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1.
目的:研究强化阿托伐他汀钙(AC)治疗对急性脑梗死(ACI)临床效果及血清低密度脂蛋白(sdLDL)水平的影响.方法:选取2015年12月~2016年12月我院收治的102例ACI患者作为观察对象.以随机数字表法分为对照组和观察组各51例.两组均采用常规ACI治疗,对照组在常规治疗的同时给予正常剂量的AC(20mg/d)治疗;观察组在接受常规治疗的同时给予强化剂量的AC(40mg/d)治疗.对比治疗前后的疗效及高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)等各项指标变化情况.结果:治疗后,观察组治愈占比45.10%(23/51),总有效率94.12%(48/51),显著高于对照组的23.53%(12/51)、78.43%(40/51);治疗后观察组血脂与炎症因子均显著低于对照组;治疗前两组颈动脉内膜中层厚度(IMT)及斑块面积均无显著差异,治疗后两组IMT及斑块面积均显著下降,观察组下降幅度明显大于对照组;治疗前两组sdLDL水平均无显著差异,治疗后1个月后及6个月观察组与对照组sdLDL水平均显著下降,观察组下降幅度明显大于对照组(P<0.05).结论:强化AC治疗ACI不仅疗效显著,还可以有效降低血脂与炎症因子指标,同时有效改善IMT值及斑块面积,sdLDL水平大幅度下降,值得临床推广.  相似文献   

2.

Background:

Various guidelines are available outlining optimal therapy for patients with acute myocardial infarction. Canadian institutions providing care for such patients have been encouraged to evaluate their care processes using specific indicators.

Objective:

To determine the proportion of patients with acute myocardial infarction discharged from a single health authority for whom acetylsalicylic acid (ASA), adrenergic β-receptor antagonists (β-blockers), angiotensin-converting enzyme (ACE) inhibitors, or 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) had been prescribed.

Methods:

Patients treated over a 12-month period (April 1, 2004, to March 31, 2005) for whom the most responsible diagnosis was acute myocardial infarction were eligible for inclusion in this review. Retrieved data included diagnosis, demographic information, comorbidities, and medications at the time of admission and discharge. Rates of discharge prescribing for the 4 drug classes were calculated for all patients and for “ideal” patients (those without documented contraindications). Rates were compared with published benchmark values.

Results:

Medical records for a total of 346 eligible patients were reviewed. Mean age was 65.3 years (standard deviation 13.4 years), and 226 (65.3%) of the patients were male. The coded diagnosis was ST-elevation myocardial infarction for 91 patients (26.3%), non-ST-elevation myocardial infarction for 164 (47.4%), and myocardial infarction not specified for 91 (26.3%). For “ideal” patients, the prescribing rates were 99.0% (308 of 311 patients) for ASA, 96.3% (310 of 322 patients) for β-blockers, 90.4% (264 of 292 patients) for ACE inhibitors, and 88.8% (278 of 313 patients) for statins.

Conclusions:

Rates of prescribing of ASA, β-blockers, ACE inhibitors, and statins for “ideal” patients discharged after treatment for acute myocardial infarction exceeded the published Canadian benchmark rates (≥ 90% for ASA, ≥ 85% for β-blockers and ACE inhibitors, ≥ 70% for statins).  相似文献   

