P-wave morphology: underlying mechanisms and clinical implications

Abstract

Increasing awareness of atrial fibrillation (AF) and its impact on public health revives interest in identification of noninvasive markers of predisposition to AF and ECG-based risk stratification. P-wave duration is generally accepted as the most reliable noninvasive marker of atrial conduction, and its prolongation has been associated with history of AF. However, patients with paroxysmal AF without structural heart disease may not have any impressive P-wave prolongation, thus suggesting that global conduction slowing is not an obligatory requirement for development of AF. P-wave morphology is therefore drawing increasing attention as it reflects the three-dimensional course of atrial depolarization propagation and detects local conduction disturbances. The factors that determine P-wave appearance include (1) the origin of the sinus rhythm that defines right atrial depolarization vector, (2) localization of left atrial breakthrough that defines left atrial depolarization vector, and (3) the shape and size of atrial chambers. However, it is often difficult to distinguish whether P-wave abnormalities are caused by atrial enlargement or interatrial conduction delay. Recent advances in endocardial mapping technologies have linked certain P-wave morphologies with interatrial conduction patterns and the function of major interatrial conduction routes. The value of P-wave morphology extends beyond cardiac arrhythmias associated with atrial conduction delay and can be used for prediction of clinical outcome of a wide range of cardiovascular disorders, including ischemic heart disease and congestive heart failure.

Figure 1

Signal‐averaged orthogonal unfiltered PTa‐wave morphology in a patient with complete atrio‐ventricular block. Note the low‐amplitude and low‐frequency Ta repolarization wave that follows P wave (dotted lines), best seen in lead Y as well as in the spatial magnitude (SM) vector. While P‐wave onset is a very distinct event, the end of the P wave may be obscured by the superimposed Ta wave that affects the morphology of the P‐wave terminal part. Solid line indicates the end of the Ta wave. The upper panel represents ECG from standard leads I, aVF and V₁ from the same patient.

Figure 2

Variability in sinus rhythm origin recorded using epicardial mapping in subjects undergoing open‐chest surgery for Wolff‐Parkinson‐White syndrome (adapted from Boineau et al. ²⁰ with permission). Isochronal maps illustrate the propagation of atrial depolarization via either Bachmann's bundle anteriorly (left panel) or via the inferior route beneath the inferior pulmonary veins (right panel). Examples of P waves from lead aVF illustrate the impact of sinus rhythm origin and propagation route on P‐wave morphology.

Figure 3

P‐wave morphology change in lead V₁ following i.v. atropine administration. Note the increase in amplitude of the negative terminal component seen in patients A (upright P wave at baseline) and B (biphasic P wave at baseline). Patient C who had negative P waves at baseline did not show any notable P‐wave morphology change despite heart rate increase in response to atropine administration.

Figure 4

Schematic illustration of mechanisms underlying the development of biphasic P waves in the sagittal plane. Interatrial conduction over posterior interatrial connections (with or without participation of Bachmann's bundle) result in posterior‐to‐anterior propagation of excitation in the left atrium, leading to positive or isoelectric P waves in the sagittal plane (upper panel, Type 1 P‐wave morphology). Interatrial conduction over Bachmann's bundle only, without contribution from posterior fibers, results in anterior‐to‐posterior activation of the left atrium and biphasic P waves in the same leads (lower panel, Type 2 morphology).