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Editorials

The Modulated Dispersion Hypothesis Confirmed in Humans

Steven Poelzing, PhD and David S. Rosenbaum, MD

From the Heart and Vascular Research Center (D.S.R.), MetroHealth Campus of Case Western Reserve University, Cleveland, Ohio; and the Nora Eccles Harrison Cardiovascular Research and Training Institute (S.P.), University of Utah, Salt Lake City, Utah.

Correspondence to David S. Rosenbaum, MD, Heart & Vascular Center, MetroHealth Campus, Case Western Reserve University, 2500 MetroHealth Dr, Hamman 330, Cleveland, OH 44109. E-mail drosenbaum@metrohealth.org

Key Words: depolarization • electrophysiology • fibrillation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Conventional teaching suggests that the initiation of arrhythmias requires an initiating "trigger" and a suitable "substrate." Moreover, the hallmark of electro-anatomic substrates for reentrant arrhythmias is spatially heterogeneous structural or electrophysiological properties. The fundamental requirement of heterogeneous refractory properties is not a new concept and was recognized by the early pioneers of cardiac electrophysiology^1,2 Under these conditions, an appropriately timed triggering beat will fail to propagate into the most refractory zones, leading to unidirectional block and reentry. One common form of spatially inhomogeneous electric properties is often referred to as "dispersion of repolarization," in which action potential duration (APD) between neighboring myocytes spanning the epicardial surface^2,3 or across the transmural wall⁴ vary to form spatial gradients of repolarization. It is the differences in ion channel composition and density between myocytes that presumably underlie spatial dispersion of repolarization.

Article see p 162

Although the "trigger" and "substrate" for arrhythmias are often considered independent phenomena, Laurita et al^5–7 previously demonstrated that a premature trigger can interact with and actively modulate spatial dispersion of repolarization through a process referred to as "modulated dispersion." According to modulated dispersion, progressive shortening of premature coupling interval will, in turn, progressively reduce dispersion of repolarization, but at very short coupling intervals dispersion of repolarization will again rise sharply. Importantly, the coupling interval–dependent modulation of repolarization gradients directly impacted vulnerability to ventricular arrhythmias, with the heart becoming relatively resistant to arrhythmia when repolarization homogenized (at intermediate coupling intervals). Subsequently, the heart became more susceptible to arrhythmias when repolarization . . . [Full Text of this Article]

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