3.
This study evaluated the effects of electroacupuncture (EA) on endothelial function and endothelial progenitor cells (EPC) in patients with cerebral infarction. In a randomized, placebo‐controlled, crossover study, 20 patients with cerebral infarction were randomized into two treatment groups: EA or placebo. Before and after each intervention, pulse amplitude tonometry (PAT) was used to assess endothelial function and peripheral blood was analyzed for the number of EPCs. Circulating EPCs were quantified by flow cytometry as CD45lowCD34+KDR2+ cells. Plasma vascular endothelial growth factor (VEGF) and interleukin (IL)‐10 levels were measured. Seven days later, crossover was performed on each group, with each group receiving the other treatment using the same protocol. The PAT hyperemia ratio ranged from 1.57 ± 0.41 to 2.04 ± 0.51 after EA, representing a significant improvement (P = 0.002); however, there was no improvement in the placebo group (P = 0.48). Circulating EPCs, as measured by flow cytometry, increased to 110.6 ± 74.3/100 μL in the EA group (P = 0.001) but did not change in the placebo group (45.9 ± 35.3/100 μL, P = 0.08). The increases in the number of EPCs and the PAT ratio after treatment were correlated (r = 0.78, < 0.001). Plasma VEGF levels increased with EA compared to baseline (261.2 ± 34.0 vs 334.9 ± 80.5 pg/mL, P = 0.003). The number of circulating EPCs was positively correlated with plasma levels of VEGF (r = 0.50, P = 0.02). In conclusion, EA induced improvement of EPC levels and the PAT ratio in patients with cerebral infarction.  相似文献   

4.
老年急性心肌梗死患者的早期康复治疗   总被引:1,自引:2,他引:1  
目的 观察老年急性心肌梗死患者实施早期康复治疗的临床效果。方法 将160例老年急性心肌梗死(AMI)患者随机分为两组,早期康复组80例,对照组80例,早期康复组在常规治疗和护理的基础上实施自行研究制定的早期康复护理方案,对照组常规治疗及护理,比较两组患者住院期间心绞痛、再梗塞、死亡发生率,活动平板运动试验,住院天数及GLQZ生活质量指标测定。结果 早期康复组与对照组相比住院期间发生心绞痛和再梗塞次数、住院天数减少,生活质量明显提高(P〈0.01),而两组住院期间死亡人数无统计学差异(P〉0.05)。结论 对老年AMI患者实施早期康复治疗护理是安全、可行的,值得在临床上推广应用。  相似文献   

5.
章祎 《中国医药》2011,6(8):902-904
目的 评估应激性高血糖对非糖尿病急性心肌梗死(AMI)患者预后的影响和意义.方法 将138例AMI患者以空腹血糖水平分为应激性高血糖组(98例)和无应激性高血糖组(40例),比较2组患者的临床特点、并发症及病死率等.结果 AMI后应激性高血糖组严重心律失常、心力衰竭、心源性休克、大面积梗死、冠状动脉2支及3支病变发生率及病死率高于无应激性高血糖组[39.8%(39/98)比12.5%(5/40)、32.7%(32/98)比10.0%(4/40)、37.8%(37/98)比12.5%(5/40)、48.0%(47/98)比15.0%(6/40)、42.9%(42/98)比15.0%(6/40)、45.9%(45/98)比12.5%(5/40)、18.4%(18/98)比5.0%(2/40),均P<0.05].应激性高血糖组肌酸激酶水平明显高于无应激性高血糖组[(521±116)U/L比(334±134)U/L,P<0.05].应激性高血糖组的左冠状动脉前降支近段、左冠状动脉回旋支近段、右冠状动脉近段的梗死面积均明显大于无应激性高血糖组[(5.10±0.88)cm2 比(3.70±1.14)cm2,(3.40±0.65)cm2比(1.20±0.54)cm2,(4.50 ±1.20)cm2比(1.80±0.91)cm2,均P<0.05].结论 应激性高血糖是AMI患者住院期间预后不良的独立预测因子和危险因素,对AMI患者应积极控制血糖水平,早发现、早处理高血糖,降低心血管事件的发生危险,以提高患者生活质量、改善其预后.
Abstract:
Objective To evaluate the influence and significance of stress-hyperglycemia on prognosis in non-diabetic patients with acute myocardial infarction(AMI). Methods All 138 AMI patients were divided, according to fasting blood glucose level, into stress-hyperglycemia group (n = 98) and non-stress-hyperglycemia group (n=40). Clinical features,complications and mortalities were compared between 2 groups. Results There was significant difference in severe arrhythmias,heart failure,cardiogenic shock,mortality and lesion incidence in 2 or 3 coronary arteries between 2 groups[(39. 8% (39/98) vs 12. 5% (5/40), 32. 7% (32/98) vs 10. 0% (4/40), 37.8% (37/98) vs 12.5% (5/40), 48. 0% (47/98) vs 15. 0% (6/40), 42. 9% (42/98) vs 15. 0% (6/40), 45.9%(45/98) vs 12.5% (5/40), 18.4%(18/98) vs5.0%(2/40), P<0.05]. Fasting blood glucose and creatine phosphokinase were higher in stress-hyperglycemia group than in non-stress-hyperglycemia group. Proximal (left anterior descending artery, circumflex artery and right coronary artery) were higher in stress-hyperglycemia group than in non-stress-hyperglycemia group[(5.10 ±0.88)cm2 vs (3.70 ±1.14)cm2 ,(3.40 ±0.65)cm2 vs (1.20± 0.54)cm2,(4.50±1.20)cm2 vs (1.80±0.91)cm2,P<0.05]. Conclusions Stress-hyperglycemia is the independent predictor and the risk factor for poor prognosis in patients with acute myocardial infarction during hospitalization. Active control of blood glucose is of importance for preventing and controling of complication and lowing of mortality.  相似文献   

