Epicardial wavefronts arise from widely distributed transient sources during ventricular fibrillation in the isolated swine heart.

It has been proposed that VF waves emanate from stable localized sources, often called "mother rotors." However, evidence for the existence of these rotors is conflicting. Using a new panoramic optical mapping system that can image nearly the entire ventricular epicardium, we recently excluded epicardial mother rotors as the drivers of Wiggers' stage II VF in the isolated swine heart. Furthermore, we were unable to find evidence that VF requires sustained intramural sources. The present study was designed to test the following hypotheses: 1. VF is driven by a specific region, and 2. Rotors that are long-lived, though not necessarily permanent, are the primary generators of VF wavefronts. Using panoramic optical mapping, we mapped VF wavefronts from 6 isolated swine hearts. Wavefronts were tracked to characterize their activation pathways and to locate their originating sources. We found that the wavefronts that participate in epicardial reentry were not confined to a compact region; rather they activated the entire epicardial surface. New wavefronts feeding into the epicardial activation pattern were generated over the majority of the epicardium and almost all of them were associated with rotors or repetitive breakthrough patterns that lasted for less than 2 s. These findings indicate that epicardial wavefronts in this model are generated by many transitory epicardial sources distributed over the entire surface of the heart.

Comparison of the temperature profile and pathological effect at unipolar, bipolar and phased radiofrequency current configurations.

With a multi-electrode catheter, phased radiofrequency (RF) delivers current between each electrode and a backplate as well as between adjacent electrodes. This study compared the tissue heating and lesion dimensions created by phased and standard RF. Ablation was performed on the in vivo thigh muscles in 5 pigs. Six lesions were created on each thigh muscle using phase angle 0 degrees RF, 127 degrees RF, 180 degrees RF with and without a backplate, and standard RF in bipolar and sequential unipolar configurations. Two plunge needles, each with 6 thermocouples 1 mm apart, were inserted into the tissue with one needle beside an electrode and the other midway between electrodes for tissue temperature measurement. The 0 degrees RF created lower tissue temperatures and smaller lesions between electrodes than those beside electrode. With 127 degrees and 180 degrees RF, tissue temperature and lesion dimensions between electrodes were similar to beside electrode, while the 127 degrees RF created higher tissue temperature and deeper lesions than 180 degrees RF (both with and without a backplate) at both sites. Standard RF bipolar ablation created similar tissue temperatures and lesion depths at both sites, but required greater power than the 127 degrees RF. Standard RF sequential unipolar ablation created only a slight temperature increase and no lesions between electrodes 3 and 4. As judged by tissue temperature, lesion depth and uniformity, and RF power requirement, 127 degrees RF may be a better energy configuration for linear ablation than the other RF modalities tested.

Atrial defibrillation thresholds of electrode configurations available to an atrioventricular defibrillator.

INTRODUCTION: Little investigation has been conducted to assess the atrial defibrillation thresholds of electrode configurations using electrodes designed for internal ventricular defibrillation (right ventricle [RV], superior vena cava [SVC], and pulse generator housing [Can]) combined with coronary sinus (CS) electrodes. We hypothesized that a CS-->SVC+Can electrode configuration would have a lower atrial defibrillation threshold than a standard configuration for defibrillation, RV-->SVC+Can. We also tested the atrial defibrillation thresholds of five other configurations. METHODS AND RESULTS: In 12 closed chest sheep, we situated a two-coil (RV, SVC) defibrillation catheter, a left-pectoral subcutaneous Can, and a CS lead. Atrial fibrillation was burst induced and maintained with continuous infusion of intrapericardial acetyl-beta-methylcholine chloride. Using fixed-tilt biphasic shocks, we determined the atrial defibrillation thresholds of seven test configurations in random order according to a multiple-reversal protocol. The peak voltage and delivered energy atrial defibrillation thresholds of CS-->SVC+Can (168+/-67 V, 2.68+/-2.40 J) were significantly lower than those of RV-->SVC+Can (215+/-88 V, 4.46+/-3.40 J). The atrial defibrillation thresholds of the other test configurations were RV+CS-->SVC+Can: 146+/-59 V, 1.92+/-1.45 J; RV-->CS+SVC+Can: 191+/-89 V, 3.53+/-3.19 J; CS-->SVC: 188+/-98 V, 3.77+/-4.14 J; SVC-->CS+ Can: 265+/-145 V, 7.37+/-9.12 J; and SVC-->Can: 516+/-209 V, 24.5+/-15.0 J. CONCLUSIONS: The atrial defibrillation threshold of CS-->SVC+Can is significantly lower than that of RV-->SVC+Can. In addition, the low atrial defibrillation threshold of RV+CS-->SVC+Can merits further investigation. Based on corroboration of low atrial defibrillation thresholds of CS-based configurations in humans, physicians might consider using CS leads with atrioventricular defibrillators.

