, 0.044 ± 0.039 uj, respectively; showing that pacing thresholds gradually decreased. It may not be necessary to pace at a high-voltage output after biphasic shocks in icds.

Not Everyone With an Ejection Fraction ≤30% Should Receive an ICD

Although the total number of deaths attributed to cardiovascular disease has decreased during recent decades, an increase in the percentage of cardiac deaths occurring suddenly (from 56% in 1989 to 63% in 1998) has actually resulted in an increase in the total number of sudden deaths in the United States.1 The problem of sudden death spans all racial and cultural groups and is equally important in men and women. It is now 40 years since continuous ECG monitoring revealed that ventricular tachycardia and ventricular fibrillation (VT/VF) are responsible for the majority of sudden deaths. Dissemination of this information resulted in a marked change in practice. Until the 1970s, physicians treated only symptomatic VTs. Therapeutic options were limited to a few antiarrhythmic drugs, administered empirically. With the advent of telemetric ECG monitoring and continuous ambulatory (Holter) ECG monitoring came the recognition that frequent and multiform ventricular ectopy often preceded episodes of VF in the acute phase of myocardial infarction (MI). Ventricular ectopy and nonsustained VT was documented 1 to 2 weeks after MI in many patients. The presence of frequent ventricular premature complexes and runs of nonsustained VT in patients with significant left ventricular dysfunction were then demonstrated to be an independent predictor of sudden cardiac death late after MI. This information then led to the practice of administering antiarrhythmic drugs to suppress ventricular ectopy under the presumption that suppression of asymptomatic ectopy would prevent sudden death. This fashion lasted almost 20 years, until the results of the Cardiac Arrhythmia Suppression Trial (CAST) trial demonstrated the harm caused by this approach.2 Thus, a sea change in the practice of cardiology had occurred, from treating only symptomatic patients to therapy aimed at primary prevention of sudden death. The initial efforts using antiarrhythmic drugs failed to reduce mortality. While many physicians …

Inappropriate implantable cardioverter defibrillator therapy delivered after sensing of arc welding

Introduction: Electromagnetic interference continues to be a life-threatening cause of ICD malfunction. This report presents an unusual case of inappropriate ICD discharge that occurred while a patient was swimming in a lake. Case Report: A 55 year old male with a history of coronary artery disease, extensive myocardial infarction, and ventricular fibrillation was first implanted with a dual-chamber ICD system on August 5, 1999 with subsequent pulse generator replacement on June 1, 2004. The new pulse generator was a Medtronic model 7274; the chronic atrial lead was a Medtronic model 6940, and the chronic right ventricular lead was a Medtronic model 6945. On July 18, 2004 the patient received two shocks. The patient reported no preceding symptoms of syncope or palpitations prior to ICD therapy. The ICD had been programmed with VT detection above 182 bpm, VF detection above 240 bpm, and ventricular sensitivity of 0.3 mV. The figure shows the intracardiac electrograms recorded during a VF episode stored that day. Electrical activity consistent with 50/60 Hz alternating current superimposed upon normal myocardial activity at 60 bpm was recorded by the ICD in several episodes that day as nonsustained VT (5-7 beats in duration) and in 3 episodes as VF. During the 11 minutes in which these “episodes” were recorded, the patient was lying on a raft in a lake. Electrical current generated during arc welding repair of a nearby dock was recorded and interpreted by the ICD as rapid ventricular activity, resulting in inappropriate therapy. Discussion: ICDs remain front-line prevention for sudden cardiac death. This unusual case report of electromagnetic interference over a long distance demonstrates a need for continued improvement of sensing algorithms.

Chronic threshold testing of implantable cardioverter defibrillators does not increase coagulation activity or platelet activation.

It is unknown if the brief periods of circulatory statis occurring with induction of VF during DFT testing in patients with an ICD activate blood coagulation processes. To address this question, coagulation activity and platelet activation were measured in peripheral venous blood samples obtained from 12 patients undergoing DFT testing under general anesthesia, 3 (n = 11) or 6 months (n = 1) after ICD implantation for recurrent ventricular arrhythmias. Five patients were anticoagulated with warfarin and two to six episodes of VF (median five) were induced per patient. Blood samples were drawn at baseline, after each DFT test and on the following morning. Coagulation activity was assessed by measuring prothrombin fragment 1 + 2 (F1 + 2) (a marker of thrombin generation), soluble fibrin (a marker of fibrin production), and D-dimer (a breakdown product of cross-linked fibrin). Platelet activation was evaluated by measuring the expression P-selectin on the platelet surface using flow cytometry. No significant changes in F1 + 2, soluble fibrin, D-dimer, or P-selectin expression occurred during DFT testing, or between baseline and morning after samples. Moreover, results were unaffected by warfarin. These findings suggest that chronic threshold testing of implantable cardioverter defibrillators is not associated with activation of blood coagulation processes.

