Journal of the American College of Cardiology Vol. 36, No.

4, 2000
© 2000 by the American College of Cardiology ISSN 0735-1097/00/$20.00
Published by Elsevier Science Inc. PII S0735-1097(00)00830-5

Hypertrophic Cardiomyopathy

Systolic Anterior Motion Begins at

Low Left Ventricular Outflow Tract Velocity
in Obstructive Hypertrophic Cardiomyopathy
Mark V. Sherrid, MD, FACC, David Z. Gunsburg, MD, Sonja Moldenhauer, MD,
Gretchen Pearle, RDCS
New York, New York
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 echocardio-
gram 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 Q wave.
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. (J Am Coll Cardiol 2000;36:
1344 –54) © 2000 by the American College of Cardiology

Systolic anterior motion (SAM) of the mitral valve is the
cause of dynamic outflow obstruction in most patients with
hypertrophic cardiomyopathy (HCM). There is agreement
that SAM is caused by the action of left ventricular (LV)
flow on the protruding mitral valve leaflet (1). The nature of
the hemodynamic force on the leaflet remains a subject of
unresolved debate (2–5). Initially, investigators hypothe-
sized that anterior motion is caused by a Venturi mecha-
nism, whereby high velocity flow in the outflow tract lifts
the mitral valve toward the septum. More recent investiga-
tions indicate that drag, the pushing force of flow, is the
dominant hydrodynamic force that initiates anterior mo-
tion, pushing the protruding mitral leaflet into the septum
(6 –9). Flow drag is the component of force on a body that
is in the direction of the flow— examples are the familiar
pushing force of rushing water or the wind. One of these
From the HCM Program, Division of Cardiology, St. Luke’s–Roosevelt Hospital
Center, Columbia University College of Physicians and Surgeons, New York, New
York. Presented in part at the American Heart Association Annual Scientific
Sessions, Atlanta, Georgia, November 8, 1999. Grants were provided by Mr. John
Lium and Mr. Munio Podhorzer.
Manuscript received December 8, 1999; revised manuscript received March 20,
2000, accepted May 1, 2000.
studies used normal canine subjects and one was an in vitro
investigation. Two were studies of HCM patients. Despite
these investigations, prominent sources describe a Venturi
mechanism for SAM (3–5). Thus, the present study of
obstructed HCM patients was undertaken in an attempt to
clarify this question.
Whenever flow traverses a surface such as the mitral
valve, both lift and drag forces are generated. Pertinent to
the present study is that lift-to-drag ratio falls with decreas-
ing velocity (10,11). During an earlier study we noticed that
color flow velocity in the left ventricular outflow tract
(LVOT) seemed low when SAM began, as deduced by
others previously (8). In the present study we reasoned that
if SAM were caused by the Venturi mechanism, we should
find high velocity flow in the LVOT at the moment of
SAM onset. Conversely, if we found low velocity at that
time, this would support a flow drag mechanism. These
early systolic velocities have not previously been measured.
Consequently, we have systematically studied the echocar-
diograms of patients with significant obstruction, specifi-
cally measuring velocity of early systolic outflow at SAM
onset.
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October 2000:1344–54 Systolic Anterior Motion Begins at Low Outflow Tract Velocity

Echocardiogram acquisition, selection and measure-

Abbreviations and Acronyms
CW ⫽ continuous wave
HCM ⫽ hypertrophic cardiomyopathy
LV ⫽ left ventricle, left ventricular
LVOT ⫽ left ventricular outflow tract
PW ⫽ pulsed wave
SAM ⫽ systolic anterior motion
METHODS
Patients. We prospectively studied 25 consecutive patients
with obstructive HCM who had resting LV outflow gradi-
ents greater than 36 mm Hg and technically adequate
echocardiograms. Mean age was 63 years (27 to 86 years);
11 were women. Patients were referred for clinical indica-
tions; medications were continued at the time of the study.
All patients had asymmetric LV hypertrophy with septal
thickness ⬎15 mm and had no apparent cause for the
hypertrophy (12). None had hypertension or aortic valve
disease. All had SAM and mitral–septal contact. The peak
pressure gradient across the LVOT was determined using
continuous wave (CW) Doppler in the apical five-chamber
view (13). All patients were in sinus rhythm.
ment. Studies were performed at rest in the left lateral
decubitus position using Hewlett-Packard Sonos 1000
echocardiographs.
