Prevention of high incidence of neurally mediated ventricular arrhythmias by afferent nerve stimulation in dogs.

BACKGROUND: This study tested the hypothesis that the high incidence of ventricular arrhythmias caused by hypothalamic stimulation during acute myocardial ischemia could be attenuated by afferent nerve stimulation and investigated the cardiac mechanisms for those effects. METHODS AND RESULTS: In 18 anesthetized dogs, stimulating electrodes were implanted in the hypothalamus and in the isolated left peroneal nerve. The chest was opened and approximately 100 plunge needles were inserted into the ventricles for 3-D activation mapping. Each animal underwent 4 episodes of 2.5 minutes of acute myocardial ischemia. The first and fourth episodes served as controls. During the second and third episodes, animals received either hypothalamic stimulation, peroneal nerve stimulation, or both. Hypothalamic stimulation significantly increased the incidence of ventricular arrhythmias. This high incidence was reduced 34% by simultaneous stimulation of the hypothalamus and peroneal nerve. 3-D mapping showed a focal origin for all ventricular arrhythmias. Hypothalamic stimulation increased the number of arrhythmic beats and decreased the coupling interval between each arrhythmic beat and the preceding beat. These effects were reduced by peroneal nerve stimulation. CONCLUSIONS: Alteration in autonomic tone by hypothalamic stimulation causes a high incidence of ventricular arrhythmias during acute myocardial ischemia that can be decreased by afferent nerve stimulation.

A new algorithm for minimizing pacemaker polarization artifact: universally applicable in permanent pacing systems.

Polarization artifacts that result from pacing may interfere with analysis of paced evoked responses during, e.g., automatic threshold tracking. We have developed a method for reduction of such artifacts that relies on the introduction of pacing stimuli during the refractory period of unipolar or bipolar paced captured beats after previous identification of a refractory period "template" or baseline. The refractory pacing stimuli cannot capture the heart, and thus any deviation from the template is due to polarization artifact alone. The artifact amplitude is measured and the precharge duration of the triphasic stimulus waveform is changed each time until artifact is minimized, as detected by repeated reversals in the polarity of the polarization artifact. In a series of 11 patients with unipolar and bipolar permanent pacing leads, mean initial artifact before balancing was 1.44 +/- 0.84 mV, which was reduced to 0.44 +/- 0.30 mV after balancing (P = 0.001). Initial precharge duration was 3.2 msec by design; mean final precharge duration was 3.30 +/- 0.34 msec. This algorithm is universally applicable in permanent pacing systems, as it is valid in unipolar and bipolar pacing and it does not require an intrinsic cardiac rhythm.

Defibrillation efficacy using two low-profile endocardial electrodes.

The hypothesis that improved energy delivery and defibrillation efficacy can be achieved by using two widely separated endocardial electrodes and a cutaneous patch electrode was explored by positioning two 6.5 F electrodes (NuMed, Hopkinton, New York) with 5 cm platinum-iridium coils in the right ventricular apex (RVA) and the right ventricular outflow (RVO) in eight dogs. In another 12 dogs, an additional electrode was positioned in the RVA. A cutaneous patch (P) was placed at the cardiac apex. Biphasic pulses were delivered, the first pulse (6 ms) positive, the second negative (2 ms). The leading edge of the second was equal to the trailing edge of the first. RVO-/P+ and RVA-RVO-/P+ were compared with RVA-/P+ at a constant voltage setting required to achieve a 60% probability of success (P60) for RVA-/P+. At a constant voltage output, the probability of success for RVA-RVO-/P+ was significantly higher (81%) than RVO-/P+ (60%) or RVA-/P+ (67%) (p less than 0.03). The current delivered was greater for RVA-RVO-/P+ (9.9 +/- 2.3 amps) than for either RVA-RVO-/P+ (8.7 +/- 1.9 amps) or RVO-/P+ (9.0 +/- 2.0 amps) (p less than 0.0001). Similarly, the impedance was significantly lower for RVA-RVO-/P+ (66 +/- 12 omega) than for RVA-/P+ (75 +/- 12 omega) and RVO-/P+ (72 +/- 9.6 omega) (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Automatic reduction of stimulus polarization artifact for accurate evaluation of ventricular evoked responses.

The ventricular evoked response, the cardiac depolarization generated in response to a pacing stimulus, is potentially useful as a sensor for rate responsive pacing and automatic threshold tracking. It is necessary to minimize the polarization artifact that results from pacing in order to sense cardiac depolarizations from the same electrodes that pace the heart. To accomplish this, a triphasic stimulus waveform consisting of precharge, stimulus, and postcharge was used. An algorithm was developed that introduced pacing stimuli during the refractory period of sensed beats, when cardiac depolarization could not occur by definition and polarization artifact could be evaluated. Precharge duration was varied until the amplitude of the polarization artifact was small compared to the evoked response. In 18 patients with temporary electrode catheters, polarization artifact was reduced from 6.8 +/- 3.4 mV to 1.9 +/- 1.1 mV after balancing (P less than 0.005). Initial precharge duration was 3200 mu sec and the mean final precharge duration was 3551 +/- 516 mu sec. In 14 patients with permanent bipolar pacing leads, polarization artifact was reduced from 3.2 +/- 3.5 mV to 0.7 +/- 0.6 mV (P less than 0.025). Final precharge duration averaged 3440 +/- 310 mu sec. Under a wide variety of pacing conditions, this algorithm simply and quickly reduces polarization artifact to a minimum to allow accurate analysis of evoked responses.

Characteristic variation in evoked potential amplitude with changes in pacing stimulus strength.

The evoked potential, the intracardiac signal generated by a pacing stimulus, shows promise as a sensor for rate-responsive pacing and automatic threshold determinations. Thus, it is important to understand factors that may alter the morphology of evoked potentials and affect accurate signal analysis. Using a computer-based pacing system emulator, stimuli at 2.5, 5.0 and 6.9 V were delivered to 12 patients through permanent bipolar pacing leads. At 2.5 V, the evoked potential amplitude measured -12.63 +/- 7.79 mV. When the pacing amplitude was increased to 5.0 and 6.9 V, the signal diminished in size or reversed in polarity, or both, averaging -0.83 +/- 7.82 mV and 0.64 +/- 7.0 mV, respectively (p less than 0.01 vs 2.5 V). Pacing at 2.5 V was performed in an additional 8 patients with temporary quadripolar electrode catheters. With the distal pole of the catheter as the cathode and the proximal 3 poles as a common anode, the evoked potential averaged -9.01 +/- 5.44 mV. With the proximal 2 poles of the catheter disconnected to make the anode equal in size and current density to the cathode, the evoked potential diminished to -0.94 +/- 11.27 mV (p less than 0.05). There is thus a decrease in the evoked potential at high stimulus amplitudes compared to that obtained at the cathodic threshold. This finding can be reproduced by manipulation of the size and current density of the anode, suggesting that anodal stimulation at the ring of permanent pacing leads may be responsible.