Anthony S. L. Tang

Stimulus-induced critical point. Mechanism for electrical initiation of reentry in normal canine myocardium.

The hypothesis was tested that the field of a premature (S2) stimulus, interacting with relatively refractory tissue, can create unidirectional block and reentry in the absence of nonuniform dispersion of recovery. Simultaneous recordings from a small region of normal right ventricular (RV) myocardium were made from 117 to 120 transmural or epicardial electrodes in 14 dogs. S1 pacing from a row of electrodes on one side of the mapped area generated parallel activation isochrones followed by uniform parallel isorecovery lines. Cathodal S2 shocks of 25 to 250 V lasting 3 ms were delivered from a mesh electrode along one side of the mapped area to scan the recovery period, creating isogradient electric field lines perpendicular to the isorecovery lines. Circus reentry was created following S2 stimulation; initial conduction was distant from the S2 site and spread towards more refractory tissue. Reentry was clockwise for right S1 (near the septum) with top S2 (near the pulmonary valve) and for left S1 with bottom S2; and counterclockwise for right S1 with bottom S2 and left S1 with top S2. The center of the reentrant circuit for all S2 voltages and coupling intervals occurred at potential gradients of 5.1 +/- 0.6 V/cm (mean +/- standard deviation) and at preshock intervals 1 +/- 3 ms longer than refractory periods determined locally for a 2 mA stimulus. Thus, when S2 field strengths and tissue refractoriness are uniformally dispersed at an angle to each other, circus reentry occurs around a critical point where an S2 field of approximately 5 V/cm intersects tissue approximately at the end of its refractory period.

Ventricular defibrillation using biphasic waveforms: The importance of phasic duration

Biphasic waveforms can be used to defibrillate the heart with less energy than that used by monophasic waveforms. In 14 anesthetized open chest dogs with large contoured defibrillation electrodes, the effect on defibrillation efficacy of varying the duration of the two phases of biphasic waveforms was studied. All combinations of 0, 1, 3.5, 6 and 8.5 ms duration were used for both the first and the second phase except for the meaningless case in which both durations were 0 ms. The 3.5-2 waveform (3.5 ms first phase and 2 ms second phase) was also tested. All the hearts were defibrillated with less than or equal to 5 joules using any of the 25 waveforms. However, biphasic waveforms with the second phase shorter than or equal to the first had significantly lower defibrillation thresholds than did those with the second phase longer than the first or than did monophasic waveforms of approximately the same total duration. A plot of defibrillation threshold current strength versus second phase duration for all biphasic waveforms with a 3.5 ms first phase did not produce a hyperbolic strength-duration curve as seen with monophasic waveforms. To verify these findings, defibrillation dose-response curves were obtained for the 3.5-2, 6-6 and 3.5-8.5 biphasic waveforms in another six dogs. The 50 and 80% successful voltage doses of the 3.5-8.5 waveforms were significantly higher than those of the other two waveforms, which were not different from one another.(ABSTRACT TRUNCATED AT 250 WORDS)

Strength-duration and probability of success curves for defibrillation with biphasic waveforms.

Certain biphasic waveforms require less energy to defibrillate than do monophasic pulses of equal duration, although the mechanisms of this increased effectiveness remain unclear. This study used strength-duration and percent success curves for defibrillation with monophasic and biphasic truncated exponential waveforms to explore these mechanisms. In part 1, defibrillation thresholds were determined for both high- and low-tilt waveforms. The monophasic pulses tested ranged in duration from 1.0 to 20.0 msec, and the biphasic waveforms had first phases of either 3.5 or 7.0 msec and second phases ranging from 1.0 to 20.0 msec. In part 2, defibrillation percent success curves were constructed for 6.0 msec/6.0 msec biphasic waveforms with a constant phase-one amplitude and with phase-two amplitudes of approximately 21%, 62%, 94%, and 141% of phase one. This study shows that if the first phase of a biphasic waveform is held constant and the second phase is increased in either duration or amplitude, defibrillation efficacy first improves, then declines, and then again improves. For pulse durations of at least 14 msec, the second-phase defibrillation threshold voltage of a high-tilt biphasic waveform is higher than that of a monophasic pulse equal in duration to the biphasic second phase (p less than 0.05), indicating that the previously proposed hypothesis of stimulation by the second phase is not the sole mechanism of biphasic defibrillation. These facts indicate the importance of the degree of tilt for the defibrillation efficacy of biphasic waveforms and suggest at least two mechanisms exist for defibrillation with these waveforms, one that is more effective for smaller second phases and another that becomes more effective as the second phase is increased.

