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J Am Coll Cardiol, 2000; 36:1344-1354 © 2000 by the American College of Cardiology Foundation |
a HCM Program, Division of Cardiology, St. Luke’s–Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, New York, USA
Manuscript received December 8, 1999; revised manuscript received March 20, 2000, accepted May 1, 2000.
Reprint requests and correspondence: Dr. Mark V. Sherrid, Division of Cardiology, 3B-30, 1000 Tenth Avenue, New York, New York 10019
msherrid{at}slrhc.org
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Abstract |
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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 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.
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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 decreasing 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 echocardiograms of patients with significant obstruction, specifically measuring velocity of early systolic outflow at SAM onset.
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Methods |
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Echocardiogram acquisition, selection and measurement. Studies were performed at rest in the left lateral decubitus position using Hewlett-Packard Sonos 1000 echocardiographs.
M-mode echocardiogram
The M-mode echocardiogram 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 Microsonics 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.
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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 different 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 observers. 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. Significance level was based on a two-tailed test. A value of p < 0.05 was considered significant.
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Results |
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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 period
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.
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Discussion |
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Velocity. It is the central premise of the Venturi theory of SAM that high velocity ejection flow causes a local underpressure 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 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 anteriorly 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.
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Canine and in vitro experiments. Without septal hypertrophy, 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).
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).
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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 midventricular 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 uncommon; patients with just basilar outflow tract hypertrophy usually just have provocable obstruction.
Instead, data indicate that midventricular septal thickening 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 contributes 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 hypertrophied segments rather than with one hypertrophied segment; SAM occurred more often when the proximal segments of the LV were thickened rather than the distal half.
Posterior leaflet SAM. The anterior motion of the posterior 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 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.
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.
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New surgical approaches address the problem of the large 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 muscles 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 important goal of myomectomy must be to extend the myomectomy 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 myomectomy 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 (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 midventricular bulge must also be addressed for complete relief of obstruction.
Dual chamber pacing with complete ventricular preexcitation through short atrioventricular delay significantly reduces outflow tract gradients (41–44). However, therapeutic 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 indicates that a decrease in Venturi forces can only play a minor role in SAM improvement. Therefore, both direct observations 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 measured. 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, geometrical and temporal observations, indicate that drag, the pushing force of flow, is the dominant hydrodynamic mechanism for SAM.
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Acknowledgments |
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Footnotes |
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References |
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. 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 
