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Published on: June 14, 2016
[SAM not only in hypertrophic cardiomyopathy]
Anna Klisiewicz1, Agnieszka Lech, Jacek Różański
1Klinika Wad Wrodzonych Serca, Instytut Kardiologii, Warszawa-Anin. aklisiewicz@ikard.pl
Insights
This case report highlights that severe left ventricular outflow tract obstruction (LVOTO) can occur via systolic anterior movement (SAM) in patients without hypertrophic cardiomyopathy. Hypovolemia and a hyperdynamic state from increased catecholamines can precipitate dynamic LVOTO.
Area of Science:
- Cardiology
- Physiology
Background:
- Left ventricular outflow tract obstruction (LVOTO) is commonly caused by hypertrophic obstructive cardiomyopathy (HOCM) leading to systolic anterior movement (SAM).
- Other conditions like dehydration, vasodilatation, and pheochromocytoma have also been linked to LVOTO.
Observation:
- A case of severe LVOTO with SAM mechanism is presented in a patient without hypertrophic cardiomyopathy.
- The patient experienced hypovolemia and a hyperdynamic state due to elevated catecholamines.
Findings:
- Dynamic LVOTO can develop in the absence of significant septal hypertrophy.
- The combination of hypovolemia and a hyperdynamic state is a critical factor in precipitating dynamic LVOTO via SAM.
Implications:
- This case broadens the understanding of potential causes for dynamic LVOTO.
- Clinicians should consider hypovolemia and hyperdynamic states in the differential diagnosis of LVOTO, even without HOCM.
- Recognizing these factors is crucial for timely diagnosis and management of dynamic LVOTO.
Abstract:
Hypertrophic obstructive cardiomyopathy with significant hypertrophy of the basal septum is the most frequently reported cause of left ventricular outflow tract obstruction (LVOTO) in the mechanism of systolic anterior movement (SAM). Additionally, other conditions such as dehydration, vasodilatation, mitral valve repair, dobutamine stress echocardiography and pheochromocytoma have been associated with LVOTO. In this report, we present a case of a patient without hypertrophic cardiomyopathy who developed severe LVOTO in the SAM mechanism. The presented case serves as a reminder that hypovolaemia together with hyperdynamic state resulting from increased catecholemines may result in the development of dynamic LVOTO.
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