Effect of heparin-induced free fatty acid elevation on myocardial oxygen consumption in man

doi:10.1016/0002-9149(77)90158-8

The American Journal of Cardiology

Volume 40, Issue 3, September 1977, Pages 365-372

https://doi.org/10.1016/0002-9149(77)90158-8 Get rights and content

Abstract

To determine whether acute elevation of plasma free fatty acids influences myocardial oxygen consumption in man, 17 patients underwent a metabolic study consisting of serial measurements of coronary sinus blood flow, heart rate and aortic blood pressure and arterial and coronary sinus determinations of oxygen, carbon dioxide, glycerol and free fatty acids both before and for 30 minutes after the intravenous administration of a bolus dose of 5,000 units of heparin. Of the 17 patients, 9 (group A) were fasting, and 8 (group B) ingested 100 g of fat 3 hours before the study in order to enhance post-heparin lipolysis.

Marked elevation of arterial free fatty acid levels was seen in each group 30 minutes after administration of heparin (group A 713 ± 21 [mean ± standard error of the mean] to 1,757 ± 139 μmoles/liter, P < 0.001; group B 721 ± 57 to 2,668 ± 332 μmoles/liter, P < 0.001); significant increase in arterial-coronary sinus free fatty acid difference was also noted (group A 139 ± 11 to 298 ± 19 μmoles/liter, P < 0.001; group B 147 ± 11 to 334 ± 35 μmoles/liter, P < 0.001). Hemodynamic variables, including mean aortic pressure, heart rate, coronary sinus blood flow and coronary vascular resistance, were unchanged. Despite the marked increase in free fatty acids, myocardial oxygen consumption was unchanged 30 minutes after administration of heparin in both groups A and B. Myocardial triglyceride formation after heparin in both groups was suggested by (1) lack of change in cardiac respiratory quotient, (2) net myocardial glycerol uptake after heparin but not in the control state, and (3) oxygen extraction ratios totaling considerably in excess of 100 percent after heparin.

The data suggest that acute elevation of plasma free fatty acids to pathophysiologic levels after heparin-induced lipolysis has no measurable effect on myocardial oxygen consumption in patients in stable condition, probably because the excess free fatty acids are stored as triglycerides rather than oxidized.

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^☆: This research was supported in part by the Specialized Center of Research for Ischemic Heart Disease, Contract 1P17HL 17667-02, the Cardiovascular Research and Training Center, Program Project Grant HL 11,310 (Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute), National Institutes of Health Grant T01LM00154, Clinical Research Unit Grant M01-RR00032-13 (General Clinical Research Centers Program, Division of Research Resources), National Institutes of Health, Bethesda, Maryland and Project 5566-01 of the Veterans Administration, Washington, D. C.

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Clinical studyEffect of heparin-induced free fatty acid elevation on myocardial oxygen consumption in man☆

Abstract

Am J Cardiol

Lancet

Lancet

Lancet

Lancet

Lancet

J Biol Chem.

J Lipid Res

Lancet

J Mol Cell Cardiol

Lancet

J Lipid Res

J Mol Cell Cardiol

J Biol Chem

Biochim Biophys Acta

Am J Cardiol

Am J Cardiol

Lancet

Am Heart J

Effect of free fatty acid on the oxygen consumption of perfused rat heart

Am J Physiol

Effect of free fatty acids on myocardial function and oxygen consumption in intact dogs

J Clin Invest

Intravenous glucose tolerance, insulin, glucose, and free fatty acid levels after myocardial infarction

Br Med J

Plasma free fatty acid and catecholamine levels in patients with acute myocardial infarction

Br Heart J

Anticoagulant therapy of coronary thrombosis with myocardial infarction

JAMA

Limited use of anticoagulants in acute myocardial infarction: analysis of 1000 “good risk” cases

JAMA

Clearing factor, a heparin-activated lipoprotein lipase

J Biol Chem

Clinical study
Effect of heparin-induced free fatty acid elevation on myocardial oxygen consumption in man☆