血栓抽吸导管在ACS急诊PCI中的临床应用研究

目的探讨血栓抽吸导管治疗在ACS常规急诊PCI中的临床疗效。方法选择2010年1月-2011年5月我院住院行急诊经皮冠状动脉介入（PCI）治疗的93例急性ST段抬高型心肌梗死和高危、极高危非ST段抬高急性冠脉综合症（ACS）患者,随机分为联用ThrombusterⅡ血栓抽吸导管治疗为A组（51例）,同期未应用血栓抽吸导管治疗为B组（42例）。比较两组患者术后心肌梗死溶栓（TIMI）血流、校正TIMI帧数（CTFC）、术后心肌呈色分级（BMG）、术后ST段抬高回落幅度及左心室射血分数（LVEF）、住院期间主要心血管不良事件（MACE）有无差异。结果 A组TIMI血流3级、CTFC、BMG、术后ST段抬高回落幅度及LVEF均优于B组,差异均有统计学意义（P〈0.05）。两组患者院内MACE发生率比较,差异无统计学意义（P〉0.05）。结论在ACS常规急诊PCI中联用ThrombusterⅡ血栓抽吸导管治疗可显著改善患者TIMI血流、心肌组织水平灌注及术后心功能,但住院期间MACE的发生率无差异。     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

糖尿病患者非高密度脂蛋白胆固醇和载脂蛋白A-Ⅰ比值与冠状动脉病变程度的相关性

目的探讨非HDL-C(NHDL-C)/载脂蛋白A-Ⅰ(apoA-Ⅰ)比值与2型糖尿病患者冠状动脉病变严重程度的相关性。方法选择因劳力性胸痛而行冠状动脉造影的2型糖尿病患者373例,依据Gensini评分三分位分为3组,低分组<8分(143例);中分组8²8分(109例);高分组>28分(121例),评价NHDL-C/apoA-Ⅰ比值与冠状动脉病变严重程度的相关性。结果 3组患者HDL-C、脂蛋白(a)、apoB、NHDL-C、NHDL-C/apoA-Ⅰ比值等比较,差异有统计学意义(P<0.05,P<0.01);Pearson相关分析和Spearman相关分析均显示,2型糖尿病患者NHDL-C/apo-A-Ⅰ比值与Gensini评分呈正相关(r=0.146,P<0.01;r=0.127,P<0.05)。多元线性回归分析显示,2型糖尿病患者NHDL-C/apoA-Ⅰ比值与冠状动脉病变严重程度独立相关(偏相关回归系数=3.361,P<0.05)。结论 NHDL-C/apoA-Ⅰ与2型糖尿病患者冠状动脉病变严重程度独立相关。     

经皮冠状动脉介入治疗右冠状动脉起源异常的不稳定型心绞痛

目的分析右冠状动脉（fight coronary artery,RCA）起源异常的不稳定型心绞痛经皮冠状动脉介入（percutaneous coronary intervention．PCI）治疗的临床特点。方法回顾性分析2005年10月至2012年10月武汉市第五人民医院收治行PCI治疗的不稳定型心绞痛合并RCA起源异常5例患者的临床资料。结果共计623例不稳定型心绞痛患者中6例合并存在RCA起源异常,其中5例罪犯血管为RCA,发生率0．96％。5例患者中男3例,女2例．中位年龄57（32～75）岁;其中RCA起源于左冠状窦3例,起源于嵴上1例,起源于主动脉前壁1例;单支血管病变4例,两支血管病变1例;4例植入药物洗脱支架1枚,1例植入药物洗脱支架2枚;5例PCI治疗围术期无夹层、血栓、心肌梗死、心力衰竭、脑卒中、死亡等并发症发生;随访14．6（6-24）个月,无心绞痛、死亡、再次冠状动脉事件入院、再次血管化等主要心血管事件发生。结论PCI治疗为RCA起源异常的不稳定型心绞痛患者提供了一种安全有效的治疗方法。     

冠状动脉瘘的研究进展

冠状动脉瘘（coronary artery fistulas,CAF）是指心脏在胚胎发育过程中,心肌窦状间隙未能退化而持续存在所形成的冠状动脉主干或其分支与某个心腔或血管形成的异常通道,是一种十分少见的先天性心血管畸形。本文复习相关文献,对CAF的诊疗进展综述如下。     

长节段心肌桥合并慢血流引发心内膜下心肌梗死1例并文献复习

心肌桥是覆盖于冠状动脉上的浅层心肌,长节段的心肌桥对冠状动脉血流影响大,可出现心绞痛及心肌梗死,冠状动脉CT血管造影（CTA）及冠状动脉造影对其有较高诊断价值。慢血流指冠状动脉造影提示冠状动脉血流为TIMI 2级及以下,可导致心肌细胞水平低灌注,引起相应部位缺血。当心肌桥及慢血流同时存在时,则明显增加心血管事件发生率,造成严重后果,本文就两者并存而引发的1例心内膜下心肌梗死进行分析。     

苦瓜总皂苷对慢性心衰大鼠Caspase-3和MMP-2表达影响

目的:探讨分析苦瓜总皂苷对慢性心衰大鼠心脏组织中Caspase-3和MMP-2表达的影响。方法:60只SD大鼠按照随机数字法分为正常组、模型组以及苦瓜总皂苷低、中和高剂量治疗组,每组12只,适应性喂养14d后给予注射盐酸去甲肾上腺素(ISO)构建心衰大鼠模型,模型建立成功后,苦瓜总皂苷低、中和高剂量组分别给予苦瓜总皂苷10、20和40 mg/(kg·d)皮下注射,注射时分散于500μL的生理盐水中,正常组和模型组则给予等量的生理盐水注射,8周后采用超声仪评价大鼠心功能指标,同时检测炎性因子TNF-α和IL-10含量,免疫组化、Western以及实时荧光定量PCR检测心肌组织中Caspase-3和MMP-2表达的特点。结果:在实验期内,模型组大鼠有明显精神萎靡,同时饮食量均降低,苦瓜总皂苷3个治疗组可明显改善上述症状,此外模型组有3只死亡,苦瓜总皂苷低、中和高剂量组分别死亡2只、2只和1只;与正常组相比,模型组LVDD和LVDS明显升高(P0.05),LVEF和LVFS明显降低(P0.05),与模型组相比,苦瓜总皂苷低剂量和中剂量组没有明显改善,而苦瓜总皂苷高剂量组LVDD和LVDS明显降低(P0.05),LVEF和LVFS则明显升高(P0.05);此外苦瓜总皂苷3个治疗组可以明显降低炎性因子TNF-α和IL-10的表达;与正常组相比,模型组Caspase-3和MMP-2表达明显升高(P0.05),与模型组相比,苦瓜总皂苷3个治疗组则可以明显降低其表达(P0.05)。结论:苦瓜总皂苷能够有效改善ISO所致的慢性心衰大鼠心功能,降低炎症反应,其机理可能与其可以抑制心脏组织中Caspase-3和MMP-2的表达有关。