{'fraction_non_alphanumeric': 0.02999747920342828, 'fraction_numerical': 0.007562389715149987, 'mean_word_length': 5.2586750788643535, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
ST-Segment Elevation in a Patient With Nausea, Vomiting, and Intracerebral Hemorrhage

A 60-year-old man who presented with nausea, vomiting, and intracerebral hemorrhage developed inferior ST-segment elevation and angina. Coronary angiography showed no coronary obstruction. The patient was found to have a small bowel obstruction causing superior translocation of the heart. Relief of obstruction caused immediate resolution of electrocardiographic changes and symptoms. (Level of Difficulty: Beginner.)

A 60-year-old man with a history of hydrocephalus with ventriculoperitoneal shunt presented with 1 day of recurrent nausea and vomiting and was found to have a small intraventricular hemorrhage noted on computed tomography (CT) of the head. Following admission, he developed sinus tachycardia and substernal, centralized, nonradiating chest pain. An electrocardiogram (ECG) showed sinus tachycardia without ST-T-wave abnormalities. His initial high-sensitivity troponin level was 23 ng/L, and it was 22 ng/L 2 hours later. Repeat CT of the head showed a stable intraventricular hemorrhage. He then had acute worsening of nausea with unchanged chest pain, thus prompting cardiology consultation. Physical examination was notable for tachycardia, regular rhythm, tachypnea, and a firm, distended, but nontender abdomen. Pulmonary and neurologic examinations were unremarkable. The chest pain was not positional. His blood pressure was 97/71 mm Hg and had been stable since admission.
A repeat ECG was obtained ( Figure 1A). Subsequent coronary angiography was angiographically normal.
CT of the chest, abdomen, and pelvis with contrast enhancement showed a mid-to-distal small bowel obstruction (SBO) and gastric distention ( Figure 1B). A nasogastric tube was placed, and 4.5 L of bilious material was evacuated, with immediate symptom resolution. Follow-up CT of the chest and ECG are shown in Figures 1C and 1D, respectively. A transthoracic echocardiogram showed normal cardiac structure and function.
What was likely the cause of the ECG findings in Figure 1A? The answer is C, superior translocation of the heart. Figure 1A shows ST-segment elevation in leads II, III, and aVF and reciprocal ST-segment depression in leads I and aVL, findings concerning for inferior wall type 1 myocardial infarction. However, coronary angiography findings were normal.
The ST-segment changes were likely the result of superior translocation of the heart from SBOinduced gastric distention that shifted the mean axis of depolarization relative to traditionally placed ECG leads. Figure 1B shows a superiorly translocated heart, which returned to a normal position following gastric decompression ( Figure 1C). Associated immediate resolution of ECG changes ( Figure 1D) suggests that the SBO-induced gastric distention was the cause of the changes. SBO causing ST-segment elevation has been described in a small number of case reports (1)(2)(3). In some cases, inferior wall ischemia from extrinsic compression of the right coronary artery has been the proposed mechanism. This was less likely in our patient with normal coronary angiography and mild myocardial injury.
According to the Fourth Universal Definition of Myocardial Infarction, the diagnosis of type 2 myocardial infarction requires a rise and/or fall in troponin. Because there was no significant change in troponin in our patient, answer option B in the foregoing multiple-choice question is incorrect.
Pericarditis (answer option A in the multiple-choice question) is unlikely given the regionality in the STsegment elevation and the nonpositional nature of the patient's chest pain.
ST-segment changes in intracerebral hemorrhage are thought to be the result of sustained sympathetic stimulation and a dysfunctional autonomic nervous system. Although this patient had risk factors for increased intracranial pressure (answer option D in the multiple-choice question), repeat cranial imaging was unchanged.