Right atrial septal electrode for reducing the atrial defibrillation threshold.

BACKGROUND: The atrial defibrillation threshold (ADFT) energy of the standard lead configuration, right atrial appendage (RAA) to coronary sinus (CS), was reduced by >50% with the addition of a third electrode traversing the atrial septum in a previous study. This study determined whether the ADFT would be lowered by a more clinically practical third electrode placed in the right atrium along the atrial septum (RSP). METHODS AND RESULTS: Sustained atrial fibrillation was induced in 8 closed-chest sheep with burst pacing and maintained with pericardial infusion of acetyl-beta-methylcholine chloride. A custom-made, dual-defibrillation catheter was placed with electrodes in the lateral RA, CS, and RSP. A separate defibrillation catheter was also placed in the RAA. ADFT characteristics of RAA-->CS and 6 other single- or sequential-shock configurations were determined in random order by using biphasic, truncated-exponential waveforms in a multiple-reversal protocol. The delivered-energy, peak-voltage, and peak-current ADFTs for the sequential-shock configuration CS-->RSP/RA-->RSP (0.53+/-0.31 J, 86+/-22 V, and 1.6+/-0.6 A, respectively) were significantly lower than those of RAA-->CS (1.14+/-0.64 J, 157+/-34 V, and 2.5+/-1.1 A, respectively). The ADFT characteristics of RAA-->CS and RA-->CS were not significantly different, nor were those of CS-->RSP/RA-->RSP and CS-->RSP/RAA--> RSP. CONCLUSIONS: The ADFT of the standard RAA-->CS configuration may be markedly reduced with an additional electrode situated at the RSP.

Improvement of defibrillation efficacy and quantification of activation patterns during ventricular fibrillation in a canine heart failure model.

BACKGROUND: Little is known about the effects of heart failure (HF) on the defibrillation threshold (DFT) and the characteristics of activation during ventricular fibrillation (VF). METHODS AND RESULTS: HF was induced by rapid right ventricular (RV) pacing for at least 3 weeks in 6 dogs. Another 6 dogs served as controls. Catheter defibrillation electrodes were placed in the RV apex, the superior vena cava, and the great cardiac vein (CV). An active can coupled to the superior vena cava electrode served as the return for the RV and CV electrodes. DFTs were determined before and during HF for a shock through the RV electrode with and without a smaller auxiliary shock through the CV electrode. VF activation patterns were recorded in HF and control animals from 21x24 unipolar electrodes spaced 2 mm apart on the ventricular epicardium. Using these recordings, we computed a number of quantitative VF descriptors. DFT was unchanged in the control dogs. DFT energy was increased 79% and 180% (with and without auxiliary shock, respectively) in HF compared with control dogs. During but not before HF, DFT energy was significantly lowered (21%) by addition of the auxiliary shock. The VF descriptors revealed marked VF differences between HF and control dogs. The differences suggest decreased excitability and an increased refractory period during HF. Most, but not all, descriptors indicate that VF was less complex during HF, suggesting that VF complexity is multifactorial and cannot be expressed by a scalar quantity. CONCLUSIONS: HF increases the DFT. This is partially reversed by an auxiliary shock. HF markedly changes VF activation patterns.

Pacing during ventricular fibrillation: factors influencing the ability to capture.

