Plasma Dipeptidyl-peptidase-4 Activities With No-reflow and Bleeding
- Conditions
- STEMINo-reflowDipeptidyl-peptidase-4PCIBleeding
- Registration Number
- NCT02849691
- Lead Sponsor
- Chinese PLA General Hospital
- Brief Summary
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.
- Detailed Description
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.
Recruitment & Eligibility
- Status
- COMPLETED
- Sex
- All
- Target Recruitment
- 747
- a diagnosis of STEMI and needed PCI
- patients with cancer
- patients who used DPP4 inhibitor
- patients who used GLP1 analogue
Study & Design
- Study Type
- OBSERVATIONAL
- Study Design
- Not specified
- Primary Outcome Measures
Name Time Method a change in the prevalence of no-reflow immediately after PCI TIMI flow grade of \<3 with a myocardial blush grade of 0-1 was defined as angiographic no-reflow
- Secondary Outcome Measures
Name Time Method in-hospital major adverse cardiac or cerebrovascular events up to 2 week after PCI (until discharge) the composite of death, nonfatal MI, or stroke
in-hospital complications up to 2 week after PCI (until discharge) defined as acute heart failure, atrial fibrillation, chest pain or re-acute myocardial infarction, complete atrioventricular block, cerebrovascular disease, ventricular fibrillation or ventricular tachycardia
in-hospital major bleeding up to 2 week after PCI (until discharge) defined as absolute hemoglobin drop (baseline to nadir)≥4g/dl, intracranial hemorrhage, retroperitoneal hemorrhage, use of red blood cell transfusion in patients with a baseline hemoglobin ≥9.0 g/dl, and use of red blood cell transfusion among patients with a baseline hemoglobin \<9.0 g/dl and a witnessed bleeding event