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.

Relative efficacy of monophasic and biphasic waveforms for transthoracic defibrillation after short and long durations of ventricular fibrillation.

BACKGROUND: Recently, interest has arisen in using biphasic waveforms for external defibrillation. Little work has been done, however, in measuring transthoracic defibrillation efficacy after long periods of ventricular fibrillation. In protocol 1, we compared the efficacy of a quasi-sinusoidal biphasic waveform (QSBW), a truncated exponential biphasic waveform (TEBW), and a critically damped sinusoidal monophasic waveform (CDSMW) after 15 seconds of fibrillation. In protocol 2, we compared the efficacy of the more efficacious biphasic waveform from protocol 1, QSBW, with CDSMW after 15 seconds and 5 minutes of fibrillation. METHODS AND RESULTS: In protocol 1, 50% success levels, ED50, were measured after 15 seconds of fibrillation for the 3 waveforms in 6 dogs. In protocol 2, defibrillation thresholds were measured for QSBW and CDSMW after 15 seconds of fibrillation and after 3 minutes of unsupported fibrillation followed by 2 minutes of fibrillation with femoral-femoral cross-circulation. In protocol 1, QSBW had a lower ED50, 16.0+/-4.9 J, than TEBW, 20.3+/-4.4 J, or CDSMW, 27.4+/-6.0 J. In protocol 2, QSBW had a lower defibrillation threshold after 15 seconds, 38+/-10 J, and after 5 minutes, 41.5+/-5 J, than CDSMW after 15 seconds, 54+/-19 J, and 5 minutes, 80+/-30 J, of fibrillation. The defibrillation threshold remained statistically the same for QSBW for the 2 fibrillation durations but rose significantly for CDSMW. CONCLUSIONS: In this animal model of sudden death and resuscitation, these 2 biphasic waveforms are more efficacious than the CDSMW at short durations of fibrillation. Furthermore, the QSBW is even more efficacious than the CDSMW at longer durations of fibrillation.

Effect of a passive endocardial electrode on defibrillation efficacy of a nonthoracotomy lead system.

OBJECTIVES: We investigated the impact of an inactive endocardial lead on the 50% effective dose (ED50%) for successful ventricular defibrillation. BACKGROUND: The presence of abandoned epicardial mesh patch electrodes detrimentally affects the defibrillation efficacy of an endocardial lead system. It is not known whether abandoned endocardial electrodes produce a similar effect. METHODS: An endocardial lead system (ENDOTAK, model 0062, Cardiac Pacemakers, Inc.) was implanted in eight dogs (mean +/- SD weight 23.7 +/- 1.0 kg). The ED50% for each of seven lead configurations was determined by a three-reversal point protocol in a balanced-randomized order with and without a second electrically passive endocardial lead system in the right ventricle (power 0.97 to detect a 50-V difference). Biphasic shocks with 80% tilt were delivered 10 s after the induction of ventricular fibrillation. In one configuration the active electrode made contact with the passive electrode in the right ventricular (RV) apex. In another configuration the active electrode was placed in a more proximal position to avoid contact. Additionally, the ED50% was determined for the endocardial lead system with a passive pacing lead positioned in the RV apex. RESULTS: ED50% values for peak voltage, peak current and delivered energy were not significantly different with or without a passive RV electrode, and this was true whether or not the active electrode touched the passive electrode. However, ED50% values were significantly higher when the active electrode was slightly proximal than when it was positioned at the apex. CONCLUSIONS: Physical contact between active and passive endocardial electrodes does not significantly alter defibrillation efficacy in this dog model. An increase in ED50% energy was caused by a slightly proximal position. Therefore, a good electrode position within the right ventricle is a more important determinant of defibrillation efficacy than is avoidance of the electrode touching a passive electrode.

Predicting the potential gradient field in ventricular fibrillation from shocks delivered in paced rhythm.

