Pacing and clinical electrophysiology : PACE
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Pacing Clin Electrophysiol · Nov 2000
Randomized Controlled Trial Clinical TrialHemodynamic assessment of right, left, and biventricular pacing by peak endocardial acceleration and echocardiography in patients with end-stage heart failure.
Multisite ventricular pacing acutely improves the hemodynamic status in heart failure, though longer-term observations require invasive procedures. The hemodynamics of multisite ventricular pacing were assessed by echocardiography and peak endocardial acceleration (PEA) measured by a pacemaker sensor. PEA variations are highly correlated with those of dP/dt. ⋯ As a result, the values of the PEA variations over a 15-minute period were significantly greater during LV pacing and BV pacing versus RV pacing (+43%, P < 0.05, and +38%, P = 0.05, respectively) and were statistically comparable between BV pacing and LV pacing (9% for LV pacing, P = NS). During various ventricular pacing configurations, PEA measurements were consistent with echocardiographic data, showing comparable hemodynamic effects of BV and LV pacing. The PEA sensor is a promising tool for long-term hemodynamic monitoring and serial evaluation of the effects of multisite ventricular pacing in heart failure patients.
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Pacing Clin Electrophysiol · Jul 1998
Randomized Controlled Trial Clinical TrialPrediction of maintenance of sinus rhythm after cardioversion of atrial fibrillation by analysis of serial signal-averaged P waves.
After cardioversion from atrial fibrillation (AF) many patients develop early recurrence of the arrhythmia. While these patients may be appropriate for immediate prophylaxis against AF recurrence their identification at the time of cardioversion is not possible. Since the signal-averaged P wave (SAPW) is abnormal in individuals with atrial arrhythmia, we assessed its utility for predicting early AF recurrence after cardioversion. ⋯ Patients with relapsing permanent AF who remain in sinus rhythm for at least 1 week after cardioversion show a fall in P wave energy within the first 24 hours. However, in these patients the technique does not predict recurrent AF within 1 week nor sinus rhythm > 4 weeks. These observations suggest persistent disordered atrial activation as a mechanism for early recurrence of AF after cardioversion.
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Pacing Clin Electrophysiol · Aug 1993
Randomized Controlled Trial Clinical TrialRandomized cross-over evaluation of two adaptive pacing algorithms for the termination of ventricular tachycardia.
In a randomized, cross-over study we evaluated the efficacy of rate adaptive constant cycle length (BURST) and autodecremental (RAMP) pacing for termination of sustained monomorphic ventricular tachycardia. ⋯ 1. Rate adaptive pacing methods for ventricular tachycardia termination are effective and safe. 2. Autodecremental RAMP pacing afford quicker ventricular tachycardia termination than constant cycle length BURST pacing. 3. The ability to terminate ventricular tachycardia is cycle length dependent with cycle length range of 300-350 msec being most responsive to pace termination.
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Pacing Clin Electrophysiol · Mar 1993
Randomized Controlled Trial Multicenter Study Clinical TrialICD versus drugs in cardiac arrest survivors: preliminary results of the Cardiac Arrest Study Hamburg.
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Pacing Clin Electrophysiol · Aug 1989
Randomized Controlled Trial Comparative Study Clinical TrialActive fixation atrial leads: randomized comparison of two lead designs.
Active fixation leads have reduced the incidence of lead dislodgement in patients with permanent pacemakers. However, theoretic concern that the tissue trauma associated with a myocardial screw-helix may increase the chronic pacing threshold of active compared to passive fixation leads has remained. Whether active fixation leads with a stimulating electrode that is independent of the fixation mechanism are associated with a lower chronic pacing threshold than leads utilizing a screw-helix for both fixation and stimulation is unknown. ⋯ At 6 weeks follow-up, there were no differences in the mean threshold voltage (1.85 +/- 0.36 vs 1.93 +/- 0.69 V), impedance (528 +/- 81 vs 530 +/- 118 ohms), or atrial electrogram amplitude (2.63 +/- 0.50 vs 2.42 +/- 0.95 mV) between the two leads. At long-term follow-up (mean 16.2 +/- 2.8 months, range 13.1-20.0 months) there were no significant differences in voltage threshold (1.65 +/- 0.61 vs 1.97 +/- 0.64 V), impedance (565.5 +/- 81.6 vs 617.7 +/- 146.7 ohms), or atrial electrogram amplitude (2.79 +/- 0.75 vs 3.10 +/- 1.53 mV). Thus, these results suggest that active fixation leads in the atrium with an electrode that is independent of the fixation mechanism do not provide chronic stimulation thresholds or electrogram amplitudes that are superior to those obtained with leads utilizing a myocardial screw-helix as both the active electrode and the fixation device.