Adjusting the timing of left-ventricular pacing using electrocardiogram and device electrograms.

Aims: Left-ventricular (LV) pacing with optimized atrio-ventricular (AV) timing may provide similar or greater benefit in comparison with bi-ventricular (BiV) pacing in a subset of cardiac resynchronization therapy (CRT) patients with sinus rhythm and preserved AV conduction. We hypothesized that the optimal device AV delays during LV pacing can be predicted using electrocardiogram (ECG) and device electrograms. METHODS AND RESULTS PATIENTS: (n= 55) with sinus rhythm and PR interval < 300 ms had their CRT devices programmed to atrial and LV pacing with a range of AVs as well as to echocardiographically optimized BiV and no ventricular pacing.

Interatrial conduction correlates with optimal atrioventricular timing in cardiac resynchronization therapy devices.

Background: Echocardiographic optimization of the atrioventricular delay (AV) may result in improvement in cardiac resynchronization therapy (CRT) outcome. Optimal AV has been shown to correlate with interatrial conduction time (IACT) during right atrial pacing. This study aimed to prospectively validate the correlation at different paced heart rates and examine it during sinus rhythm (Sinus).

Optimal atrioventricular delay in CRT patients can be approximated using surface electrocardiography and device electrograms.

Unlabelled: Electrocardiographic AV Delay Adjustment.

Background: Optimization of the atrioventricular (AV) delay (AVD) may result in an improvement in cardiac resynchronization therapy (CRT) outcome. Previous studies have shown positive correlation between interatrial conduction time measured invasively during the implant procedure and optimal AVD determined postimplant using Doppler echocardiography.

Prediction of interatrial and interventricular electromechanical delays from P/QRS measurements: value for pacemaker timing optimization.

Unlabelled: Cardiac pacing creates spurious delays between and within the cardiac chambers. These are: 1. Left atrial (LA) transport delay (ATD) either sensed (s) or paced (p), (time from right atrial P-wave to the end of LA transport (mitral Doppler A-wave)).

Dynamics of virtual electrode-induced scroll-wave reentry in a 3D bidomain model.

Functional reentry in the heart can be caused by a wave front of excitation rotating around its edge. Previous simulations on the basis of monodomain cable equations predicted the existence of self-sustained, vortex-like wave fronts (scroll waves) rotating around a filament in three dimensions. In our simulations, we used the more accurate bidomain model with modified Beeler-Reuter ionic kinetics to study the dynamics of scroll-wave filaments in a 16 x 8 x 1.

Virtual electrode theory explains pacing threshold increase caused by cardiac tissue damage.

The virtual electrode polarization (VEP) effect is believed to play a key role in electrical stimulation of heart muscle. However, under certain conditions, including clinically, its existence and importance remain unknown. We investigated the influence of acute tissue damage produced by continuous pacing with strong current (40-mA, 4-ms biphasic pulses with 4-Hz frequency for 5 min) on stimulus-generated VEPs and pacing thresholds.

Nonlinear effects in subthreshold virtual electrode polarization.

Introduction of the virtual electrode polarization (VEP) theory suggested solutions to several century-old puzzles of heart electrophysiology including explanation of the mechanisms of stimulation and defibrillation. Bidomain theory predicts that VEPs should exist at any stimulus strength. Although the presence of VEPs for strong suprathreshold pulses has been well documented, their existence at subthreshold strengths during diastole remains controversial.

Anode-break excitation during end-diastolic stimulation is explained by half-cell double layer discharge.

The phenomenon of anodal-break excitation during end-diastolic stimulation of the heart was discovered many years ago by B. Hoffman. Yet, the existence and mechanistic explanation of this effect remain controversial.

Mechanisms of make and break excitation revisited: paradoxical break excitation during diastolic stimulation.

Onset and termination of electric stimulation may result in "make" and "break" excitation of the heart tissue. Wikswo et al. (30) explained both types of stimulations by virtual electrode polarization.