RESUMO
Objective:To investigate the safety and efficacy of tirofiban therapy in acute cerebral infarction patients having broadened therapeutic time window.Methods:Eighty-four acute cerebral infarction patients having broadened therapeutic time window (the onset time was within 4.5-8 h), admitted to our hospital from January 2016 to May 2018, were chosen in our study. Forty-two patients (treatment group), with the informed consent of himself or his family, received emergent cerebral angiography and treated with tirofiban (the load of tirofiban was pumped via the microductal artery, and the maintenance load was continuously pumped intravenously for 48 h) right after the angiography; the other 42 patients (control group) received emergent cerebral angiography and treated with intensive antiplatelet aggregation therapy right after the angiography; intensive lipid-lowering therapy was given in both groups. The efficacy, safety and follow-up rehabilitation were compared between the two groups. According to the locations of acute cerebral infarction, patients in the treatment group were divided into anterior circulation infarction subgroup ( n=24) and posterior circulation infarction subgroup ( n=18); the efficacy and follow-up rehabilitation were compared between the two subgroups. Results:Patients from the treatment group had significantly lower National Institutes of Health Stroke Scale (NIHSS) scores 48 h, 7 d, and 10 d after treatment, and significantly higher NIHSS score difference values before and after treatment than those from control group ( P<0.05); the proportion of patents having good prognosis (modified Rankin scale [mRS] scores≤2) in the treatment group 3 months after treatment (78.57%) was significantly higher than that in the control group (52.38%), and the Barthel index in the treatment group 3 months after treatment (94.76±11.67) was significantly higher than that in the control group (85.00±15.17, P<0.05). Patients from the posterior circulation infarction subgroup had significantly lower NIHSS scores 48 h, 7 d, and 10 d after treatment, and significantly higher NIHSS score difference values before and after treatment than those from anterior circulation infarction subgroup ( P<0.05); the proportion of patents having good prognosis in the posterior circulation infarction subgroup 3 months after treatment (94.44%) was significantly higher than that in the anterior circulation infarction subgroup (66.67%, P< 0.05). There were no statistically significant differences in platelet count and coagulation tests between the treatment group and control group, and between the posterior circulation infarction subgroup and anterior circulation infarction subgroup ( P>0.05). Conclusion:Tirofiban could improve the prognoses of patients with acute cerebral infarction in broadened therapeutic time window, enjoying high effectiveness and safety, which are more obvious in the posterior circulation infarction.
RESUMO
Objective To investigate the effects of high density lipoprotein (HDL) on thrombin-activated platelet al-pha-granulemembrane protein (CD62P) and lysosome intact membrane protein (CD63) expressions in vitro. Methods The equivalent volume of washed platelets prepared by hand was preincubated with HDL (1 g/L) in 37℃water for 15 minutes, which was then stimulated with different concentrations of thrombin (0.5 U/mL, 1 U/mL and 10 U/mL) for 10 minutes in wa-ter of 37℃. Meanwhile another three groups of washed platelets were incubated with thrombin (0.5 U/mL, 1 U/mL and 10 U/mL) for 10 minutes, respectively. The CD62P and CD63 from each sample were analyzed by flow cytometry (FCM). Results The CD62P positive rates of HDL-preincubated groups were significantly lower than those of different concentrations of thrombin groups (0.5 U/mL,1 U/mL and 10 U/mL) in the absence of HDL (11.55%± 1.34% vs 18.14%± 1.50%, 17.19%± 0.17% vs 26.24%± 0.77% and 19.79%± 0.32% vs 80.38%± 5.66%,P ＜ 0.01). Meanwhile, The CD63 positive rates of HDL-preincubated groups were also significantly lower than those of thrombin-treated (0.5 U/mL, 1 U/mL and 10 U/mL) groups without HDL, namely,2.92%±0.22%vs 8.09%±0.48%(P＜0.001), 4.20%±0.98%vs 14.15%±1.39%(P＜0.001) and 5.12%± 0.09% vs 24.48%± 1.71%(P ＜ 0.01). Conclusion HDL inhibits the expression of CD62P and CD63 on throm-bin-stimulated platelets in vitro.
RESUMO
Objective To study the nlanifestation and the clinical significance of the cerebral angiography of the isehemic cerebrovascular diseases.Methods Digital sublraction angiography(DSA)was taken in 312 patients with cerebral infarction and transient ischemic attack(TLA).The distribution of the lesion in the extra/intracranial arteries was compared.Results Cerebral angiography showed that the stenosis and occlusion was dominant in the intracranial arteries at the cerebral infarction in the internal carotid artery system and vertebrobasilar artery system[59.57%(56/94)and 61.90%(26/42)].TIA of internal carotid artery system was mainly because of stenosis of intracranial arteries (68.75%,22/32).TIA of vertebrobasilar artery system was mainly because of stenosis of extracranial arteries(61.70%,29/47).Conclusions The diseases of the intracranial arteries are the main causes of cerebral infarction(including internal carotid artery system and vertebrobasilar artery system) and TIA of internal carotid artery system. The diseases of the extracranial arteries are main causes of TIA of vertebrobasilar artery system.
