Matter of Fat: Are Lipids Antiarrhythmic?

Abstract

After the occlusion of a coronary vessel in the heart, ischemia and subsequent infarction of cardiac tissue occurs because of an inadequate supply of blood, resulting in a deficiency of oxygen and glucose to the muscle cells. Within minutes, there are apparent changes in the ECG indicating cardiac cellular electric disorders, namely ST elevation myocardial infarction (MI). Because the processes postocclusion are complicated, the complex nature has been dissected into different facets in various in vitro studies. Solutions can be made to mimic ischemia and superfused over paced multicellular and single-cell preparations of cardiac tissues. Under these conditions, one can apply voltage clamp/Ca2+ imaging to define how specific biochemical changes that occur during this acute period affect ion channel behavior and signaling pathways. Single cells can be subjected to hypoxia, uncouplers of the mitochondrial oxidative chain, inhibitors of glycolysis, solutions containing a high concentration of K+ and low H+, and solutions deficient in glucose, amphiphiles, free radicals, catecholamines, as well as stretch. Professor Carmeliet1 summarized these data in his 1999 review. This list is by no means complete and ignores the consequences of certain agents, for example, unabated reactive oxygen species that are potentiated by an ischemia-induced shift in anaerobic metabolism. This generates superoxide anion on reperfusion. Reactive oxygen species can modify protein structure and function in fundamental ways, one of which is by forming reactive lipid species from the oxidation of lipids.2 However, in most studies the experimental tissues used are from normal hearts. Article see p 1481 The study of Baartscheer et al3 in this issue focuses on the effects of changes in the lipid composition of the membrane and ion channel function before the acute effects of …