INTRODUCTION: Recent studies showed that pacing atrial and ventricular fibrillation (VF) is possible. The studies presented here determined which parameters influence the efficacy of a pacing train to capture fibrillating ventricular myocardium. Electrode type, current strength, order of pacing trains, polarity, and VF morphology preceding the pacing trains were investigated. METHODS AND RESULTS: A 504-electrode recording plaque sutured to the right ventricle of pig hearts was used to record the activations of VF and those resulting from the pacing stimulation. Capture of VF by pacing was determined by observing an animated display of the first temporal derivative of the electrograms. A series of electrodes in a line captured the heart more frequently during VF than did a point electrode. Increasing the current strength to 10 x diastolic pacing threshold increased the incidence of capture, but increasing this strength further did not. The second or third train of 40 stimuli had greater capture rates than did the first train during the same VF episode. Anodal and cathodal unipolar, and bipolar stimulation were equally efficacious in capturing VF. VF activation during the 1-second interval preceding pacing was more organized for pacing trains that captured than those that did not. The highest incidence of capture, 46% to 61% of pacing trains, occurred with a line of electrodes at 10 x diastolic pacing threshold delivered by the second or third train. CONCLUSION: The probability of a pacing train capturing fibrillating myocardium can be influenced by the pacing protocol parameters.

Reduction of atrial defibrillation threshold with an interatrial septal electrode.

BACKGROUND: The standard lead configuration for internal atrial defibrillation consists of a shock between electrodes in the right atrial appendage (RAA) and coronary sinus (CS). We tested the hypothesis that the atrial defibrillation threshold (ADFT) of this RAA-->CS configuration would be lowered with use of an additional electrode at the atrial septum (SP). METHODS AND RESULTS: Sustained atrial fibrillation was induced in 8 closed-chest sheep with burst pacing and continuous pericardial infusion of acetyl-ss-methylcholine. Defibrillation electrodes were situated in the RAA, CS, pulmonary artery (PA), low right atrium (LRA), and across the SP. ADFTs of RAA-->CS and 4 other lead configurations were determined in random order by use of a multiple-reversal protocol. Biphasic waveforms of 3/1-ms duration were used for all single and sequential shocks. The ADFT delivered energies for the single-shock configurations were 1.27+/-0.67 J for RAA-->CS and 0. 86+/-0.59 J for RAA+CS-->SP; the ADFTs for the sequential-shock configurations were 0.39+/-0.18 J for RAA-->SP/CS-->SP, 1.16+/-0.72 J for CS-->SP/RAA-->SP, and 0.68+/-0.46 J for RAA-->CS/LRA-->PA. Except for CS-->SP/RAA-->SP versus RAA-->CS and RAA-->CS/LRA-->PA versus RAA+CS-->SP, the ADFT delivered energies of all of the configurations were significantly different from each other (P:<0. 05). CONCLUSIONS: The ADFT of the standard RAA-->CS configuration is markedly reduced with an additional electrode at the atrial SP.

A telemetry system for the study of spontaneous cardiac arrhythmias.

The characteristics of spontaneous cardiac arrhythmias leading to sudden cardiac death are largely unknown. To study arrhythmias in animal models, an eight-channel implantable radio telemetry system has been developed to record continuously cardiac electrograms over a period of weeks to months, with maintenance restricted to changing batteries. The inputs are connected in a unipolar manner. Each channel has a gain of fifty and is AC coupled, band limited to 0.07-260 Hz. The signals are digitized with 12 bits resolution at 1000 samples/s. The amplifiers, analog-to-digital converter, and control logic are packaged in an implantable unit. An umbilical cable is passed through the skin to an external backpack unit for power and data transmission. A custom serial interface card, a PC/104 form factor 25-MHz 80386-based single-board computer with a PCMCIA wireless local area network (WLAN) card, and battery power supply make up the backpack. Data are read into the parallel port of the computer, buffered, then transmitted over the WLAN to the laboratory network where it can be analyzed and archived. Approximately 12 h of 14,000 bytes/s data can be collected with each set of batteries. The system is suitable for continuous monitoring of animal models of spontaneous arrhythmias and sudden cardiac death.