Comparison of the internal defibrillation thresholds for monophasic and double and single capacitor biphasic waveforms

Implantable cardiac defibrillators are now an accepted form of therapy for patients with life-threatening ventricular arrhythmias that cannot be controlled by antiarrhythmic drugs. These devices could be made even more acceptable if they were smaller, had increased longevity and the surgical procedure for implantation was less invasive. Reducing the energy requirements for internal defibrillation with use of a nonthoracotomy system would make all of these goals achievable. Monophasic and double and single capacitor biphasic waveforms were compared in 14 anesthetized dogs (25.5 +/- 2.2 kg) with use of a nonthoracotomy lead system that has previously been shown to distribute the delivered voltage throughout the heart more equally. Cathodal catheter electrodes were placed in the right ventricular apex and outflow tract. The anodal electrode was a large cutaneous R2 patch placed over the left side of the chest. The mean energy requirement for defibrillation when a single capacitor biphasic waveform was used was significantly less (6.4 +/- 2.6 J) than that for either the double capacitor biphasic or the monophasic waveform (18.0 +/- 8.0 and 17.4 +/- 8.0 J, respectively) of the same duration. Unexpectedly, the leading edge voltage for the phase I of the single capacitor biphasic waveform was significantly less (266 +/- 51 V) than that for either the double capacitor biphasic or the monophasic waveform (336 +/- 76 and 427 +/- 117 V, respectively). In conclusion, in large dogs, defibrillation is possible at low energy levels with a single capacitor biphasic waveform.

Three-dimensional potential gradient fields generated by intracardiac catheter and cutaneous patch electrodes.

BackgroundDefibrillation may be improved if electrode configurations can be found that create a larger and more even voltage gradient field across the heart. This study determined the magnitude of the shock gradient fields generated by four nonthoracotomy electrode configurations for defibrillation. Methods and ResultsIn six dogs, a catheter was inserted containing a right ventricular apical electrode V) and a right atrial electrode (A). A cutaneous patch electrode (P) was placed on the left lateral thorax. Shock potentials were recorded simultaneously from 128 electrodes in the left ventricular and right ventricular subepicardium and subendocardium, ventricular septum, and atria. With the chest closed, 50-mA shocks were given during diastole via the following lead configurations: V→A (V, cathode; A, anode); V→P; V→A+P; and V+A→P. Potential gradients were calculated at the subepicardium and subendocardium in millivolts per centimeter per volt of shock. In most dogs, the V→A+P configuration produced higher gradients throughout the ventricles than did V→A, V→P, or V+A→P. The maximum potential gradient was smaller for the V+A→P configuration than for V→A, V→P, or V→A+P. The gradient fields for the configurations with the catheter alone or combined with P were uneven. ConclusionsIt is possible to estimate shock gradient fields in three dimensions. Of the four configurations tested, V→A+P produced the highest gradients and V+A→P produced the lowest high gradient. The gradient fields were uneven throughout the ventricles.

Effect of Ebstein's anomaly on short- and long-term outcome of surgically treated patients with Wolff-Parkinson-White syndrome.

BackgroundEbsteins anomaly is the most commonly occurring congenital abnormality associated with the Wolif-Parkinson-White (WPW) syndrome. However, the effects of Ebsteins anomaly on the risks and benefits of surgical ablation of accessory pathways in patients with WPW syndrome are unknown Methods and ResultsThis study compared the long-term outcome of 38 WPW patients with Ebsteins anomaly undergoing accessory pathway ablation to a reference population of 384 similarly treated patients without the anomaly. Ebsteins anomaly was mild in 21 patients (55%) and moderate-to-severe in 17 patients (45%). Sixteen patients (42%) required tricuspid valve surgery, and 23 (61%) had an atrial septal defect or patent foramen ovale repaired. Baseline clinical characteristics and preoperative clinical arrhythmias were similar in both groups. Ten-year survival was 92.4% and 91.2% for patients with and without Ebsteins anomaly, respectively (p = NS). During a mean follow-up of 6.2±3.8 and 5.3±3.6 years, 82% of patients with and 90% without Ebsteins anomaly had either clinically insignificant or no arrhythmias, and 18% versus 10% reported symptoms suggesting arrhythmias lasting longer than 1 minute, respectively. Atrial fibrillation was reduced postoperatively to 9% (p < 0.00l) in patients with and to 4% (p < 0.00l) in those without the anomaly. Fewer hospitalizations were reported postoperatively by 90% versus 96% of patients with and without Ebsteins anomaly; 9.4% versus 6.0% of patients were disabled at follow-up, respectively (p = NS) ConclusionsPatients with Ebsteins anomaly are improved significantly after accessory pathway ablation. The presence of this anomaly should not preclude accessory pathway ablation in these patients.

