Comparison of PD1+T Cell Expression in Peripheral Blood for Cardiac Function Prognosis in Patients With Acute MI

NCT ID: NCT05251987

Last Updated: 2022-02-23

Basic Information

• Recruitment Status: UNKNOWN
• Total Enrollment: 100 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2021-10-01
• Study Completion Date: 2022-12-30

Brief Summary

Comparison of high PD1+ T cell and low PD1+ T cell expression in peripheral blood for cardiac function prognosis in Patients with acute myocardial infarction

Detailed Description

Myocardial infarction is a serious common disease in human beings. Although many patients with acute myocardial infarction survive with the improvement of medical technology in recent years, studies have shown that cardiac remodeling caused by myocardial remodeling after myocardial infarction can still lead to heart failure. Severe heart failure is the main cause of death. Myocardial infarction is a process in which multiple cells interact and participate in post-infarction repair. The pathophysiological processes include early angiogenesis, myocardial compensatory hypertrophy and chronic rational myocardial remodeling and fibrosis. Accordingly, how immune inflammatory cells regulate angiogenesis and fibroblast activation during chronic myocardial remodeling are important therapeutic targets for improving the prognosis of myocardial infarction.Each phase after myocardial infarction has its characteristic pathophysiological changes. Studies have shown that immune inflammatory cells T cells are involved in the whole process of regulating the repair of myocardial infarction. Immune studies have shown that PD1/PD-L1, as a second stimulation signaling pathway besides the antigen TCR of T cells, has the ability to inhibit THE activity of T cells, so the inhibition of PD1/PD-L1 has become a research hotspot in the field of tumor therapy. A large number of studies have focused on the regulation mechanism of PD1/PD-L1 signaling pathway in tumor immune cell activity. Regarding PD1/PD-L1 as the mechanism of immune cell function change in non-tumor lesions, studies based on primary pulmonary hypertension and sarcoidosis have shown that PD1-positive CD4+ cells exhibit a process of promoting fibrosis. Therefore, blocking PD1 antibody can inhibit and improve pulmonary fibrosis. These data suggest that PD1 positive cells are involved in the pathologic process of pulmonary fibrosis. Preliminary data showed that PD1 expression levels were differentiated in peripheral blood of patients with acute myocardial infarction. Further study on the expression and corresponding role of PD1/PD-L1 signaling pathway in ventricular remodeling may provide a new target for the treatment of myocardial infarction remodeling.

This is a perspective, self-controlled cohort study. This study aims to Compare high PD1+ T cell and low PD1+ T cell expression in peripheral blood for cardiac function prognosis in Patients with acute myocardial infarction.

Conditions

PD1; Acute Myocardial Infarction

Study Design

• Observational Model Type: COHORT
• Study Time Perspective: PROSPECTIVE

Study Groups

High PD1+ T Cell Expression

high PD1+ T cell expression in peripheral blood

PD1+ T Cell Expression

Intervention Type: BIOLOGICAL

The expression of PD1+ T cells was detected by flow cytometry in peripheral blood

Low PD1+ T Cell Expression

low PD1+ T cell expression in peripheral blood

PD1+ T Cell Expression

Intervention Type: BIOLOGICAL

The expression of PD1+ T cells was detected by flow cytometry in peripheral blood

Interventions

PD1+ T Cell Expression

The expression of PD1+ T cells was detected by flow cytometry in peripheral blood

Intervention Type: BIOLOGICAL

Eligibility Criteria

Inclusion Criteria

1. Over 18 years of age;

2. Understand oral confirm to accept the risks and benefits of this experiment could bring He (she) or its legal representative in experiment related to provide written informed consent before surgery;

3. Was diagnosed with st-elevation acute myocardial infarction;

4. Based on the visual assessment of coronary angiography of coronary artery stenosis degree is 50% and the row stenting patients;

5. The target vessels are limited to the main coronary arteries (including the left anterior descending, left circumflex, and right coronary arteries).

Exclusion Criteria

1. Pregnant or lactating women; Patients with previous malignant tumors or mental diseases; Recent major trauma/trauma, or surgical treatment; Drug, drug and alcohol abusers; Those who have been receiving antitumor drugs, immunosuppressants, hormones and antibiotics for a long time; People with blood-borne infectious diseases (including hepatitis B, c, syphilis, AIDS, etc.);

2. People with immune deficiency diseases or autoimmune diseases; Liver and kidney dysfunction; Aortic dissection, pulmonary embolism, acute myocarditis or severe valvular disease; One who is in the acute phase of any illness (influenza, pneumonia, gastroenteritis, skin disease, etc.).

• Minimum Eligible Age: 18 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: Yes

Sponsors

First People's Hospital of Hangzhou

OTHER

Sponsor Role: collaborator

Second Affiliated Hospital, School of Medicine, Zhejiang University

OTHER

Sponsor Role: lead

Responsible Party

Responsibility Role: SPONSOR

Principal Investigators

Jianan Wang, MD, PhD

Role: STUDY_CHAIR

2nd Affiliated Hospital, School of Medicine at Zhejiang University

Xinyang Hu, MD, PhD

Role: STUDY_DIRECTOR

2nd Affiliated Hospital, School of Medicine at Zhejiang University

Locations

The Second Affiliated Hospital of Zhejiang University, School of Medicine

Hangzhou, Zhejiang, China

Site Status: RECRUITING

Countries

China

Central Contacts

Jianan Wang, MD, PhD

Role: CONTACT

wangjianan111@zju.edu.cn

+86 0571 87784808

Changle Ke, PhD

Role: CONTACT

keheart@zju.edu.cn

+86 15757102667

Facility Contacts

Jianan Wang, MD, PhD

Role: primary

wangjianan111@zju.edu.cn

+86 0571 87784808

Changle Ke, PhD

Role: backup

keheart@zju.edu.cn

+86 15757102667

Other Identifiers

2021-0725

Identifier Type: -

Identifier Source: org_study_id