Three-dimensional mapping of spontaneous ventricular arrhythmias in a canine thrombotic coronary occlusion model.

INTRODUCTION: Ventricular tachycardia (VT) and ventricular fibrillation (VF) induced by thrombotic coronary occlusion were mapped in three dimensions in ten dogs. METHODS AND RESULTS: Thrombotic occlusion was induced using a wire to deliver current to the proximal left circumflex artery (LCX). In nine dogs, nonsustained VT (NSVT) arose from numerous focal sites. Sustained VT was initiated in six dogs (VT group) by a focus near or in the ischemic region. VT was maintained by a focus in the ischemic border in three dogs and by macroreentry that involved both the ischemic and nonischemic regions in the other three dogs. In five dogs, VT degenerated into VF due to intramural reentry in different locations. Mean total activation time (AT), the time for activation to traverse the ventricles, for a sinus beat when LCX current was first applied was 40 +/- 4 msec. In the four dogs in which VT occurred 3 to 7 minutes after total occlusion, sinus AT increased to 98 to 146 msec just before VT. Sinus AT in the four dogs without VT was always <98 msec. Mean AT of the first ten cycles of VT was significantly longer in those VTs that degenerated into VF (169 +/- 29 msec) than in those that did not (81 +/- 12 msec). CONCLUSION: Thrombotic LCX occlusion induced NSVT in 90%, VT in 60%, and VF in 50% of dogs. Focal mechanisms caused most NSVTs and VT initiation. VT was maintained by a focus near or in the ischemic region or by macroreentry involving both the ischemic and nonischemic regions. AT identified animals in which VT occurred soon after LCX occlusion and in which VT progressed to VF.

Estimation of 3-D conduction velocity vector fields from cardiac mapping data.

A method to estimate three-dimensional (3-D) conduction velocity vector fields in cardiac tissue is presented. The speed and direction of propagation are found from polynomial "surfaces" fitted to space-time (x, y, z, t) coordinates of cardiac activity. The technique is applied to sinus rhythm and paced rhythm mapped with plunge needles at 396-466 sites in the canine myocardium. The method was validated on simulated 3-D plane and spherical waves. For simulated data, conduction velocities were estimated with an accuracy of 1%-2%. In experimental data, estimates of conduction speeds during paced rhythm were slower than those found during normal sinus rhythm. Vector directions were also found to differ between different types of beats. The technique was able to distinguish between premature ventricular contractions and sinus beats and between sinus and paced beats. The proposed approach to computing velocity vector fields provides an automated, physiological, and quantitative description of local electrical activity in 3-D tissue. This method may provide insight into abnormal conduction associated with fatal ventricular arrhythmias.

Continuous telemetry from a chronic canine model of sudden cardiac death.

INTRODUCTION: We sought to develop a continuously telemetered animal model of sudden cardiac death (SCD) to study the role of existing infarcts and acute ischemia in fatal arrhythmias. METHODS AND RESULTS: A telemetry system capable of recording eight channels of electrophysiologic data continuously and chronically has been developed. To demonstrate the use of this technology in an animal model of sudden death, 12 anesthetized dogs were instrumented with eight electrodes located in endocardium of the right side of the heart, epicardium of the left ventricle (LV), or in the subcutaneous tissues. The left anterior descending (LAD) coronary artery was occluded for 90 minutes and reperfused to produce LV infarction. A copper wire was placed in the left circumflex (LCX) coronary artery to cause intimal injury in a second arterial bed. The telemetry unit recorded deaths in seven animals between 19 to 64 hours after surgery. Five animals that did not experience SCD by the fifth postoperative day served as controls. There were three modes of SCD: complex ventricular ectopy that degenerated into ventricular fibrillation (VF, n = 4); normal sinus rhythm that suddenly degenerated into VF (n = 1); and bradycardia (RR intervals >1,000 msec) that lasted >3 minutes and preceded VF (n = 2). ST segment changes were significantly greater in the LCX-bed electrograms for tachyarrhythmic compared to bradyarrhythmic deaths (mean +/- SD; 4.0 +/- 3.4 mV and 0.2 +/- 0.8 mV, respectively). Fast Fourier transform showed the peak frequency of VF 10 seconds after onset was significantly higher in the five dogs with initial tachyarrhythmias compared with the VF that followed profound bradycardia (6.5 +/- 3.1 Hz and 3.7 +/- 0.6 Hz, respectively). Computer-assisted planimetry of postmortem heart slices revealed that infarcts in the two dogs with bradycardic events were larger (19.7% +/- 2.2% of the LV and septal mass) than in the five dogs with tachyarrhythmias (7.7% +/- 2.4%) or in the five control dogs (11.9% +/- 8.1%). CONCLUSION: It is possible to record via telemetry the events leading to SCD in an animal model. Continuous telemetry monitoring demonstrated that both tachyarrhythmias and bradyarrhythmias ultimately resulted in VF in an animal model of SCD. Animals with tachyarrhythmic deaths had greate ischemia in the LCX bed, smaller preexisting infarcts, and higher VF peak frequency than animals with bradyarrhythmic deaths.

