Lipids and cardiac arrhythmia.
In any discussion of lipids and heart disease it is beneficial from the outset to recognise that at least three different pathological processes may be involved. The first of these is atherosclerosis which involves the deposition of "fat" in the coronary vessels, another is thrombogenesis which describes the formation of blood clots in the coronary vessels, and the third is arrhythmia which refers to disorders in the beating of the heart which may become sufficiently serious to cause sudden cardiac death (SCD). Also it is this disturbance in the rhythmic beating of the heart which is responsible for much of the mortality from 'heart attacks' which occur 'outside-of-hospital' in societies like U.S.A., U.K. and Australia. It is this latter condition of cardiac arrhythmia which is the major concern of this review. Because it is often difficult to differentiate the role of lipids in 'heart disease' in man, it has frequently been assumed that all dietary fatty acids have similar effects on the different processes involved, and many unwarranted generalisations have been made which have led to conflicts of opinion amongst physicians and confusion in the lay public. From the animal studies discussed in this review, it is apparent that dietary fatty acids have an important role to play in determining the vulnerability of the myocardium to develop serious ventricular fibrillation (VF) and potentially lethal cardiac arrhythmia. In general, diets rich in saturated fatty acids promote a state of myocardial vulnerability, whilst diets rich in PUFA significantly diminish the probability of developing lethal disorders in cardiac rhythm when the heart is placed under pharmacological (or emotional) stress, or deprived of sufficient blood flow and supply of oxygen. Very recent experiments with the monounsaturated fatty acid (MUFA) oleic acid clearly demonstrate that, at least in rats subjected to ligation of their coronary artery, this acid is not 'neutral' as has been suggested by some for its role in atherosclerosis, but in fact is indistinguishable from saturated fatty acids in its effect in promoting arrhythmia during either regional ischaemia or reperfusion arrhythmia in this animal model of SCD.(ABSTRACT TRUNCATED AT 400 WORDS)
Charnock
J S
JS
Cardiac Research Unit, Glenthorne Laboratory, CSIRO, Australia.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000378:metabolism*; D016757:Death, Sudden, Cardiac / Q000209:etiology; D004041:Dietary Fats / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D051379:Mice; D017202:Myocardial Ischemia / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism
D004041:Dietary Fats