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Eicosanoids represent a family of compounds derived primarily from arachidonic acid. It is now known that arachidonic acid can undergo metabolism via at least three distinct pathways, although the most readily understood are those resulting in prostaglandin or leukotriene formation via cyclooxygenase and 5-lipoxygenase, respectively. These products can be synthesized by the heart or can be released from accumulating neutrophils under various pathological conditions. Eicosanoids possess a wide array of pharmacological actions that could be of importance either in the initiation or modulation of various cardiac diseases. Here, we review the potential importance of eicosanoids to ischemic heart disease. Data are cited that examine the potential importance of these compounds to experimentally induced cardiac injury as well as clinically observed ischemic heart disease. Particular emphasis is placed on recent studies that document the relevance of endogenously synthesized arachidonic acid metabolites as well as the consequence of modulating eicosanoid synthesis through pharmacological or dietary means on cardiac injury under experimental or clinical situations.
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Morris Karmazyn (1989) studied this question.
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