A Rare Case of Transient Inferior ST Segment Elevation
The patient is an 86-year-old white male with a past medical history of hypertension and a 12-year history of a hiatal hernia. He does not have a history of diabetes, hyperlipidemia, or coronary artery disease. He is a non-smoker, active for his age, and has no recent history of chest pain. The patient takes 25 mg of metoprolol twice a day for his hypertension and 40 mg of omeprazole daily for GERD.\nThe patient presented to the emergency department with a chief complaint of persistent nausea. He received an abdominal film during his work-up which revealed a large hiatal hernia, which along with his persistent nausea, the possibility of gastric volvulous was entertained []. The patient subsequently underwent an abdominal CT scan that ruled out gastric volvulous and demonstrated a large hiatal hernia in which the stomach was almost entirely in the thorax []. An electrocardiogram while patient was in Emergency Department revealed new ST segment elevation in the inferior leads without reciprocal changes []. The patient continued to have persistent nausea and started to develop pleuritic left sided chest pain. His vital signs remained stable with a temperature of 98.4, 16 respirations a minute, heart rate of 70, blood pressure of 156/63, and an oxygen saturation of 98% on room air. He was admitted for 24-h observation. His cardiac markers remained within normal limits. An echocardiogram revealed no wall motion abnormalities and a preserved ejection fraction.\nDuring the hospitalization, the patient had a number of episodes of large volume emesis, resulting in dramatic improvement of his symptoms. Repeat electrocardiogram revealed resolution of the ST segment elevation []. The patient received supportive care during his hospitalization and was referred to cardiothoracic surgery at discharge. Two months later, the patient received a laparoscopic Nissen fundoplication. The procedure and post-operative course were without complications and the patient has been in good health since the surgery.\nArrhythmias such as atrial tachycardia, atrial fibrillation, supraventricular tachycardia, paroxysmal atrial flutter as well as electrocardiographic changes such as T wave inversion have been reported with large hiatal hernias in previous case reports. The exact mechanism of these electrocardiographic changes is not well understood. Kounis and colleagues hypothesized that an increase in direct or indirect pressure to the global surface of the heart caused electrical alternation seen on electocardiography.[] Schilling and colleagues hypothesized two theories in their case of paroxysmal atrial flutter. First, that compression of the heart caused either ischemic changes or an anatomic conduction block causing the reentry. Second, that the hiatal hernia may cause compression of the vagal innervation to the heart causing electrocardiographic changes.[]\nPatients with large hiatal hernias have been reported to have cardio-pulmonary symptoms as well as electrocardiographic and echocardiographic manifestations in several case reports. These findings are reviewed in []. Hokamaki and colleagues described an interesting case of a 79-year-old woman who developed diffuse ST segment elevation after decompression of a large hiatal hernia.[] In their report, they hypothesize that rapid decompression of the hiatal hernia may have caused pericardial inflammation resulting in pericarditis. Tursi and colleagues also hypothesized that their finding of a supraventricular arrhythmia may have been caused by pericardial irritation.[]\nOur case represents a patient with focal ST segment elevation of the inferior leads, a new electrocardiographic finding associated with large hiatal hernias. The exact mechanism of these electrocardiographic changes is not known. We hypothesize that the focal ST segment elevation in the inferior leads could be related to torsion or compression of the epicardial artery from direct pressure from the hiatal hernia. These electrocardiographic changes could also be related to rotational changes of the heart associated with compression from the hiatal hernia. This may also explain the changing depth and duration of the inferior Q-waves. Regardless of the exact cause of these electrocardiographic changes, once the patient's had repeated episodes of large volume emesis, his hiatal hernia decompressed leading to resolution of his electrocardiographic findings.