title: Dietary fatty acids and myocardial function.
abstract: It is widely recognized that dietary polyunsaturated fatty acids (PUFA's) and cholesterol can profoundly influence the development of atherosclerotic plaques in coronary vessels, which may lead to myocardial infarction. The possibility that dietary fatty acids may also directly influence cardiac function has received less attention. We therefore reviewed the evidence of the effects of dietary fatty acids, in particular n-3 and n-6 PUFA's, on myocardial phospholipid fatty acid composition and cardiovascular performance. Heart organelles appear to incorporate uncommon fatty acids like 22:1 and trans- 18:1. Diets enriched with 22:1 induce myocardial lipidosis. N-9, n-6 and n-3 families compete among membrane C20 and C22 acids. Several studies have dealt with the relation between diet-induced changes of cardiac membrane (sarcolemma, sarcoplasmic reticulum and mitochondria) phospholipids and membrane function. In view of the variety of diets used and of the membrane functions studied, the results do not permit equivocal interpretation. Several investigators have reported an altered stress response of the heart due to a change of PUFA's in the diet. In rats fed with a low 18:2n-6/18:3n-3 ratio combined with relatively low amounts of saturated fatty acids, a high incidence of myocardial lesions has been observed. Pigs are less sensitive but more susceptible to the development of vitamin E deficiency, when the dietary PUFA content is high. Increased contractility and coronary flow rate have been reported for Langendorff-perfused hearts of rats fed 18:2n-6-rich diets. The effects on coronary flow rate are possibly related to alterations in eicosanoid synthesis, which may also contribute to the reduction by n-6 or n-3 PUFA's in infarct size, magnitude of recovery of function and suppression of reperfusion arrhythmias following release of a coronary artery ligation. On the other hand, increased peroxidation of membrane lipids, due to their high content of n-3 PUFA, may be deleterious.
authors.affiliation: Department of Biochemistry, Medical Faculty, Erasmus University Rotterdam, The Netherlands.
authors.forename: J M
authors.initials: JM
authors.lastname: Lamers
authors.forename: J M
authors.initials: JM
authors.lastname: Hartog
authors.forename: P D
authors.initials: PD
authors.lastname: Verdouw
authors.forename: W C
authors.initials: WC
authors.lastname: Hülsmann
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000517:prevention & control; D002395:Catecholamines / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects; D004042:Dietary Fats, Unsaturated / Q000378:metabolism / Q000494:pharmacology*; D005227:Fatty Acids / Q000378:metabolism / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D008563:Membrane Lipids / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism
chemical_list: D002395:Catecholamines; D004042:Dietary Fats, Unsaturated; D005227:Fatty Acids; D008563:Membrane Lipids; D010743:Phospholipids