RESUMO
BACKGROUND: Ambulatory blood pressure monitoring can sensitively and objectively reflect blood pressure level, which is closely related to target organ damage and disease prognosis. In hypertension, vascular endothelial damage is the most common lesion to target organs. There is little known about how ambulatory pulse pressure correlates to large artery elasticity and vascular endothelial function. OBJECTIVE: To investigate changes of large artery elasticity and of vascular endothelial function in patients with primary hypertension using an automatic pulse wave velocity determinator and ultrasound techniques, and to analyze the correlation of ambulatory pulse pressure to large artery elasticity and vascular endothelial function.DESIGN: A non-randomized concurrent control clinical observation. SETTING: Diagnosis and Treatment Center for Coronary Heart Disease, the 305 Hospital of Chinese PLA. PARTICIPANTS: A total of 156 inpatients and/or outpatients, who were recently confirmed with primary hypertension, were recruited for this study between June 2005 and April 2007. Patients consisted of 114 males and 42 females. All patients averaged 56 ± 4 years of age (range: 40-75). Inclusive criteria: Corresponding to diagnostic standards for preventing and treating hypertension instituted in 2004 by Chinese scholars. Confirmed as primary hypertension within 1 month. Not receiving any blood pressure lowering, hypolipidemic or nitrate-like drug treatments. Written informed consents for laboratory measurements were obtained from all subjects. The study was approved by the hospital's Ethics Committee. METHODS: According to the mean pulse pressure over 24 hours, all patients were assigned into 3 groups: Group A (mean pulse pressure ＜ 40 mm Hg, n=92), group B (40 mm Hg ≤ mean pulse pressure ＜ 60 mm Hg, n=39) and group C (mean pulse pressure ＞ 60 mm Hg, n=25). In each group, daytime pulse pressure and night-time pulse pressure, as well as 24-hour mean pulse pressure were measured using a non-invasive portable ambulatory blood pressure monitor (ABPM-04, Meditech Inc, USA). Carotid-femoral and carotid-radial arterial pulse wave velocities were measured using an automatic pulse wave velocity determinator to evaluate large artery dilation. Blood flow mediated and nitroglycerin-dependent dilatation of the brachial artery was determined using a high-resolution ultrasound technique to evaluate vascular endothelial function. MAIN OUTCOME MEASURES: Correlations of ambulatory pulse pressure to large artery dilation and arterial endothelial function. RESULTS: All 156 patients were included in the final analysis. Correlation of ambulatory pulse pressure to large artery dilation: Carotid-femoral arterial pulse wave velocity was significantly positively correlated to daytime pulse pressure, night-time pulse pressure and 24-hour mean pulse pressure, with coefficient of partial correlation being 0.310, 0.281 and 0.303, respectively, P ＜ 0.01). There were no significant correlations of carotid-radial arterial pulse wave velocity to daytime pulse pressure, night-time pulse pressure or 24-hour pulse pressure (P ＞ 0.05). Correlation of ambulatory pulse pressure to arterial endothelial function: There was a linear relationship between ambulatory pulse pressure and blood flow-mediated blood vessel dilatation values. Linear correlation analysis was performed, taking ambulatory pulse pressure as an independent variable, and endothelial-dependent dilatation as a dependent variable. Results demonstrated that blood flow-mediated blood vessel dilatation was significantly negatively correlated to daytime pulse pressure, night-time pulse pressure and 24- hour mean pulse pressure (r = -0.684, -0.597, -0.668, P ＜ 0.01). There was no correlation of ambulatory pulse pressure to non-endothelial-dependent blood vessel dilatation. CONCLUSION: Ambulatory pulse pressure increase is closely related to large artery elasticity decrease and injury to endothelial function in patients with primary hypertension.
RESUMO
Objective To explore the effect of IL-1? and IL-6 on MMP-3 gene expression in human coronary artery smooth muscle cells.Methods We used IL-1?(20 ?g/L) and IL-6(10 ?g/L) to stimulate human coronary artery smooth muscle cells,which were co-culture for 0,2,4,8,24,36 h.IL-1?(0,5,20,40 ?g/L) and IL-6(0,5,10,50 ?g/L) were used to stimulate human coronary artery smooth muscle cells,which were co-cultured for 6 h.Then we detected the gene expression by fluorescent quantitation PCR.Results In the same concentration of IL-1? and IL-6,gene expression was up-regulated at 2 h,at 8 h the expression reached the peak,then began to descend.In different concentration of IL-1? and IL-6,gene expression was up-regulated with the dose of IL-1? and IL-6(IL-1?: r=0.907,P=0.000;IL-6: r=0.919,P=0.000).There were significant differences in MMP-3 expression among different groups(IL-1?: F=24.047,P=0.000;IL-6: F=14.081,P=0.001).There were no significant differences in matrix metalloproteinase-3 between IL-1? 20 and 40 ?g/L groups(P=0.154) and between IL-6 5 ?g/L and 10 ?g/L(P=0.292).Conclusion It suggests that IL-1? and IL-6 can promote MMP-3 gene expression in human coronary artery smooth muscle cells,and it may be one of the mechanisms of inflammation effect in acute coronary syndrome.