Serum total and lipid-bound sialic acid levels following acute myocardial infarction

Although serum total sialic acid has been shown to be a cardiovascular risk factor, with elevated levers associated with increased cardiovascular mort ality and also with cerebrovascular disease, the reason for the elevation i n serum sialic acid content remains obscure. It has been shown that an incr eased output of serum proteins by the liver due to some type of acute phase reaction may be one of the possible sources of an increased serum sialic a cid concentration in patients with myocardial infarction. An increase in th e activity of sialidase, which cleaves the terminal sialic acid residues fr om oligosaccharides, glycoproteins and gangliosides, may also play an impor tant role in the elevation of serum total sialic acid in myocardial infarct ion. Elevated serum total sialic acid in the blood might result either from the shedding or secreting of sialic acid from the cell membrane surface, o r releasing of cellular sialic acid from the cell into the bloodstream due to cell damage after myocardial infarction. The purpose of the present stud y is to investigate serum total and lipid-bound sialic acid and the enzymes serum lactate dehydrogenase, creatine kinase and aspartate aminotransferas e in patients with acute myocardial infarction, at 24 h post-infarction (da y 1), 48 h post-infarction (day 2) and 72 h post-infarction (day 3). A poss ible role of cell damage in the elevation of serum total and lipid-bound si alic acid levels in these patients was also evaluated. In this study, 40 pa tients with myocardial infarction ranging in age from 42 to 68 years, and 2 6 healthy volunteers ranging in age from 45 to 71 years were included. Seru m total sialic acid determination was carried out by the thiobarbituric aci d method of Warren and lipid-bound sialic acid by the method of Katopodis. Our data shows that a) there is a gradual increase in the levels of serum t otal sialic acid and lipid-bound sialic acid during the first three days af ter the acute myocardial infarction and b) the elevation in serum total sia lic acid revels correlates with the elevation in lactate dehydrogenase acti vity only on day 1 following infarction. Therefore, either the shedding or secreting of sialic acid from the cell or cell membrane surface may be part ly responsible for an increased serum sialic acid concentration especially on day 1 following myocardial infarction.