M-MODE ECHOCARDIOGRAM. The M-mode echocardio-
gram recordings were made from the parasternal window
during the same examination and within 5 min of the
Doppler tracings. A modified electrocardiographic (ECG)
lead I was continuously recorded. The mitral valve area of
interest was magnified and recorded at 100 mm/s sweep
speed. Views showing the mitral coaptation point and the
most SAM of the mitral valve were recorded on videotape.
The M-mode views were correlated with the two-
dimensional (2-D) view to avoid mistakenly recording
chordal SAM.
Tracings of SAM with both a clear mitral coaptation
point and continuity with mitral–septal apposition were
subsequently selected for measurement using a Nova Mi-
crosonics analysis computer. We measured the time interval
from Q-wave onset till the first abrupt systolic anterior
movement of the mitral valve. We measured the RR interval
for each M-mode beat selected. Figure 1 illustrates the
M-mode and Doppler measurements.

Figure 1. (Left) Continuous wave (CW) Doppler tracings were recorded in the five-chamber view through the LVOT as shown by the dashed line. Pulsed
wave (PW) Doppler tracings were recorded in the LV at a point 2.5 cm apical of the mitral coaptation point and 1 cm from the septum, in LV outflow,
as marked with the X. This location is the AMV point, apical of the mitral valve. (Right) The time interval Q-SAM is the interval from Q-wave onset
to SAM onset. The velocity V-SAM is the CW velocity in the outflow tract at the time interval Q-SAM. Ar ⫽ atrial reflected wave.
1346 Sherrid et al.
Systolic Anterior Motion Begins at Low Outflow Tract Velocity
CONTINUOUS WAVE DOPPLER. Continuous wave (CW)
Doppler was performed from the apex, through the area of
mitral–septal contact. We avoided contamination of this
signal by flow from mitral regurgitation and by flow from
the aortic valve or aorta. Doppler flow velocity tracings were
recorded on videotape at 100 mm/s sweep speed.
PULSED WAVE DOPPLER. In the apical five-chamber view,
the pulsed Doppler sample volume was placed in the LV,
2.5 cm apical of the mitral valve coaptation point and 1 cm
from the interventricular septum, near the centerline of
ejection color flow. We refer to this point as the AMV
point, apical of the mitral valve (14,15). The 2-D image
apical of the mitral valve was magnified to assure proper
placement of the sample volume. We recorded beats that
had high peak velocities and minimal spectral dispersion.
Small sample volume and low filter settings were used.
DOPPLER TRACE SELECTION AND MEASUREMENTS. Beats
were excluded if they did not show laminar flow, or showed
an attenuated envelope. We selected several M-mode,
pulsed wave (PW), and CW Doppler beats matched for
similar RR intervals; for individual patients there was ⬍3%
variation in mean RR intervals between modalities. Selected
Doppler traces were digitized into the analysis computer.
Doppler and M-mode measurements were made by differ-
ent investigators. For Doppler traces, we measured the
preejection period as the time from the beginning of the
ECG Q wave to the onset of ejection.
THE LV OUTFLOW VELOCITY AT SAM ONSET. 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 onset to SAM onset from
multiple M-mode tracings. Next, we measured the CW
velocity in the outflow tract at that same time interval
following the Q wave. The CW trace with the closest RR
interval to the mean M-mode RR interval was selected. On
this tracing we digitally magnified the early systolic area of
interest. Using digital calipers, the CW velocity at the time
of SAM onset was determined by two independent observ-
ers. This measurement is shown in Figure 1. The average
velocity measurement of the two observers was determined,
as was the interobserver variation.
As we found that SAM began before ejection onset in
more than half the patients, we examined the Doppler LV
intraventricular flow that occurred during this preejection
period. During this time, the Ar wave is a prominent
preejection flow (16 –19). Both peak Ar velocity and the
time from Q-wave onset to peak Ar velocity were measured.
Statistics. Continuous data are presented as mean ⫾ SEM
(range). The Student group t tests were calculated for
comparisons of means. Relations between different variables
were assessed by Pearson’s correlation coefficient. Signifi-
cance level was based on a two-tailed test. A value of p ⬍
0.05 was considered significant.
