About this trial
To identify plasma multi-omics biomarkers that predict left ventricular adverse remodeling (LVAR) and major adverse cardiovascular events (MACE) in patients with acute ST-segment elevation myocardial infarction, and to investigate the molecular pathways linked to LVAR and MACE.
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
Age ≥18 years and ≤80 years.
Chest pain lasting >30 minutes, and
ST-segment elevation in at least two contiguous leads: ≥0.2 mV in leads V2-V3 (≥0.2 mV for men, ≥0.15 mV for women) or ≥0.1 mV in other leads, or new-onset left bundle branch block.
Reperfusion therapy: Symptom onset to first medical contact ≤12 hours, and successful primary PCI (culprit vessel opened, post-procedure TIMI flow grade 3).
Disqualifiers
Non-atherosclerotic MI: coronary embolism, spasm, aortic dissection, myocarditis, Takotsubo.
Prior HF (NYHA ≥II);
Severe CKD (eGFR <30 mL/min/1.73m² or dialysis);
Severe liver disease (Child-Pugh B/C);
Trial population
The study population includes individuals diagnosed with acute ST-segment elevation myocardial infarction (MI), selected by the site personnel according to predefined inclusion criteria. The cohort comprises 1,000 patients, whose baseline clinical characteristics and plasma biomarkers will be assessed.
Trial design
Cohort
Prospective
Treatments tested in this trial
Diagnostic Test: echocardiography and blood collection
Other interventionBlood samples were collected from all patients at enrollment (within 24 hours after primary PCI), at days 3-5, and at months 1, 3, and 6 after enrollment. Echocardiography was performed at enrollment (baseline, within 24-48 hours after admission), and at months 1, 3, and 6 after enrollment.
Treatment groups
Trial outcomes
Primary outcomes
major adverse cardiovascular events
Identify T0 plasma multi-omics biomarkers that predict cardiac death, myocardial infarction, heart failure, and stroke.
Secondary outcomes
adverse cardiac remodeling
To assess the predictive ability of multi-omics biomarkers in T0 plasma for adverse cardiac remodeling, and to identify new candidate markers for forecasting this condition.
Sponsors and contacts
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Beijing Anzhen Hospital
Lead sponsor
Beijing Jishuitan Hospital
Collaborator
Institute of Biophysics, Chinese Academy of Sciences
Collaborator