Abnormal P-wave Morphology is a Predictor of Atrial Fibrillation Development and Cardiac Death in MADIT II Patients

Overview

Journal Ann Noninvasive Electrocardiol

Specialty Cardiology & Vascular Diseases

Date 2010 Feb 12

PMID 20146784

Citations 24

Authors

Fredrik Holmqvist

Pyotr G Platonov

Scott McNitt

Slava Polonsky

Jonas Carlson

Wojciech Zareba

Arthur J Moss

Affiliations

Soon will be listed here.

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.

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