Abstract
BackgroundSoluble urokinase plasminogen activator receptor (suPAR) is a proinflammatory biomarker associated with immune activation and fibrinolysis inhibition. Plasminogen activator inhibitor (PAI‐1) is associated with excessive fibrin accumulation, thrombus formation, and atherosclerosis. The relationship between cross‐coronary suPAR and PAI‐1 production and endothelial dysfunction remains unknown.Methods and ResultsSeventy‐nine patients (age 53±10 years, 75% women) with angina and normal coronary arteries or mild coronary artery disease (<40% stenosis) on angiogram underwent acetylcholine assessment of epicardial endothelial dysfunction (mid–left anterior descending coronary artery diameter decrease >20% after acetylcholine) and mircovascular endothelial dysfunction (coronary blood flow change <50% after acetylcholine). Simultaneous left main and coronary sinus suPAR and PAI‐1 levels were measured in each patient before acetylcholine administration, and cross‐coronary suPAR and PAI‐1 production rates were calculated. Patients’ characteristics, except for age (51±10 versus 57±9, P=0.02), and resting coronary hemodynamics were not significantly different between patients with (26%) versus without (74%) epicardial endothelial dysfunction. Patients’ characteristics and resting coronary hemodynamics were not significantly different between those with (62%) and those without (38%) mircovascular endothelial dysfunction. Patients with mircovascular endothelial dysfunction demonstrated local coronary suPAR production versus suPAR extraction in patients with normal microvascular function (median 25.8 [interquartile range 121.6, −23.7] versus −12.7 [52.0, −74.8] ng/min, P=0.03). Patients with epicardial endothelial dysfunction had higher median coronary PAI‐1 production rates compared with those with normal epicardial endothelial function (1224.7 [12 940.7, −1915.4] versus −187.4 [4444.7, −4535.8] ng/min, P=0.03).ConclusionssuPAR is released in coronary circulation of patients with mircovascular endothelial dysfunction and extracted in those with normal microvascular function. Cross‐coronary PAI‐1 release is higher in humans with epicardial endothelial dysfunction.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.