The pathogenesis of post-cardiac injury syndronme was studied prospectively in 62 patients who underwent coronary bypass grafting. Preoperative and serial postoperative titres of actin and myosin antibodies were measured by an enzyme linked immunosorbent assay. Perioperative cumulative release of serum aspartate and alanine aminotransferases, lactate dehydrogenase, and creatine kinase was calculated by approximation formulas that are used to estimate infarct size. Complete post-cardiac injury syndrome developed in eight (13%) patients and an incomplete syndrome developed in 16 (26%). There was a significant correlation between frequency and intensity of the syndrome and the ratio of postoperative to preoperative titres of actin and myosin antibodies. Furthermore, there was a significant correlation between the cumulative release of lactate dehydrogenase, serum aspartate aminotransferase, and creatine kinase and the number of coronary vessels that were grafted, but no correlation was found between the incidence of post-cardiac injury syndrome and the number of coronary bypasses grafted or between the cumulative enzyme release and the postoperative immunological response against the major contractile proteins, actin and myosin. The amount of enzymes released during coronary bypass surgery seems to be a good indicator of the extent of myocardial damage during operation but it does not determine either the incidence of post-cardiac injury syndrome or the postoperative immunological response against the main contractile proteins actin and myosin.Post-cardiac injury syndrome is a frequent complication of cardiac surgery' -7; it is seen less often after acute myocardial infarction,7 8 despite the generally more severe myocardial damage produced by infarction. Furthermore, post-cardiac injury syndrome was found to be significantly more frequent after valve replacement surgery than after coronary bypass operation.69 According to Engle et al more severe myocardial damage after valve replacement explains this observation.9 Aortic valve replacement gives rise to a greater cumulative enzyme release of creatine kinase, creatine kinase MB, and a hydroxybutyrate dehydrogenase than coronary artery bypass grafting which in turn gives rise to greater cumulative enzyme release than mitral valve replacement.10o 1 Thus the reason for the significantly Requests for reprints to Dr Ivan De Scheerder, higher frequency of post-cardiac injury syndrome after valve replacement surgery than after coronary artery bypass grafting remains controversial. De Scheerder etal demonstrated that the difference in occurrence of post-cardiac injury syndrome after cardiac surgery and acute myocardial infarction correlated well with the difference of post-cardiac injury humoral immune response against myocardial tissue and the major contractile proteins, actin and myosin,7 suggesting that this immune response is important in the pathogenesis or postcardiac injury syndrome.We have studied the correlation between the tissue damage during coronary artery bypas...
The aim of this study was to determine whether substituting enzymatically interesterified butter for native butter in the usual diet affects lipid and lipoprotein levels in man. Parameters studied were serum total cholesterol, LDL-cholesterol, HDL-cholesterol, free cholesterol, phospholipids, triglycerides, apoA1 and apoB and the fatty acid composition of serum triglycerides, free fatty acids, phospholipids and cholesterol esters. Subjects were healthy volunteers and a controlled design was used. The only mathematically significant difference found when interesterified butter was substituted for butter was an about 7% lower fraction of oleic acid in the serum cholesterol esters (p = 0.005). In contrast to an earlier study where chemically interesterified butter fat was substituted for native butter, no indications are found in this study that replacing native butter by enzymatically interesterified butter, in amounts normally consumed, may have any beneficial effect on health.
is a haemoglobin-binding acute phase protein with three genetic types: Hp 1-1, Hp 2-1, Hp 2-2. We investigated 45 patients during the first 48 hours of acute myocardial infarction, and studied determinant factors and clinical correlates. Upon hospital admission, serum haptoglobin concentration was increased (1.95 ± 0.94 g/1, mean ± SD, P < 0.001) versus the reference population (0.97 ± 0.46 g/l, n = 107), independent of haptoglobin type: 1.84 ± 0.64 g/1 (Hp 1-1, n = 11) (P < 0.01), 1.98 ± 0.79 g/l (Hp 2-1, n = 25) (P < 0.001), 1.98 ± 1.58 g/l (Hp 2-2, n = 9) (P < 0.001). Moreover, during the first hours of hospitalization, a temporal lowering of haptoglobin was observed suggesting acute haemolysis, independent of the haptoglobin type. Minimal serum haptoglobin was reached 9.6 ± 5.8 hours after admission. The amplitude of the haptoglobin decrease correlated with initial serum haptoglobin (r = 0.78) and was more pronounced (P < 0.05) in men (0.53 ± 0.57 g/1) than in women (0.18 ± 0.17 g/1). Decrease of serum haptoglobin did not correlate with infarct size (based on creatine kinase-MB release). Out of the other acute phase proteins measured upon admission, only C-reactive protein was significantly increased (P < 0.05). During the next 36 hours, haptoglobin increased as a result of the acute phase response to myocardial injury. Our findings suggest that acute myocardial infarction is also preceded by an acute phase response, characterized by an initial high haptoglobin and followed by a temporal haptoglobin decrease due to haemolysis.
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