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October 2000:1344–54
RESULTS
In the 25 patients, a total of 98 M-mode tracings, 159 CW
Doppler tracings and 151 PW Doppler tracings were
digitized and analyzed. There were an average of 4
M-mode, 7 CW Doppler and 6 PW Doppler tracings per
patient. The mean peak LVOT gradient was 82 ⫾
6 mm Hg (range 40 to 150). The mean time of SAM onset
was 71 ⫾ 5 ms (range 34 to 155 ms) after the ECG Q wave.
The mean CW Doppler velocity in the LVOT at the time
of SAM onset was 89 ⫾ 8 cm/s (range 43 to 193). In 67%
of the patients, SAM began at velocities of less than
100 cm/s. Representative tracings in six patients are shown
in Figures 2 and 3. Data on the 25 patients are shown in
Table 1. There was little interobserver variability between
the measured CW velocities at SAM onset. The mean
interobserver difference was 8 cm/s (range 1 to 26); corre-
lation between the two measurements was good, r ⫽ 0.97.
The RR intervals. In the 25 patients as a group, little
difference was seen in the mean RR intervals of the analyzed
M-mode, CW and PW Doppler tracings; the mean RR
intervals were 868 ⫾ 25, 872 ⫾ 25, and 874 ⫾ 25 ms,
respectively. For individual patients, the mean difference
between the average RR intervals of the M-mode and CW
tracings was 24 ⫾ 3 ms (range 2 to 48 ms). The mean
difference between the average RR intervals of the M-mode
and PW tracings was 20 ⫾ 3 ms (range 0 to 48 ms).
Preejection SAM. In 17 patients (68%), the onset of SAM
occurred before the onset of ejection flow recorded on both
CW and PW Doppler. In these patients with preejection
SAM, M-mode SAM began earlier than in the patients
with SAM beginning after ejection onset, at 62 ⫾ 4
compared with 92 ⫾ 11 ms after Q-wave onset (p ⫽ 0.03).
Examples of patients with early SAM are shown in Figures
2 and 3.
INTRAVENTRICULAR FLOW DURING THE PREEJECTION PE-
RIOD. We observed preejection flow both within the LV
and also within the LVOT in all patients. The predominant
flow during this time period is the Ar wave, seen as a flow
directed away from the transducer (16 –19), shown in
Figures 1 through 3. In the LV at the AMV point, the mean
peak velocity of the Ar wave was 69 ⫾ 4 cm/s (range 35 to
108); mean acceleration to peak of the Ar wave was 1,217 ⫾
111 cm/sec2. Peak Ar wave velocity occurred 53 ⫾ 4 ms
after Q-wave onset.
DISCUSSION
In this study we have found that Doppler velocity measure-
ments in the LVOT do not support the hypothesis that
Venturi forces cause SAM. Whenever flow traverses a
surface such as the mitral valve, both lift and drag forces are
generated. Drag, the pushing force of flow, is the compo-
nent of force that is in the same direction as flow. An
example is the pushing force of water on the paddle of a
JACC Vol. 36, No. 4, 2000 Sherrid et al. 1347
October 2000:1344–54 Systolic Anterior Motion Begins at Low Outflow Tract Velocity

Figure 2. M-mode (top), continuous wave (middle), and pulsed wave Doppler (bottom) tracings of two patients. Patient 3 is on the left and patient 14
is on the right. In both patients, the left dashed line indicates time of Q-wave onset. The right solid line indicates the time of SAM onset. In both patients
SAM onset begins at a time of low velocity both in the outflow tract and in the LV. In both patients SAM begins before the onset of ejection, during the
Ar wave (16 –19). Both M-mode and Doppler tracings were recorded on the same study, within a 5-min interval, and were selected for matched RR
intervals. Vertical calibrations of CW and PW tracings are at 1-m/s and 20-cm/s intervals, respectively.

waterwheel. Lift refers to Venturi forces produced by high
velocity flow over the surface of an object causing the object
to move perpendicular to flow. An example is the force
produced as a horizontal airplane wing moves through the
air, lifting it vertically. For any object the relative impor-
tance of lift as compared with drag is dependent upon three
factors: 1) velocity of flow, 2) shape, and 3) orientation
relative to flow (10,11).
