Rare Case of Acute Pancreatitis Presenting With ST-Segment Elevation

Abstract

When first presented, ST-segment elevation on EKG (electrocardiogram) requires close scrutiny. The most concerning of possible diagnoses is acute coronary syndrome, yet it is not the only clinical entity that can cause ST-segment elevation. Herein, we present a case of a 62-year-old male current smoker with past medical history of uncontrolled diabetes, hypertension, and hyperlipidemia presenting with abdominal pain for 1 week duration. His initial admission EKG illustrated ST-segment elevation; however, his clinical presentation, lack of anginal symptoms, normal bedside transthoracic echocardiogram, and normal range troponin were not indicative of myocardial infarction. In fact, he was found to have elevated lipase and CT findings consistent with acute pancreatitis. This case highlights an uncommon presentation of pancreatitis and illustrates the importance of obtaining a comprehensive clinical history when evaluating patients to ensure patient’s receive efficient and appropriate care.

Introduction

When ST-segment elevation is seen on electrocardiogram, acute coronary syndrome (ACS) is the first clinical entity that must be considered. However, there are many pathologies that can mimic myocardial injury on EKG that one must be aware of; such as pericarditis, aortic dissection, pulmonary embolism, Takotsubo cardiomyopathy, hyperkalemia, and acute intra-abdominal pathologies, like cholecystitis and pancreatitis. Although incidence of pancreatitis mimicking ACS is not entirely clear within a recent study, it was found within 50% of patient’s presenting with acute pancreatitis.^1,2 In fact, the EKG can detect an acute myocardial infarction with 81% sensitivity, but only 69% specificity. ³ Herein this article, we discuss a patient who presents with ST-segment elevation secondary to acute pancreatitis to stress the importance of obtaining a clear clinic picture before initiating treatment that could have potential adverse consequences.

Case Presentation

A 62-year-old male current tobacco smoker of 20 pack/years with a past medical history of uncontrolled, noninsulin-dependent diabetes, hypertension, and hyperlipidemia presents to the hospital due to worsening abdominal pain for the past week.

The patient was in his normal state of health until 1 week prior to presentation, when he began to develop constant, diffuse abdominal pain, worse in his epigastric region. He had associated symptoms of nausea, vomiting, and generalized weakness. He originally thought that the abdominal pain would resolve on its own, but when it began to worsen he decided to come to the hospital. He denies any chest discomfort, shortness of breath, palpitations, or loss of consciousness. He reports a previous history of heavy alcohol use, which he denies for the past 10 years. His home medications included metformin 500 mg twice a day and Losartan 25 mg daily, which he took irregularly.

Upon admission to the hospital, his vital signs were within normal limits. His physical exam was significant for tenderness to palpation in the epigastric region. There were no abnormal heart sounds, jugular venous distention, or abnormal lung sounds. His admission EKG (Figure 1) revealed ST-segment elevation within the inferior leads II, III, and aVF. Due to this concerning EKG, his troponin was taken, which was within normal range at 0.034 ng/mL at admission, <0.030 ng/mL 2 hours after (normal range < 0.040 ng/mL). Cardiology service was emergently consulted from the emergency room due to ST-segment elevation seen on EKG. With discussion with the interventional cardiology team, an emergent limited bedside transthoracic echocardiogram (TTE) performed (Figure 2), to rule out any wall motion abnormalities indicative of myocardial infarction or presence of pericardial effusions, both of which were not seen. Patient continued to deny any anginal symptoms, only severe abdominal pain for a week’s duration.

Figure 1.

EKG on admission: This EKG illustrates ST-segment elevation within leads II, III, and aVF (seen in red circle) which are typically indicative of an inferior wall myocardial infarction.

Figure 2.

STAT Limited TTE: There was normal left and right ventricular size, systolic function, wall motion with ejection fraction estimated at 60% to 65%, making it less likely for acute coronary syndrome. There was also no evidence of pericardial effusion or valvular abnormalities.

His additional lab work was significant for elevated white blood cell count 17.2 µL (normal range: 4.0-11.0 µL) and elevated lipase 129 µ/L (normal range: 12-53 µ/L). His thyroid-stimulating hormone was within normal limits, HbA1c was 12.5%, lipid panel revealed low-density lipoprotein (LDL) of 110 mg/dL (goal: <75 mg/dL), and brain natriuretic peptide was 104.0 pg/mL (normal range: <100.0 pg/mL). No electrolyte abnormalities were noted.

