Why the study?
The interaction of cellular architecture and metabolic and ionic changes causing arrhythmogenesis in ischemic myocardium remains poorly understood.
This review highlights the need for advanced experimental methods, such as mathematical and transgenic mouse models, to better understand the fundamental mechanisms of ischemia-related ventricular arrhythmias.
In ischemic myocardium, cellular architecture and heterogeneous changes in metabolic and ionic conditions interact to cause spatial and temporal heterogeneity of electrical properties predisposing to lethal ventricular arrhythmias. Yet, the details of their interaction, vis-à-vis the initiation and maintenance of reentry, remain poorly understood. Future studies are needed to address the mechanisms of the initial premature beat, reentry, and formation of wavebreaks contributing to ventricular fibrillation. New experimental methods including mathematical and transgenic mouse models are promising techniques to study these phenomena and thereby provide new insights into the fundamental mechanisms of ischemia-related arrhythmias.
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Wayne E. Cascio (2001) conducted a review in Myocardial Ischemia.
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