It allowed the right ventricular pacemaker to escape and, by causing temporal dispersion of repolarization after the conducted QRSs, facilitated reentrant ventricular premature complexes with retrograde atrial conduction
that reset the sinus node, thus slowing it further.
P-wave dispersion (PWD) is an electrocardiographic measurement, which reflects a disparity in an atrial conduction
Objective: The aim of our study was to investigate total atrial conduction time and left atrial (LA) mechanical function in patients with isolated coronary artery ectasia (ICAE).
The total atrial conduction time (PA-tissue Doppler imaging (TDI) duration) was assessed by measuring the time interval between the beginning of the P wave on the surface ECG and point of the peak A wave on TDI from LA lateral wall just over the mitral annulus.
Total atrial conduction
time is measured as the time delay between the onset of the P-wave (preferably in lead II) of the surface electrocardiogram and the peak A'-wave on the tissue Doppler tracing of the left atrial (LA) lateral wall (PA-TDI duration).
Atrial fibrillation (AF) is known to induce atrial electrical remodeling (AER), which includes shortening, maladaptation, and increased dispersion of atrial effective refractory period (AERP) as well as decreased atrial conduction
velocity (1, 2).
Recent findings showed that AF induces atrial electrical remodeling, increases dispersion of atrial effective refractory period and decreases atrial conduction
The device via foreign body reaction might lead to an inflammatory response within the atrial myocardial tissue thus increasing the atrial conduction
P-wave dispersion is considered to reflect the discontinuous and inhomogeneous propagation of sinus impulses and the prolongation of atrial conduction
Objective: P-wave dispersion (PWD) is an electrocardiographic measurement, which reflects a disparity in an atrial conduction
P-wave maximum duration in any of the 12-lead surface ECGs was calculated and used as a marker of prolonged atrial conduction
The mechanisms that predispose HCM patients to develop AF are variable and include genetic factors, structural abnormalities, as well as prolonged and impaired atrial conduction
due to atrial myopathy.