Velocity. It is the central premise of the Venturi theory of
SAM that high velocity ejection flow causes a local under-
pressure in the LVOT, which pulls the protruding mitral
leaflet toward the septum. In this study, we show that SAM
actually begins very early in systole at a time when velocity
in the LVOT is normal. Specifically, SAM begins at a time
when mean outflow tract velocity is 89 cm/s (range 43 to
193), a velocity not unlike that routinely recorded in the
LVOT of normal patients without SAM (20).
Decreased velocity significantly decreases lift in two ways,
and decreases its importance compared with drag forces. First,
lift falls because it is roughly proportional to the square of
velocity. Second, for any given shape, the ratio of lift to drag
falls with decreasing velocity (10,11). At lower velocity, profile
drag increases because increased contact of the fluid with the
surface leads to increased friction with flow. Lower velocity
1348 Sherrid et al. JACC Vol. 36, No. 4, 2000
Systolic Anterior Motion Begins at Low Outflow Tract Velocity October 2000:1344–54

Figure 3. Four patients with obstructive HCM. In all cases the M-mode echocardiograms showing SAM onset are on top and the Doppler tracings are
below. For the two patients on the left, the M-mode is compared with the CW Doppler tracings in the LVOT. For the two patients on the right, the
M-mode is compared with the PW Doppler tracings in the LV at the AMV point. In all, the left dashed line indicates Q-wave onset. The right solid
line indicates SAM onset. In all four patients SAM onset occurs at a time of low velocity, before the beginning of ejection. In the two patients on the right,
SAM onset begins during the Ar wave. Both M-mode and Doppler tracings were recorded on the same study, within a 5-min interval, and were selected
for matched RR intervals. Vertical calibrations of CW and PW Doppler tracings are at 1-m/s and 20-cm/s intervals, respectively.

allows viscosity to do its work. The difficulty of flying at low
speed is an example of falling lift/drag ratio at lower velocity.
The modest outflow velocities we have measured indicate
that, at the time of SAM onset, the magnitude of the
Venturi force is much smaller than previously assumed; high
velocities needed to generate significant Venturi forces are,
in fact, not present. Therefore, the Venturi mechanism
cannot be the main cause of SAM.
Flow drag: Geometric shape and orientation relative to
flow. Besides velocity, the other factors that determine the
relative importance of lift and drag are shape and orientation
relative to flow (10,11), in this case between the mitral valve
and the LV intraventricular flow (6,8). Available data with
regard to these geometric relations indicate that drag is the
dominant hydrodynamic mechanism for SAM (6 –9).
In obstructive HCM the mitral valve leaflets are anteri-
orly positioned, relatively large, and residual portions of
leaflets extend past the coaptation point and protrude into
the outflow tract (1,7,21–23). The anterior displacement
puts the mitral valve into the edge of the flow stream of LV
ejection, subjecting the mitral valve to the hemodynamic
force of ejection flow (1).
This LVOT narrowing and anterior position of the
mitral coaptation point can be cited as evidence for either
Venturi or drag (pushing) mechanisms, as the narrowing
could play a role in both mechanisms. On the one hand,
flow velocity must increase as it enters the narrowed outflow
tract producing Venturi (lift) forces (24,25). Such Venturi
forces are necessarily present. On the other hand, narrowing
of the LVOT and the anterior position of the coaptation
point also places the protruding leaflet into the edge of the
flow stream, subject to the pushing force of flow that strikes
the undersurface of the leaflet (6 –9,23). The flow drag
mechanism is illustrated in Figure 4. Thus, the LVOT
narrowing provides the substrate for, and is evidence to
support, both theories. This has been a source of confusion
in the debate.
Additional data show that drag forces are more important
than Venturi for causing SAM.
Canine and in vitro experiments. Without septal hyper-
trophy, SAM and obstruction can be induced in normal
dogs by anterior displacement of the papillary muscles with
ligatures (7). In an in vitro model, SAM does not occur
when the valve has its normal posterior coaptation point,
regardless of how high velocities are elevated in the LVOT.
Not until the valve is mechanically lifted into the outflow
stream and chordal slack is introduced does SAM occur
(9,26).
