Giant Hiatal Hernia as a Contributing Physiological Stressor to Cardiopulmonary Dysfunction: A Case Report

Abstract Background Extracardiac thoracic pathology can significantly alter cardiac physiology and mimic primary heart disease, particularly in older adults with multiple comorbidities. Case Summary An 89-year-old woman with known aortic stenosis and heart failure presented with one week of progressive, positional dyspnea and wheezing. Transthoracic echocardiography demonstrated severe global left ventricular systolic dysfunction with an estimated ejection fraction of approximately 30%, a dilated left atrium (dimension 4.77 cm, volume 100 mL), and markedly elevated filling pressures evidenced by a medial e’ velocity of 3.16 cm/s, mitral E velocity of 103 cm/s, and E/e’ ratio of 32.6. Aortic valve assessment revealed hemodynamic features of low-flow, low-gradient severe aortic stenosis, with a mean gradient of 26–28 mmHg, a valve area of 0.68 cm2 by continuity equation, a dimensionless index of 0.25, and a stroke volume index of 29.4 mL/m2. Notably, right ventricular size and systolic function were preserved despite estimated pulmonary artery systolic pressure of 40–45 mmHg, a pattern physiologically discordant with the degree of left-sided dysfunction. Chest computed tomography revealed a giant paraesophageal hiatal hernia measuring 10–12 cm, with intrathoracic migration of the stomach causing extrinsic compression of the left atrium and posterior cardiac structures. Troponin was negative, and no electrocardiographic evidence of acute ischemia was identified. The observed left ventricular dysfunction is likely multifactorial, with extracardiac compression acting as a contributing physiological stressor in the context of underlying low-flow severe aortic stenosis. Discussion This case highlights the importance of recognizing extracardiac causes of cardiopulmonary deterioration and integrating multimodality imaging into diagnostic reasoning, particularly when hemodynamic findings are physiologically discordant.