PANCREATITIS-INDUCED ACUTE ST SEGMENT ELEVATION AND REGIONAL WALL MOTION ABNORMALITY

Abstract

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Acute myocardial infarction (AMI) mimics causing ST segment elevation present a diagnostic conundrum for physicians. Recognition of uncommon causes of AMI mimics is essential in reducing patient exposure to unnecessary intervention. CASE PRESENTATION: A 49-year-old male with a past medical history of hypertension presented to the emergency with a chief complaint of severe epigastric pain radiating to his back. He had undergone ERCP earlier in the day for removal of a common bile duct (CBD) stone. Severe epigastric tenderness was observed on physical exam. Laboratory evaluation revealed WBC count of 25700/mcL, Hb 19.8 g/L, BUN 25 mg/dL, creatinine 1.3 mg/dL, alkaline phosphatase 188 IU/L, AST 42 IU/L, ALT 89 IU/L, total bilirubin 1.4 mg/dL, amylase 1059 IU/ L, lipase 21,417 units/L and troponin < 0.015 ng/mL. CT scan of the abdomen revealed an enlarged pancreas with surrounding fat stranding and the presence of a distal CBD stone. EKG was unremarkable (figure 1). The following day, the patient developed tachycardia and reported recurrent epigastric pain. He denied chest pain. EKG evidenced sinus tachycardia, 2-3mm convex ST segment elevation in inferior leads, 1-2mm ST depression in the anterolateral leads was also observed (figure 2). Serial troponin I levels were within the undetectable range. Repeat EKG after 3 hours showed tachycardia with no ST segment elevation (figure 3). Echocardiography revealed a small area of dyskinesia in the inferoseptal wall of the left ventricle. Patient was managed without percutaneous coronary intervention (PCI), thrombolysis or anticoagulation. Patient’s hospital stay was complicated by pancreatic necrosis, abscess, pseudocyst formation, and sepsis. He was discharged on day 19 after recovery. DISCUSSION: The most common EKG changes in pancreatitis are secondary to metabolic derangements such as hypocalcemia, hyponatremia, hypokalemia, hypomagnesemia, and insulin-induced hypoglycemia. QT prolongation, ST depression, U waves, and low amplitude T wave changes are frequently seen. On the other hand, ST elevation is rarely seen. Proposed mechanisms for ST elevation and wall motion abnormality include the cytotoxic effect of proteolytic enzymes on cardiac myocytes, a cardiobiliary reflex resulting in increased vagal tone, coronary vasospasm, exacerbation of underlying coronary artery disease, or coronary thrombus formation from increased platelet adhesiveness and/or pancreatic enzyme induced coagulopathy [1,2,3]. Takotsubo stress cardiomyopathy has been linked to pancreatitis in several reports. Hypothesized pathomechanisms for this transient myocardial dysfunction include catecholamine excess and sympathetic stimulation [2]. CONCLUSIONS: Acute pancreatitis may mimic EKG and echocardiography findings of AMI. In selected cases, knowing this can help avoid unnecessary PCI, thrombolysis or anticoagulation which may lead to serious hemorrhagic complications. Reference #1: Coppola G, Carità P, Corrado E, Borrelli A, Rotolo A, Guglielmo M, et al. ST segment elevations: Always a marker of acute myocardial infarction? Indian Heart Journal. 2013 Jul;65(4):412–23. Reference #2: Yu ES, Lange JJ, Broor A, Kutty K. Acute Pancreatitis Masquerading as Inferior Wall Myocardial Infarction: A Review. Case Rep Gastroenterol. 2019 Aug;13(2):321–35. Reference #3: Ro TK, Lang RM, Ward RP. Acute pancreatitis mimicking myocardial infarction: evaluation with myocardial contrast echocardiography. Journal of the American Society of Echocardiography. 2004 Apr;17(4):387–90. DISCLOSURES: No relevant relationships by Maryam Moghareh, source=Web Response No relevant relationships by Prashank Neupane, source=Web Response No relevant relationships by Zed Seedat, source=Web Response No relevant relationships by Touqir Zahra, source=Web Response