Lecithin: cholesterol acyltransferase and lysolecithin in coronary atherosclerosis.
Of 100 arteriographically examined, hospitalized, male patients, those without myocardial infarctions were divided into the following categories: zero-, one-, two-, and three-vessel disease; patients diagnosed with myocardial infarction were classified separately. The fasting plasma samples from these patients were examined for concentrations of triglycerides and total cholesterol, lipoprotein profile, lecithin: cholesterol acyltransferase (LCAT) activity, and lysolecithin ( LPC) concentration. Those parameters in this group which are commonly determined were consistent with the clinical classification of these patients. Of those remaining parameters, the LCAT activity was increased as the severity of coronary atherosclerosis increased and the changes in the activity of this enzyme were appropriately reflected by increases in LPC concentration and decreases in the proportion of the plasma cholesterol unesterified. The results of this study suggest that increased, rather than decreased, plasma LCAT activity and increased LPC concentrations are characteristic of coronary atherogenesis. The plasma concentrations of LPC observed in these atherosclerotic patients are more than sufficient to qualify this substance for its previously proposed roles of mediator of transmembrane diffusion of LDL and as an inhibitor of platelet aggregation.[1]References
- Lecithin: cholesterol acyltransferase and lysolecithin in coronary atherosclerosis. Wells, I.C., Peitzmeier, G., Vincent, J.K. Exp. Mol. Pathol. (1986) [Pubmed]
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