Abnormal P-wave morphology is a predictor of atrial fibrillation development and cardiac death in MADIT II patients

Abstract

Background: Several ECG-based approaches have been shown to add value when risk-stratifying patients with congestive heart failure, but little attention has been paid to the prognostic value of abnormal atrial depolarization in this context. The aim of this study was to noninvasively analyze the atrial depolarization phase to identify markers associated with increased risk of mortality, deterioration of heart failure, and development of atrial fibrillation (AF) in a high-risk population with advanced congestive heart failure and a history of acute myocardial infarction.

Methods: Patients included in the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) with sinus rhythm at baseline were studied (n = 802). Unfiltered and band-pass filtered signal-averaged P waves were analyzed to determine orthogonal P-wave morphology (prespecified types 1, 2, and 3/atypical), P-wave duration, and RMS20. The association between P-wave parameters and data on the clinical course and cardiac events during a mean follow-up of 20 months was analyzed.

Results: P-wave duration was 139 + or - 23 ms and the RMS20 was 1.9 + or - 1.1 microV. None of these parameters was significantly associated with poor cardiac outcome or AF development. After adjustment for clinical covariates, abnormal P-wave morphology was found to be independently predictive of nonsudden cardiac death (HR 2.66; 95% CI 1.41-5.04, P = 0.0027) and AF development (HR 1.75; 95% CI 1.10-2.79, P = 0.019).

Conclusion: Abnormalities in P-wave morphology recorded from orthogonal leads in surface ECG are independently predictive of increased risk of nonsudden cardiac death and AF development in MADIT II patients.

Figure 1

Schematic illustration of the three P‐wave morphology classes. Type 1 is characterized by a right‐to‐left (positive lead X), superior‐to‐inferior (positive lead Y) and posterior‐to‐anterior activation pattern (negative lead Z). Type 2 is also characterized by positive signals in lead X and Y, but the biphasic signal in lead Z indicates a more complex activation pattern (posterior‐to‐anterior‐to‐posterior). Type 3 P‐wave morphology also exhibits a positive signal in lead X, and a biphasic signal in lead Z, as does type 2, but the signal in lead Y reflects the retrograde activation of the left atrium (superior‐to‐inferior‐to‐superior). The two morphologies within the red rectangle are illustrations of two distinct patterns seen among the atypical P waves. The meaning of these patterns are yet to be elucidated.

Figure 2

The Kaplan‐Meier graph for P‐wave morphology as a predictor of AF development. As illustrated by the curves there is a progressive and proportional increase in risk of AF development from type 1 to type 2 to type 3/atypical.

Figure 3

The Kaplan‐Meier graphs show the univariate association between the different P‐wave morphologies and all‐cause mortality (A); cardiac death (B); nonsudden cardiac death (C); sudden cardiac death (D); CHF hospitalization (E); and the combined end point of CHF hospitalization and cardiac death (F). Notably, for all analyzed variables (with sudden cardiac death as the one exception) the increase in risk seems to be highest for the type 3 or atypical P‐wave morphologies and lowest for the type 1 P‐wave morphology.