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Background: While reentry within the ventricular myocardium (VM) is responsible for the maintenance of short-duration ventricular fibrillation (SDVF; VF duration <1 minute), Purkinje fibers (PFs) are important in the maintenance of long-duration ventricular fibrillation (LDVF; VF duration >1 minute).Objective: The purpose of this study was to test the hypothesis that the mechanisms of defibrillation may also be different for SDVF and LDVF.Methods: A multielectrode basket catheter was deployed in the left ventricle of eight beagles. External defibrillation shocks were delivered with a ramp-up protocol after SDVF (20 seconds) and LDVF (150 seconds). Earliest VM and PF activations were identified after the highest energy shock that failed to terminate VF and the successful shock.Results: Defibrillation was successful after 36 +/- 12 and 181 +/- 14 seconds for SDVF and LDVF, respectively. The time after shock delivery until earliest activation was detected for failed shocks and was significantly longer after LDVF (138.7 +/- 24.1 ms) than after SDVF (75.6 +/- 8.7 ms). Earliest postshock activation after SDVF typically initiated in the VM (14 of 16 episodes), while it always initiated in the PF (16 of 16 episodes) after LDVF. Sites of earliest activity during sinus rhythm correlated with sites of earliest postshock activation for PF-led cycles but not for VM-led cycles.Conclusion: Earliest recorded postshock activation is in the Purkinje system after LDVF but not after SDVF. This difference raises the possibility that the optimal defibrillation strategy is different for SDVF and LDVF. [ABSTRACT FROM AUTHOR]

Background: Knowledge of transmural V(m) changes is important for understanding the mechanism of long-duration ventricular fibrillation (LDVF).Objective: The purpose of this study was to measure transmural V(m) changes during LDVF.Methods: V(m) was recorded optically at up to 8 transmural points separated by 1.5 mm in the left ventricle of Langendorff-perfused canine hearts (n = 6) using a bundle of optical fibers (optrode) during 10 minutes of LDVF followed by 3 minutes of VF with reperfusion. Measurements were grouped into 4 layers: epicardium, subepicardium, midwall, and subendocardium.Results: Activation rates (ARs) and action potential durations (APDs) decreased, whereas diastolic intervals (DIs) increased during LDVF in all transmural layers (P < .05). After approximately 3 minutes of LDVF, ARs were faster and DIs shorter in the midwall and subendocardium than in the epicardium and subepicardium (P < .05). Activations persisted at the subendocardium but disappeared from other layers after approximately 8 minutes of VF in the majority of hearts. There were no transmural differences in APD during LDVF or during pacing before and after LDVF (P > .05). Restitution plots showed no functional relationship between APD and DI in any layer at any stage of LDVF. Partial reperfusion during VF for 3 minutes restored transmural synchronicity of activation and eliminated gradients in activation parameters.Conclusion: V(m) dynamics evolve differently at different transmural layers. The subendocardium maintains persistent and the fastest activation during 10 minutes of LDVF, suggesting it contains the source of VF wavefronts. There are no transmural APD gradients and no restitution relationship between APD and DI at any transmural layer, indicating these are not the primary factors in the mechanism of LDVF. [ABSTRACT FROM AUTHOR]

