不同剂量阿托伐他汀对不稳定型心绞痛预后的影响

目的观察不同剂量阿托伐他汀对不稳定型心绞痛预后的影响。方法将2005年10月～2008年10月收治的128例不稳定性心绞痛患者随机分为两组,每组64例,观察组常规治疗加上阿托伐他汀40mg/d,对照组常规治疗加上阿托伐他汀20mg/d。两组均在治疗前及治疗后90d测定血脂四项、C反应蛋白(CRP)和NO浓度,并且观察再发心绞痛、心肌梗死及心脏性死亡等不良心血管事件的发生情况。结果两组治疗后血脂水平有不同程度的降低,与对照组比较,观察组降低的更明显(P<0.05),两组治疗后CRP降低而NO升高,观察组与对照组比较效果更明显(P<0.05),两组患者不良事件发生情况,观察组与对照组比较明显降低(P<0.05)。结论阿托伐他汀强化治疗能改善不稳定型心绞痛患者的预后,每天剂量40mg是安全的,他汀类药物对冠心病患者防治有重要意义。     

美国“六大药方”防控冠心病

近年来,冠心病的发病率呈逐年上升趋势。2001年,美国做了一项关于心血管病和脑中风医疗费用开支的专项调查,美国2001年心血管疾病总计花     

慢病毒Hoxa3载体的构建及其对人脐静脉内皮细胞迁移和血管新生的影响

目的构建慢病毒Hoxa3载体,观察其对人脐静脉内皮细胞(HUVEC)的转染效率,研究其对细胞迁移和血管新生的影响,并探讨Hoxa3促进血管新生的机制。方法以基因合成法从聚合酶链式反应文库获取人Hoxa3基因,酶切后插入慢病毒骨架载体,以三质粒联合转染293T细胞获得慢病毒Hoxa3载体,并进行滴度测定。转染HUVEC,获取最大转染效率。转染HUVEC后分对照组和慢病毒Hoxa3转染组,进行HUVEC迁移实验和小管形成实验,观察Hoxa3对HUVEC迁移和小管形成的影响。Western blot检测慢病毒Hoxa3载体转染HUVEC后尿激酶型纤溶酶原激活物受体(uPAR)和基质金属蛋白酶14(MMP-14)蛋白表达的变化。结果成功构建慢病毒Hoxa3载体,病毒的滴度为8×1011TU/L; 30 MOI慢病毒载体对HUVEC的转染效率达到99%以上。Western blot结果显示慢病毒Hoxa3载体转染HUVEC后Hoxa3能够有效在HUVEC中表达。与对照组比较,慢病毒Hoxa3载体转染HUVEC后显著增强HUVEC的迁移和小管形成,显著增加uPAR和MMP-14蛋白的表达(P0.05)。结论成功构建的慢病毒Hoxa3载体可促进HUVEC的迁移和小管形成,其作用机制可能为上调HUVEC的uPAR和MMP-14蛋白表达。     

冠状动脉支架置入后支架内的血栓问题：形成的因素及其防治

目的：探讨冠状动脉支架置入后血栓形成的机制及防治情况。方法：由第一作者应用计算机检索维普数据库(http://www.cqvip.com/)与冠状动脉支架置入后血栓形成有关的文献,检索时限为2000-01/2009-10。检索关键词：冠状动脉,支架植入术,血栓。对资料进行初审,并查看每篇文献后的引文。纳入标准：①支架内血栓形成的机制及危险因素。②支架内血栓的预防及治疗。排除标准：重复研究或较陈旧文献。依据纳入排除标准共保留相关文献28篇。结果: 支架内血栓形成是冠心病介入治疗的严重并发症,可对人体造成灾难性的后果。与普通金属支架比较,药物洗脱支架可明显减少再狭窄率和靶病变的血运重建率。置入支架后可发生早期、晚期、极晚期支架内血栓形成,其发生机制并不完全相同。抗血小板、抗凝、调脂治疗可能降低支架内血栓的发生率。个体化手术及个体化药物治疗,在解决冠状动脉血运重建的同时,可减少再狭窄率和降低支架血栓的发生率。结论：在期待新型支架的同时,对每例患者,应仔细评估支架内血栓形成的各种危险因素,做到个体化手术及个体化药物治疗。在冠状动脉血运重建的同时,减少再狭窄率和降低支架内血栓的发生率。     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

前列地尔脂肪乳剂对急性心肌梗死心肌缺血-再灌注损伤的保护作用

目的探讨溶栓前应用前列地尔脂肪乳剂(Lipo-PGE1)对急性心肌梗死(AMI)患者心肌缺血/再灌注(I/R)损伤的影响.方法首次发病6h之内的AMI患者,予尿激酶溶栓治疗,临床再通者24例为对照组.在溶栓前予Lipo-PGE110μg静脉注射临床再通者32例为前列地尔组.统计2h内心电图ST段抬高指数(∑STI)下降≥50%率与ST段完全回落率.记录再灌注心律失常(RA).测定溶栓前即刻及溶栓后3h血清丙二醛(MDA)与超氧化物岐化酶(SOD)活性.2周后超声心动图检查测定梗死部位收缩期室壁增厚率(AT)、左室收缩末期容量(LVESV)与左室射血分数(LVEF). 结果与对照组比较前列地尔组心电图∑STI下降≥50%率ST段完全回落率显著提高;频发室早与室速发生率降低;MDA与SOD再灌注前后的差值减少再灌注治疗2周后AT、LVEF均提高,LVESV减少. 结论Lipo-PGE1可以减轻过氧化损伤,有助于溶栓后ST段完全回落,降低再灌注时室早、室速的发生率,改善左室功能.     

经皮冠状动脉介入治疗术中心室颤动4例

心室颤动是经皮冠状动脉介入治疗(PCI)术中的严重并发症.本文对2000年4月-2004年3月我院298例PCI术中出现的心室颤动4例,分析报告如下.     

冠心病心肌梗塞恢复期的心功能评价

我们应用心阻抗图微波来观察分析心便恢复期患者的心脏收缩时间间期及心输出量，观察其梗塞部位、时间及异常Q波对心功能的影响，以指导病人康复期的保健及生活是非常必要的。材料与方法一、恢复期组40例急性心肌梗塞病人，均有典型病史，血清酶港变化和心电图所证实。急性发病后2个月病情稳定者，男29例，女11例，年龄33—74岁，平均59．8岁。急性心梗后时间：2个月一3年ZI例，3年一5年12例，5年以上7例。梗塞部位：前间壁15例，广泛前壁11例，下壁14例。恢复期心电图改变：相应导联仍在Q波或QS波31例，Q波消失9例。二、对照组40例与恢…