JACC Vol. 36, No. 4, 2000 Sherrid et al. 1349
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Table 1. Doppler and M-Mode Measurements in 25 Patients With Systolic Anterior Motion
(SAM)
Age LVOTG Q to SAM PEP/PW PEP/CW v at SAM
Patient (yrs) Gender (mm Hg) (ms) (ms) (ms) (cm/s)
Early SAM
1 72 M 64 34 59 51 91
2 65 M 47 51 109 99 75
3 52 M 40 41 83 64 80
4 40 M 100 78 88 79 48
5 83 F 75 62 68 81 60
6 57 F 68 57 84 78 44
7 77 M 64 62 74 85 71
8 48 M 125 96 116 106 81
9 69 M 58 46 81 N/A N/A
10 74 F 100 54 84 108 170*
11 42 M 77 73 91 80 44
12 85 F 80 51 62 60 61
13 66 M 68 90 100 110 63
14 77 M 45 75 84 81 92
15 87 F 78 66 87 75 100*
16 68 F 120 42 65 61 74
17 86 F 54 71 112 90 53
Average 68 74 (⫾6) 62 (⫾4) 85 (⫾4) 82 (⫾4) 75 (⫾8)
Late SAM
18† 32 F 75 67 68 57 44
19† 27 M 40 82 91 74 126
20† 42 M 75 58 55 62 43
21 49 M 150 103 92 91 114
22 62 F 144 87 81 79 133
23 78 M 120 155 116 103 167
24 75 F 70 75 60 55 118
25 70 F 125 110 73 56 193
Average 54 100 (⫾14) 92 (⫾11) 80 (⫾7) 72 (⫾6) 117 (⫾19)
Total Average 63 82 (⫾6) 71 (⫾5) 83 (⫾4) 78 (⫾4) 89 (⫾9)
*A velocity ⱖ100 cm/s was measured in two patients with “Early SAM.” In these patients, SAM coincided with the Ar-wave.
†In three patients, onset of ejection in PW/CW occurred around the beginning of SAM; those patients were considered as “Late
SAM.”
LVOTG ⫽ left ventricular outflow tract gradient; Q to SAM ⫽ onset of Q wave to beginning of systolic anterior motion;
PEP ⫽ preejection period (onset of Q wave to ejection); PW ⫽ pulsed wave Doppler; CW ⫽ continuous wave doppler; v at
SAM ⫽ velocity at beginning of SAM.

In HCM patients: Orientation, shape, temporal and
Doppler velocity evidence. In patients, a high angle of
attack of Doppler color flow relative to the protruding leaflet
of the mitral valve has been found; this orientation precludes
significant Venturi effects and implicates drag (6). In the
apical five-chamber view, local flow direction comes from an
angle lateral of the protruding leaflet. The mean angle at
time of mitral coaptation was lateral by 21°; mean angle just
before septal contact increased to 45° (6). At these high
angles relative to flow, drag is the dominant hydrodynamic
force on the leaflet. This is illustrated in Figure 5. Flow
pushes on the underside of the protruding leaflet (6 –9), as
drawn in Figure 4 and imaged in a patient in Figure 6.
Critical overlap exists between the inflow and outflow
portions of the LV that allows flow drag to catch the leaflet
(6,27).
The leaflet is swept by the pushing force of flow into the
septum. As it moves toward the septum the angle relative to
flow increases and constricting drag forces are correspond-
ingly increased as the leaflet presents a greater surface
relative to flow (Fig. 5) (6). An example of this phenomenon
is a widely open door in a drafty corridor. The door starts
moving slowly; it then accelerates as drag increases because
the door presents a larger area, until it slams shut (28).
Shape of the mitral valve. The mitral valve was not
designed for lift. To the contrary, the valve has a sharp
anterior edge with no streamlining, and there is a concavity
under the cowl of the protruding leaflet. It resembles other
biologic structures with high drag coefficient (Fig. 5) (10).
The midseptal bulge. Besides the anterior position of the
mitral valve, another contributor to the initial positive angle
of attack is the midseptal bulge. In patients with obstructive
HCM and resting gradients, hypertrophy of the midven-
tricular septum is the rule, occurring in 92% of patients (29).