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8.
目的:对比研究不同年龄层次急性心肌梗死( AMI)患者的临床特点及冠脉病变特点。方法序贯入选AMI患者226例,按年龄层次分为青年组、中老年组及高龄组。比较3组人群的临床特征及冠脉造影结果。结果两两比较3组患者高血压病比例、总胆固醇、低密度脂蛋白、甘油三酯、高密度脂蛋白组间差异均无统计学意义(P>0.05)。青年组中年组吸烟比例较中老年组、高龄组明显增高,与其比较差异有统计学意义( P<0.05)。3组患者发病至入院时间、入院至导管室时间随年龄增加,逐渐升高。高龄组糖尿病史、血肌酐、肌酸激酶、肌酸激酶同工酶MB、肌钙蛋白I与青年组、中老年组相比差异均具有统计学意义( P<0.05)。比较高龄组患者与青年组、中老年组患者Gensini评分差异均具有统计学意义( P<0.05)。青年组与中老年组患者Gensini评分之间差异无统计学意义( P>0.05)。结论急性心肌梗死在不同年龄层次患者中的临床特点及病变程度不尽相同,其发病机制可能略有不同。不同年龄层次急性心肌梗死的特点对于临床诊疗具有重要意义。  相似文献   

9.
目的 探讨阿托伐他汀序贯疗法在急性心肌梗死(AMI)患者中的应用效果.方法 按照随机对照原则将132例AMI患者分为观察组和对照组各66例,观察组患者给予阿托伐他汀序贯疗法,对照组患者给予口服阿托伐他汀20 ng/d治疗.观察两组患者入院后24 h、4周、8周的早晨空腹血脂变化,包括甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、肌酸激酶(CK).结果 观察组患者治疗4周后的血TC、TG、LDL-C水平分别为(4.09±0.68)、(1.52±0.39)、(2.68±0.90)mmol/L,均低于对照组患者的(4.81±0.97)、(1.62±0.47)、(2.93±0.83)mmol/L,差异均有统计学意义(P<0.05).观察组患者治疗8周后的血TC、TG、LDL-C水平分别为(3.64±0.19)、(1.31±0.64)、(1.60±0.33) mmol/L,均低于对照组患者的(4.19±0.28)、(1.44±0.82)、(2.53±0.66) mmol/L,差异均有统计学意义(P<0.05);观察组患者的血ALT、AST、CK、HDL-C水平与对照组相比,差异均无统计学意义(P>0.05).结论 阿托伐他汀序贯疗法对AMI患者具有较好的调脂效果,值得临床推广使用.  相似文献   

