Uncommon cause of ST elevation.

A 73-year-old man presented with severe postprandial epigastric pain that did not radiate. He had 6 episodes of emesis followed by retching. The character of the pain was different from past anginal symptoms. At his local emergency department, a chest roentgenogram revealed air presumably within a large intrathoracic hiatal hernia (Figure 1). Computed tomography was notable for the stomach being almost entirely intrathoracic and distended with an organo-axial volvus configuration (Figure 2). A nasogastric tube was inserted, and he was transferred to our institution. His medical history included hiatal hernia, hypertension, dyslipidemia, diabetes mellitus, and chronic kidney disease. He had undergone coronary artery bypass grafting 26 years previously with vein grafts to his left anterior descending artery and right coronary artery. Ten years ago, he had redo surgery with a left internal mammary artery to the left anterior descending artery. His medications included aspirin, -blocker, angiotensin receptor blocker, statin, and nitrates. He was afebrile; his pulse was 73 bpm and blood pressure was 169/87 mm Hg. Chest examination revealed a significant systolic upper sternal lift with normal chest auscultation. His abdomen was not tender. He had normal leukocyte count, creatinine of 1.5 mg/dL (normal values, 0.8 to 1.3 mg/dL), and lactate of 2.92 mg/dL (0.6 to 2.3 mmol/L). Initial troponin I was 0.02 ng/mL ( 0.01 ng/mL). A telemetry alarm alerted for ST-segment elevation (STE), and ECG revealed prominent anterior STE (Figure 3). The patient denied dyspnea or chest pain. Intravenous heparin was initiated and aspirin therapy was continued. Emergency bedside transthoracic echocardiogram demonstrated left ventricular geometric distortion with asynchronous contraction pattern and hyperdynamic left ventricular function with ejection fraction of 70% without regional wall motion abnormalities (Movie I in the online-only Data Supplement). Serial troponin assessment remained flat without significant delta. Serial ECG assessment revealed persistent STE, and the patient remained asymptomatic. Repeat transthoracic echocardiogram was unchanged. Heparin was discontinued. An upper endoscopy was performed with suctioning of a large amount of retained liquid. The examination demonstrated a massive hiatal hernia with a large antral ulceration and smaller ulcerations within the gastric body and fundus. Selected ulcers were treated endoscopically, and intravenous proton pump inhibitor started. Thirty-six hours after admission and after stomach Figure 1. Portable anterior-posterior chest x-ray with arrows delineating air within the intrathoracic stomach. Figure 2. Chest computed tomography demonstrating the hiatal hernia (HH) compressing cardiac structures: left atrium (LA), left ventricle (LV), and right ventricle (RV).