This midseptal bulge is often associated with basilar or
whole septal thickening (29,30). Resting gradients are
uncommon in patients with only subaortic basilar septal
thickening; in these patients resting gradients are found in
just 12% (29). If it were Venturi forces from acceleration
into a small outflow tract that caused resting obstruction,
then isolated basilar hypertrophy and subaortic narrowing
should commonly cause resting obstruction. But this is
1350 Sherrid et al.
Systolic Anterior Motion Begins at Low Outflow Tract Velocity
Figure 4. The pushing force of flow. Intraventricular flow relative to the
mitral valve in the apical five-chamber view. In obstructive HCM the
mitral leaflet coaptation point is closer to the septum than normal (1). The
protruding leaflets extend into the edge of the flowstream and are swept by
the pushing force of flow toward the septum. Flow pushes the underside of
the leaflets (arrow) (6 –9). Note that the midseptal bulge redirects flow so
that it comes from a relatively lateral and posterior direction; on the
five-chamber view, flow comes from “right field” or “one o’clock” direction.
This contributes to the high angle of attack relative to the protruding
leaflets. Also note that the posterior mitral leaflet is shielded and separated
from outflow tract flow by the cowl of the anterior leaflet. Venturi flow in
the outflow tract cannot be lifting the posterior leaflet because there is little
or no area of this leaflet exposed to outflow tract flow. Venturi forces
cannot be causing the anterior motion of the posterior leaflet.
uncommon; patients with just basilar outflow tract hyper-
trophy usually just have provocable obstruction.
Instead, data indicate that midventricular septal thicken-
ing is generally a necessary condition for resting SAM with
mitral–septal contact (29). We have observed that this
occurs because the midseptal bulge forces the outflow to
sweep from a relatively posterior and lateral direction in the
LV, as shown in Figures 4 and 6. When viewed in the
echocardiographic apical five-chamber view, flow comes
from “right field” or “one o’clock” direction. This contrib-
utes to a high angle of attack relative to the protruding
mitral leaflet (6). Klues and colleagues (30) reported that
SAM was more common in patients with several hypertro-
phied segments rather than with one hypertrophied seg-
ment; SAM occurred more often when the proximal seg-
ments of the LV were thickened rather than the distal half.
Posterior leaflet SAM. The anterior motion of the poste-
rior mitral leaflet is evidence for the drag mechanism. In
89% of patients with SAM and obstruction, the posterior
leaflet moves anteriorly as well (31,32). However, the
posterior leaflet is separated from the flow in the LVOT by
the cowl of the anterior leaflet (Fig. 4). Venturi forces in the
LVOT cannot be lifting the posterior leaflet because there is
little or no area of the posterior leaflet that is exposed to
LVOT flow. In light of this and the previously mentioned
JACC Vol. 36, No. 4, 2000
October 2000:1344–54
Figure 5. (Left) In the example of a wing, as it moves from a position
parallel to flow to a more angled orientation, flow separates from the upper
surface, lift decreases, and drag increases (10,11). (Top) Lift is the
dominant force up to an angle of approximately 15° relative to air flow.
(Middle and bottom) Above 15°, separation occurs and lift is greatly
attenuated because the rapid flow and its local decrease in pressure are no
longer in contact with the top surface. Lift is lost, drag forces are dominant,
and the wing stalls (10,11). The angle between flow and a surface is referred
to as the angle of attack. Streamlines are shown with continuous arrows;
forces on the wing are shown with larger gray arrows. (Right) Similarly, in
HCM the magnitude of flow drag on the protruding mitral leaflet is
directly related to the angle between the local direction of LV flow and the
protruding leaflet. (Middle) The angle between the direction of local flow
and the protruding leaflet of the mitral valve is the angle of attack, ␣. The
anterior position of the protruding leaflet contributes to the angle of attack.
Also, the midseptal bulge redirects flow so that local flow comes from a
relatively posterior direction as it curves around the septum. Color flow
Doppler defines local flow direction (6). Measured angle of attack was high
at the moment of coaptation, mean 12° in the parasternal view, and mean
21° in the apical five-chamber view. High angles preclude significant
Venturi forces and implicate drag. (Bottom) As the leaflet is pushed
toward the septum, both the angle and drag forces increase markedly.
observations, it is concluded that the posterior leaflet is
pushed anteriorly. This mechanism is shown in Figure 6. Is
it likely that the anterior and posterior leaflets, which share
a coaptation plane, have different causes for SAM? It is
more reasonable that the anterior motion of the anterior
leaflet is caused by the same force that triggers the abnormal
posterior leaflet motion; both are caused by flow drag.