10.
目的观察急性心肌梗死(AM I)患者尿激酶溶栓治疗的疗效、安全性及预后。方法选择符合溶栓治疗适应证、无溶栓治疗禁忌证急性心肌梗死(AM I)患者46例作为观察组,另选取30例有溶栓禁忌或不同意进行溶栓治疗的急性心肌梗死患者作为对照组。对两组疗效进行比较,对其再通情况和治疗后并发症、病死率进行比较分析。结果观察组在6h内和6~12h内以及总的再通率均高于对照组,差异有统计学意义(P<0.05);对照组的病死率、并发症均高于观察组,差异有统计学意义(P<0.05)。结论尿激酶溶栓治疗急性心肌梗死可以显著改善患者的预后,提高血管的再通率,减少病死率和并发症,是一种安全有效的再灌注疗法。  相似文献   

11.
Many cytokines have been reported to be increased in human and animal models with cardiovascular diseases. Myocardial infarction (MI) is accompanied with an inflammatory reaction which induces cardiac dysfunction and remodeling. The inflammatory reaction has been investigated in animal models of MI or myocardial ischemia-reperfusion injury. The mechanisms by which cytokine cascade is activated in the infarcted myocardium have been recently elucidated. Several hematopoietic growth factors including interleukin-3 (IL-3), IL-6, granulocyte-macrophage colony-stimulating factors (GM-CSF), granulocyte colony-stimulating factor (G-CSF), and stem cell factor (SCF) have been reported to be positive regulators of granulopoiesis and act at different stages of myeloid cell development. G-CSF plays a critical role in regulation of proliferation, differentiation, and survival of myeloid progenitor cells. G-CSF also causes a marked increase in the release of hematopoietic stem cells (HSCs) into the peripheral blood circulation, a process termed mobilization. Although cardiac myocytes have been considered as terminally differentiated cells, it has been recently reported that there are many proliferating cardiac myocytes after MI in human heart. After it was demonstrated that bone marrow stem cells (BMSCs) can differentiate into cardiac myocytes, myocardial regeneration has been widely investigated. Recently, G-CSF has been reported to improve cardiac function and reduces mortality after acute MI. Although the mechanism by which G-CSF ameliorates cardiac dysfunction is not fully understood, there is the possibility that G-CSF may regenerate cardiac myocytes and blood vessels through mobilization of BMSCs. In the future, cytokine-mediated regeneration therapy may become to be a novel therapeutic strategy for MI.  相似文献   

12.
The β-1 adrenergic receptor blocker metoprolol is primarily metabolized by the polymorphic enzyme cytochrome P 450 2D6 (CYP2D6), an enzyme with substantial genetic heterogeneity. Our purpose was to investigate the impact of CYP2D6 metabolism on clinical effects and tolerability of metoprolol in patients after myocardial infarction (MI). We included 136 patients with MI discharged on treatment with metoprolol with a recommendation to the general practitioner (GP) to increase the metoprolol dose up to 200 mg/day within 2 months if possible. At follow-up, metoprolol dosage after up-titration, metoprolol steady-state trough plasma concentrations, hemodynamic parameters, potential metoprolol-induced adverse drug reactions and number of visits to the GP were measured. CYP2D6 genotyping including the reduced-function variant alleles CYP2D6*9, CYP2D6*10 and CYP2D6*41 was performed after end of follow-up. According to the genotype-defined CYP2D6 phenotypes, 30% of the patients were metoprolol extensive metabolizers (EMs), 55% intermediate metabolizers (IMs) and 13% poor metabolizers (PMs; carriers of non-coding and reduced-function variant included). Dose-adjusted metoprolol trough concentrations were significantly higher in IM (2-fold) and PM (6.2-fold) groups vs. the EM group (p < 0.001). Only 35% of patients in the PM group achieved the primary end point, i.e. reaching at least 85% of the expected maximum heart rate (HR) during exercise, compared with 78% in the EM group (p < 0.01), and maximum observed HR at exercise was significantly lower in the PM group vs. the EM group (129 ± 5 vs. 142 ± 2 bpm, p < 0.007). In contrast, metoprolol maintenance dose, blood pressure, exercise capacity, number of visits at the GP and frequency and severity of self-reported potential metoprolol-related adverse drug reactions were not significantly different between the groups. Using a comprehensive CYP2D6 genotyping panel, the present study demonstrates a > 6-fold increase of dose-adjusted plasma metoprolol trough concentration in CYP2D6 PMs vs. EMs with a parallel lower increase in achieved maximum HR during exercise but without association between genotype and frequency or severity of self-reported adverse drug effects. This may indicate that CYP2D6 PMs potentially could benefit of the increased plasma concentration per dose in a naturalistic setting.  相似文献   

