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

NCT ID: NCT02849691

Last Updated: 2016-07-29

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

747 participants

Study Classification

OBSERVATIONAL

Study Start Date

2014-01-31

Brief Summary

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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

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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.

Conditions

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Dipeptidyl-peptidase-4 STEMI PCI No-reflow Bleeding

Study Design

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Observational Model Type

COHORT

Study Time Perspective

RETROSPECTIVE

Study Groups

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Quartile 1

Quartile 1 of plasma DPP4 activity

No interventions assigned to this group

Quartile 2

Quartile 2 of plasma DPP4 activity

No interventions assigned to this group

Quartile 3

Quartile 3 of plasma DPP4 activity

No interventions assigned to this group

Quartile 4

Quartile 4 of plasma DPP4 activity

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

* a diagnosis of STEMI and needed PCI

Exclusion Criteria

* patients with cancer
* patients who used DPP4 inhibitor
* patients who used GLP1 analogue
Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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Chinese PLA General Hospital

OTHER

Sponsor Role lead

Responsible Party

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Li Jing Wei

Dr.

Responsibility Role PRINCIPAL_INVESTIGATOR

References

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Windecker S, Bax JJ, Myat A, Stone GW, Marber MS. Future treatment strategies in ST-segment elevation myocardial infarction. Lancet. 2013 Aug 17;382(9892):644-57. doi: 10.1016/S0140-6736(13)61452-X.

Reference Type BACKGROUND
PMID: 23953388 (View on PubMed)

Zhong J, Rajagopalan S. Dipeptidyl Peptidase-4 Regulation of SDF-1/CXCR4 Axis: Implications for Cardiovascular Disease. Front Immunol. 2015 Sep 25;6:477. doi: 10.3389/fimmu.2015.00477. eCollection 2015.

Reference Type BACKGROUND
PMID: 26441982 (View on PubMed)

Zhong J, Maiseyeu A, Davis SN, Rajagopalan S. DPP4 in cardiometabolic disease: recent insights from the laboratory and clinical trials of DPP4 inhibition. Circ Res. 2015 Apr 10;116(8):1491-504. doi: 10.1161/CIRCRESAHA.116.305665.

Reference Type BACKGROUND
PMID: 25858071 (View on PubMed)

Connelly KA, Zhang Y, Advani A, Advani SL, Thai K, Yuen DA, Gilbert RE. DPP-4 inhibition attenuates cardiac dysfunction and adverse remodeling following myocardial infarction in rats with experimental diabetes. Cardiovasc Ther. 2013 Oct;31(5):259-67. doi: 10.1111/1755-5922.12005.

Reference Type BACKGROUND
PMID: 22963483 (View on PubMed)

Shigeta T, Aoyama M, Bando YK, Monji A, Mitsui T, Takatsu M, Cheng XW, Okumura T, Hirashiki A, Nagata K, Murohara T. Dipeptidyl peptidase-4 modulates left ventricular dysfunction in chronic heart failure via angiogenesis-dependent and -independent actions. Circulation. 2012 Oct 9;126(15):1838-51. doi: 10.1161/CIRCULATIONAHA.112.096479. Epub 2012 Oct 3.

Reference Type BACKGROUND
PMID: 23035207 (View on PubMed)

Other Identifiers

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DPP4a-noreflow

Identifier Type: -

Identifier Source: org_study_id