Lp-PLA2 and Coronary Atherosclerosis in Humans (AIM 1 and II)
|Coronary Atherosclerosis Endothelial Dysfunction||Other: Blood sampling from the Coronary Sinus and Aorta Procedure: Intravascular Ultrasound of the coronary artery.|
|Study Design:||Intervention Model: Single Group Assignment
Masking: None (Open Label)
Primary Purpose: Diagnostic
|Official Title:||Lp-PLA2, Progenitor Cells and Coronary Atherosclerosis in Humans|
- Lp-PLA2 Assessment [ Time Frame: baseline endothelial function assessment 6 months ]AIM 1: To assess the relationship between the 3 inflammatory measures of the Lp-PLA2 pathway (Lp-PLA2 mass, Lp-PLA2 activity and LysoPC) with endothelial function (as measured by the percent change in CAD (coronary artery disease) [Ach] and by the length of segments with endothelial dysfunction and plaque vulnerability (as measured by the necrotic core percent volume). AIM II: To assess the association between the percent of Lp-PLA2 residing on LDL and endothelial function (again measured by percent change in CAD [Ach], percent change in CBF (coronary blood flow)[Ach], and the length of endothelial dysfunction).
|Study Start Date:||February 2009|
|Study Completion Date:||June 2015|
|Primary Completion Date:||June 2015 (Final data collection date for primary outcome measure)|
Other: Blood sampling from the Coronary Sinus and Aorta
Aim I: Hypothesis: The extent of endothelial dysfunction will correlate with production of Lp-PLA2 and oxidative stress and correlates with the tissue characteristics of plaque vulnerability. The investigators will define the systemic and coronary gradient and production of markers of inflammation and oxidative stress and the presence of coronary endothelial dysfunction in patients with early coronary atherosclerosis.
Aim II: Hypothesis: The distribution of Lp-PLA2 on the LDL is associated with greater coronary endothelial dysfunction and correlates with the degree coronary atherosclerosis and plaque vulnerability. The investigators will define the distribution of Lp-PLA2 in patients with early coronary atherosclerosis and endothelial dysfunction.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01557088
|United States, Minnesota|
|Rochester, Minnesota, United States, 55905|
|Principal Investigator:||Amir Lerman, MD||Mayo Clinic|