Background: An intravascular, percutaneously placed implantable defibrillator (InnerPulse percutaneous intravascular cardioverter-defibrillator [PICD]) with a right ventricular (RV) single-coil lead and titanium electrodes in the superior vena cava (SVC) and the inferior vena cava (IVC) has been developed., Objective: The purpose of this study was to compare defibrillation thresholds (DFTs) of the PICD to those of a conventional implantable cardioverter-defibrillator (ICD) in canines., Methods: Eight Bluetick hounds were randomized to initial placement of either a PICD or a conventional ICD. For PICD DFTs, a single-coil RV defibrillator lead was placed in the RV apex, and the device was positioned in the venous vasculature with electrodes in the SVC and IVC. With the conventional ICD, an RV lead was placed in the RV apex and an SVC coil was appropriately positioned. The ICD active can (AC) was implanted in a subcutaneous pocket formed in the left anterior chest wall and connected to the lead system. DFT was determined by a three-reversal, step up-down method to estimate the 80% success level. Two configurations were tested for the conventional ICD (#1: RV to SVC+AC; #2: RV to AC). A single configuration (RV to SVC+IVC) was evaluated for the PICD., Results: Mean PICD DFT was 14.8 ± 1.53 (SE) J. Conventional #1 configuration demonstrated mean DFT of 20.2 ± 2.45 J and #2 of 27.5 ± 1.95 J. The PICD had a significantly lower DFT than the better conventional ICD configuration (#1; mean difference 5.4 ± 2.1 J, P <.05, paired t-test, N = 8)., Conclusion: The new intravascular defibrillator had a significantly lower DFT than the conventional ICD in this canine model., (Copyright © 2011 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background: Cycle length (CL) increases as ventricular fibrillation (VF) progresses., Objective: 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., Methods: 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., Results: 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., Conclusion: 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.

Ventricular fibrillation (VF), despite its declining incidence as a cause of sudden cardiac death, is still a major health problem. The underlying mechanisms for the maintenance of VF are still disputed. Studies suggest that VF is unlikely one static mechanism but rather a dynamic process of electrical derangement that changes with duration. The 2 principal proposed mechanisms of VF are multiple wavelets and mother rotors. Most studies of these proposed mechanisms for VF maintenance have been during the first minute of VF. However, the time to external defibrillation in the community and pre-hospital settings, where the majority of sudden cardiac death occurs, ranges from 4 to 10 min and the time to defibrillation seems crucial because the odds of survival worsen with delay. Recent studies during the first 10 min of VF suggest that Purkinje fibers are important in maintaining VF after the first 1 to 2 min, either as a part of a reentrant circuit or as a source of focal activations.

Background: Knowledge of the shock potential gradient (nablaV) and postshock activation is limited to internal defibrillation of short-duration ventricular fibrillation (SDVF)., Objective: The purpose of this study was to determine these variables after external defibrillation of long-duration VF (LDVF)., Methods: In six pigs, 115-20 plunge needles with three to six electrodes each were inserted to record throughout both ventricles. After the chest was closed, the biphasic defibrillation threshold (DFT) was determined after 20 seconds of SDVF with external defibrillation pads. After 7 minutes of LDVF, defibrillation shocks that were less than or equal to the SDVF DFT strength were given., Results: For DFT shocks (1632 +/- 429 V), the maximum minus minimum ventricular voltage (160 +/- 100 V) was 9.8% of the shock voltage. Maximum cardiac nablaV (28.7 +/- 17 V/cm) was 4.7 +/- 2.0 times the minimum nablaV (6.2 +/- 3.5 V/cm). Although LDVF did not increase the DFT in five of the six pigs, it significantly lengthened the time to earliest postshock activation following defibrillation (1.6 +/- 2.2 seconds for SDVF and 4.9 +/- 4.3 seconds for LDVF). After LDVF, 1.3 +/- 0.8 episodes of spontaneous refibrillation occurred per animal, but there was no refibrillation after SDVF., Conclusion: Compared with previous studies of internal defibrillation, during external defibrillation much less of the shock voltage appears across the heart and the shock field is much more even; however, the minimum nablaV is similar. Compared with external defibrillation of SDVF, the biphasic external DFT for LDVF is not increased; however, time to earliest postshock activation triples. Refibrillation is common after LDVF but not after SDVF in these normal hearts, indicating that LDVF by itself can cause refibrillation without requiring preexisting heart disease.