Shock coordinated with high power of morphology electrogram improves defibrillation success in patients with implantable cardioverter defibrillators.

Animal studies have suggested that the success of defibrillation may depend on the properties of VF waveform obtained from the morphology electrogram (ME) at the time of the shock. The reliable identification of depolarization events in the fibrillatory signal can be achieved using adaptive estimation of the instantaneous signal power (P). The aim of this study was to investigate if a high P of the ME (P(ME)) was related to ventricular DFT and if the upslope in ME can be associated with the depolarization event. A total of 575 VF (mean duration 10 s) episodes recorded and stored during ICD implantation in 77 patients with ventricular arrhythmias were used for analysis. The DFT was defined using a double step-down test. The values of P(ME) immediately before pulse delivery (P(shock)) and shock outcomes were registered. The differences between P(shock) of successful and failed defibrillation were tested with the Mann-Whitney U test. The relationship between individual medians of P(shock) (P(med)) and DFT was analyzed using the Kruskall-Wallis H-test. The coincidence between identified depolarization and upslope in ME was tested using the chi-square test. A P value of 0.05 was set for an error probability. The P(shock) in case of failed defibrillation was significantly lower than P(shock) in successful cases by the pulses of any strength (P < 0.001). The test revealed a significant inverse correlation between P(med) and DFT with P < 0.001. The depolarization corresponded to the upslope of ME in 85% of cases. This study demonstrated that a high value of instantaneous power of ME indicates the optimal time for shock delivery. The implementation of this algorithm in ICDs may improve the defibrillation efficacy.

Transthoracic monophasic and biphasic defibrillation in a swine model: a comparison of efficacy, ST segment changes, and postshock hemodynamics

Objective: Biphasic waveforms for transthoracic defibrillation (DF) have been tested extensively after brief (15 s) episodes of VF in animal models and in patients undergoing electrophysiologic testing. The purpose of this study was to compare the effects mono- and biphasic waveforms for DF on postdefibrillation ST segments and left ventricular pressure, markers of myocardial injury, after more extended periods of VF (30 and 90 s). Methods: 21 anesthetized and instrumented swine were randomized to truncated exponential monophasic or biphasic waveform DF. VF was induced electrically and 30 s later, DF with the designated waveform was attempted with a shock dose of 200 J. If unsuccessful, 300 J and then 360 J were administered if necessary. Following return to control hemodynamic values and normalization of the surface ECG, VF was again induced and, after 90 s, DF was attempted as in the 30 s VF period. CPR was not performed during VF and each animal was countershocked with only one waveform for both VF episodes. Waveforms were compared for frequency of first shock defibrillation success, surface ECG indicators of myocardial injury (ST segment changes at 10, 20, and 30 s after countershock) and time to return to pre-VF hemodynamics after successful DF, an indicator of postshock ventricular function. Results: Successful first shock conversion rates at 30 and 90 s were 60 and 63% for monophasic and 64 and 82% for biphasic (NS). Biphasic DF after 30 s produced ST segment changes (measured 10 s after DF) in 1/10 animals while six of eight animals in the monophasic group showed ST segment changes ( P=0.013). After 90 s of VF, ST segment changes were observed in 6/8 in the monophasic group and 2/10 in the biphasic group ( P=0.054). Differences in the time to hemodynamic recovery (return to control peak left ventricular pressure) were not observed between biphasic and monophasic waveforms after 30 or 90 s of VF. Conclusions: Monophasic and biphasic transthoracic defibrillation are equally effective in terminating VF of 30 and 90 s duration and restoring a perfusing rhythm. The biphasic waveform produced less ECG evidence of transient myocardial injury. However, there was no difference in the rate of return to control hemodynamics. ST segment changes following countershock of VF of brief duration are transient and of questionable significance.

Deterministic nonlinearity in ventricular fibrillation.

We provide numerical evidence that the electrocardiogram data collected from pigs during induced ventricular fibrillation cannot be described by a monotonic nonlinear transformation of linearly filtered noise. To establish this we use surrogate techniques and apply two test statistics: (1) the Takens' maximum likelihood estimator of the Grassberger-Procaccia correlation dimension and (2) an improved correlation dimension estimation routine. The improved dimension estimates provide evidence that the correlation dimension of the underlying dynamics during the episode of VF in the first 30 s is slightly less than 6. This result is consistent and reproducible among subjects. (c) 2000 American Institute of Physics.

