Author + information
- Sérgio Barra, MD⁎ (, )
- Rui Providência, MD, MSc and
- Luís Paiva, MD, MSc
- ↵⁎Cardiology Department, Coimbra's Hospital and University Centre, Quinta dos Vales 3041-801 S. Martinho do Bispo, Coimbra, Portugal
We read with great interest the results of the recent meta-analysis performed by Wu et al. (1), in which the researchers suggested that early repolarization pattern (ERP), defined as an elevation ≥0.1 mV of the J point in the inferior and/or lateral leads, is consistently associated with higher risk for arrhythmia death but not cardiac death or all-cause death. Their findings also revealed a low to intermediate absolute incidence of arrhythmia death in patients with ERP. These findings are valuable to our current understanding of the true risk associated with ERP.
First, although an increased arrhythmic risk has once more been documented, the absolute increase in risk is low, supporting the notion that otherwise healthy patients are extremely unlikely to die from this condition. Therefore, cost effectiveness of primary prevention strategies may be very hard to attain.
Second, although bias due to misclassification may have played a role, the fact that only arrhythmic risk was shown to increase in the presence of ER suggests that this electrocardiographic pattern was probably associated with a change in the mechanism underlying the fatal event rather than a higher risk for death.
Most importantly, ERP has never been shown to consistently increase arrhythmic risk in the absence of additional proarrhythmic triggers. Depression of the epicardial action potential plateau in ER may create a transmural repolarization gradient that is not arrhythmogenic by itself, but further increases in the net repolarizing current, with additional loss of the action potential dome, and dispersion of repolarization may create an electric substrate conducive to malignant ventricular arrhythmias. Under certain conditions known to predispose to ST-segment elevation, such as ST-segment elevation myocardial infarction (MI), or to additional repolarization heterogeneity, such as hypokalemia and heart failure, patients with ERP may be at increased arrhythmic risk. Recent studies support the important role of additional proarrhythmic triggers in the pathogenesis of ER, especially in the case of acute myocardial ischemia (2–5). A prospective study composed of patients at high coronary risk could add some robustness to these theses in the event that a higher arrhythmic risk was detected in those with ERP. Moreover, inclusion of low-risk coronary patients only, eventually based on Framingham risk stratification, could help us better evaluate the potential intrinsic arrhythmogenic nature of ER.
Although the authors highlighted that increased transmural heterogeneity of ventricular repolarization may be the mechanism involved, it is of note that some researchers have reported that repolarization abnormality markers, such as T-wave alternans and QT dispersion, do not differ between patients with and without J-waves, whereas the incidence of late potentials (a depolarization abnormality marker) in idiopathic ventricular fibrillation J-wave groups is higher than in non–J-wave groups (6). The contribution of various pathophysiological mechanisms in ER syndrome seems as likely as in the Brugada syndrome.
In the first 2 forest-plots, the I2 is more than 90%, illustrating a very high heterogeneity. Interpretation of data arising from pooling of such a heterogeneous group of studies may compromise the overall validity of the meta-analysis. Moreover, the fact that there are no funnel-plots provided makes us wonder about a potential publication bias in this meta-analysis.
Although physicians should be aware of the potential arrhythmogenic role of ERP, there is no evidence to support different primary prevention strategies for patients with ER. Nevertheless, prevention of arrhythmic triggers, such as acute myocardial ischemia, through more aggressive prevention of coronary artery disease might mitigate the apparent association between ER duration and arrhythmic mortality.
- American College of Cardiology Foundation
- Wu S.H.,
- Lin X.X.,
- Cheng Y.J.,
- Qiang C.C.,
- Zhang J.
- Tikkanen J.T.,
- Wichmann V.,
- Junttila M.J.,
- et al.
- Naruse Y.,
- Tada H.,
- Harimura Y.,
- et al.