Background: Measurements of intramural membrane potential (Vm) would greatly increase knowledge of cardiac arrhythmias and defibrillation. Optrodes offer the possibility for three-dimensional Vm mapping, but their signal quality has been inadequate., Objective: The purpose of this work was to improve optrode signal quality and use optrodes to measure intramural distribution of action potentials and shock-induced Vm changes in porcine hearts., Methods: Optrodes were made from seven optical fibers 225 or 325 microm in diameter. Fiber ends were polished at a 45 degrees angle, which improved light collection and allowed their insertion without a needle. Fluorescent measurements were performed in isolated porcine hearts perfused with Tyrode's solution or blood using Vm-sensitive dye RH-237 and a 200-W Hg/Xe lamp., Results: The signal-to-noise ratio for 325-microm fibers was 44 +/- 23 in blood-perfused hearts (n = 5) and 106 +/- 45 in Tyrode's-perfused hearts (n = 3), which represents an approximately four-fold improvement over previously reported data. There was close correspondence between optical and electrical measurements of activation times and action potential duration (APD). No significant intramural APD gradients were observed at cycle lengths up to 4 s and in the presence of dofetilide or d-sotalol. Application of shocks (5-50 V/cm) produced large intramural Vm changes (up to approximately 200% action potential amplitude), possibly reflecting a combined effect of tissue discontinuities and optrode geometry., Conclusions: A substantial improvement of optrode signal quality was achieved. Optical measurements of APD and activation times matched electrical measurements. Optrode measurements revealed no significant intramural APD gradients. Application of shocks caused large intramural Vm changes that could be influenced by the optrode geometry.

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.

I am deeply grateful and honored to receive the 2006 Distinguished Scientist Award from the Heart Rhythm Society. Many outstanding individuals have received this award since it was established in 1982, and it is humbling to realize that my small feet are walking in the footsteps of these giants. I would be remiss if I did not thank the numerous colleagues, fellows, and students who performed most of the work leading to the papers of which I am a coauthor.

Intravascular ventricular defibrillation and intravascular atrial defibrillation have many similarities. An important factor influencing the outcome of the shock is the potential gradient field created throughout the ventricles or the atria by the shock. A minimum potential gradient is required throughout the ventricles and probably the atria in order to defibrillate. The value of this minimum potential gradient is affected by several factors, including the duration, tilt, and number of phases of the waveform. For shock strengths near the defibrillation threshold, earliest activation following failed shocks arises in a region in which the potential gradient is low. The defibrillation threshold energy can be decreased by adding a third and even a fourth defibrillation electrode in regions where the shock potential gradient is low for the shock field created by the first two defibrillation electrodes and giving two sequential shocks, each through a different set of electrodes. However, the addition of more electrodes and sequential shocks complicates both the device and its implantation. Because patients are conscious when the atrial defibrillation shock is given, they experience pain during the shock, which is one of the main drawbacks of intravascular atrial defibrillation. Unfortunately, the pain threshold for defibrillation shocks is so low that a shock less than 1 J is uncomfortable and is not much less painful than shocks several times stronger. Therefore, even though electrode configurations exist that have lower atrial defibrillation threshold energy requirements than the atrial defibrillation threshold with standard defibrillation electrode configurations used in implantable cardioverter-defibrillators (ICDs) for ventricular defibrillation, they are not clinically practical because their shocks are almost as painful as with the standard ICD electrode configurations. Such electrode configurations would make the ICD more complicated, leading to greater difficulty and longer time required for implantation.

Background: Acute pericardial tamponade is a life-threatening complication of invasive cardiovascular procedures. Survival depends on early recognition and treatment. A diagnostic test to detect pericardial fluid accumulation before a significant fall in blood pressure and without contamination of the sterile field would be valuable., Objective: We tested the hypothesis that fluoroscopic excursion of the cardiac silhouette decreases early in the course of acute pericardial tamponade and precedes hemodynamic compromise., Methods: The pericardial space of seven pigs was accessed by a sub-xiphoid puncture. Tamponade was produced by intrapericardial saline infusion at 20-25 mL/minute until the pericardial pressure equalized with right ventricular end diastolic pressure or the systolic blood pressure reached 40 mmHg. Supine fluoroscopic images were obtained every 2 minutes in the left anterior oblique view with simultaneous echocardiography. The fluoroscopic heart silhouette was digitized, and the maximum excursion during the cardiac cycle was quantified by custom software. The qualitative excursion of the fluoroscopic heart silhouette on randomly selected video images was also graded by two independent observers who were blinded to the time course of the experiment and the hemodynamics., Results: During progressive pericardial fluid accumulation, the cardiac silhouette excursion quantified by the custom software (p < 0.001) and by video rating (p < 0.0001) was significantly reduced within 2 minutes. A statistically significant fall in blood pressure compared with baseline did not occur until 6 minutes (89 +/- 21 vs. 121 +/- 15 mmHg, p < 0.001). The interobserver agreement was very close, with a kappa statistic of 0.78. The reduction in cardiac silhouette excursion was apparent as soon as the effusion was detected by echocardiography., Conclusion: Cardiac silhouette excursion becomes reduced early in the course of acute pericardial fluid accumulation. This fluoroscopic observation can be used to detect impending pericardial tamponade before hemodynamic collapse.

