Why the study?
Do additional proarrhythmic triggers like acute myocardial ischaemia unmask the malignant nature of early repolarization patterns to cause sudden cardiac death?
Do additional proarrhythmic triggers like acute myocardial ischaemia unmask the malignant nature of early repolarization patterns to cause sudden cardiac death?
This review highlights the potential role of proarrhythmic triggers, such as acute myocardial ischaemia, in transforming benign early repolarization patterns into malignant variants associated with sudden cardiac death.
Early repolarization patterns warrant vigilance during acute ischaemia; leaves open prospective validation of malignant risk stratification.
The majority of individuals with early repolarization (ER) patterns have a benign prognosis. However, recent case-control series and population studies have established a significant association between ER and an increased risk of arrhythmic death. There is a common agreement that J-waves, particularly of large amplitude, dynamic, and present in multiple leads, are more prevalent in patients with idiopathic ventricular fibrillation, but the distinction between benign and malignant electrocardiographic variants of ER is still a controversial subject. Some authors have proposed the increased dispersion of repolarization or delayed fragmented depolarization in individuals with J-waves would place them at increased arrhythmic risk, but only in the presence of additional proarrhythmic factors or triggers. The scientific community has therefore embraced research for the identification of those proarrhythmic triggers that could unmask the malignant nature of certain ER variants. This manuscript aims at reviewing very recently published data relating ER patterns and sudden cardiac death in the presence of additional proarrhythmic triggers, in particular acute myocardial ischaemia, focusing on possible pathophysiological and electrogenic mechanisms and therapeutic implications.
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Barra et al. (2012) studied this question.
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