Abstract

Fatty acids are the preferred physiological substrate for oxidative energy production in the heart (Neely et al., 1972, 1974). On the other hand, there is good evidence to believe that the high levels of non-esterified fatty acids observed in patients after myocardial (Kurien et al., 1966; Oliver, 1972; Opie, 1975) infarction may be harmful to jeopardized myocardium. Thus, fatty acids have been associated with increased risk of arrhythmias in both patients and experimental animals exposed to myocardial ischaemia (Mjos et al., 1974; Mjos, 1978). High levels of fatty acids have also been shown to depress recovery of mechanical function in both hypoxic rat hearts (Henderson et al., 1970) and ischaemic swine hearts (Liedtke et al., 1978).

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