Finally, the last ingredient necessary for SAM is chordal
slack. Without a reduction in chordal tension, no SAM
would occur because the leaflets would be tethered (8,9,23).
Systolic anterior motion can be described as anteriorly
directed mitral valve prolapse. This analogy has merit; in
both conditions, the mitral valve is often large and is pushed
by flow from its normal systolic position, resulting in mitral
regurgitation.
In summary, geometric data indicate that the necessary
conditions for SAM are anterior position of the mitral
coaptation point (which puts the valve into the edge of
the outflow stream), positive angle of attack between
outflow and the protruding leaflet, and chordal slack.
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Figure 6. Flow strikes the undersurface and lateral aspect of the mitral valve very early in systole, causing SAM. Two echocardiographic views of one patient
with obstructive HCM are shown; resting gradient ⫽ 54 mm Hg. (Left) Apical five-chamber view. (Top left) The 2-D image shows the protruding mitral
leaflet on the first frame in systole that showed mitral coaptation. Arrowhead points to mitral valve. O indicates outflow tract. (Bottom left) The same view
showing the first systolic frame with color flow. Color flow is seen lateral to the leaflet tips (arrow). These images show the event graphically drawn in Figure
4. (Right) Apical three-chamber view. (Top right) The 2-D image again shows the protruding mitral leaflet on the first frame in systole that showed mitral
coaptation. Arrowhead points to mitral valve. (Bottom right) This shows the same view of the first systolic frame with color flow. Color flow is seen
posterior to the leaflet tip (arrow). Note that color flow velocity is low on both views. On 2-D imaging, the next systolic frames showed fully developed SAM
on both views. On color flow, the next systolic frames showed aliasing in the outflow tract. The mitral leaflets are medially and anteriorly positioned into
the edge of the flow stream. Low velocity flow strikes the undersurface of valve leaflets; they are swept toward the septum by the pushing force of flow.

The geometric conditions for SAM are met in another
condition where obstruction occurs, despite the absence of
septal hypertrophy. Following mitral annuloplasty certain
patients develop, as a complication, SAM. The mitral
coaptation point has been shown to be anteriorly displaced
into the outflow tract by the ring (33). Consequently,
surgical techniques have been developed to ensure that the
postoperative mitral coaptation point is posterior in the LV,
explicitly out of the way of the outflow stream with its
attendant drag (34,35).
In the present work, we have shown that rapid ejection
flow velocity in the LVOT is not a necessary condition for
SAM. In addition, we found that SAM begins before
ejection onset in two-thirds of the patients. That SAM
often occurs before ejection begins was first reported in
1987; in 10 patients on 2-D echocardiography SAM was
seen to begin before the aortic valve opened (8). These
temporal data, confirmed in the present work, support the
drag hypothesis, rather than Venturi. In patients with
preejection SAM, the early motion has been observed to be
associated with a prominent LV preejection flow (36).
Figure 7 summarizes the evidence in the debate between
Venturi and drag forces as the cause of SAM.
Therapeutic implications. Recently, new methods to re-
lieve obstruction have been developed: revised surgical
techniques (37– 40), dual chamber pacing (41– 44) and
percutaneous transluminal septal myocardial ablation
(45,46). Interventions are not always successful (47), and the
reason for heterogeneity in response is not clear (43).
Despite active research in treatment, the hemodynamic
mechanism of obstruction has hitherto remained controver-
sial (2–5). By clarifying the circumstances and the nature of
the dynamic force that causes obstruction, the present study
should help explain how novel treatments work and also
could permit their refinement. This understanding is of
crucial importance for the development of future treatment
strategies.
New surgical approaches address the problem of the large
1352 Sherrid et al.
Systolic Anterior Motion Begins at Low Outflow Tract Velocity
Figure 7. Evidence in the debate between Venturi (lift) and drag (pushing)
force as the dynamic cause for SAM. References are enumerated in the text.
ASH ⫽ asymmetric septal hypertrophy.
protruding mitral valve and its contribution to obstruction;
the operation described by McIntosh reduces by plication
the size of the anterior mitral leaflet, adding this to
myomectomy (37). Another frees the bound papillary mus-
cles from the surrounding LV muscle. This allows more
normal posterior mitral coaptation, explicitly out of the
outflow stream and its drag forces (38,39). As Messmer
states: “This relieves the obstructive component of the
mitral valve, which is rarely due to the often cited and never
proved Venturi effect but has its origin rather in pathologic
insertion of subvalvular apparatus” (38).
