Key result
Acute MI is linked to early free fatty acid spikes and later cholesterol drops, potentially thyroxine-driven.
Observational
Acute myocardial infarction is associated with early, dynamic changes in serum lipids and fatty acids, hypothesized to be driven by thyroxine-mediated beta-lipoprotein degradation.
Post-MI lipid shifts should not alter practice; leaves open thyroxine as driver of beta-lipoprotein changes.
Disturbances in serum lipids and in their fatty acid composition have been studied during the early phase of acute myocardial infarction. A rise in free fatty acids was observed within 2–6 hours after onset of pain, and on the 3rd‐4th day a decline in concentrations of cholesterol and phospholipids together with changes in their fatty acid composition. Linoleate percentages decreased, while arachidonate and palmitate increased. For triglycerides elevations in palmitate and oleate and a decline in lino‐leate were observed in the same period. It is concluded that an increase in β‐lipoprotein degradation—and not a decline in their synthesis—is the mechanism responsible for lowering of cholesterol and phospholipids. Various endocrine factors occurring in response to stress may be involved in the mechanisms leading to lipoprotein degradation, but thyroxine is the only hormone having nearly the same effect on lipid metabolism as that of acute serious illness. It is postulated that alterations in the free thyroxine level contribute more to the homeostatic response to serious illness than has been generally believed hitherto, and that thyroxine is the main cause of the changes in β‐lipoproteins observed after myocardial infarction.
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Knut Kirkeby (1972) conducted an observational in Acute myocardial infarction. Acute myocardial infarction was evaluated on Changes in serum lipids and fatty acid composition. Acute myocardial infarction was associated with an early rise in free fatty acids followed by a decline in cholesterol and phospholipids, postulated to be driven by thyroxine.
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