Severe pulmonary disease as a driver of dynamic left ventricular outflow tract obstruction in stress cardiomyopathy

Dynamic left ventricular outflow tract obstruction (LVOTO) is a recognized complication of stress cardiomyopathy and can mimic hypertrophic obstructive cardiomyopathy (HOCM) even in the absence of structural hypertrophy. In critically ill patients with severe pulmonary disease, preload, afterload, and contractility can be altered which may exacerbate obstruction.

A 76-year-old woman with interstitial lung disease and microscopic polyangiitis receiving immunosuppressive therapy presented with progressive dyspnea and shock. Transthoracic echocardiography demonstrated systolic anterior motion (SAM) of the mitral valve and a dynamic LVOT gradient which increased with Valsalva maneuver. Coronary angiography showed no obstructive coronary artery disease. Cardiac magnetic resonance imaging demonstrated normal left ventricular wall thickness with hypokinesis of the mid-to-apical segments suggestive of stress cardiomyopathy. Her clinical course was complicated by COVID-19 pneumonia, recurrent shock, mechanical ventilation, and progressive right ventricular dysfunction. Repeat echocardiography demonstrated persistent dynamic obstructive physiology despite the absence of structural cardiac disease. Treatment required careful preload optimization, vasopressor selection, and respiratory support, as interventions commonly used for shock and pulmonary edema risked worsening LVOTO.

This case highlights stress cardiomyopathy complicated by dynamic LVOTO presenting with pseudo-HOCM physiology. Clinical complications of severe pulmonary disease, respiratory failure, and right ventricular dysfunction likely amplified the preload-dependent obstruction and contributed to refractory hemodynamic instability. Due to standard shock therapies paradoxically worsening obstruction, early echocardiographic recognition and physiology-guided management are critical in this population.