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临床试验/NCT02849691
NCT02849691已完成不适用

Plasma Dipeptidyl-peptidase-4 Activities With No-reflow and Bleeding

Chinese PLA General Hospital0 个研究点目标入组 747 人开始时间: 2014年1月最近更新:
适应症

试验速览

阶段
不适用
状态
已完成
发起方
入组人数
747
主要终点
a change in the prevalence of no-reflow

研究概览

简要总结

Dipeptidyl-peptidase-4 (DPP4) is an important regulator of incretins and inflammation, and participates in the pathophysiological process of acute myocardial infarction (AMI). However clinical data of DPP4a in AMI patients is sparse. This study was to investigate the role of plasma DPP4 activity (DPP4a) in patients with ST-segment elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention (PCI). This was a analysis of consecutive patients conducted at a tertiary referral center from January 2014 to October 2015. The investigators included 747 STEMI-patients, treated with PCI from January 2013 to October 2015. Blood samples were collected immediately at admission. The patients were divided into four groups according to DPP4a quartile.

详细描述

ST-segment elevation myocardial infarction (STEMI) is an acute manifestation of coronary heart disease, remaining a frequent cause of death.A better understanding of risk factors and pathogenic mechanisms underlying STEMI may help improve the prognosis and life quality of these patients.Dipeptidyl peptidase 4 (DPP4) is an exopeptidase expressed on the surface of diverse cells, cleaving off amino-terminal dipeptides with either L-proline, L-alanine or serine at the penultimate position. As a cell surface protein, it participates in immune regulation, signal transduction and apoptosis. DPP4 also circulates as a soluble form in the plasma. Soluble DPP4 came from either membrane type clearance or secreted by cells like endothelial cells, with enzymatic activity. Plasma DPP4 activity (DPP4a) are elevated in several diseases, including type 2 diabetes, obesity, atherosclerosis and osteoporosis. Basic studies have showed that DPP4 inhibition leads improved survival and heart function after cardiac ischemia-reperfusion (I/R) injury, and this is partly due to activation of AKT (pAKT), pGSK3 and ANP pathways. Also inhibition of DPP4 can alleviate atherosclerosis and heart failure. Accordingly, one could hypothesize that high DPP4a may worsen myocardial I/R injury, causing poorer cardiovascular outcomes. However, no study has evaluated whether DPP4a is associated with adverse clinical outcomes in STEMI patients.

研究设计

研究类型
Observational
观察模型
Cohort
时间视角
Retrospective

入排标准

性别
All
接受健康志愿者

入选标准

  • a diagnosis of STEMI and needed PCI

排除标准

  • patients with cancer
  • patients who used DPP4 inhibitor
  • patients who used GLP1 analogue

结局指标

主要结局

a change in the prevalence of no-reflow

时间窗: immediately after PCI

TIMI flow grade of \<3 with a myocardial blush grade of 0-1 was defined as angiographic no-reflow

次要结局

  • in-hospital major adverse cardiac or cerebrovascular events(up to 2 week after PCI (until discharge))
  • in-hospital complications(up to 2 week after PCI (until discharge))
  • in-hospital major bleeding(up to 2 week after PCI (until discharge))

研究者

发起方
Chinese PLA General Hospital
申办方类型
Other
责任方
Principal Investigator
主要研究者

Li Jing Wei

Dr.

Chinese PLA General Hospital

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