Abstract 15077: Plasma Macrophage Migration Inhibitory Factor and Angiopoietin-2 Levels During Venoarterial Extracorporeal Membrane Oxygenation Support

• Published in: Circulation (New York, N.Y.) Vol. 138; no. Suppl_1 Suppl 1; p. A15077
• Main Authors: Vuthoori, Ravi, Miller, Edmund, Heaney, Cassandra, Lin, Ke, Wang, Ping, Fernandez, Harold, Lima, Brian, Majure, David, Maybaum, Simon
• Format: Journal Article
• Language: English
• Published: by the American College of Cardiology Foundation and the American Heart Association, Inc 06.11.2018
• ISSN: 0009-7322; 1524-4539

IntroductionMacrophage migration inhibitory factor (MIF) is an inflammatory cytokine with expression and release mediated by oxidative stress and hypoxia. Angiopoietin-2 (Ang-2) is a modulator of vascular permeability. Both have been linked to poor outcomes in cardiogenic shock (CS). Both proteins are rapidly released from intracellular storage during stress and can have profound effects on the cardiopulmonary vasculature. We studied plasma concentrations of MIF and Ang-2 in 9 patients with CS supported with VA ECMO.MethodsAll patients had baseline blood samples taken within 24 hrs of ECMO. Repeat samples were drawn on stable patients prior to ECMO decannulation. Plasma MIF and Ang-2 were evaluated using commercially available enzyme linked immunosorbent assay (R&D Systems Inc., Minneapolis, MN).ResultsNine patients (63±5 yrs) supported with VA ECMO for post-MI (6), post-cardiotomy (2), and other CS (1) were studied. At baseline (n=9, within 24 hrs of ECMO), HR 77±15 bpm, MAP 82±30 mmHg, SaO2 98±4%. At follow-up (n=4, 4-12 days of support), HR 81±11 bpm, MAP 82±8 mmHg, SaO2 = 99±0.5%. During ECMO support, there was a reduction in lactate (9.2±6.7 vs 0.9±0.2 mmol/L, p< 0.02) and pressor requirement (Inotrope Score 48±63 vs 3.1±2.3). At baseline, both MIF and Ang-2 were significantly elevated as compared to 9 controls (606.2±545.0 vs 1.5±0.7 ng/mL, p<0.05; 52.1±58.4 vs 3.3±0.7 ng/mL, p<0.05, respectively) (Fig 1). Clinical improvements during ECMO were associated with decreases in MIF and Ang-2 at follow up (69.6±26.5 ng/mL; 13.4±7.7 ng/mL, respectively) which were no longer significantly different from controls.ConclusionOur preliminary data suggest that CS is associated with significant derangement of plasma MIF and Ang-2 that improves with mechanical hemodynamic support. Further study could lead to a better understanding of their role in CS and may identify novel targets for therapy.