Abstract
This chapter discusses the various mechanisms by which phospholipid turnover is controlled, along with the consequences of altered phospholipid turnover on arrhythmias formation. The changes to the phospholipid membrane including the alterations in phospholipid turnover rates and alterations in the composition of the phospholipids membrane contribute to the development of arrhythmias. Phospholipids of the sarcolemmal and sarcoplasmic reticulum membranes of the heart are composed of two main classes, diacyl phospholipids and plasmalogen phospholipids. Combined, these phospholipids form a lipid bilayer that contains the integral membrane ion channels and pumps that determine the electrophysiological function of cardiac cells. During and following an ischemic insult, the composition of these diacyl and plasmalogen phospholipids can change rapidly, resulting in a change in the electrophysiological stability of the cell. During ischemia, fatty acid oxidation is inhibited, leading to an accumulation of fatty acid metabolites. Some of these metabolites, particularly long chain acyl-CoA and long chain acylcarnitine, are amphiphic compounds that can interact with the phospholipid membrane and contribute to arrhythmias formation. Although the overall myocardial phospholipid content does not change during short periods of ischemia, the accumulation of lysophospholipids can be detected readily in this time frame. The formation of lysophospholipids can occur within minutes of the onset of ischemia. The release of lysophospholipids has also been observed in patients undergoing stress tests after coronary artery bypass grafting.
Published Version
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