13.
目的比较直接经皮冠状动脉内介入治疗 (PCI)与静脉溶栓治疗急性心肌梗死 (AMI)患者近期和长期的临床疗效。方法入选AMI患者 4 7例 ,2 5例患者接受静脉溶栓治疗 ,2 2例患者接受直接PCI治疗 ,比较两组患者临床和住院期间及随访期间超声心动图结果。结果溶栓组住院死亡率高于直接PCI组 (P <0 .0 5 )。溶栓组血管再通率为 5 2 0 % ;直接PCI组血管再通率为 10 0 % ,达到TIMI 3级血流。AMI后 1周左室射血分数 (LVEF) :溶栓组为 4 4 3± 11 6 % ,直接PCI组为 6 4 5±9 1% ,两组比较有显著性差异 (P <0 .0 5 )。溶栓成功者其AMI后 1周LVEF也明显低于直接PCI组 (47 2± 9 6 %VS 6 4 5± 9 1% ,P <0 .0 5 )。溶栓组因溶栓失败行补救性PCI者为 2 4 0 % ,IRA开通率为 10 0 % ,其AMI后 1周及 3、6个月的LVEF略低于直接PCI组 ,但两组比较无显著性差异 (P>0 .0 5 )。溶栓组因存在梗死后心肌缺血症状行择期PCI的比率高于直接PCI组 ,两组比较有显著性差异 (2 8 0 %VS0 % ,P <0 .0 5 )。结论与溶栓治疗比较 ,直接PCI能使IRA安全有效充分开通 ,可更好地改善患者近期和长期心功能 ,降低住院死亡率。补救PCI也能有效地开通IRA ,获得TIMI13级血流 ,挽救濒死心肌 ,改善心功能。  相似文献   

14.
目的观察亚冬眠疗法在急性心肌梗死治疗中的疗效,探讨其对急性心肌梗死患者的心肌保护作用并推测其可能机制。方法人选69例患者随机分为干预组和对照组,两组均给予常规治疗。干预组在常规治疗的基础上,给予冬眠合剂半量每4~6h静脉滴注,观察其体温、血压、心率、呼吸,测定心肌酶谱肌酸激酶同工酶(CK-MB)平均值、血浆去甲肾上腺素(NE)、血清钾离子(K^+)和镁离子(Mg^2+)含量,记录心律失常、心力衰竭、死亡例数和平均住院天数。结果干预组心肌酶谱肌酸激酶平均值明显小于对照组,体温、血压、血浆NE含量和住院天数均明显低于对照组(P〈0.01)。血清K^+、Mg^2+含量高于对照组(P〈0.05),心律失常和心力衰竭例数较对照组减少(P〈0.05)。结论亚冬眠疗法可降低急性心肌梗死患者体温和血压,减少应激性NE释放,有效维持心功能,减少电解质紊乱、心律失常等并发症的发生,缩短了住院时间,是急性心肌梗死治疗的一种安全有效的方法。  相似文献   

