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Influence of alprostadil on preventing left ventricular remodeling after acute myocardial infarction
Received date: 2016-04-19
Online published: 2016-06-30
To investigate the clinic effect of alprostadil on preventing left ventricular remodeling after acute myocardial infarction (AMI). A total of 73 cases of AMI were randomly divided into two groups: basic treatment group and alprostadil treatment group. Both groups were given basic treatments such as rest, oxygen inhalation, dual antiplatelet therapy. Alprostadil was intravenously injected in the alprostadil treatment group, 10 μg once a day for 7 days. Left ventricular end-diastolic dimension (LVDd), left ventricular end-systolic dimension (LVDs), interventricular septal thickness (IVST), left ventricle posterior wall end-diastolic (LVPWd), ejection fraction (EF) and E/A ratio were measured by echocardiography on the 3rd and the 28th days after treatment. Compared to the 3rd day after treatment, LVDd, LVDs, IVST, LVPWd, EF, E/A ratio in the basic treatment group had no significant changes on the 28th day after treatment. LVDd, LVDs, E/A ratio in the alprostadil treatment group on the 28th day after treatment were significantly reduced in comparison with the 3rd day after treatment (P <0.05) while IVST and LVPWd showed no significant changes. Alprostadil improves cardiac function after acute myocardial infarction in short term, but has no influence on preventing left ventricular remodeling.
ZHAN Li1,2, XU Jiahong1 . Influence of alprostadil on preventing left ventricular remodeling after acute myocardial infarction[J]. Journal of Shanghai University, 2016 , 22(3) : 371 -375 . DOI: 10.3969/j.issn.1007-2861.2016.03.015
[1] 高晓津, 杨进刚, 杨跃进, 等. 中国急性心肌梗死患者心血管危险因素分析[J]. 中国循环杂志, 2015(3): 206-210.
[2] Hori M, Nishida K. Oxidative stress and left ventricular remodelling after myocardial infarction [J]. Cardiovascular Research, 2009, 81: 457-464.
[3] Liu S, Yin T, Wei X, et al. Downregulation of adiponectin induced by tumor necrosis factor alpha is involved in the aggravation of post traumatic myocardial ischemia/reperfusion
injury [J]. Crit Care Med, 2011, 9: 1935-1943.
[4] Turer A T, Hill J A. Pathogenesis of myocardial ischemia-reperfusion injury and rationale for therapy [J]. Am J Cardiol, 2010, 106: 360-368.
[5] Yun B, Lee H, Ghosh M, et al. Serine hydrolase inhibitors block necrotic cell death by preventing calcium overload of the mitochondria and permeability transition pore formation [J]. J Biol Chem, 2014, 289: 1491-1504.
[6] Frangogiannis N G. Targeting the inflammatory response in healing myocardial infarcts [J]. Curr Med Chem, 2006, 13: 1877-1893.
[7] 中华医学会心血管病学分会, 中华心血管病杂志编辑委员会. 急性ST段抬高型心肌梗死诊断和治疗指南[J]. 中华心血管病杂志, 2010, 38: 675-690.
[8] Henry T D, Atkins J M, Cunningham M S, et al. ST-segment elevation myocardial infarction: recommendations on triage of patients to heart attack centers: is it time for a national policy for the treatment of ST-segment elevation myocardial infarction? [J]. J Am Coll Cardiol, 2006, 47: 1339-1345.
[9] Li J, Yang P, Li A, et al. Cardioprotective effect of liposomal prostaglandin E1 on a porcine model of myocardial infarction reperfusion no-reflow [J]. J Zhejiang Univ-Sci B: Biomed &
Biotechnol, 2011, 12: 638-643.
[10] Enrique M S, James H T, Noelia C, et al. Beneficial effects of intra-arterial and intravenous prostaglandin E1 in intestinal ischaemia—reperfusion injury [J]. Interact Cardiovasc Thorac Surg, 2014, 18: 466-474.
[11] Hsieh C C, Hsieh S H, Chiu J H, et al. Protective effects of n-acetylcysteine and a prostaglandin E1 analog, alprostadil, against hepatic ischemia: reperfusion injury in rats [J]. J Tradit Complement Med, 2014, 4: 64-71.
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