NCT06833918

Brief Summary

The pathophysiology of acute myocardial infarction is multifaceted, involving numerous biological processes. The crosstalk between cuproptosis and remodeling biomarkers may be implicated in the pathogenesis of AMI. Combining cuproptosis, LIPCAR, and α-SMA cardiac recovery analysis may enable more precise identification of diagnostic biomarkers that help for future improvement of treatment and prognosis

Trial Health

65
Monitor

Trial Health Score

Automated assessment based on enrollment pace, timeline, and geographic reach

Enrollment
50

participants targeted

Target at P25-P50 for all trials

Timeline
13mo left

Started Mar 2025

Typical duration for all trials

Status
not yet recruiting

Health score is calculated from publicly available data and should be used for screening purposes only.

Trial Relationships

Click on a node to explore related trials.

Study Timeline

Key milestones and dates

Study Progress53%
Mar 2025Jul 2027

First Submitted

Initial submission to the registry

January 13, 2025

Completed
1 month until next milestone

First Posted

Study publicly available on registry

February 19, 2025

Completed
10 days until next milestone

Study Start

First participant enrolled

March 1, 2025

Completed
1.8 years until next milestone

Primary Completion

Last participant's last visit for primary outcome

January 1, 2027

Expected
6 months until next milestone

Study Completion

Last participant's last visit for all outcomes

July 1, 2027

Last Updated

February 19, 2025

Status Verified

January 1, 2025

Enrollment Period

1.8 years

First QC Date

January 13, 2025

Last Update Submit

February 13, 2025

Conditions

Outcome Measures

Primary Outcomes (2)

  • The present study will include two groups: First group: 50 AMI patients and Second group (control): 50 age and gender matched healthy volunteers without history of pre-existing or existing cardiovascular comorbidities with normal cardiac enzymes

    The followings markers will be investigated in plasma samples: 1. LIPCAR, STAT3 and DDIT3 using quantitative real-time polymerase chain reaction (qRT-PCR) 2. α-SMA using western blot analysis 3. Troponin T using ELISA expression 4. Serum levels of fasting blood glucose (FBG), total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C), oxidized low-density lipoprotein (ox-LDL) using chemical methods (spectrophotometry). The Friedewald formula will be used to compute low-density lipoprotein cholesterol (LDL-C): LDL-Cholesterol =Total cholesterol- (HDL-Cholesterol +Triglycerides/5).

    2 years

  • AMI is a myocardial injury event induced by rupture of atherosclerotic plaques and thrombosis. Rapid and accurate identification of AMI in accordance with reducing myocardial cell death has become a critical component for early diagnosis and improvement

    The followings markers will be investigated in plasma samples using quantitative real-time polymerase chain reaction (qRT-PCR): 1. LIPCAR, 2. STAT3, 3. DDIT3, 4. α-SMA and 5. Troponin T * To measure LIPCAR, STAT3 and DDIT3 expression in AMI patients for identifying their role in the pathogenesis of AMI, that could enable further research on its role as a potential therapeutic target. * To detect the relationship between LIPCAR, STAT3 and DDIT3 expression and Age, gender, BMI, diabetes mellitus (DM), hypertension (HTN), dyslipidaemia,smoking, and obesity. * To detect the relationship between α-SMA protein expression and cardiac regeneration and repair, so that healthcare providers can make more informed decisions regarding treatment strategies, allowing for tailored pharmacological or intervention approaches based on individual patient needs and significantly enhancing heart function and improving the overall quality of life for patients recovering from myocardial infarction.

    2 years

Interventions

The followings markers will be investigated in plasma samples: 1. LIPCAR, STAT3 and DDIT3 using quantitative real-time polymerase chain reaction (qRT-PCR) 2. α-SMA using western blot analysis 3. Troponin T using ELISA expression 4. Serum levels of fasting blood glucose (FBG), total cholesterol (TC), triglycerides (TG), and high-density lipoprotein cholesterol (HDL-C), oxidized low-density lipoprotein (ox-LDL) using chemical methods (spectrophotometry). The Friedewald formula was used to compute low-density lipoprotein cholesterol (LDL-C): LDL-Cholesterol =Total cholesterol- (HDL-Cholesterol +Triglycerides/5).

Eligibility Criteria

Sexall
Healthy VolunteersYes
Age GroupsChild (0-17), Adult (18-64), Older Adult (65+)
Sampling MethodNon-Probability Sample
Study Population

The present study will include 50 AMI patients diagnosed and screened based on criteria including persistent chest pain, electrocardiogram changes, and high-sensitivity cardiac troponin I (cTnI) and T testing during their hospital admission to the cardiac catheter unit, department of cardiology, faculty of medicine, Assiut university hospital. Patient features will be anonymously analysed in addition to 50 age and gender matched healthy volunteers without history of cardiovascular diseases or other organ issues, no pre-existing or existing cardiovascular symptoms like chest pain during their routine physical examinations in the hospital, normal cardiac enzyme cTnI and T levels, coronary artery stenosis \<50% on coronary angiography, and normal ECG parameters as a control group

You may qualify if:

  • All patients will be subjected to full history taking, meticulous general examination, and local cardiac examination
  • Age ≥ 18 years
  • AMI diagnosis : clinical, laboratory (troponins level), ECG and coronary angiography indicated occlusion or (≥50% stenosis of any coronary artery or its major branches)

You may not qualify if:

  • Patients with aortic coarctation,
  • Coronary artery bypass grafting surgery,
  • Coronary intervention,
  • Congestive heart failure,
  • Rheumatic heart disease,
  • Presence of coronary myocardial bridges,
  • Organic cardiac disease such as combined heart valve disease,
  • Congenital heart defects,
  • Any inflammatory diseases like myocarditis or pericarditis, traumatic cardiac injury or other primary heart diseases,
  • Dilated cardiomyopathy,
  • Hypertrophic cardiomyopathy,
  • Patients complicated with malignant arrhythmias.
  • Patients with severe haematological disease,
  • Infection as tuberculosis,
  • Pulmonary embolism,
  • +7 more criteria

Contact the study team to confirm eligibility.

Sponsors & Collaborators

Biospecimen

Retention: SAMPLES WITH DNA

Blood Sample Collection For plasma isolation a total of 5 ml of peripheral antecubital venous blood will be obtained in the morning after an overnight fast from each patient within 24 h of the onset of myocardial infarction and from healthy controls in EDTA-containing tubes. The plasma will be separated by centrifugation at 800 g for 10 min. The supernatant plasma samples will be divided into RNase-free Eppendorf tubes and stored at - 80 until analysis.

MeSH Terms

Interventions

Blood Specimen Collection

Intervention Hierarchy (Ancestors)

Specimen HandlingClinical Laboratory TechniquesDiagnostic Techniques and ProceduresDiagnosisPuncturesSurgical Procedures, OperativeInvestigative Techniques

Central Study Contacts

Study Design

Study Type
observational
Observational Model
CASE CONTROL
Time Perspective
PROSPECTIVE
Target Duration
6 Months
Sponsor Type
OTHER
Responsible Party
PRINCIPAL INVESTIGATOR
PI Title
Dr

Study Record Dates

First Submitted

January 13, 2025

First Posted

February 19, 2025

Study Start

March 1, 2025

Primary Completion (Estimated)

January 1, 2027

Study Completion (Estimated)

July 1, 2027

Last Updated

February 19, 2025

Record last verified: 2025-01