15.
依达拉奉对急性脑梗死患者血管内皮功能的影响   总被引:1,自引:1,他引:1  
目的 观察依达拉奉对急性脑梗死患者血管内皮细胞功能的保护作用.方法 选择急性脑梗死患者260例,随机分为治疗组和照组,各130例,对照组口服阿司匹林100 mg,1次/d,辛伐他汀20mg,睡前服;治疗组在对照组治疗的基础上加用依达拉奉30 mg静脉滴注,2次/d,共14 d.分别于治疗前和治疗后第1、3、7、14、21天测定血浆NO、血浆内皮素1、血浆可溶性血栓调节蛋白(sTM)和血管性血友病因子(vWF),并观察中国卒中量表(CSS)、日常生活能力量表(ADL)评分及循环内皮细胞数.结果 对照组治疗后第3、7、14、21天血浆NO浓度分别为(8.19±3.29)、(9.26±4.32)、(10.17±5.28)、(9.86±4.76)μg/L,sTM浓度分别为(5.67±0.63)、(7.64±0.71)、(9.85±1.26)、(7.89±1.12)μg/L,vWF浓度分别为(52.47±7.13)%、(76.59±8.17)%、(86.52±9.16)%、(68.94±7.52)%,ADL评分分别为(39.99±9.14)、(43.64±9.73)、(48.36±9.85)、(46.78±8.94)分.治疗组治疗后第3、7、14、21天血浆NO浓度分别为(9.85±4.57)、(12.57±5.39)、(15.42±6.73)、(13.28±5.68)μg/L,sTM浓度分别为(9.79±0.82)、(12.93±1.04)、(21.26±3.12)、(15.86±2.85)μg/L,vWF浓度分别为(78.95±6.73)%、(125.61±11.89)%、(216.75±32.85)%、(178.73±25.83)%,ADL评分分别为(53.68±9.s3)、(58.79±11.25)、(69.72±13.61)、(68.63±11.29)分.在治疗后第3、7、14、21天,治疗组血浆NO、sTM、vWF浓度及ADL评分均明显高于对照组(P<0.05),而血浆内皮素1浓度、CSS评分及循环内皮细胞数均明显低于对照组(P<0.05).结论 依达拉奉能有效保护急性脑梗死患者血管内皮细胞功能,减轻内皮细胞的损伤与脱落入血.
Abstract:
Objective To investigate the effeets of edaravone on endothelial cell function in patients with acute cerebral infarction.Methods Two hundred and sixty patients with acute cerebral infarction were randomly divided into treatment group(n=130)and control group(n=130).Treatment group received edaravone injection (30 mg,bid)based on the routine therapy.The Nitric oxide(NO),endothelin-1,plasma soluble thrombomodulin (sTM),yon willebrand factor(vWF),China stroke scale(CSS)score,daily living skills rating scale(ADL)Score and the number of cireulation endothehal cell at the time of 1,3,7,14,21 d after treatment were determined.CSS,ADL SCOre and circulatory endothelial cell number were observed.Results Plasma NO concentration of the control respectively;sTM concentration was(5.67±0.63),(7.64±0.71),(9.85±1.26),(7.89±1.12)μg//L,respec-tively;vWF concentration was(52.47±7.13),(76.59 4-8.17),(86.52±9.16),(68.94±7.52)%respectively;ADL score was(39.99±9.14),(43.64±9.73),(48.36±9.85),(46.78±8.94)points.while the data of the treatment group were(9.85±4.57),(12.57 ±5.39),(15.42±6.73),(13.28±5.68)μg/L;(9.79±0.82),(12.93±1.04),(21.26±3.12),(15.86±2.85)μg/L;(78.95±6.73),(125.61±11.89),(216.75 4-32.85).(178.73±25.83)%;(53.68±9.83),(58.79±11.25),(69.72±13.61),(68.63±11.29)points,re-spectively.Compared with the control group,the serum concentration of NO,sTM,vWF and ADL score of the treat-ment group were significantly inereased.However,the serum concentration of ET-1,CSS score and the number of circulation endothelial cell were markedly decreased.Conclusion Edaravone protects the endothelial cell effectively by decreasing the endothelial cell injury.  相似文献   

