Abstract
Sudden cardiac death due to ventricular tachyarrhythmias is a threatening cause of mortality in patients after acute myocardial infarction [1, 2]. The risk for subsequent arrhythmic events is highest in those patients in whom an arrhythmogenic substrate is modulated by trigger factors [2]. The anatomical substrate usually develops in the border zone of a myocardial scar where bundles of muscle cells are separated by fibrotic barriers producing a fractionation of the activation wave front and slowing of conduction [3, 4]. In those areas an adequate trigger (e.g. VPB, ischemia, etc.) may then initiate re-entrant tachycardia which is considered to be a common complication of remote myocardial infarction [5–7]. Since effective means for termination of sustained ventricular arrhythmias and prevention of sudden arrhythmic death might currently be considered (e.g. implantable cardioverter-defibrillator) noninvasive identification of high risk patients is highly desirable. One challenging method is the non-invasive assessment of the anatomical substrate from which actual electrical derangement may generate.
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Faber, T.S., Malik, M. (1996). Signal averaged electrocardiogram. Current applications and limitations. In: Oto, M.A. (eds) Practice and Progress in Cardiac Pacing and Electrophysiology. Developments in Cardiovascular Medicine, vol 183. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0219-0_7
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