Dynamic LVOT Obstruction as a Cause of Hemodynamic Instability in Takotsubo Syndrome

Scritto il 30/07/2026
da Simran Tanna

J Investig Med High Impact Case Rep. 2026 Jan-Dec;14:23247096261475113. doi: 10.1177/23247096261475113. Epub 2026 Jul 30.

ABSTRACT

Takotsubo syndrome (TTS) frequently presents with chest pain, ST-segment elevation, and troponin elevation, closely mimicking acute coronary syndrome, and can be complicated by acute heart failure and cardiogenic shock. In a subset of patients, dynamic left ventricular outflow tract obstruction (LVOTO) with systolic anterior motion (SAM) of the mitral valve contributes to hemodynamic instability and requires a distinct therapeutic approach. We report a 79-year-old woman admitted for evaluation of biliary and pancreatic ductal dilation who developed acute chest pain followed by dizziness and hypotension during hospitalization. Electrocardiography demonstrated anterolateral ST-segment elevations, and HS troponin I peaked at 7,594 ng/L. Emergent coronary angiography revealed mild, non-obstructive coronary artery disease, while left ventriculography demonstrated apical akinesis with basal hyperkinesis consistent with TTS. Persistent hypotension despite intravenous fluids prompted bedside echocardiography, which demonstrated severe left ventricular systolic dysfunction with basal hypercontractility and SAM. Transthoracic echocardiography confirmed severe dynamic LVOTO (peak gradient 126 mmHg) with moderate mitral regurgitation and reduced ejection fraction (25%-30%). Phenylephrine was initiated with prompt improvement in blood pressure and symptoms, while inotropes and afterload-reducing agents were avoided. With cautious volume resuscitation and beta-blockade after stabilization, serial echocardiography demonstrated reduction in LVOT gradient and improvement in mitral regurgitation. This case highlights the importance of early echocardiography in hypotensive patients with suspected TTS, the need for mechanism-directed management when dynamic LVOTO is present, and suggests that the distribution of regional wall motion abnormalities may influence the development of obstructive physiology.

PMID:42531595 | DOI:10.1177/23247096261475113