Key result
Prevention of adduction of highly reactive lipid species (isoketals) formed via lipid peroxidation is suggested to have antiarrhythmic effects in the post-myocardial infarction substrate.
This review highlights the mechanistic role of isoketals in ischemic arrhythmias and proposes that preventing their adduction could serve as a novel antiarrhythmic strategy.
Isoketal adduction prevention may reduce post-MI arrhythmias; hypothesis-generating and should not yet change practice.
Unabated reactive oxygen species (ROS) are potentiated by an ischemia-induced shift in anaerobic metabolism, which generates superoxide anion upon reperfusion and reintroduction of oxygen. ROS can modify protein structure and function in fundamental ways, one of which is by forming reactive lipid species from the oxidation of lipids. In this review, we discuss these pathways and discuss the literature that shows that these species can produce dramatic effects on cardiac ion channel function (eg, Na+ channel function). Furthermore, we review what is known about the generation of such in the highly remodeled post myocardial infarction substrate. We suggest prevention of adduction of these highly reactive compounds would be antiarrhythmic.
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Boyden et al. (2007) conducted a review in Ischemic Arrhythmias. Prevention of adduction of highly reactive lipid species (isoketals) was evaluated. Prevention of adduction of highly reactive lipid species (isoketals) formed via lipid peroxidation is suggested to have antiarrhythmic effects in the post-myocardial infarction substrate.
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