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Objective To investigate the efficacy and safety of warfarin in the prevention of cerebral infarction in nonvalvular atrial fibrillation (NVAF). Methods One hundred and thirty-six NVAF patients were randomized into warfarin group [receiving adjusted-dose warfarin,international normalized ratio(INR)was 2.0 - 3.0], aspirin group( receiving aspirin 100 mg/d) and control group (treated without anticoagulants )by random digits table. Followed up 18 months, and the main end point events and adverse effect of the three groups were compared. Results In 136 cases,4 cases lost,and 77 cases(58.3%) were male. The mean dose of warfarin was(2.5 ± 1.0) mg. During the follow-up period, main end point events occurred in 12 cases,with 1 case (2.50%, 1/40) in warfarin group, 4 cases(9.52%, 4/42 ) in aspirin group and 7 cases ( 14.00%, 7/50)in control group. There was no significant difference in main end point events among the three groups ( x2 =2.084,P =0.353). But in the patients with 3 or above risk factors,there was significant difference in the survival curve among the three groups ( x2 = 6.404, P = 0.041 ). The incidence rate of bleeding was higher in warfarin group than that in aspirin group,but there was no significant difference [5.00%(2/40) vs. 2.38%(1/42),P ＞ 0.05]. Conclusions Warfarin can improve survival rate especially in the patients with 3 or above risk factors,and the complication of bleeding occurs mostly when INR ＞ 3.0.Under closed monitoring (INR 2.0-3.0),adjusted-dose warfarin is safety and efficacy.
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Objective To investigate the effect of high glucose on the number and proliferation, migration and adhesion of peripheral endothelial progenitor cells (EPCs). Methods Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin coated culture dishes. After 7 days of culture, several groups of attached cells were incubated with glucose in a series of concentrations (15, 25, 35, 45mmol/L) for different durations (6, 12, 24 and 48h). EPCs were characterized as adherent cells which were double positive for DiLDL uptake and lectin binding by direct fluorescent staining demonstrated under a laser scanning confocal microscope. EPCs were further documented by demonstrating the expression of KDR, VEGFR 2 and AC133 with flow cytometry. EPCs proliferation, migration and in vitro vasculogenesis activity were assayed with MTT assay, modified Boyden chamber assay and in vitro vasculogenesis kit, respectively. EPCs adhesion assay was performed by replating MNCs on fibronectin coated dishes, and then the adherent cells were counted. Results Incubation of isolated human MNCs with high glucose concentration decreased the number of EPCs, and this effect was most prominant when glucose concentration was 45mmol/L, and incubated for 24 hours (approximately 1 fold decrease, P
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AIM: To study the effects of hydrogen peroxied (H 2O 2) on cell proliferation and transcription of gelatinase A (MMP-2) and its inhibitor (TIMP-2) in vascular smooth muscle cells (VSMC). METHODS: Cell proliferation and toxicity by H 2O 2 were tested through MTT. The expression of MMP-2 mRNA and TIMP-2 mRNA in VSMC were evaluated by RT-PCR. RESULTS: The present study showed that H 2O 2 (more than 300 ?mol/L)was lethal to VSMC. 0 01-50 ?mol/L H 2O 2 promoted proliferation of VSMC in a time-dependant manner. A value (optical density) was reached to peak at 24 h after continuing stimulation of 10 ?mol/L H 2O 2. MMP-2/?-actin mRNA ratio significantly increased after stimulation with 1 ?mol/L?10 ?mol/L H 2O 2. TIMP-2/?-actin mRNA ratio was not significantly fluctuated at 12 h?24 h?36 h?48 h after continuing stimulation with 1 ?mol/L, 10 ?mol/L, and 50 ?mol/L H 2O 2.CONCLUSION: H 2O 2 at suitable concentrations stimulated proliferation of VSMC and induced transcription of MMP-2 gene in VSMC. There was no effect of H 2O 2 on transcription of TIMP-2 gene in VSMC. These results imply that H 2O 2 takes part in the pathological course of vascular remodeling through VSMC.