A method of defibrillation threshold determination that utilizes low-strength shocks delivered in a benign rhythm would be desirable. Because the two-dimensional epicardial potential gradient (PG) is a shock parameter that is linked to defibrillation, we examined whether the epicardial PG measured for shocks delivered in paced rhythm could be used to predict the PG for defibrillation-strength shocks delivered in ventricular fibrillation (VF). In six open-chest pentobarbital-anesthetized pigs with left ventricular apex and right atrial internal defibrillation patches, we measured the epicardial PG field for shocks delivered in paced rhythm and during VF. We determined that there was a linear relationship between epicardial PG and shock strength for shocks delivered in paced rhythm. However, prediction of the PG measured for shocks in VF from those measured in paced rhythm resulted in a statistically significant overestimation of the PG in VF. We conclude that, for equivalent strength shocks, the epicardial PG field is weaker for shocks delivered in VF. This change in the potential gradient field can have an effect on defibrillation threshold estimates that are based on shocks delivered in paced rhythm.

Evaluation of an automatic cardiac activation detector for bipolar electrograms.

The identification of local activation events in bipolar cardiac electrograms, the first step of isochronal map construction, is a time-consuming and difficult process. Owing to the variability among bipolar activation complexes and the lack of practical knowledge concerning the relationship of the bipolar waveform to action potential characteristics, a set of empirical rules to guide the assignment of local activation times have been adopted. A computer program, called AP, has been designed, which implements these rules in the form of a syntactic analyser. Canine epicardial recordings were used to evaluate AP by comparing local activation times, assigned by AP, with times assigned independently by three investigators. The Hermes-Cox model for detector evaluation and a bootstrap statistical method were used in conjunction with ROC analysis to evaluate the ability of AP to detect events. Analysis of discrepancies among investigator-assigned times showed that the reliabilities of AP event detection and AP-assigned times were comparable to those of the investigators. The methods used in system design and evaluation are applicable to a broad range of problems in the detection and localisation of waveform components.

High-current stimuli to the spared epicardium of a large infarct induce ventricular tachycardia.

BACKGROUND: Previous studies have demonstrated that both ventricular tachycardia (VT) and ventricular fibrillation (VF) may begin as figure-eight reentry: VT with a longer cycle length from spared tissue adjacent to an infarct by programmed stimulation and VF with a shorter cycle length from noninfarcted tissue by a large premature S2 stimulus. These results suggest that the type of tissue or cycle length of the arrhythmia rather than the mode of induction determines whether the figure eight becomes sustained VT or degenerates into VF. Thus, a protocol similar to that by which a VF threshold is determined may induce VT rather than VF when performed in the spared tissue over an infarct. METHODS AND RESULTS: In 10 dogs, 4 days after occlusion-reperfusion of the left anterior descending coronary artery, 10 S1 stimuli were delivered from a total of 34 right and left ventricular sites outside the infarct. An epicardial S2 stimulus over the infarct was increased in 10-mA steps and introduced in diastole at decreasing cycle lengths of 5 msec until VT or VF was induced. Sustained monomorphic figure-eight VT was induced from 24 S1 sites and VF from nine (p = 0.03). The mean cycle lengths for the initial six arrhythmic cycles was 152 +/- 33 msec for VT and 115 +/- 13 msec for VF (p less than 0.001). Mean transmural infarct extent was 80% in five dogs with only VT, 63% in three dogs with both VT and VF, and 15% in two dogs with only VF. Different morphologies of VT were induced by changing the S1 site, the S2 strength, or the S1S2 coupling interval. In 25 of the 34 arrhythmias, the central part of the initial figure-eight pathway was oriented opposite the S1 activation sequence in that region. CONCLUSIONS: A large S2 stimulus over a nontransmural infarct induces VT if the spared myocardium is thin. This study introduces a useful technique for inducing sustained monomorphic VT in which the location and direction of the figure-eight pathway are known a priori and in which different morphologies of sustained VT can be produced by changing the S1 site.