Abstract 11617: Peripheral Venous Congestion Increases Circulating Levels of Activated CD62E+ Endothelial Microparticles in Humans
Background: Circulating levels of endothelial microparticles (EMPs) increase with worsening functional class and independently predict future cardiovascular events in congestive heart failure (CHF) patients. EMPs are likely involved in the pathogenesis of the CHF as they promote inflammation, vascular dysfunction, and coagulation. The mechanisms underlying their production in CHF remain unclear.
Methods: To experimentally model venous congestion (VC), we developed a novel method, wherein the venous arm pressure was increased to 30 mmHg above baseline by inflating a tourniquet cuff around one arm (congested) for 120 minutes, with the other arm serving as the control (non-congested). Five healthy subjects (4 males, age 33±9 years) were studied. Blood was sampled simultaneously in both arms at baseline; after 60 and 120 minutes of VC; and finally at 60 minutes after cuff release (venous decongestion). Circulating CD62E+ EMPs, phenotypic for endothelial cell activation, and CD31+CD42b- EMPs, phenotypic for endothelial cell apoptosis, were quantified using flow cytometry.
Results: No adverse event was observed. Arterial O2 saturation did not change after 120 minutes of VC. Compared to baseline, CD62E+ EMPs significantly increased during 120 minutes of VC in the congested arm (figure) but not in the control arm (not shown). CD62E+ EMPs normalized after 60 minutes of decongestion. CD31+/CD42b- EMPs did not increase in response to VC.
Conclusion: Peripheral venous congestion acutely stimulates release of CD62E+ EMPs, phenotypic for endothelial cell activation, which rapidly resolves after venous decongestion. These findings support the hypothesis that VC might contribute to the progression of CHF through endothelial cell injury and release of activated (pro-inflammatory and pro-coagulant) EMPs.
- © 2013 by American Heart Association, Inc.