Plasma post heparin lipoprotein lipase activity (LLA) has been studied in patients with hyper- and hypothyroidism and in rabbits made thyrotoxic with thyroxine. The hypothyroid patients had high triglyceride and low LLA values as compared with a control group of healthy subjects. Statistically highly significant negative correlation was found between the triglycerides in fasting patients and the post heparin LLA, indicating a causal relationship, possibly with disturbance of chylomicron degradation due to low LLA in the arterial wall. However, relatively low LLA values were also demonstrated in hyperthyroid patients as well as in rabbits following treatment with thyroxine for 3 weeks. A stimulating effect of the thyroid hormones on the synthesis and degradation of lipoprotein lipase may be a possible explanation for these apparently contradictory findings.

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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.

No abstract

Studies of the fatty acid composition in cholesterol esters, phospholipids and triglycerides in serum have been made in 73 men with acute myocardial infarction (AMI) and in 32 healthy men of comparable age. Of the patients 36 had previously had a myocardial infarction or a history of angina pectoris, while for the other 37 the present attack was their first symptom of coronary heart disease (CHD). Significant differences in fatty acid composition were observed between the two groups of patients with higher percentages of linoleic acid in patients with old CHD. Since linoleic acid proportions in serum to a large extent reflect dietary habits, it is thought that patients with an old CHD have been more assiduous in following diet recommendations given to the whole population, advocating “cholesterol‐lowering diets”, than subjects with no history of cardiac disease. It is concluded that data concerning fatty acid composition in patients with a history of old CHD cannot be used to evaluate dietary habits prior to the manifestation of CHD. It was demonstrated that in patients with an AMI as the first manifestation of CHD linoleic acid percentages were lower than in controls. The finding indicates dietary habits in the patients characterized by a high intake of saturated and monosaturated fats, low intake of essential fatty acids, and possibly a high intake of simple sugars. Differences were also observed in pentaenoic and hexaenoic acids, with higher values in the patient group. This finding does not support the assumption that pentaenoic and hexaenoic acids are significant in the prevention of CHD. In a smaller number of patients, admitted to the hospital within 6 hours after the initial attack of pain, studies were made on admission and on the following morning. These studies gave no indication of important changes in fatty acid composition occurring during the first 24 hours of the disease; and since all studies reported here were performed within 24 hours after onset of the attack, the results are probably representative of preinfarction fatty acid composition.