New observations on atrial fibrillation before and after surgical treatment in patients with the Wolff-Parkinson-White syndrome

The records of 342 patients who received surgical treatment for the Wolff-Parkinson-White syndrome between 1968 and 1986 were reviewed to evaluate the characteristics of atrial fibrillation. The patients were classified into two groups according to the presence (n = 166) or absence (n = 176) of documented episodes of atrial fibrillation preoperatively. The mean follow-up duration was 6 years (range 2 to 20). As compared with reports based on smaller patient groups and shorter follow-up, the study revealed several new findings. 1) During follow-up, nine patients in the atrial fibrillation group developed recurrent atrial fibrillation after a successful operation; five of these nine patients did not have associated heart disease. 2) All three patients with a history of atrial fibrillation and an accessory pathway conducting in the anterograde direction only had a successful surgical procedure and no postoperative atrial fibrillation. 3) The cycle length of atrioventricular (AV) reciprocating tachycardia was significantly shorter in the atrial fibrillation group (304 +/- 42 ms, mean +/- SD) than in the no-atrial fibrillation group (321 +/- 54 ms, p less than 0.005), and the cycle length of AV reciprocating tachycardia that degenerated into atrial fibrillation (289 +/- 26 ms) was shorter than that for the AV reciprocating tachycardia without subsequent atrial fibrillation (316 +/- 51 ms, p less than 0.005). 4) Sustained atrial fibrillation was induced in 30% of patients without a history of atrial fibrillation. 5) Atrial fibrillation occurred in four patients with an accessory pathway that conducted only in the retrograde direction.(ABSTRACT TRUNCATED AT 250 WORDS)

Basic Mechanisms of Ventricular Defibrillation

Recordings were made simultaneously from many electrodes placed on and in the hearts of animals to study the basic principles of ventricular defibrillation. The findings are listed below. Earliest activations following a shock slightly lower in strength than needed to defibrillate (a subthreshold defibrillation shock) occur in those cardiac regions in which the potential gradients generated by the shock are weakest. Activation fronts after subthreshold shocks do not appear to be continuations of activation fronts present just before the shock. An upper limit exists to the strength of shocks that induce fibrillation when given during the “vulnerable period” of regular rhythm. This upper limit of vulnerability correlates with and is similar in strength to the defibrillation threshold. To defibrillate, a shock must halt the activation fronts of fibrillation without giving rise to new activation fronts that reinduce fibrillation. The response to shocks during regular rhythm just below the upper limit of vulnerability is similar to the response to subthreshold defibrillation shocks. Shocks during regular rhythm initiate rotors of reentrant activation leading to fibrillation when a critical point is formed, at which a certain critical value of shock potential gradient field strength intersects a certain critical degree of myocardial refractoriness. This critical point may explain the existence of the upper limit of vulnerability. The critical point may also partially explain the finding that the relationship between shock strength and the success of the shock in halting fibrillation is better represented by a probability function rather than by a discrete threshold value. Very high potential gradients, approximately an order of magnitude greater than needed for defibrillation, have detrimental effects on the heart, including conduction block, induction of arrhythmias, decreased wall motion, and tissue necrosis.

Calculating endocardial potentials from epicardial potentials measured during external stimulation

A boundary integral method for calculating the potential field generated by external stimulation at locations within the heart using realistic heart geometry and samples of the potential taken from the epicardial surface is presented. This method assumes the heart is homogeneous and isotropic. To test the method epicardial and endocardial measurements are made in dogs during transthoracic pacing stimuli. From the epicardial potential measurements the endocardial potential values are predicted and compared with the measured data. Despite the seemingly gross assumptions, the mean correlation coefficient between the measured and predicted potentials for three dogs and eleven stimulation electrode configurations was 0.985, and the mean rms error was 17%.<<ETX>>

On the Trail of Ventricular Tachycardia or the Adventure of the Unspeckled Band

An important goal of cardiac electrophysiology is identification of the anatomic region that gives rise to an arrhythmia even when the arrhythmia is not present. When a technique is developed to achieve this goal, its most direct application will be to the surgical treatment of ventricular tachycardia (VT). Because of two problems, electrical mapping to identify the arrhythmogenic region during surgery is a lengthy procedure that has been reported to be successful in only about 64% of cases.’ One, it can be difficult or impossible to induce the clinical arrhythmia during surgery. Two, mapping with a hand-held probe may require several minutes to record individually from all desired locations.’ If the VT does not last this long before halting or degenerating into fibrillation, it must be reinduced. Laser3 and electrical4 ablative techniques may soon allow definitive treatment of VT in the cardiac electrophysiology catheterization laboratory, where the second problem is also critical because the induced arrhythmia may cause hemodynamic collapse before mapping is complete. A major reason for the development of analog and digital multi-channel mapping systems has been to circumvent the second problem by recording simultaneously from all electrodes during a single beats5 An easier way to solve both problems would be to develop a simple technique to localize the arrhythmogenic region without having to induce the arrhythmia. One proposed technique is pace mapping in which electrical stimu-