Abstract 14812: Acute Venous Congestion Enhances Vasoconstriction, Inflammation, Oxidative stress and Endothelial Activation and in Compensated Ambulatory Patients with Systolic Heart Failure on Stable Medical Regimen
Background: Accumulating evidence suggests that venous congestion (VC) begins to occur weeks before symptoms worsen, requiring hospitalization for acute decompensated heart failure (ADHF). Whether VC itself enhances vasoconstriction, inflammation, oxidative stress and endothelial activation, thereby promoting progression to decompensation in HF patients is currently unknown.
Methods: 42 ambulatory patients with NYHA functional class II or III, an LVEF <40%, no evidence of VC on physical exam and on stable medical therapy were studied. To experimentally model VC, venous arm pressure was increased to 30 mmHg above baseline by inflating a pressure cuff around the dominant arm. Blood was sampled from test and control arm (lacking an inflated cuff) before and after 90 minutes of venous congestion. Plasma concentrations of endothelin-1 (ET-1), interleukin-6 (IL-6), and vascular cell adhesion molecule 1 (VCAM-1) were determined using quantitative immunoassay kits. 8,12-iso-Isoprostane F-2alpha-VI was measured in plasma by liquid chromatography tandem mass spectrometry.
Results: The age of the study cohort was 53±12 years, 29% were female, 31% had an ischemic etiology and the LVEF was 22±8%. Plasma levels of ET-1 (marker of vasoconstriction), IL-6 (marker of inflammation), 8,12-iso-Isoprostane F-2alpha-VI (marker of oxidative stress) and VCAM-1 (marker of endothelial activation) significantly increased in the congested arm after 90 minutes of experimental VC. No adverse event was observed during the test.
Conclusions: The current study provides the first direct evidence that peripheral VC is sufficient to increase plasma ET-1, IL-6, VCAM-1 and 8,12-iso-Isoprostane F-2alpha-VI. Our preliminary findings support the hypothesis that VC might be a causal contributor (as opposed to a consequence) to the pathophysiology of ADHF via its influence on vasoconstriction, inflammation, oxidative stress and endothelial activation.
Author Disclosures: Y. Hayashi: None. D. Onat: None. K. Wong: None. S. Cremers: None. A. Harxhi: None. M.M. Ahmad: None. N. Uriel: Honoraria; Modest; Thoratec, heartware. U.P. Jorde: None. H.N. Sabbah: None. T.H. LeJemtel: None. R.T. Demmer: None. P.C. Colombo: None.
- © 2014 by American Heart Association, Inc.