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冠状动脉粥样硬化斑块形成是冠心病的病理基础,贯穿疾病发生与进展的整个过程。近年来国内外大量关于动脉粥样硬化的研究证实,降脂治疗不仅能稳定斑块,甚至能“逆转斑块”。本文对冠状动脉粥样硬化斑块逆转的机制、临床证据、治疗策略的最新研究进展进行概述。 相似文献
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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. 相似文献
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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。 相似文献
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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。 相似文献
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冠状动脉瘘的研究进展 总被引:1,自引:0,他引:1
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。 相似文献
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<正>1病例资料患者男性,80岁,因"发作性胸痛10余年,再发加重9 h"入院。患者10年前曾因"不稳定性心绞痛"行冠状动脉旁路移植术,术后严格实施冠心病二级预防药物治疗,无心绞痛发作。9 h前,患者再次频繁缺血性胸痛发作,口服硝酸甘油片等抗心绞痛药物无效而入院。既往有原发性高血压(高血压)病史20余年,规律服药治疗,血压控制尚可,否认糖尿病及风湿结缔组织疾病病史。入院体检:体温36.5℃,脉搏92bpm,呼吸20bpm,血压140/90 mmHg 相似文献
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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. 相似文献
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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. 相似文献
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