FATTY-ACID ACCUMULATION AND ABNORMAL LIPID DEPOSITION IN PERIPHERAL AND BORDER ZONES OF EXPERIMENTAL MYOCARDIAL INFARCTS

  • 1 January 1978
    • journal article
    • research article
    • Vol. 19  (3) , 276-283
Abstract
Dogs (28) 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: time course and location of abnormal lipid accumulation after infarction, degree of muscle-cell injury associated with increased lipid deposition and whether uptake of fatty acid from the circulating fat pool contributes to lipid accumulation in certain myocardial regions. Myocardial lipid accumulation apparently begins as early as 6 h after proximal LAD occlusion. Increased lipid deposition occurs as nonmembrane-bound lipid droplets in muscle cells with and without ultrastructural evidence of irreversible injury. Analysis of tissue uptake of i.v. 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. TLC showed that most of the label was associated with the triglyceride fraction when radiolabeled fatty acid was injected 6 or 24 h after LAD occlusion. These myocardial cellular and topographical alterations probably should 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.