Due to his elevated lipase and presentation of severe abdominal pain with prolonged duration, a CT scan of his abdomen and pelvis (Figure 3) was performed, which revealed acute pancreatitis with associated pancreatic tail abscess in the background of chronic pancreatitis. General surgery was consulted, and there was no indication for surgery at this time. He was diagnosed with acute on chronic pancreatitis and was treated appropriately with intravenous hydration and pain control, which he recovered from and was discharged home within 3 days of hospitalization. His EKG upon discharge showed return to normal sinus rhythm without evidence of ST elevation (Figure 4). However, due to his significant cardiovascular risk factors, he was scheduled for additional outpatient follow-up with cardiology.

Figure 3.

CT Abdomen Pelvis w/wo contrast: (A) coronal plane, (B) axial plane. The image illustrates inflammation of the pancreatitis indicating acute pancreatitis with associated pancreatic tail abscess, which is labeled with the measurements seen on the image.

Figure 4.

EKG on discharge, day 3: This EKG illustrates normal sinus rhythm without evidence of previous ST-segment elevation that was seen in leads II, III, and aVF.

Discussion

According to the ACC/AHA 2025 guidelines, the initial diagnosis and classification of ACS is based on clinical history, symptomatology, EKG, and cardiac troponin. ACS can be further classified into 3 related conditions: unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction (STEMI). If a STEMI is diagnosed, the patient is evaluated for immediate reperfusion therapy at a percutaneous coronary intervention capable center. ⁴ The most concerning risks of cardiac catheterization include inducing myocardial infarction, stroke, coronary artery dissection, pericardial effusion, cardiac tamponade, or need for urgent coronary artery bypass graft surgery. ⁵ It is necessary to have high suspicion for STEMI beyond ST-segment changes due to noted risks of unnecessary intervention.

Since the 1930’s, ischemic EKG changes have been seen in cases of pancreatitis. ⁶ Pancreatitis typically will mimic T wave and ST-segment abnormalities in 25% of acute cases, but presentation within ST-segment elevation is still rare. ⁶ If a case of pancreatitis does present with ST-segment elevation, an inferior wall STEMI pattern is the most frequently seen. ⁷ There has been no correlation noted between elevation in amylase and lipase levels and significance of EKG changes. ¹

Interestingly, the exact pathophysiology of ST-segment elevation in acute pancreatitis is unknown. Pancreatitis occurs due to activation of proteolytic enzymes that will increase the active trypsin within the pancreas. The lysosomal enzymes will cause rupture of the vacuoles, then releasing trypsin. The release of trypsin causes autodigestion of the pancreatic tissue causing severe epigastric pain for the patient and elevation of pancreatic enzymes.^2,8

Pancreatitis can result in hypovolemia and hypotension causing coronary hypoperfusion and electrolyte disturbances, which may result in ST-segment changes. Another explanation is that there can be direct damage of myocytes secondary to proteolytic enzymes. Trypsin modifies permeability of membranes that can result in direct membrane injury, inducing necrosis and worsening electrolyte disturbance, which can exhibit EKG abnormalities. Since the pancreas is located posterior and retroperitoneal, it is theorized that there is a transdiaphragmatic translocation of inflammation during pancreatitis, which explains why it typically mimics inferior wall myocardial injury. In cases of severe acute pancreatitis, cardiac and pulmonary manifestations are often present. It may affect rhythm and contractility of the heart, which can result in EKG changes showing T wave flattening and ST-segment depression. These changes are typically reversible with treatment of pancreatitis. ⁹

Often to assist with the diagnosis of ACS, a TTE will be used to assess wall motion abnormalities. Unfortunately, this may not always lead to a clear diagnosis. Acute pancreatitis can also cause transient regional wall motion abnormalities, referred to as myocardial stunning, and not all ACS presents with wall motion abnormalities. Therefore, as with our case, it is important to get the full clinical picture before initiating ACS protocol. An elevation in ST-segment without evidence on TTE of wall motion abnormalities, anginal symptoms, elevation in troponin, makes ACS a less likely etiology.

Conclusion

When presented with acute ST-segment elevation, ACS should always be on top of the differentials due to its high risk of mortality, but other clinical entities can mimic myocardial injury on an EKG; including, intra-abdominal pathologies, like acute pancreatitis. This case is an important example that clinical history and symptomatology play a vital role in diagnosis. Obtaining a full history allows us to ensure the safety of our patients by providing an appropriate level of care and reducing their risk of harm.