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Fatty Acid Accumulation and Abnormal Lipid Deposition in Peripheral and Border Zones of Experimental Myocardial Infarcts

University of Texas (Southwestern) Medical School, Dallas, Texas

Correspondence: For reprints contact: James T. Willerson, Ischemic Heart Center, L5.134, The University of Texas Health Science Ctr., 5323 Harry Hines Blvd., Dallas, TX 75235.

ABSTRACT

Twenty-eight dogs with acute anterior myocardial infarcts due to proximal occlusion of the left anterior descending coronary artery (LAD) were studied at various periods following the occlusion to determine: (a) the time course and location of abnormal lipid accumulation after infarction, (b) the degree of muscle-cell injury associated with increased lipid deposition, and (c) whether uptake of fatty acid from the circulating fat pool contributes to lipid accumulation in certain myocardial regions. The findings show that myocardial lipid accumulation begins as early as 6 hr after proximal LAD occlusion. The increased lipid deposition occurs as non-membrane-bound lipid droplets in muscle cells with and without ultra-structural evidence of irreversible injury. Analysis of tissue uptake of intravenously injected [¹⁴C] oleic acid conjugated with albumin revealed relatively selective concentration of label in the peripheral and border regions of the infarct, but occasionally even the central subendocardial portion of the infarct concentrated the fatty acid. Thin-layer chromotography showed that most of the label was associated with the triglyceride fraction when the radiolabeled fatty acid was injected 6 or 24 hr after LAD occlusion. These myocardial cellular and topographical alterations will have to be considered when labeled fatty acids are used for imaging acute myocardial infarcts and/or if attempts are made to identify myocardial fat-laden cells scintigraphically.

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