Abstract
The epidemiological studies of Kromann and Green1 on the low mortality rate of Greenland Inuits from ischemic heart disease led to the suggestion by Bang et al2 that despite the high total fat intake of the Eskimos, this low mortality rate was due to the abundance of n-3 fatty acids from seafood in their diet. This hypothesis initiated research by many investigators into possible antiatherogenic effects of n-3 PUFAs. Much has been learned regarding physiological and biochemical changes induced by this class of essential fatty acids that could have potential antiatherogenic effects; nevertheless, controversy persists in the current literature regarding the clinical evidence for beneficial effects from fish ingestion (the major dietary source of n-3 fatty acids) on the development of coronary heart disease.3 4 Studies seeking a resolution to the potential antiatherogenic effects of n-3 PUFA will undoubtedly continue.5 Meanwhile, on the basis of earlier sporadic suggestions that n-3 PUFA might possess antiarrhythmic effects,6 7 McLennan and coworkers8 9 pursued this possibility. They showed in feeding studies in rats that when saturated fats or olive oil is the major dietary fat, a high incidence of fatal, irreversible VF occurs from experimental coronary artery ligation, which was significantly reduced when the dietary fat was vegetable oil but was essentially abolished by fish oil. They have confirmed their basic finding in marmosets.10 It is not our purpose in this brief review to discuss possible antiatherogenic effects of n-3 PUFA or the role of coronary heart disease in causing malignant ventricular arrhythmias. Clearly, coronary heart disease is the major clinical setting in which malignant ventricular arrhythmias occur today, and myocardial ischemia is the most common trigger eliciting such arrhythmias. Rather, we will focus on our recent studies on the mechanism of the apparent antiarrhythmic actions …
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