.1. Endothelial Damage And Acute Myocardial Infarction 2.ace Gene Insertion / Deletion Polymorphism And Plasma Ace Level And Myocardial Infarction

Vascular endothelium is now believed to be an active participant in the maintenance of vascular tone and regulation of blood flow. Endothelium also prevents platelet and leukocyte activation on the luminal side of the vessel wall. The functional intact endothelium plays a major role in maintaining vascular homeostasis and thrombus-free surface. Disturbance in the structure and function of endothelium are associated with vasoconstriction and intravascular thrombosis in atherosclerosis and acute myocardial infarction.Using the circulating endothelial cells (CEC) as an endothelial injury indica-tor,and the plasma level of endothelin(ET-1) as the functional marker of the vascular endothelial cells, a dynamic study was taken in 41 patients with AMI and 21 normal individuals. The CEC were isolated and counted by Percoll solution density gradient centrifugation from the blood samples, The CEC were identified by FVIII-R Ag by an indirect immunoflurescent assay. The plasma concentration of ET-1 was measured by radioimmunoassay kit. The CEC and plasma ET-1 were measured 4-7 times over a 72h period after acute myocardial infarction(AMI). All patients with AMI were divided into two groups: in Group A included 26 patients with uncomplicated AMI, Group B 15 patients with hemodynamic or ischemic sequlae. The plasma ET-1 levels in Group A rose sharply after the onset of chest pain reached a peak level of 10.30±2.96pg/ml (P<0.01, compared with values in control subjects). and returned gradually towards a normal range by 72h, the number of CEC showed a similar course of changes, reaching a peak of 11.40±3.06 cells/0.9ul at 4h, but remaining elevated by 72h (p<0.01, compared with values in control subjects). Patients in group B demonstrated a similar rapid increase in plasma ET-1 and the number of CEC to peak values of 12.96±223pg-/ml and 15.20±2.28cells/0.9ul respectively; however, plasma ET-1 and the number of CEC remained elevated in these patients, becoming significantly different from values in group A in each time point. There was no correlation between peak value in creatine kinase and peak ET-1 or peak CEC in either group. Furthermore, left ventricular ejection fraction did not correlate with the increases in ET-1 and CEC in either group, while a significant positive correlation was present between ET-1 and CEC in both group.ConclusionThe rapid increase in plasma ET-1 and CEC associated with the onset of infarction suggests that they may provide markers of endothelial perturbation in the early phase of coronary ischemia or even contribute to alterations in myocardial perfusion. The sustained increase in plasma ET-1 and CEC in patients demonstrating complications of myocardial infarction might reflect continuing ischemia or marked depression in ventricular function in patients.