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Myocardial Uptake of Circulating Triglycerides in Nondiabetic Patients With Heart Disease

¹ Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota
² Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota

Address correspondence and reprint requests to John M. Miles, MD, Endocrine Research Unit, Mayo Clinic, 200 First St. SW, Rochester, MN 55905. E-mail: miles.john{at}mayo.edu

Abbreviations: FFA, free fatty acid; LPL, lipoprotein lipase; LPL_c, myocardial LPL

Animal studies indicate that oversupply of fatty acids derived from the action of cardiac lipoprotein lipase (LPL) on plasma lipoproteins may contribute to myocardial dysfunction. However, the contribution of circulating triglycerides to myocardial fatty acid supply in humans is not known. Six postabsorptive nondiabetic subjects who were scheduled for diagnostic coronary angiography were studied. ¹⁴C oleate and a lipid emulsion labeled with ³H triolein were infused to assess myocardial uptake of free fatty acids (FFAs) and triglycerides, as well as myocardial spillover of LPL-generated fatty acids. Six paired blood samples were taken from the femoral artery and the coronary sinus. Coronary sinus concentrations of unlabeled triglycerides were slightly, but not significantly, lower than arterial (P = 0.12), whereas labeled triglyceride concentrations were significantly lower in the coronary sinus than in the artery (P < 0.05; extraction fraction 11%). Triglycerides and FFAs accounted for 17% and 83%, respectively, of myocardial fatty acid uptake. Systemic and myocardial fractional spillover of LPL-generated fatty acids was 49.0 ± 7% and 34.7 ± 13%, respectively. The myocardium was a minor contributor to systemic triglyceride uptake (3%) and a trivial contributor to systemic FFA production (0.5%). These results indicate that circulating triglycerides may be a significant source of fatty acids for myocardial respiration.

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