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Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic
M V Sherrid1, D Z Gunsburg, S Moldenhauer
1Division of Cardiology, St. Luke's-Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, New York, USA. msherrid@slrhc.org
Insights
In obstructive hypertrophic cardiomyopathy, systolic anterior motion (SAM) is caused by flow drag, not the Venturi effect. This finding clarifies the hemodynamics of this condition.
Area of Science:
- Cardiology
- Fluid Dynamics
- Medical Imaging
Background:
- Obstructive hypertrophic cardiomyopathy (HCM) is associated with systolic anterior motion (SAM).
- The underlying mechanism of SAM, whether Venturi or flow drag, remains debated.
- Understanding SAM's cause is crucial for managing HCM.
Purpose of the Study:
- To investigate the hydrodynamic mechanism responsible for systolic anterior motion (SAM) in obstructive hypertrophic cardiomyopathy (HCM).
- To differentiate between the Venturi effect and flow drag as the primary cause of SAM.
Main Methods:
- Echocardiography was used to study 25 patients with obstructive HCM.
- Mitral valve M-mode and Doppler (CW and PW) tracings were analyzed.
- Left ventricular outflow tract (LVOT) velocity at SAM onset was measured relative to Q-wave timing.
Main Results:
- Systolic anterior motion (SAM) onset occurred at a mean of 71 ms after Q-wave.
- Mean LVOT velocity at SAM onset was 89 cm/s, considered normal.
- In 68% of cases, SAM initiated before LV ejection was detected by Doppler.
Conclusions:
- Systolic anterior motion (SAM) begins at normal LVOT velocities.
- The Venturi mechanism is insufficient to explain SAM due to low forces at onset.
- Flow drag is identified as the dominant hydrodynamic force causing SAM in obstructive HCM.
Objectives:
The purpose of this study was to determine whether the dynamic cause for mitral systolic anterior motion (SAM) is a Venturi or a flow drag (pushing) mechanism.
Background:
In obstructive hypertrophic cardiomyopathy (HCM), if SAM were caused by the Venturi mechanism, high flow velocity in the left ventricular outflow tract (LVOT) should be found at the time of SAM onset. However, if the velocity was found to be normal, this would support an alternative mechanism.
Methods:
We studied with echocardiography 25 patients with obstructive HCM who had a mean outflow tract gradient of 82 +/- 6 mm Hg. We compared mitral valve M-mode echocardiogram tracings with continuous wave (CW) and pulsed wave (PW) Doppler tracings recorded on the same study. A total of 98 M-mode, 159 CW, and 151 PW Doppler tracings were digitized and analyzed. For each patient we determined the LVOT CW velocity at the time of SAM onset. This was done by first determining the mean time interval from Q-wave to SAM onset from multiple M-mode tracings. Then, CW velocity in the outflow tract was measured at that same time interval following the Qwave.
Results:
Systolic anterior motion began mean 71 +/- 5 ms after Q-wave onset. Mean CW Doppler velocity in the LVOT at SAM onset was 89 +/- 8 cm/s. In 68% of cases SAM began before onset of CW and PW Doppler LV ejection.
Conclusions:
Systolic anterior motion begins at normal LVOT velocity. At SAM onset, though Venturi forces are present in the outflow tract, their magnitude is much smaller than previously assumed; the Venturi mechanism cannot explain SAM. These velocity data, along with shape, orientation and temporal observations in patients, indicate that drag, the pushing force of flow, is the dominant hydrodynamic force that causes SAM.
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