Molecular and Morphologic Characterization of Circulating Endothelial Cells (CEC)
The primary hypothesis of this study is that circulating endothelial cells (CECs) harbor key genetic and structural characteristics predisposing individuals to acute atherosclerotic plaque rupture and heart attack.
Acute Myocardial Infarction
|Study Design:||Observational Model: Cohort|
|Official Title:||Comprehensive Molecular and Morphologic Characterization of Circulating Endothelial Cells|
- The primary endpoint is complete molecular profiling of CEC's in up to 250 patients with a diagnosis of acute myocardial infarction (MI) and up to 25 healthy controls. [ Time Frame: 2 years ] [ Designated as safety issue: No ]
Biospecimen Retention: Samples With DNA
Blood for each patient will be collected from arterial access established as part of standard of care or via venipuncture. Blood must be collected in the order listed below. By drawing the PAX gene tube first, the likelihood of contamination of the sample with vessel wall endothelial cells is decreased.
- x 8.5 ml PAX gene (blue top) tube
- x 10 ml EDTA purple top tubes
Follow-up visits: (healthy controls only)
- x 5 ml red top (discard)
- x 10 ml EDTA purple top tube
|Study Start Date:||January 2010|
|Estimated Study Completion Date:||December 2016|
|Estimated Primary Completion Date:||March 2016 (Final data collection date for primary outcome measure)|
Patients undergoing open vascular surgery on arterial structures to better define optimal laboratory and collection techniques for isolation of CECs.
Healthy controls will be recruited from the general medical population, community.
Acute Myocardial Infarction
Patients with acute myocardial infarction with or without ST segment deviation.
Endothelial injury and inflammation are pivotal underlying processes that put patients at risk for catastrophic vascular events including acute myocardial infarction (heart attack) and stroke. We seek to accelerate scientific discovery through clinically meaningful, innovative translational research, and are collaborating in a trans-disciplinary effort to define the DNA sequence of CECs and that of germ line DNA, along with RNA sequencing, mRNA expression profiling, and ultrastructural characterization of CECs in order to better understand the mechanisms leading to acute arterial plaque rupture and embolization of arterial endothelial cells in patients with acute myocardial infarction. This will enable us to create a molecular fingerprint that could identify and preempt individuals from suffering from such debilitating vascular conditions.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01005485
|Contact: Emily Spencer, PhDfirstname.lastname@example.org|
|Contact: Sarah Topol, BSN, RNemail@example.com|
|United States, California|
|La Jolla, California, United States, 92037|
|Principal Investigator: Eric Topol, M.D.|
|Principal Investigator:||Eric Topol, M.D.||Scripps Translational Science Institute|