Dofetilide-Induced Microvolt T-Wave Alternans

Marcantoni, Ilaria; Laratta, Rosita; Mascia, Guido; Ricciardi, Leonardo; Sbrollini, Agnese; Nasim, Amnah; Morettini, Micaela; Burattini, Laura

doi:10.1109/embc.2019.8857486

Cited by 1 publication

(1 citation statement)

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“…It has been known for several decades that APD alternans is suppressed or inhibited by verapamil (Marcantoni et al, 2019), caffeine (Wang et al, 2014), BayK8644 (Saitoh et al, 1988), nisoldipine (Saitoh et al, 1988), and ryanodine (Sun et al, 2018), all of which point to a mechanism related to [Ca 2+ ] i handling. Substantial follow-up studies have suggested that disturbances in every-other-beat [Ca 2+ ] i cycling constitute the main cause of AP alternans (Picht et al, 2006;Wang et al, 2014;Sun et al, 2018;Liu et al, 2019;Oropeza-Almazan and Blatter, 2020).…”

Section: Alternans Due To Instabilities Of [Ca 2+ ] I Handlingmentioning

confidence: 99%

Electrophysiological Mechanisms Underlying T-Wave Alternans and Their Role in Arrhythmogenesis

et al. 2021

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T-wave alternans (TWA) reflects every-other-beat alterations in the morphology of the electrocardiogram ST segment or T wave in the setting of a constant heart rate, hence, in the absence of heart rate variability. It is believed to be associated with the dispersion of repolarization and has been used as a non-invasive marker for predicting the risk of malignant cardiac arrhythmias and sudden cardiac death as numerous studies have shown. This review aims to provide up-to-date review on both experimental and simulation studies in elucidating possible mechanisms underlying the genesis of TWA at the cellular level, as well as the genesis of spatially concordant/discordant alternans at the tissue level, and their transition to cardiac arrhythmia. Recent progress and future perspectives in antiarrhythmic therapies associated with TWA are also discussed.

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