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Published at www.nejm.org November 16, 2009 (10.1056/NEJMoa0907589)

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ABSTRACT

Background Early repolarization, which is characterized by an elevation of the QRS–ST junction (J point) in leads other than V₁ through V₃ on 12-lead electrocardiography, has been associated with vulnerability to ventricular fibrillation, but little is known about the prognostic significance of this pattern in the general population.

Methods We assessed the prevalence and prognostic significance of early repolarization on 12-lead electrocardiography in a community-based general population of 10,864 middle-aged subjects (mean [±SD] age, 44±8 years). The primary end point was death from cardiac causes, and secondary end points were death from any cause and death from arrhythmia during a mean follow-up of 30±11 years. Early repolarization was stratified according to the degree of J-point elevation (0.1 mV or >0.2 mV) in either inferior or lateral leads.

Results The early-repolarization pattern of 0.1 mV or more was present in 630 subjects (5.8%): 384 (3.5%) in inferior leads and 262 (2.4%) in lateral leads, with elevations in both leads in 16 subjects (0.1%). J-point elevation of at least 0.1 mV in inferior leads was associated with an increased risk of death from cardiac causes (adjusted relative risk, 1.28; 95% confidence interval [CI], 1.04 to 1.59; P=0.03); 36 subjects (0.3%) with J-point elevation of more than 0.2 mV in inferior leads had a markedly elevated risk of death from cardiac causes (adjusted relative risk, 2.98; 95% CI, 1.85 to 4.92; P<0.001) and from arrhythmia (adjusted relative risk, 2.92; 95% CI, 1.45 to 5.89; P=0.01). Other electrocardiographic risk markers, such as a prolonged QT interval corrected for heart rate (P=0.03) and left ventricular hypertrophy (P=0.004), were weaker predictors of the primary end point.

Conclusions An early-repolarization pattern in the inferior leads of a standard electrocardiogram is associated with an increased risk of death from cardiac causes in middle-aged subjects.

Source Information

From the Institute of Clinical Medicine, Department of Internal Medicine, University of Oulu, Oulu (J.T.T., M.J.J., H.V.H.); the Department of Internal Medicine, Päijät-Häme Central Hospital, Lahti (O.A., A.L.A., T.K.); and the National Institute for Health and Welfare, Helsinki (H.A.R., A.R.) — all in Finland.

This article (10.1056/NEJMoa0907589) was published on November 16, 2009, at NEJM.org.

Address reprint requests to Dr. Huikuri at the Institute of Clinical Medicine, Department of Internal Medicine, Center of Excellence in Research, University of Oulu, P.O. Box 5000, 90014 Oulu, Finland, or at heikki.huikuri{at}oulu.fi.

Full Text of this Article

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