Key result
Ischemic calcium mishandling drives ectopy and reentry, highlighting potential novel antiarrhythmic targets.
Altered intracellular calcium handling plays a critical role in the genesis of ventricular arrhythmias during acute ischemia, presenting potential novel targets for antiarrhythmic therapy.
May identify calcium-handling pathways as antiarrhythmic targets in ischemia; leaves open clinical translation pending prospective trials.
Acute ischemia results in deadly cardiac arrhythmias that are a major contributor to sudden cardiac death (SCD). The electrophysiological changes involved have been extensively studied, yet the mechanisms of ventricular arrhythmias during acute ischemia remain unclear. What is known is that during acute ischemia both focal (ectopic excitation) and nonfocal (reentry) arrhythmias occur, due to an interaction of altered electrical, mechanical, and biochemical properties of the myocardium. There is particular interest in the role that alterations in intracellular calcium handling, which cause changes in intracellular calcium concentration and to the calcium transient, play in ischemia-induced arrhythmias. In this review, we briefly summarize the known contributors to ventricular arrhythmias during acute ischemia, followed by an in-depth examination of the potential contribution of altered intracellular calcium handling, which may include novel targets for antiarrhythmic therapy.
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Baumeister et al. (2016) conducted a review in Acute Ischemia and Ventricular Arrhythmias. Altered intracellular calcium handling was evaluated. Alterations in intracellular calcium handling during acute ischemia play an important role in both ectopic excitation and reentrant activity, presenting potential novel targets for antiarrhythmic therapy.
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