16.
目的观察辛伐他汀对急性心肌梗死(AMI)患者血清高敏C-反应蛋白(hs-CRP)、内皮素-1(ET-1)、心肌肌酸激酶同功酶(CK-MB)的影响,探讨辛伐他汀在斑块稳定性和炎症反应中的作用。方法选取AMI患者56例,按发病前是否因心绞痛、血脂异常服用过辛伐他汀分为治疗组25例,服用辛伐他汀(20mg,1次/d)4周以上与对照组31例,未服用辛伐他汀。采用放射免疫法、酶联免疫吸附法检测2组患者血清hs-CRP、ET-1、CK-MB水平。结果治疗组血浆hs-CRP、ET-1、CK-MB水平低于对照组,差异有统计学意义(P〈0.05)。结论辛伐他汀可抑制炎症反应,改善内皮功能,稳定粥样斑块,缩小心肌梗死范围。  相似文献   

17.
目的:探讨瑞替普酶静脉溶栓辅助应用依诺肝素替代普通肝素抗凝治疗急性心肌梗死(AMI)的安全性与有效性。方法:86例AMI患者在瑞替普酶静脉溶栓时随机分为依诺肝素组(45例)和静脉普通肝素组(41例),2周后行冠状动脉造影及冠脉介入治疗(PCI)。观察临床再通率、血管开通率、急性期并发症、出血及不良反应发生率。结果:依诺肝素组与普通肝素组临床再通率、血管开通率比较差异无统计学意义(P〉0.05)。两组急性期并发症发生率比较差异无统计学意义(P〉0.05)。依诺肝素组出血并发症低于静脉普通肝素组,两组比较差异有统计学意义(P〈0.05)。结论:瑞替普酶并依诺肝素用于AMI再灌注治疗是安全有效的。  相似文献   

18.
Macrophage colony-stimulating factor, which induces proliferation and differentiation, and activation of monocytes and macrophages, plays an important role in the vulnerability of atheromatous plaques as well as the formation of atherosclerotic lesions. We measured serum concentrations of macrophage colony-stimulating factor in patients with acute myocardial infarction and also investigated the effects of early administration of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker on circulating macrophage colony-stimulating factor levels in these patients. The patients were divided randomly into 3 therapeutic groups; perindopril, candesartan, and control (without perindopril and candesartan) groups, and the drugs were administered within 24 to 36 hours after the onset of acute myocardial infarction. Serum macrophage colony-stimulating factor concentrations in acute myocardial infarction patients at the time of admission were significantly higher than those in healthy control subjects. The macrophage colony-stimulating factor levels in the patients decreased gradually after admission, but remained significantly higher than those in control subjects for 14 days. There were no significant differences in serum macrophage colony-stimulating factor levels among the 3 therapeutic groups during this study period. In conclusion, circulating macrophage colony-stimulating factor levels are elevated during the course of acute myocardial infarction, and inhibition of the renin-angiotensin system by angiotensin-converting enzyme inhibitor or angiotensin receptor blocker does not affect these levels.  相似文献   

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20.
亚冬眠疗法对急性心肌梗死患者心肌保护作用的研究   总被引:1,自引:0,他引:1  
目的探讨亚冬眠疗法对急性心肌梗死患者的心肌保护作用并推测其可能机制。方法入选患者随机分为干预组和对照组,在常规治疗的基础上,干预组予冬眠合剂持续泵入,观察其体温、血压、心率、呼吸频率变化,测定血浆去甲肾上腺素(NE)(、血清钾离子(K )和镁离子(Mg2 )含量,记录住院天数和心律失常、心力衰竭、死亡例数。结果干预组体温、血压、血浆NE含量和住院天数均明显低于对照组(P<0.01),血清K 、Mg2 含量高于对照组(P<0.05),心律失常和心力衰竭例数较对照组减少(P<0.05)。结论亚冬眠疗法可降低急性心肌梗死患者体温和血压,减少应激性NE释放,有效维持心功能,减少电解质紊乱、心律失常等恶性后续反应,缩短了住院时间。  相似文献   

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