2026 FSA Podium and Poster Abstracts

Introduction: Cardiovascular instability remains a leading cause of morbidity during liver transplantation (LT), particularly during reperfusion, when abrupt hemodynamic and metabolic shifts may precipitate severe hypotension and myocardial stress. We present a case of intraoperative MI during LT in a patient with extensive coronary artery disease, highlighting the use of venoarterial extracorporeal membrane oxygenation (VA-ECMO) as a bridge to emergent coronary revascularization after failed conventional therapy.  

Case Description: A 64-year-old male with alcoholic cirrhosis (MELD 30), CAD, hypertension, hyperlipidemia, and type 2 diabetes mellitus presented for LT. His CAD-LT score was 19, indicating high risk for obstructive CAD. Preoperative coronary angiography demonstrated maximal revascularization status post three-vessel CABG (2022) and PCI (2024). Transthoracic echocardiography showed normal left ventricular systolic function (EF 55–59%) without regional wall-motion abnormalities. Cardiology cleared him for LT, noting acceptable hemodynamics and no cardiac contraindications. He denied chest pain, dyspnea, or functional limitations, and his vital signs were stable preoperatively. 

Following dissection, inferior vena cava clamping, and hepatectomy, norepinephrine (0.04 mcg/kg/min) and vasopressin (0.03 mcg/min) were initiated and titrated to maintain a mean arterial pressure (MAP) > 60 mmHg. Upon reperfusion, MAP acutely dropped to 47 mmHg with systolic pressures in the 50s. Escalating product resuscitation, increased vasopressor support, initiation of an epinephrine infusion, and bolus administration of epinephrine (299 mcg), vasopressin (16 U), calcium chloride (1,000 mg), sodium bicarbonate (100 mEq), and hydroxocobalamin failed to correct persistent vasoplegia and worsening shock. The patient developed tachycardia with new ST-segment elevations. 

Cardiology and cardiac anesthesia were consulted emergently. Intraoperative transesophageal echocardiography revealed severe anteroseptal hypokinesis consistent with acute MI and cardiogenic shock. After multidisciplinary discussion, VA-ECMO was initiated as a bridge to coronary reperfusion. Following completion of the vascular anastomosis and placement of a biliary drain, the abdomen was temporarily closed. The patient was cannulated for VA-ECMO in the operating room and transferred directly to the catheterization laboratory for urgent revascularization. 

Discussion/Conclusion: Acute MI during LT is rare but carries a high risk of mortality, particularly when masked by the vasoplegia commonly encountered after graft reperfusion. In patients with significant underlying CAD, new or refractory hypotension that does not respond to standard post-reperfusion interventions should raise immediate suspicion for myocardial ischemia rather than isolated vasoplegic shock. Because the definitive treatment for MI is urgent coronary revascularization, early recognition is critical to prevent progression to severe ventricular dysfunction, worsening end-organ perfusion, and cardiogenic shock. In this setting, short-term mechanical circulatory support plays an essential role. Options such as intra-aortic balloon pump (IABP) may augment coronary perfusion but offer limited support in profound hypotension or severe ventricular dysfunction. VA-ECMO offers immediate, complete cardiopulmonary support that can be initiated directly in the OR. By maintaining systemic perfusion and unloading the myocardium, ECMO serves as an effective bridge to PCI when acute intraoperative MI is suspected. In our case, early TEE identification of new wall-motion abnormalities and persistent hemodynamic collapse prompted rapid initiation of VA-ECMO, allowing safe transfer to the catheterization laboratory for definitive revascularization.