An observational study in Myocardial Inflammation and Myocardial Infarction, sponsored by Ann & Robert H Lurie Children's Hospital of Chicago. Completed at 1 site in United States. Open to participants aged Up to 19 Years. Per ClinicalTrials.gov, last updated 2021-08-12.
Sponsored by Ann & Robert H Lurie Children's Hospital of Chicago · Observational
The relationship between the immune system and the myocardium after myocardial ischemia is an evolving field of research. Crosstalk occurs between macrophages and cardiac myocytes to promote cardio-protection and resolution of inflammation after myocardial ischemia and reperfusion injury (MI/R injury).
Myeloid-epithelial-reproductive tyrosine kinase (MerTK), a member of the TAM family of tyrosine kinase receptors (Tyro-Axl-MerTK), is a macrophage receptor that mediates efferocytosis, anti-inflammatory signaling, and resolution of inflammation. After MI/R injury, intact MerTK is necessary for the phagocytosis of dead cardiac myocytes and to promote anti-inflammatory signaling. Proteolytic cleavage of MerTK to its inactive form, soluble MER, restricts the capacity of macrophages to phagocytize dead cardiac myocytes and impairs MerTK-dependent anti-inflammatory signaling resulting in suppressive effects on cardiac remodeling and function.
The Thorp lab at Northwestern University has previously measured soluble MER levels in both adult mice and humans and found that soluble MER concentrations increase after MI/R injury. In adult MI patients, soluble MER was measured post coronary artery reperfusion and was found to be increased (average 3200 pg/mL compared to 1700 pg/mL) compared to controls with stable cardiovascular disease. Based on murine data, the lab further postulated that reperfusion injury may directly interfere with MerTK-dependent cardiac repair as reactive oxygen species formed during reperfusion injury induce proteolytic cleavage of MerTK to soluble MER.
Myocardial infarctions are rare events in pediatric patients. However, pediatric hearts are exposed to periods of hypoperfusion, ischemia, and inflammation during times of stress such as cardiac bypass and critical illness, and it is unknown how soluble MER levels change in response to these events. Thus, I was interested in investigating how soluble MER levels change after MI/R injury induced by cardiac bypass as well as in the utility of soluble MER as a biomarker of cardiac inflammation and injury in pediatric patients.
2,744 studies on the registry are indexed under Myocardial Infarction; 418 are open to participants now.
This study's enrollment of 50 is below the median of 500 across 983 observational studies indexed under Myocardial Infarction.
Browse Myocardial Infarction studies →Ann & Robert H Lurie Children's Hospital of Chicago is the lead sponsor of 176 studies on the registry; 30 are open to participants now.
Of its 10 completed or terminated interventional studies of FDA-regulated products, 5 (50%) have results posted.
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Pediatric patients with congenital heart disease presenting to Lurie Children's Hospital for corrective or palliative heart surgery and will be undergoing cardiac bypass.
Exclusion Criteria:
Blood samples obtained from patients ages from birth-19 years-old as well as cyanotic and acyanotic cardiac lesions who underwent cardiac bypass.
Other: Change in Soluble MER Concentration
Measuring change in soluble MER Concentration post compared to pre bypass for each patient.
Change in Soluble MER Concentration
Time frame: 5/10/2019-12/31/2020
Utility of soluble MER as a biomarker of inflammation and injury
Time frame: 5/10/2019-12/31/2020
Plan to share: Undecided
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Ann & Robert H Lurie Children's Hospital of Chicago