[The relationship between the level of circulating endothelial progenitor cells CD34+; and carotid artery arteriosclerosis in youth and middle aged patients with essential hypertension].

OBJECTIVE: To explore the relationship between the level of circulating endothelial progenitor cells (EPCs) CD34+ with the Framingham cardiovascular risk factors, or with the carotid artery intima-media thickness (IMT), and to evaluate the value of circulating EPCs CD34+ level as a cytological marker of early vascular lesion in youth and middle aged essential hypertension (EH) patients. METHODS: A total of 62 patients with EH aged between 25 to 45 were enrolled as study group and 20 healthy people were enrolled as control group. EH patients were stratified with cardiovascular risk factors according to Framingham risk factors score into low-risk group with 18 cases, mid-risk group with 14 cases, high-risk group with 17 cases, and extremely high-risk group with 13 cases. The level of circulating EPCs CD34+, carotid artery IMT were respectively measured. The relationship between the level of circulating EPCs CD34+ and Framingham cardiovascular risk factors score, carotid artery IMT was analyzed. RESULTS: The level of circulating EPCs CD34+ was gradually decreased with an increase of the Framingham risk factors score in each hypertensive subgroup [low-risk group: (0.12+/-0.02)%, mid-risk group: (0.07+/-0.03)%, high-risk group: (0.04+/-0.03)%, extremely high-risk group: (0.01+/-0.01)%], and they were significantly lower than that in control group [(0.15+/-0.03)%], and there was a significant difference among hypertensive subgroups (P<0.05 or P<0.01). Carotid artery IMT was significantly thicker among hypertensive subgroups [low- risk group: (0.80+/-0.07) mm, mid-risk group: (1.11+/-0.08) mm, high-risk group: (1.26+/-0.10) mm, extremely high-risk group: (1.45+/-0.09) mm], and there was a significant difference between each hypertensive group and that of control group [(0.73+/-0.08) mm, all P<0.01]. There was also statistical significance among hypertensive subgroups (P<0.05 or P<0.01). There was a negative correlation between the level of circulating EPCs CD34+ and Framingham risk factors score (r=-0.875, P<0.01), and also a negative correlation with carotid artery IMT (r=-0.852, P<0.01). CONCLUSION: There was a significant correlation between the level of circulating EPCs CD34+ with Framingham risk factors score and also carotid artery IMT in EH patients. Circulating EPCs CD34+ could be a cytological marker of early vascular lesion in hypertension patients.

[Evolution of fibrinolysis status with D-dimer level and the rate of plasminogen activator inhibitor type-1/D-dimer in acute coronary syndrome patients complicated with impaired glucose tolerance].

OBJECTIVE: To study the status of fibrinolytic inhibition in patients with acute coronary syndrome (ACS) complicated with impaired glucose tolerance (IGT) and to evaluate the effect of fibrinolytic inhibition on treatment and prognosis. METHODS: The subjects were divided into three groups included 39 patients with ACS without diabetes mellitus, 37 patients with IGT+ACS and 36 patients with ACS+noninsulin-dependent diabetes mellitus (NIDDM). Twenty healthy people were randomized to be control group. The plasma levels of tissue type plasminogen activator (t-PA), plasminogen activator inhibitor type-1 (PAI-1) and plasma D-dimer were detected by enzyme linked immunoadsorbent assay (ELISA) technique. The index of status of fibrinolysis was detected with the plasma levels of PAI-1, D-dimer and the ratio of PAI-1/D-dimer. This index was used to evaluate the status of fibrinolytic inhibition and the clinical out come in patients with AMI. RESULTS: Plasma level of PAI-1 was significantly higher in IGT+ACS patients and NIDDM +ACS patients than that in ACS(P<0.05), but the plasma level of D-dimer raised from basic level was significantly lower in IGT+ ACS patients and NIDDM+ACS patients than that in ACS (P<0.05). The ratio of PAI-1/D-dimer was significantly higher in IGT+ACS patients and NIDDM +ACS patients than that in ACS or in control group (P<0.01). For AMI patients in treatment groups, the rate of reperfusion after the thrombolytic was significantly lower and the rate of incidences in pump failure was significantly higher in IGT+ACS patients and NIDDM+ACS patients than that in ACS, too (P<0.01 and P<0.05). The incidences of serious arrhythmia, re-infarction and death were also higher in IGT+ACS patients and NIDDM +ACS patients. CONCLUSION: The fibrinolytic inhibition is existed in IGT+ACS group patients. The plasma level of D-dimer combined with the ratio of PAI-1/D-dimer could be used to be the evidence and to be the index to evaluate the status of fibrinolytic inhibition and prognosis.