Background: A single stationary mother rotor has been hypothesized to be responsible for maintenance of ventricular fibrillation (VF) in the guinea pig. Previous studies have pointed to the ventricular septum as a possible location for a mother rotor in the pig heart., Objectives: The purpose of this study was to test the hypothesis that a mother rotor is located in the septum., Methods: In seven open-chest pigs, we mapped the first 20 seconds of electrically induced VF simultaneously from the posterior left ventricle (LV) and right side of the septum with two electrical arrays. Each array contained 504 electrodes (21 x 24) spaced 2 mm apart in the LV and 1.5 mm apart in the septum., Results: The percentage of VF wavefronts that formed reentrant circuits was significantly lower in the septum (1% +/- 1% [mean +/- SD]) than in the LV (2% +/- 1%). The peak frequency during VF also was significantly smaller in the septum (8.6 Hz +/- 3.0 Hz) than in the LV (10.4 Hz +/- 3.4 Hz). The mean direction of spread of activation of VF wavefronts was away from the region where the posterior LV free wall intersects the posterior septum in both the LV and septum., Conclusions: The lower incidence of reentry and lower peak frequency in the mapped region of the septum than in the LV indicate that a mother rotor is not present in swine on the RV side of the septum. The mean directions of the VF activation sequences in the LV and septum suggest that if a mother rotor is present during the first 20 seconds of VF, it exists where the posterior LV free wall joins the septum, the region where the posterior papillary muscle inserts.

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.

Objective: The objective of this study was to test the hypothesis that on the epicardium of the in vivo human heart, ventricular fibrillation (VF) consists of chaotic small wavefronts that constantly change paths., Background: Despite the significance of VF to cardiovascular mortality, little is known about the wavefronts that constitute VF in humans., Methods: In 9 patients undergoing cardiac surgery, a single VF episode was induced by rapid pacing immediately after institution of cardiopulmonary bypass while recordings were made from 504 electrodes spaced 2 mm apart in a 20 cm(2) plaque held against the anterior left ventricle epicardium. A total of 26 segments of VF, each 2 s long, were analyzed. A computer algorithm identified individual wavefronts and classified them into groups that followed similar activation sequences., Results: The mean activation rate was 5.8 +/- 1.8 (mean +/- SD) cycles/s. The wavefronts during each epoch were grouped into 9.4 +/- 7.1 different activation pathways, and 8.3 +/- 2.3 wavefronts followed each pathway. Individual wavefronts spread to activate an area of 5.1 +/- 3.0 cm(2) in the mapped region. The majority of the wavefronts propagated into the mapped region and/or propagated out of the mapped region into adjacent tissue, suggesting that the wavefronts were larger than 5.1 cm(2). Reentry was identified in only 16 of the 26 (62%) 2-s segments, always completed <2 cycles, and lasted for 9.5 +/- 6.6% of these 16 epochs, which is 5.8% of the total duration of all the segments analyzed., Conclusion: VF wavefronts on the human epicardium are usually large, repeatedly follow distinct pathways, and only occasionally reenter. If these results for the left ventricular epicardium are representative of those for the entire ventricular mass, they do not support the hypothesis that human VF consists of small, constantly changing wavefronts, but rather suggest that there is significant organization of human VF.