Objectives-Cardiac myocytes secrete apolipoprotein (apo)B-containing lipoproteins. Their function may be the removal of triglycerides when -oxidation of fatty acids is decreased, eg, during hypoxia. To test this hypothesis, we examined heart biopsies from patients undergoing coronary artery bypass graft (CABG, nϭ13) (MTP). ApoB forms the structural backbone of the triglyceride-rich lipoproteins acquiring neutral lipids during its translation and translocation into the lumen of the endoplasmatic reticulum. 1 MTP transfers the lipids onto the apoB polypeptide. 2 The apoB and MTP genes are expressed in the liver, intestine, and yolk sac. [1][2][3][4] In addition, the apoB and MTP genes also are expressed by cardiac myocytes, which secrete apoBcontaining lipoproteins. [5][6][7] In the intestine the apoB mRNA is edited, resulting in formation of a truncated apoB, ie, apoB48. The apoB mRNA is not edited in the heart, 5 and the heart secretes lipoproteins containing the full-length apoB, ie, apoB100. 7 The physiological importance of lipoprotein secretion from the heart is unknown. It has been proposed that lipoprotein formation in the heart serves as a pathway for removing triglycerides that are not used as fuel. 5,7 In the healthy heart, -oxidation of fatty acids provides Ϸ70% of the energy. 8 However, during ischemia, glucose becomes the major energy substrate. 9 Studies of experimentally infarcted rat and dog hearts have shown accumulation of lipid droplets in the border zone of the infarcted area. 10