Case Report: Pancreatitis Mimics STEMI

Many conditions outside of acute coronary syndrome (ACS) mimic ST-elevation myocardial infarction (STEMI), but only a handful of cases have reported ST-elevations (STE) in the setting of pancreatic inflammation where underlying ACS was excluded.1,2 While acute pancreatitis can involve electrocardiographic changes in up to 50 percent of cases, the exact mechanism causing STE remains unknown.3,4 Patients with ST segment elevation in the absence of classic ACS symptoms presents a dilemma for emergency physicians. Epigastric pain often raises concern for both cardiovascular and abdominal pathologies, including pancreatitis. Given the paucity of data and mechanistic uncertainty, a standard management protocol does not currently exist for patients with coexisting pancreatitis and ST segment elevation. Our case seeks to make emergency physicians aware of this phenomenon as recognition is essential in reducing patient exposure to unnecessary and potentially harmful interventions.

FIGURE 1: Initial EKG were notable for a leukocytosis of 23.19 k/uL, lipase of 87 U/L and an initial negative troponin of 3 ng/L HEART score of 1. The patient denied any chest pain or shortness of breath. A repeat ECG completed shortly after epigastric pain was controlled showed dynamic STE in aVL, V1 and aVR with diffuse ST depressions (see Figure 2). (Click to enlarge.)

A 60-year-old female presented to the emergency department with acute epigastric pain radiating to the back, nausea and vomiting. Pertinent medical history included atrial fibrillation with unclear adherence to apixaban, hypertension, peripheral artery disease status-post superficial femoral artery stent placement and chronic pancreatitis. The day prior to presentation, the patient was in her usual state of health and had been drinking wine coolers. Symptoms had been ongoing for nearly 22 hours prior to presentation. She was hypertensive and tachycardic with otherwise normal vital signs. On physical exam, she had epigastric pain to deep palpation without peritoneal signs or skin changes.

During the initial work-up, her ECG revealed STE measuring approximately 1 mm in V1, V2. There was also STE approximately 1 mm in I and aVL with diffuse ST depressions in the inferior leads, V3-V6 and aVR (see Figure 1).

FIGURE 2: Given concern for myocardial ischemia, cardiology was consulted and the patient was placed on ticagrelor and aspirin with transport arranged for emergent cardiac catheterization. Near complete pain control was achieved with a combination of nitroglycerin and morphine. During the delay to transport, a CT angiogram of the chest, abdomen and pelvis was completed and notable for peripancreatic acute on chronic inflammatory changes (see Figure 3). No evidence of pulmonary embolism, aneurysm or dissection was found. (Click to enlarge.)

The patient symptomatically improved throughout her stay, vitals stabilized, and repeat troponins remained negative. Her leukocytosis and elevated lipase both trended down to  within normal values. Her repeat ECG prior to discharge was normal sinus rhythm with resolution of ST changes. She was ultimately discharged on aspirin and atorvastatin, with continuation of apixaban and discontinuation of ticagrelor.

Intra-abdominal etiologies with occurrence of ST-elevation myocardial infarction are rare. With 36 cases involving pancreatic inflammation described in literature, the pathophysiology remains unknown. Interestingly, an inferior wall ST-elevation myocardial infarction has been the most frequent pattern reported.2 Proposed hypothesis as described by Hsu et al., include (1) vagally mediated reflexes, (2) metabolic and electrolyte abnormalities, (3) direct toxic effects of pancreatic enzymes on myocardium, (4) coronary artery vasospasm, (5) hemodynamic instability or systemic inflammatory response, (6) prothrombotic derangement, and others including (7) takotsubo cardiomyopathy.2,4,5,6 In our case, STE in I, aVL and inferior depressions suggested a lateral infarction with a repeat ECG with STE in aVR with diffuse ST-depressions. The patient’s normal electrolytes, catheterization and echocardiogram lead us to suspect the etiology could be related to direct toxic effects, vasospasm or systemic inflammatory response.

FIGURE 3: The patient was taken for left heart catheterization given the dynamic ECG changes in the setting of epigastric pain. Findings were without obstructive lesions and notable only for 20-30 percent stenosis of the left anterior descending artery. An echocardiogram soon after demonstrated a normal left ventricular systolic function with minimal pericardial effusion and no major valvular abnormalities. (Click to enlarge.)

Despite the low frequency, acuity remains high when considering the importance of misdiagnosis leading to invasive treatment and testing. Missing ACS has fatal consequences, as does converting acute pancreatitis to hemorrhagic pancreatitis with thrombolytics.7,8 Catheterization itself carries the complications of dissections, perforations and bleeding. Yu et al.2 describe their patient developing a stroke following PCI, in the setting of pancreatitis induced STE. In the absence of guidelines, a multidisciplinary approach to the clinical situation may be most appropriate. Even still, pseudo-myocardial infarction associated with acute pancreatitis must be a diagnosis of exclusion.9,10 The lethality of true myocardial infarction warrants cardiology consultation for angiography, as opposed to use of thrombolytics.

The presentation serves as another instance where STE signaled systemic disease unrelated to a flow-limiting coronary lesion.11 While our patient’s ECG findings could have represented occlusion, the clinical context proved to be an important factor in avoiding thrombolytics as transport was arranged for angiography. There is both a circumspect and nuanced approach to diagnosing and managing myocardial infarctions. To guide clinical management, the risks and benefits of cardiac interventions must be weighed with factors such as the patient’s stability and likelihood of other diagnoses to make the most appropriate disposition.

Dr. Knoedler is a resident physician at Georgetown University Hospital & Washington Hospital Center.

Dr. Koo is an attending physician and assistant professor in emergency medicine on staff at MedStar St Mary’s Hospital and Medstar Washington Hospital Center.

Dr. Hockstein is an attending physician in emergency medicine and critical care medicine and is on staff at Medstar Georgetown University Hospital.

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