Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) Induced Myocardial Injury is Mitigated by Endovascular Variable Aortic Control (EVAC) Background The cardiac effects of resuscitative endovascular balloon occlusion of the aorta (REBOA) are largely unknown. We hypothesized that increased afterload from REBOA would lead to cardiac injury, and that partial flow using endovascular variable aortic control (EVAC) would mitigate this injury. Methods Eighteen anesthetized swine underwent controlled 25% blood volume hemorrhage. Animals were randomized to either Zone 1 REBOA, Zone 1 EVAC, or no intervention (control) for 45 minutes. Animals were then resuscitated with shed blood, observed during critical care, and euthanized after a six-hour total experimental time. Left ventricular function was measured with a pressure-volume catheter and blood samples were drawn at routine intervals. Results The average cardiac output during the intervention period was higher in the REBOA group [9.3 (8.6-15.4) L/min] compared to the EVAC group [7.2 (5.8-8.0) L/min, P=0.01] and the control group [6.8 (5.8-7.7) L/min, P<0.01]. At the end of the intervention, the preload recruitable stroke work (PRSW) was significantly higher in both the REBOA and EVAC groups compared to the control group [111.2 (102.5-148.6) and 116.7 (116.6-141.4) versus 67.1 (62.7-87.9), P=0.02 and P<0.01, respectively]. The higher PRSW was maintained throughout the experiment in the EVAC group, but not in the REBOA group. Serum troponin concentrations after six hours were higher in the REBOA group compared to both the EVAC and control groups (6.26±5.35 ng/mL versus 0.92±0.61 ng/mL and 0.65±0.38 ng/mL, P=0.05 and P=0.03, respectively). Cardiac intramural hemorrhage was higher in the REBOA group compared to the control group (1.67±0.46 vs 0.17±0.18, P=0.03), but not between the EVAC and control groups. Conclusions In a swine model of hemorrhagic shock, complete aortic occlusion resulted in cardiac injury, although there was no direct decrease in cardiac function. EVAC mitigated the cardiac injury and improved cardiac performance during resuscitation and critical care. Level of Evidence not applicable for basic science study Name and address for correspondence: Carl A Beyer, 2315 Stockton Boulevard, Room OP 512, Sacramento, CA 95817, 916-734-2724 | Fax: 916-734-5633, E-mail: cbeyer@ucdavis.edu Disclaimer: The views expressed in this material are those of the authors and do not reflect the official policy of the US Government, the Department of Defense, the Department of the Air Force, the Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., the University of California Davis, or Wake Forest University. Meetings: Awarded second prize at the 16th biennial Strandness Symposium, March 3-7, 2019, Wailea, HI. © 2019 Lippincott Williams & Wilkins, Inc.