P-wave signal averaging. High tech or an expensive alternative to the standard ECG?

A trial fibrillation is the most common sustained arrhythmia treated by cardiologists and inter-nists, occurring in 0.4% of the general population and in 2% to 4% of those over age 60 years.1'2 Several small studies of coronary artery bypass grafting (CABG) have shown an incidence of postoperative atrial fibrillation ranging from 5% to as high as 40%. Recent large studies by Taylor et a12 and Fuller et a13 reported 19% and 28.4% incidences of post-CABG atrial fibrillation, respectively, and these results may be more representative of the true incidence in the population undergoing CABG. Several investigators have noted a correlation between both increasing age and the lack of ,8-blockade and the incidence of post-CABG atrial fibrillation, but other clinical correlates have not been consistently demonstrated. Post-CABG atrial fi-brillation usually occurs within 72 hours after surgery.4 Although often benign and self-limited, complications may occur in a small proportion of patients and may result in significant sequelae and increased length of hospitalization. Atrial fibrillation is more common in CABG patients who suffer postoperative stroke than in patients who do not,2 suggesting a possible causal relation. Hemodynamic compromise and/or the development of chronic atrial fibrillation resulting from post-CABG atrial fibrillation are rare.5 See p 2618 The mechanism of maintenance of atrial fibrillation involves the presence of a number of independent wavelets of depolarization traveling through the atrium. The initiating events are multifactorial but can include enhanced vagal or sympathetic tone and hemodynamic alterations, with or without atrial premature complexes. In order to maintain a critical number of simultaneously circulating wavelets in the atria, the wavelength (a product of conduction velocity and refractory period) must be small. Studies in humans have demonstrated that intra-atrial conduction delays (more marked in the right atrium), and short right atrial refractory periods The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. characterize patients with atrial fibrillation and flutter .6-8 Atrial conduction delays may result from active cell membrane abnormalities and nonuniform anisot-ropy caused by myofibril hypertrophy or interstitial fibrosis in dilated atria and possibly from other factors such as left atrial hypertension, atrial infarction, inflammation in pericarditis, or after cardiac surgery, atrial trauma. Autonomic tone also plays an important role in enhancing atrial vulnerability to fibrillation, but the interactions between vagal and adrenergic tone and their effects on atrial refractoriness, dispersion of re-fractoriness, and intra-atrial conduction delay are …