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AIM: To investigate whether homocysteine (Hcy) has influences on endothelial progenitor cell (EPCs) number and activity from peripheral blood. METHODS: Total mononuclear cells (MNCs) were plated on fibronectin-coated culture dishes and cultured for 7 days, and then attached cells were stimulated with Hcy or vehicle control for 6 h, 12 h, 24 h and 48 h. The adhesion, proliferation, migration and in vitro vasculogenesis activity of EPCs were assayed, respectively. RESULTS: Incubation of isolated human MNCs with Hcy dose and time-dependently decreased the number of EPCs with maximum at 200 (?mol/L) for 24 hours (35.7?6.7 vs 62.5?10.6, P
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AIM: The purpose of this study was to determine whether the signal transduction systems were activated at the molecular atrial tissue level in patients with atrial fibrillation (AF) and whether atrial expression of extracellular-signal regulated kinase (ERK) and protein phosphatases is altered. METHODS: Atrial tissue sample of 30 patients undergoing cardiac surgery were examined. 20 patients had AF, 10 patients had no history of AF. The mRNA expression of calcineurin B and MKP-1 were detected by semi-quantitative RT-PCR. ERK1 and phospho-ERK1 were analyzed at the protein level by Western blot. RESULTS: Western blot analysis showed that atrial fibrillation did not induce significant change in ERK1 expression level in the left atrium. In contrast , phospho-ERK1 content was increased in the patients with AF in comparison with those who had sinus rhythm (SR). The mRNA expression of calcineurin B and MKP-1 in the patients with AF were significantly higher than that in patients with SR. CONCLUSION: The activation of extracellular-signal regulated kinase and protein phosphatases may have correlation with the initiation or maintenance of atrial fibrillation.
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AIM: To evaluate effects of diltiazem on platelet hyperreactivity in situations associated with endothelial injury and their possible relationship to cytosolic calcium concentration. METHODS: Blood samples were collected at 7 time points from 35 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) who received combined diltiazem and aspirin/ticlopidine therapy or aspirin/ticlopidine therapy alone. Platelet expression of glycoprotein Ⅱb/Ⅲa and cytosolic calcium concentration were measured, respectively, by whole blood flow cytometry and fluorospectrophotometry. The effects of diltiazem of different concentrations on expression of glycoprotein Ⅱb/Ⅲa were also studied in vitro in blood samples from patients with chronic stable angina. RESULTS: Of the two treatments, aspirin/ticlopidine therapy did not prevent an acute increase of expression of glycoprotein Ⅱb/Ⅲa 5 minutes and 10 minutes after first inflation and 10 minutes after PTCA, whereas combined diltiazem and aspirin/ticlopidine therapy had a significant inhibitory effect. In the group receiving aspirin/ticlopidine therapy, there was a short-term elevation of platelet [Ca~(2+)]i immediately following PTCA which was significantly reduced by diltiazem treatment. Expression of glycoprotein Ⅱb/Ⅲa was significantly inhibited in vitro by diltiazem in the concentration of 200 ?g/L or higher, but not 50 ?g/L. CONCLUSIONS: Combined diltiazem and aspirin/ticlopidine therapy significantly inhibited platelet activation that continued in the presence of conventional aspirin/ticlopidine treatment. Antiplatelet effects of diltiazem were probably a consequence of reduction of platelet [Ca~(2+)]i and may only be achieved in higher than therapeutic concentrations. [
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AIM: We examined the effect of interleukin- 2 (IL-2) on calcium handlin g of rat cardiomyocytes. METHODS: The effects of steady state an d transient chan ges in stimulus frequency on the intracellular calcium transient were investigat ed in the isolated ventricular myocytes with spectrofluorometry technique. RESULTS: Under the steady state (0.2 Hz), IL-2 at 2?10 5 U/L decr eased the peak [Ca 2+ ] i and amplitude of the [Ca 2+ ] i transient, increas ed the diastolic calcium level, and prolonged the decay of the calcium transient . At 1.25 mmol/L of extracellular [Ca 2+ ], when increasing the stimulus frequency from 0.2 to 1.0 Hz, diastolic calcium level and peak [Ca 2+ ] i as well as the amplitude of the transient were inc reased. The positive frequency relationship was blunted in the IL-2-treated myoc ytes and this was not normalized by increasing extracellular [Ca 2+ ] t o 2.5 mmol/L . The caffeine induced Ca 2+ release was increased with increase in stimu lus freq uency. IL-2 inhibited the frequency relationship of caffeine induced Ca 2+ releas e. The restitution was not different between control and IL-2 groups at the 1.25 mmol/L of extracellular [Ca 2+ ], which was slowed in IL-2-treated myo cytes when t he extracellular [Ca 2+ ] was increased to 2.5 mmol/L. CONCLUSIO NS: It is concluded that the blunted frequency response of IL-2-treated myocytes was resulted from the decrease in SR Ca 2+ release, which was related to depression of SR funct ion. Despite the evidence of depressed SR Ca 2+ uptake, the restitution o f ca lcium transient at 1.25 mmol/L of extracellular [Ca 2+ ] remains uncha nged, which maybe due to the increase in the Na +/Ca 2+ exchanger activi ty.