Effect of altering the left ventricular pressure on epicardial activation time in dogs with and without pacing-induced heart failure.

BACKGROUND: The influence of an increased left ventricular end-diastolic pressure (LVEDP) on the development of lethal arrhythmias in chronic heart failure is unclear. We investigated the effect of chronic and acute LVEDP increase on the epicardial activation time of sinus (SB) and paced (PB) beats. METHODS: Six dogs underwent rapid ventricular pacing at 220-280[emsp4 ]beats/min for 6-14 weeks for induction of heart failure. On the study day, baseline (ba) LVEDP was determined for the surviving heart failure animals (HF-ba), and for seven control animals (C-ba). The epicardial activation time (EAT, time between the earliest and latest epicardial activation) for five consecutive SB and five ventricular PB during the baseline hemodynamic state were recorded using a 504 electrode mapping-sock. In the control animals a 2-litre volume (vl) was infused over 10[emsp4 ]min to acutely increase the LVEDP (C-vl) to a level comparable to the chronic increased LVEDP of the HF-ba. The same volume challenge was performed in two HF animals (HF-vl) and the EAT for SB and PB was redetermined. RESULTS: Three of six HF animals died during induction of heart failure. In the three remaining HF animals, chronic LVEDP increased from 6+/-1 to 17+/-10.8[emsp4 ]mmHg (P=0.07), EAT for SB increased by 68 % compared to control animals (HF-ba vs. C-ba, P<0.05). In contrast, in the control animals the acute rise in LVEDP from 6.8+/-4.5 to 14.7+/-6.2 mmHg P<0.05), shortened the EAT for SB (C-ba vs. C-vl, P<0.05). A similar decrease in EAT for SB caused by acute volume load was seen in the HF animals, but did not reach significance due to the small sample size (one of the three remaining HF animals died of spontaneous ventricular fibrillation before the volume load). Chronic LVEDP elevation significantly prolonged the EAT for PB from 72+/-11 to 120+/-31[emsp4 ]ms (C-ba vs. HF-ba) while acute LVEDP increase had no significant effect on EAT for PB. CONCLUSION: Chronic HF increases LVEDP and prolongs EAT, while an acute increase in LVEDP shortens the EAT for sinus beats. A prolongation of EAT in heart failure may make the heart more susceptible to ventricular arrhythmias and electromechanical dissociation.

Electrode impedance: an indicator of electrode-tissue contact and lesion dimensions during linear ablation.

Pre-ablation impedance was evaluated for its ability to detect electrode-tissue contact and allow creation of long uniform linear lesions with a multi-electrode ablation catheter. The study consisted of 2 parts, both of which used the in vivopig thigh muscle model. In part 1, a 7 Fr. multi-electrode catheter was held in 3 electrode-tissue contact conditions: (1) non-contact; (2) light contact with a 30g downward force; and (3) tight contact with a 90g downward force. Impedances were measured in unipolar, modified unipolar and bipolar configurations using a source with frequencies from 100Hz to 500kHz. Compared with non-contact, the impedance increased 35 +/- 22 % with 30g contact pressure and 68 +/- 40% when the contact pressure was increased to 90g across the range of frequencies studied. In part 2, the same catheter was held against the tissue with different forces. Pre-ablation impedance was measured using a 10kHz current. Phased radiofrequency energy was applied to the 5 electrodes simultaneously using 10W power at each electrode for 120s. A total of 32 linear lesions were created. The lesion dimensions correlated with pre-ablation impedance. A unipolar impedance > or = 190 Omega indicates 95% possibility to create a uniform linear lesion of at least 3mm depth with our ablation system. We conclude that pre-ablation impedance may be a useful indicator for predicting electrode-tissue contact and the ability to create a continuous and transmural linear lesion with a multi-electrode catheter.

