Case Presentation: A 67-year-old female with a medical history of coronary artery disease, hypertension, and hyperlipidemia presented to the hospital with several days of worsening epigastric pain and chest pain. The pain had a band-like distribution with radiation to her back and no clear aggravating or alleviating factors. She reported chills and one day of nausea but denied vomiting, shortness of breath, or diaphoresis. Her coronary artery disease had been diagnosed five years earlier after a non-ST elevation myocardial infarction (NSTEMI), for which she received a right coronary artery (RCA) stent. On presentation, her electrocardiogram (ECG) revealed new ST-segment elevations in the inferior leads (II, III, aVF) with reciprocal changes in leads I and aVL (figure 1). Serial high-sensitivity troponin levels remained within normal limits, making acute coronary syndrome (ACS) less likely. Due to the concerning ECG findings and prior history of NSTEMI, she underwent emergent left heart catheterization, which revealed non-obstructive coronary arteries with a widely patent RCA stent. Further laboratory testing showed an elevated lipase of 662 U/L, and a computed tomography (CT) scan of the abdomen revealed peripancreatic stranding consistent with acute pancreatitis. A transthoracic echocardiogram also demonstrated a small pericardial effusion. She was treated supportively with intravenous fluids and pain management. Her symptoms resolved, and she was discharged two days later.
Discussion: Acute coronary syndromes (ACS) are commonly diagnosed based on clinical presentation, ECG findings, and cardiac biomarkers. Prompt recognition and intervention are essential for improving outcomes in ACS. However, it is critical to recognize that not all ST-segment elevations indicate an acute coronary event. Here we present a case of acute pancreatitis associated with new ST-elevations on ECG. Several mechanisms have been proposed to explain ECG changes seen in patients with acute pancreatitis. Some of the hypothesized mechanisms include metabolic derangements, myocarditis, coronary artery vasospasm, and pericarditis among others (1). Regardless of exact mechanism, acute pancreatitis is an important etiology to keep in mind when evaluating a patient with new ECG changes.
Conclusions: This case underscores the importance of a comprehensive clinical evaluation when assessing patients with ST-segment elevations on ECG. While ACS remains a critical diagnosis to rule out, clinicians must consider alternative causes of ST-segment elevations, such as pericarditis. The clinical presentation, in conjunction with appropriate diagnostic testing, plays a key role in avoiding unnecessary invasive procedures and ensuring that patients receive the appropriate treatment for their underlying condition. Keeping a broad differential and recognizing atypical causes of ECG changes can improve patient outcomes.