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Objective To evaluate safety and effect of percutaneous balloon mitral valvuloplasty(PBMV) for patients with rheumatic mitral stenosis and left atrial thrombi.Methods PBMV was performed in 27 patients with rheumatic mitral stenosis and left atrial thrombi. 19 cases of left atrial fresh thrombi revealed by transesophageal echocardiography (TEE) received warfarin orally for 3-6 months before PBMV. Results PBMV was successful in all cases of mitral stenosis and left atrial thrombi. Left atrial fresh thrombi was completely resolved in 9 cases and became smaller chronic organized thrombi in 10 cases after warfarin anticoagulation treatment among 19 cases of left atrial fresh thrombi revealed by TEE. In 5 cases of left atrial chronic organized thrombi shown only transthoracic echocardiography and without anticoagulation treatment, one case had cerebral embolism. No complication occurred in other cases.Conclusions The study showed that patients with rheumatic mitral stenosis and atrial fibrillation should have routine TEE. PBMV for rheumatic mitral stenosis with left atrial thrombi after anticoagulation treatment is safe and effective.
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0.05).Compared with SHR group,left ventricular weight mass index decreased significantly in SHR-A group(P
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AIM: To clarify the effect of the specific sodium-hydrogen antiporter HOE642 on ischemia/reperfusion(I/R) injury including apoptosis, and the relationship between its effect and the time of HOE642 administration. METHODS: The isolated rat heart model were randomly divided into group A and B. Furthermore, the rat hearts in group A were divided into four subgroups including I/R, HOE-Pr+I/R, HOE-Is+I/R and HOE-Re, also the rat hearts in group B were divided into the following subgroups including control, I/R and HOE642+I/R. The LVDP, LVEDP, arrythmia coronary flow and the enzymatic activity in myocardium were measured in group A, and TUNEL method was applied to probe apoptosis in group B. RESLUTS: It was found that the LVEDP, arrythmias and the enzymatic activity including CK-MB and LDH were significantly lower in group HOE-Pr+I/R than that in group I/R, while the LVDP was obviously higher in HOE-Pr+I/R than that in I/R. The administration of HOE642 during ischemia could decrease LVEDP, arrythmias and enzymatic activity in myocardium, but not the LVDP. Furthermore, the results showed that HOE642 could inhibit apoptosis induced by ischemic/reperfusion injury. CONCLUSIONS: HOE642 is an effective cardio-protector in case of ischemic/reperfusion injury especially when it is applied before ischemia. The inhibition of apoptosis might be involved in the mechanisms underlying the protective effect of HOE642.
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AIM: The aim of this study was to study the changes of rabbit heart electrophysiological properties caused by increasing left ventricular afterload, and to assess the effects of streptomycin or verapamil on these changes. METHODS: The rabbit heart preparation in situ was used,and the afterload of left ventricle was increased by clipping in part the root of ascending aorta. The changes of heart electrophysiological parameters including relative refractory period (RRP),effective refractory period (ERP),monophasic action potential duration (MAPD_ 90 ) and ventricular fibrillation threshold(VFT) were observed before and after altering the afterload of left ventricle and were compared in the absence and presence of streptomycin or verapamil. RESULTS: The rising of left ventricular afterload [(72?11)mmHg] led to shortening of RRP,ERP and MAPD_ 90 ,and to descent of VFT ( P 0.05) except increasing of VFT ( P
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Objective To investigate the effects of rapamycin on the number and function of peripheral blood endothelial progenitor cells (EPCs). Methods Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. After 7-day culture, adherent cells were treated with rapamycin in a series of final concentrations of 1.0, 2.0, 5.0?g/ml for 6, 12, 24, and 48h. EPCs were identified as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining as demonstrated under a laser scanning confocal microscope. EPCs were further documented by demonstrating the expression of VEGFR-2, AC133 and CD34 with flow cytometry. EPCs proliferation and migration were assayed with MTT assay and modified Boyden chamber assay, respectively. EPCs adhesion assay was performed by replating them on fibronectin-coated dishes, and then adherent cells were counted. In vitro vasculogenesis activity was assayed by in vitro vasculogenesis kit. Results Incubation of isolated human MNCs with rapamycin resulted in a decrease in the number of EPCs, and rapamycin also decreased EPCs proliferative, migratory, adhesive and in vitro vasculogenesis capacity in both concentration and time dependent manners. Conclusion Rapamycin decreases the number, proliferative, migratory, adhesive and in vitro vasculogenesis capacity of EPCs.