Novel methods to evaluate controlled reperfusion techniques in cardiac surgery.

BACKGROUND: This manuscript describes two novel techniques that may be useful for comparing methods to reperfuse the heart during cardiac operations. These techniques are based on measurements of intra-myocyte ion content and the analysis of reperfusion arrhythmias. METHODS: Myocyte ion content was measured in normal porcine hearts before and after ischemia (cardioplegic arrest, CP arrest) using atomic absorption spectroscopy. A cobalt-EDTA complex served as the extra-cellular marker. Cobalt-EDTA was infused into the aorta together with blood or cardioplegia (CP) solution. Myocardial biopsies were taken prior to CP arrest and upon successful defibrillation 5 min after initiating reperfusion. Ventricular fibrillation (VF) was recorded prior to ischemia, and then during reperfusion. VF wavefront (WF) morphology and propagation patterns were analyzed using computer algorithms. Electrophysiologic variables for measuring VF included the multiplicity index (a descriptor of VF organization), the number of WFs detected (nwaves/s) and the mean peak first derivative of electrogram voltage with respect to time (mp d V/dt). RESULTS: Intra-cellular sodium content increased, while intra-cellular magnesium content decreased between control and reperfusion measurements (p < 0.05). Electrophysiologic recovery was characterized by increasingly rapid depolarization (i.e. more negative mp d V/dt) and an increasing nwaves/s during the first minute of post-CP reperfusion. CONCLUSIONS: Atomic absorption spectroscopy and computer-based analysis of reperfusion VF successfully measured metabolic and electrophysiologic events that occurred during controlled reperfusion. These methods may be useful for comparing controlled reperfusion techniques.

High-resolution mapping and histologic examination of long radiofrequency lesions in canine atria.

INTRODUCTION: Catheter ablation may prevent conduction of multiple atrial wavefronts and/or reduce the critical mass of atrial myocardium required to sustain fibrillation. The purpose of this study was to examine the effect of radiofrequency (RF) energy application on conduction in canine atria by performing high-density epicardial mapping and careful histologic examination of the ablation zone. METHODS AND RESULTS: RF energy was applied to the right atrial endocardium in nine anesthetized mongrel dogs in an attempt to create a line of conduction block spanning the vertical length of a 504-channel epicardial mapping plaque. The mean length and width of the histologically determined ablation zone was 34 +/- 4 and 7.3 +/- 2.6 mm, respectively. No thrombus was present. Conduction block that spanned the mapping plaque in 6 of 9 animals was matched histologically by continuous transmural necrosis in five. In one, only a portion of the ablation zone was transmural; the remainder was wide but nontransmural. In 2 of 3 animals with conduction, a narrow region was present where continuous transmural necrosis was absent. In the other animal, conduction was present despite continuous transmural necrosis. CONCLUSION: Conduction block usually occurred when continuous transmural necrosis was present, and conduction usually persisted when continuous transmural necrosis was absent. However, important exceptions were observed, including block when the ablation zone was wide but nontransmural, and conduction despite a thin line of continuous transmural necrosis.

Predicting the relative efficacy of shock waveforms for transthoracic defibrillation in dogs.