As discussed above, the impact of the midventricular
septal bulge is to redirect LV flow so that it comes from a
relatively postero-lateral direction. Consequently, an impor-
tant goal of myomectomy must be to extend the myomec-
tomy resection far enough down toward the apex to allow
flow to track more anteriorly and medially along the
surgically reduced septum and away from the mitral valve
(23,38,39). Adequate extent of the myomectomy past the
tip of the anterior mitral leaflets was stressed by Morrow
(48) and others (23). A large decrease in the angle of attack
of flow relative to the mitral valve has been shown after
successful myomectomy; flow is made more parallel to the
mitral valve (49). A recent modification extends resection to
the deepest portion of the septum, to ensure complete
resection of the midseptal bulge (38,39); 90% of patients
had no postoperative SAM. Conversely, failure of myomec-
tomy to alleviate SAM is often due to inadequate excision;
in many such cases only the basal septum has been resected
without resection farther down to the midventricle
JACC Vol. 36, No. 4, 2000
October 2000:1344–54
(47,50,51). Such considerations also apply to site selection
for percutaneous alcohol ablation procedures. Targeting the
basal septum alone will likely be inadequate; the midven-
tricular bulge must also be addressed for complete relief of
obstruction.
Dual chamber pacing with complete ventricular preexci-
tation through short atrioventricular delay significantly re-
duces outflow tract gradients (41– 44). However, therapeu-
tic effect is often incomplete; SAM persists with mean
gradients of 30 to 55 mm Hg after three months of pacing
(43,44). The mechanism by which pacing benefits SAM is
unclear at this time (52). One hypothesis is that pacing
might cause asynchronous or paradoxical septal motion,
widening the outflow tract and decreasing Venturi forces
(42). However, septal paradox is only rarely seen (41,52).
Jeanrenaud (52) did find a modest decrease in regional
septal wall motion but there was no uniform correlation
between the magnitude of decreased septal motion and
percent gradient reduction. Also, the present research indi-
cates that a decrease in Venturi forces can only play a minor
role in SAM improvement. Therefore, both direct observa-
tions and pathophysiology indicate that the mechanism by
which pacing reduces SAM is more complex than just a
widening of the outflow tract (52).
Study limitations. The M-mode tracings of SAM and
Doppler tracings were not done simultaneously. Rather,
they were done sequentially, within 5 min. This could have
influenced results. However, tracings for M-mode, CW,
and PW Doppler analyses were selected for matched RR
intervals, and many tracings were selected and measured (4
M-mode and 7 CW Doppler beats). The mean RR intervals
between modalities were quite close. For individual patients,
the mean difference between the average RR intervals of the
M-mode and CW tracings was 24 ⫾ 3 ms (range 2 to
48 ms). No patients with atrial fibrillation were examined in
this study. Interventricular pressures were not directly mea-
sured. In the parasternal M-mode view, as the mitral valve
moves anteriorly, the point with SAM onset and the point
of mitral–septal contact may not be on the same M-mode
line. For this study, clear registration of SAM onset was
deemed essential, sometimes to the detriment of the point
of mitral–septal contact.
Conclusions. In patients with obstructive HCM we have
shown that the onset of SAM of the mitral valve is a low
velocity phenomenon. At SAM onset, though Venturi
forces are necessarily present in the outflow tract, their
magnitude is much smaller than previously assumed. This
velocity data, combined with other experimental, geometri-
cal and temporal observations, indicate that drag, the
pushing force of flow, is the dominant hydrodynamic
mechanism for SAM.
Acknowledgment
We would like to acknowledge the work of Mrs. Carmen
Stockfisch who prepared this manuscript.
JACC Vol. 36, No. 4, 2000
October 2000:1344–54 Systolic Anterior Motion Begins at Low Outflow Tract Velocity
Reprint requests and correspondence: Dr. Mark V. Sherrid,
Division of Cardiology, 3B-30, 1000 Tenth Avenue, New York,
New York 10019. E-mail: msherrid@slrhc.org.
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