孟增慧,韦 宏,李光男,高艳辉,杨庆辉.前列腺素E1治疗冠状动脉微血管病变的临床研究[J].,2019,19(16):3164-3167 |
前列腺素E1治疗冠状动脉微血管病变的临床研究 |
Effects of Prostaglandin E1 in Patients with Coronary Microvascular Disease |
投稿时间:2019-03-23 修订日期:2019-04-18 |
DOI:10.13241/j.cnki.pmb.2019.16.033 |
中文关键词: 冠状动脉微血管病变 前列腺素E1 西雅图心绞痛量表 血栓调节蛋白 |
英文关键词: Coronary microvascular disease Prostaglandin E1 Seattle angina questionnaire TM |
基金项目:2015年中国冠心病微血管病变研究基金项目;2016年黑龙江博士后资助基金项目(LBH-Z16126) |
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中文摘要: |
摘要 目的:本研究旨在探索前列腺素E1(PGE1)对冠状动脉微血管病变(CMVD)治疗的效果及其可能的机制。方法:92例CMVD患者随机分为PGE1治疗组(47例)及常规治疗组(45例)。PGE1治疗组给予PGE1静脉注射,10 μg/次,一日一次。常规治疗组给予等剂量生理盐水静脉注射,一日一次。两组治疗时间均为10天。通过治疗前后各组的西雅图心绞痛量表评分、血清血栓调节蛋白(TM)水平、血清超氧化物歧化酶(SOD)水平观察PGE1对CMVD的治疗效果。结果:PGE1治疗组在西雅图心绞痛量表中的5个维度(躯体活动受限程度、心绞痛频率、心绞痛稳定状态、治疗的满意程度、疾病认识)评分均高于常规治疗组(P均<0.05)。此外,PGE1治疗组患者血清TM水平较常规治疗组显著下调(PGE1治疗组18.25±7.84 vs 常规治疗组23.1±9.11,P<0.05),血清SOD水平两组间无统计学差异(PGE1治疗组78.23±18.61 vs 常规治疗组71.01±19.1,P=0.07)。结论:PGE1能够缓解CMVD患者的心绞痛状态,提高CMVD患者的生活质量,其机制可能与下调血清TM水平、保护冠状动脉微血管内皮细胞有关。 |
英文摘要: |
ABSTRACT Objective: In this study, we assessed the effect of prostaglandin E1(PGE1) in coronary microvascular disease(CMVD)and explored the underlying mechanisms. Methods: 92 patients with CMVD were randomly divided into a PGE1-treatment group(n=47, PGE1 10ug/d, iv drip) and a control group(n=45, comparable dose of physiological saline). The whole therapeutic course was 10 days. The score of Seattle angina questionnaire(SAQ), the level of thrombomodulin(TM) and superoxide dismutase(SOD) were measured at baseline and after treatment. Results: PGE1-treatment group improved all SAQ items(physical limitation, angina frequency, angina stability, treatment satisfaction, disease perception) compared with control. Furthermore, the level of TM decreased in PGE1-treatment group compared with control.(PGE1 group: 18.25±7.84 vs control group: 23.1±9.11, P<0.05). There were no statistical differences between the two groups at the level of SOD(PGE1 group: 78.23±18.61 vs control group: 71.01±19.1, P=0.07). Conclusion: PGE1 may play a therapeutic role of CMVD patients in relieving angina and improving the quality of life by decreasing the level of TM and protecting the endothelial cells of coronary microvascular. |
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