STUDY OBJECTIVE: Previous work has shown that a passive membrane model using a parallel resistor-capacitor circuit is capable of predicting optimal waveforms for transvenous defibrillation. This study tested the ability of that model to predict optimal waveforms for transthoracic defibrillation. METHODS: This study was divided into 3 parts, each of which determined transthoracic defibrillation thresholds (DFTs) in 6 dogs for several different waveform shapes and durations. For each part, strength-duration relationships were determined from both experimental and model data and then compared with test model predictions. Part 1 DFTs were determined at various durations for 3 different monophasic waveforms-the ascending ramp, descending ramp, and square waveform. Part 2 DFTs were determined for 3 biphasic waveforms. Phase 1 was a 30-ms ascending ramp, and phase 2 was an ascending ramp, a descending ramp, or a square waveform. Part 3 DFTs were determined for 3 biphasic waveforms with very short second-phase durations. Phase 1 was a 30-ms ascending ramp, and phase 2 was a descending ramp. RESULTS: For part 1, the model was able to predict the relative defibrillation efficacy of the 3 monophasic waveforms ( P < .05). For parts 2 and 3, the model was able to predict the biphasic waveforms with the lowest DFTs. These predictions were based on the criterion that the model response at the end of the second phase should return to or slightly pass the model response value at the beginning of the first phase. CONCLUSION: The resistor-capacitor model successfully predicted the relative defibrillation efficacy of several different waveforms delivered transthoracically.

Inducibility of sustained ventricular tachycardia in a closed-chest ovine model of myocardial infarction.

The two goals of this study were (1) to develop a closed-chest animal model of monomorphic ventricular tachycardia; and (2) to investigate the effect of dual site pacing on inducibility of ventricular tachycardia. In the first part of the study, 10 of 14 sheep underwent successful induction of myocardial infarction by temporary balloon occlusion of the left anterior descending coronary artery. After a follow-up period of 21-43 days, sustained monomorphic ventricular tachycardia could be induced during programmed electrical stimulation using a "clinical" stimulation protocol in 8 of the 10 sheep. The number of ventricular tachycardia episodes per animal varied between 5 and 70. Ventricular fibrillation was never induced during programmed electrical stimulation. Ventricular tachycardia episodes lasted from 30 seconds up to 15 minutes and were terminated by antitachycardia pacing or DC cardioversion. In the second part of the study, the effect of dual site stimulation on ventricular tachycardia inducibility was investigated. High current stimuli from an area within the infarcted zone were given with the S1 programmed stimulation protocol. This dual site stimulation showed no effect on ventricular tachycardia induction during programmed electrical stimulation. This animal model shows a high induction rate of sustained monomorphic ventricular tachycardia in the chronic phase of myocardial infarction. The high incidence of ventricular tachycardia inducibility provides a reliable tool to study new techniques for the prevention of ventricular tachyarrhythmias.

The influence of ventricular fibrillation duration on defibrillation efficacy using biphasic waveforms in humans.

OBJECTIVES: The purpose of this study was to prospectively investigate the influence of ventricular fibrillation (VF) durations of 5, 10 and 20 s on the defibrillation threshold (DFT) during implantable cardioverter-defibrillator (ICD) implantation. BACKGROUND: Although the DFT using monophasic waveforms has been shown to increase with VF duration in humans, the effect of VF duration on defibrillation efficacy using biphasic waveforms in humans is not known. METHODS: Thirty patients undergoing primary ICD implantation or pulse generator replacement were randomly assigned to have the DFT determined using biphasic shocks at two durations of VF each (5 and 10 s, 10 and 20 s or 5 and 20 s). RESULTS: There was no statistically significant difference in the mean DFT comparing VF durations of 5 s (9.5+/-6.0 J) and 10 s (10.8+/-7.0 J) (p=0.4). The mean DFT significantly increased from 10.9+/-6.1 J at 10 s of VF to 12.6+/-5.6 J (p=0.03) at 20 s of VF, and from 7.0+/-3.5 J at 5 s of VF to 10.5+/-6.3 J (p=0.04) at 20 s of VF. An increase in the DFT was observed in 14 patients as VF duration increased. There were no clinical characteristics that differentiated patients with and without an increase in the DFT. CONCLUSIONS: Defibrillation efficacy decreases with increasing VF duration using biphasic waveforms in humans. Ventricular fibrillation durations greater than 10 s may negatively affect the effectiveness of ICD therapy.