Significance of r-on-t phenomenon in early ventricular tachyarrhythmia susceptibility after acute myocardial infarction in the thrombolytic era

We investigated the clinical significance and mechanism of the R-on-T phenomenon in the current thrombolytic era as potential precipitant of R-on-T–induced early ventricular tachyarrhythmias in patients with a thrombolysed acute myocardial infarction. We also examined the role of QT dispersion on ventricular vulnerability and its association with R-on-T–initiated ventricular tachyarrhythmias. A total of 93 patients underwent 24-hour Holter monitoring starting at hospital admission before thrombolysis. Patients were classified into 2 groups: those with (n = 76) and those without (n = 17) reperfusion according to electrocardiographic criteria. All R-on-T ventricular premature complexes (VPCs) and R-on-T–initiated arrhythmic events (ventricular tachycardia [VT], ventricular fibrillation) were counted to estimate arrhythmia density and severity in 2 time periods during and after completion of thrombolysis. Measurements of QT and QTc intervals and dispersion parameters were obtained on the 12-lead electrocardiogram before thrombolysis and at 24 hours in patients with and without R-on-T VTs. Overall, R-on-T VPCs were rarely observed (1.8% of total VPCs over 24 hours), occurring more frequently during than after thrombolysis (at a rate of 8 vs 0.6 VPCs/hour, p = NS) and at a higher rate during thrombolysis in nonreperfused than in perfused patients (15 vs 8/hour, p = NS). Three VF episodes were observed in 1 reperfused patient, and all were R-on-T initiated. Episodes of nonsustained R-on-T VTs (3.3% of total VTs over 24 hours) appeared more frequent during than after thrombolysis (at a rate of 0.8 vs 0.05 VPCs/hour, p = NS), and compared with non–R-on-T VTs they were significantly faster (374 ± 56 ms vs 411 ± 69 ms; p <0.05), with a trend toward longer duration. Our findings indicate that R-on-T VPCs and R-on-T VTs are early rare features in acute myocardial infarction, and do not serve as triggers of severe ventricular tachyarrhythmia. The study of ventricular repolarization did not elicit an identifiable risk factor of R-on-T VT susceptibility.

Incessant ventricular fibrillation attacks in a patient with Brugada syndrome

A 42-year-old man was hospitalized for investigation of repeated episodes of ventricular fibrillation (Vf). Electrocardiogram (ECG) showed typical features of Brugada syndrome. Echocardiography, coronary angiography and endomyocardial biopsy specimen were normal. 123I-MIBG scintigraphy showed homogeneous reduction of uptake. The patient demonstrated 17 episodes of Vf in 1 day, but these were terminated by direct cardioversion. Spectral analysis of heart rate variability demonstrated increased sympathetic activity followed by Vf attacks.

Proarrhythmic Effects of Pinacidil are Partially Mediated Through Enhancement of Catecholamine Release in Isolated Perfused Guinea-pig Hearts

The contribution of adrenergic stimulation to the proarrhythmic effects of pinacidil (30μM), an opener of ATP-sensitive potassium channels (K+ATP), was tested in an isolated guinea-pig heart model of global ischemia (10 min) and reperfusion (10 min). None (0%) of the control hearts (n=10) elicited arrhythmias during ischemia or reperfusion. In the pinacidil-treated group, one heart (5%) experienced episodes of ventricular tachycardia (VT)/fibrillation (VF) during normoxia. During ischemia, 63% (12 out of 19) of pinacidil-treated hearts exhibited episodes of VT or VF. Hearts not in VT or VF (n=7) at the time of reperfusion, exhibited 71% VT and 43% VT/VF upon reperfusion. Proarrhythmic effects of pinacidil during ischemia or reperfusion were completely reversed by glyburide (n=9; 10μM), a K+ATPantagonist, or nadolol (n=9; 3μM), aβ-adrenergic antagonist. Isoproterenol (n=10; 50 nM), aβ-adrenergic agonist, induced a 20% incidence of ischemic VT and VF, and a 70% incidence of reperfusion VF, while methoxamine (n=10; 10μM), anα-adrenergic agonist, demonstrated little proarrhythmia (20% VT/VF at reperfusion only). Proarrhythmic effects of isoproterenol were reversed by nadolol, but not glyburide. Pinacidil caused a slight potentiation of tachycardia induced by a bolus injection of tyramine (30μg), an indirectly acting sympathomimetic, but bolus injections of pinacidil (100μg) had no effect on heart rate. Nisoxetine, a catecholamine uptake1 inhibitor, had no proarrhythmic effects when given alone. Catecholamine levels were reduced in pinacidil-treated hearts relative to vehicle-treated. In conclusion, it is suggested that the proarrhythmic effects of pinacidil following global ischemia and reperfusion in the isolated perfused guinea-pig heart appears to involve stimulation ofβ-adrenoceptors. These proarrhythmic effects of pinacidil do not appear to be mediated solely through direct opening of K+ATP, but rather through an indirect enhancement of catecholamine release.