S191 Severe Acute Pancreatitis Is Associated With Left Ventricular Dysfunction With Preserved Ejection Fraction

Introduction: Vascular leak during acute pancreatitis is assumed to cause severity, making fluid resuscitation the main treatment. However, pulmonary edema complications from fluid overload during the WATERFALL trial suggest underlying left ventricular dysfunction. Therefore, we compared early cardiac injury, left ventricular dysfunction, and EF% in patients developing severe acute pancreatitis (SAP) vs those developing mild or moderate acute pancreatitis (MMAP). Methods: Patients presenting with acute pancreatitis to Mayo Clinic Arizona or the Phoenix VA Medical Center between May 2017 and February 2024 were included. Those with pre-existing heart failure, ischemic heart disease, valvular heart disease, chronic pancreatitis, pancreatic cancer, pancreatic surgery, pregnant women, history of stage 4 renal failure or dialysis were excluded. Patients were classified as SAP or MMAP based on the Revised Atlanta Criteria. Fluid status, admission serum CK-MB, NT-Pro BNP, echocardiography, and clinical outcomes were compared between the 2 groups. Results: Age, sex, race, and BMI were similar between the 23 SAP and the 237 MMAP patients. All SAP patients developed persistent organ failure and 10 required ICU admission (43% vs 0% in MMAP, P = 0.0001). Four required pressors (17% vs 0%, P = 0.0001), and had longer hospital stay (17 ± 22 vs 3 ± 3 days, P = 0.0001) vs MMAP. Compared to MMAP patients, SAP patients had lower mean arterial pressure (90 ± 2 vs 105 ± 16 mmHg). The drop in hematocrit value (%) from the day of admission vs the day of echocardiography (median day 2 in both groups) trended to be higher in SAP (-8.3 ± 5.5 vs –4.6 ± 5.9, P = 0.09), compared with the MMAP group. SAP patients had lower end-diastolic volume (88 ± 31 mL vs 149 ± 160 mL, P = 0.03) and lower stroke volume (57 ± 19 mL vs 70 ± 16 mL, P = 0.02), while both groups had preserved %EF (65 ± 9% and 62 ± 5%, P = 0.09). SAP patients had higher markers of cardiac injury (CK-MB 46 ± 35 vs 26 ± 14 pg/mL, P = 0.03) and higher markers of heart failure (NT-Pro BNP 347 ± 1278 vs 73 ± 618 pg/mL, P = 0.002) vs MMAP patients. Conclusion: SAP patients have elevated cardiac injury and heart failure markers on admission. Despite adequate fluid resuscitation, SAP patients had lower end-diastolic volume and stroke volume but normal EF% compared to MMAP. Thus, cardiac injury and left ventricular dysfunction with preserved ejection fraction are present in early SAP. These contribute to the fluid overload, hypotension, and the severity of pancreatitis.