PGY3 Internal Medicine Northern Ontario School of Medicine Sudbury, Ontario, Canada
Case background: A 72-year-old female with no prior medical history presented to the emergency department with a 5-day history of nausea and vomiting. These symptoms began approximately one day after eating at a restaurant and were initially attributed to possible food poisoning. She reported persistent abdominal discomfort but denied chest pain, palpitations, dyspnea, or orthopnea. She had no history of hypertension, diabetes, dyslipidemia, coronary artery disease and was a life-long non-smoker. Her only home medication was as-needed cetirizine.
Initial laboratory investigations revealed a sodium of 132 mmol/L, potassium 3.2 mmol/L, chloride 92 mmol/L and a creatinine of 437 μmol/L (baseline unknown). Venous blood gas showed a pH of 7.50, pCO2 36 mmHg, bicarbonate 28 mmol/L and lactate 1.5 mmol/L. High sensitivity troponin I was 55 ng/L (ULN 16 ng/L). Chest X-ray showed small lung volumes with bilateral atelectasis. A baseline ECG was obtained, which demonstrated an isolated Q wave in lead III and non-specific ST/T changes (Table 1A). She was admitted to general internal medicine for fluid resuscitation and supportive management of nausea and vomiting.
Later that evening, the patient experienced an acute desaturation event requiring escalation to 10L/min via a non-rebreather mask (NRB). She reported a “heartburn’’ sensation approximately one hour prior but this did not recur. ECG obtained at that time demonstrated ST-segment elevations in the inferior leads and V3-V6 (Table 1B) with ST depression in 1 and aVL, and prolongation of the QT interval. High-sensitivity troponin I was 45 ng/L. This was interpreted by the computer algorithm as an inferior ST-elevation myocardial infarction (STEMI), prompting an emergent cardiology consultation.
At the bedside, she was tachycardic (HR 118), with blood pressure 111/80 mmHg and SpO2 95% on 10L NRB. Cardiovascular examination was unremarkable; JVP was not elevated, there was no pedal edema, no crackles, and no murmurs. The abdomen was markedly distended with diffuse mild tenderness.
Point-of-care ultrasound (PoCUS) demonstrated normal biventricular function without regional wall motion abnormalities. Serial high sensitivity troponin I was 50 ng/L and 49 ng/L at 2- and 4-hours, respectively, after the initial ECG. Given the absence of typical anginal symptoms, dynamic ECG changes, or significant troponin rise, and normal cardiac function on PoCUS, the cardiac catheterization lab was not activated after the case was reviewed with the on-call interventional cardiologist. Empiric antiplatelet and anticoagulant therapy was initiated, including ASA 160 mg chewed, clopidogrel 300 mg orally, and IV heparin 5000 units.
Given the atypical presentation and significant hypoxia, CT chest with contrast was ordered to evaluate for pulmonary embolism and aspiration pneumonia. The scan demonstrated a markedly distended fluid-filled stomach compressing the inferior and inferolateral segments of the left ventricle (Figure 1A, B).
Radiology recommended urgent abdominal imaging. A non-contrast CT abdomen/pelvis revealed a high-grade small bowel obstruction (SBO) with a clear transition point in the posterior pelvis. An NG tube was urgently inserted for decompression resulting in marked clinical improvement and subsequent resolution of ECG changes (Table 1C).
A formal transthoracic echocardiogram (TTE) one day later showed a normal-sized left ventricle with hyperdynamic systolic function (LVEF >65%), and no regional wall motion abnormalities. The right ventricle was normal based on limited visualization, and there was no hemodynamically significant valvular pathology or pericardial effusion.
A coronary CT angiogram (CCTA) was later performed, which demonstrated a right-dominant system with no evidence of plaque or stenosis in the right coronary or left circumflex arteries. A mild-to-moderate burden of calcified plaque was noted in the proximal LAD, causing at most 25–49% stenosis. Total coronary calcium score was 139. There was also evidence of improvement in gastric distension (Figure 1C, D).
After NG decompression and supportive care, the patient’s oxygenation and abdominal distention improved significantly. Following discussion with the general surgery team regarding potential operative management of the SBO, further doses of ASA and clopidogrel were held as her presentation was not felt to be consistent with acute coronary syndrome (ACS). She underwent surgical management for SBO three days later without any cardiac complications.
Management Challenges: This case exemplifies a rare but critical mimic of acute myocardial infarction. ST-segment elevation, particularly in the absence of classic ischemic symptoms, dynamic biomarker changes, or wall motion abnormalities, should prompt clinicians to consider non-cardiac etiologies. In this patient, severe gastric and esophageal distention secondary to high-grade small bowel obstruction produced mass effect on the inferior and inferolateral segments of the left ventricle, likely resulting in the transient ECG changes described.
Previous case reports have documented similar findings, including gastrointestinal distention, mediastinal masses, and even acute pancreatitis mimicking ST-elevation myocardial infarction. The proposed mechanism of SBO and gastric distention leading to ST elevation involves direct mechanical compression of the inferior myocardium or alteration of autonomic tone leading to coronary hypoperfusion and localized ECG abnormalities.
This case also highlights the importance of interdisciplinary collaboration. Cardiology’s initial empiric treatment for suspected STEMI was appropriately de-escalated once gastrointestinal pathology was identified, preventing potential bleeding complications in the setting of surgical management.
This case underscores that gastrointestinal and mediastinal pathologies can produce ST-segment elevation in the absence of myocardial infarction. ECG findings must always be interpreted in the broader context of the patient’s clinical presentation, biomarker trends, and cardiac imaging. Early integration of PoCUS and additional diagnostic imaging can be instrumental in avoiding unnecessary activation of the cardiac catheterization lab. In cases where ACS is suspected but the presentation is atypical, particularly in the absence of chest pain or biomarker elevation, clinicians must maintain a broad differential to ensure accurate diagnosis and safe management.
