lschacmic heart disease is a major cause of death in the western world. The manifestation of this disease can be chest pain, heart attack or sudden cardiac death. Coronary heart disease (CHD) mortality is positively related to dietary saturated fat [I] . Such diets are correspondingly low in polyunsaturated fatty acids, in particular linoleic acid [2]. There is now ample support from cross-sectional and longitudinal studies that diets low in polyunsaturated fatty acids, whether of plant or fish oil origin, i.e. n 6 or ti 3 , may predispose to CHD 131. Ventricular fibrillation, a chaotic disturbance of the normal rhythm of the heart, occurs during the early, and hence potentially reversible, phase of an acute heart attack and is the principal cause of sudden cardiac death. It is not possible t o predict those who are at risk of imminent sudden cardiac death, because of the nature of the disease. Most of our current knowledge of factors predisposing to ischaemic arrhythmias has been derived from animal models. Acute myocardial ischaemia is induced by ligation of a major coronary artery and the resultant early appearance of arrhythmias is similar to that in man (heart models are widely used t o test the efficacy of anti-arrhythmic treatment in vivo or in vitro). Detailed recommendations on the conduction of such experiments have been proposed to ensure adequate group sizes, uniform definition of serious arrhythmias and awareness o f the requirement to exclude the influence of confounding factors (i.e. ischaemic area, heart rate, etc.) 141. Early studies examined the effect of large dietary supplements of linoleic acid-rich oils. Linoleic acid-rich diets, fed over varying periods ( 12 weeks12 months), reduced ischaemic ventricular fibrillation in anaesthetized and conscious rats [ 5-71. The polyunsaturated to saturated fatty acid (I ' / .S) ratios were extremely high (/'/S 6) and bear little resemblance to the human diet ( / ' / .S= 0.3), and dietary vitamin and mineral intake are not always balanced. The mechanisms of the reduction in arrhythmias is assumed to be due t o increased availability of arachidonic acid in myocardial phospholipids for prostanoid synthesis [ 71.