The relationship between systolic anterior motion of the mitral valve and the left ventricular outflow tract Doppler in hypertrophic cardiomyopathy In an attempt to investigate the role of left ventricular blood outflow in the generation of systolic anterior motion (SAM) of the mitral valve in patients with hypertrophic cardiomyopathy, we precisely analyzed the temporal relation of SAM and the left ventricular outflow tract (LVOT) systolic Doppler events obtained at the maximal mitral-septal apposition or equivalent area in eight patients with severe SAM, in five patients with mild/moderate SAM, and in seven patients with no SAM, using M-mode and pulsed Doppler echocardiography; the results were compared with those in 10 normal subjects. In all 13 patients with SAM, the timing of SAM generation corresponded to the LVOT Doppler events either between the onset of SAM and the onset of Doppler (r = 0.834, p < 0.0001) or between the peak of SAM and the peak of Doppler (r = 0.836, p < 0.0001). The excursion rate of the development of SAM showed a correlation with the LVOT blood outflow acceleration (r = 0.828, p < 0.0001). The timing of SAM resolution also correlated with the Doppler events, either between the offset of SAM and the offset of Doppler (r = 0.795, p < 0.001) or the end of SAM and the end of Doppler (r = 0.859, p < 0.0001). The LVOT blood outflow deceleration showed a correlation with the regression rate of SAM (r = 0.668, p < 0.013). The LVOT blood outflow acceleration was significantly higher in patients with severe SAM than in patients with mild/moderate SAM or no SAM. This study suggests that the high LVOT blood outflow acceleration in early systole possibly plays an important part in the generation of the Bernoulli pressure drop and results in anterior motion of the mitral valve. At mid-systole, a drag force and/or suction effect of pressure drop produced by continuous outflow blood may sustain the anterior motion of the mitral valve. At late systole, as the blood flow decelerates, the regression of SAM then occurs. (AM HEART J lgg1;122:1671.)
Chung-Sheng Lin, MD, Kuo-Shuen Chen, MD, Ming-Cheng Lin, MD, Men-Chin Fu, MD, and Shu-Mei Tang, BS. Taichung, Taiwan, Republic
Since echocardiographic recording of systolic anterior motion (SAM) of the mitral valve in patients with hypertrophic cardiomyopathy (HCM) was observed, several mechanisms have been proposed to explain this motion, l-i0 but the Venturi theory1 has been most widely accepted. This hypothesis states that rapid ejection in the early phase of systole through a narrowed left ventricular outflow tract (LVOT) produces a high-velocity stream above the mitral valve that, according to Bernoulli’s equation, decreases the pressure above the valve, drawing it anteriorly. However, despite recent studies using From the Departmentof Internal Medicine, Chung Shari Medical and Dental College Hospital. Received for publication Jan. ‘7, 1991; accepted May 1, 1991. Reprint requests: Chung-Sheng Lin, MD, 23 Sec. 1, Taichung Kang Rd., Taichung, Taiwan 40334, Republic of China. 4/l/32948
of China
hemodynamic monitoring,“, l2 two-dimensional echocardiography,2-7F galo, l3 and Doppler echocardiography,14-17 several questions are still unanswered regarding the relationship between velocities in the LVOT, the pattern of flow in the ascending aorta, and SAM of the mitral valve.18 Previous Doppler studies in patients with HCM concentrated on analyzing the Doppler aortic flow to correlate the events of SAM. However, Doppler aortic studies fail to explain many of the observed features of SAM.18 In this study, we analyzed the pulsed Doppler obtained at the maximal mitral-septal apposition to gain further insight into the relationship of SAM and Doppler and to attempt to fmd the mechanism of SAM. METHODS Patient
secutive
selection.
patients
with
Echocardiographic studies of 20 conHCM were evaluated. All patients 1671
1672
December 1991 American Heart Journal
Lin et al.
.
I
D=+ Mild/Mod
SAM
-
SAMER=+
Fig. 2. Method of pulsed Doppler echocardiographic examination. The sample volume was placed at the region between the maximal anterior apposition of the mitral valve and the interventricular septum from the apical long-axis view. LA, Left atrium; LV, left ventricle; RV, right ventricle; Ao, aorta.
SAMRR=+ Fig.
1. Scheme
showing
(A) and deceleration
calculation
of flow acceleration
(D), SAM excursion rate (SAMER), rate (SAMRR) in patients with severe
and SAM regression SAM (upper panel) and mild/moderate SAM (lower panel). VI and Vs are peak Doppler flow velocities of A wave and B wave, respectively. SAM, Systolic anterior motion of the mitral valve.
showed diagnostic quality Doppler and M-mode echocardiographic studies. Ten normal subjects without any heart disease were selected for control studies. All patients and normal subjects were in normal sinus rhythm. HCM was diagnosed by characteristic clinical findings and the demonstration of left ventricular hypertrophy without cavity dilatation or any known cause of hypertrophy. All patients with HCM demonstrated a ventricular septal thickness of more than 15 mm and a diastolic septal-to-left ventricular free wall ratio of at least 1.5 below the level of the mitral valve on an M-mode echocardiogram. The magnitude of SAM was classified using a modification of the classification proposed by Gilbert et al.lg The SAM was defined as mild if the minimal mitral-septal distance was greater than 10 mm, as moderate SAM if this distance was 10 mm or less but with no mitral-septal contact, and as severe SAM if there was either brief or prolonged mitral-septal contact. Among 20 patients with HCM, eight
patients were classified in the severe SAM group, five patients were classified in the mild/moderate SAM group, and seven patients were classified in the no SAM group. Ultrasound system. All echocardiographic studies were performed using a phased-array echocardiographic color Doppler system (Hewlett-Packard Co., Medical Products Group, Andover, Mass.). The pulsed Doppler examination of this system is performed under simultaneous guidance of a two-dimensional color Doppler image. A 2.5 MHz transducer was used in this study. Echocardiograms of this study were recorded on the strip charts at paper speeds of 50 to 100 mm/set. M-mode echocardiography. M-mode echocardiograms were obtained with the patients and normal subjects in the supine position. Ventricular septal and left ventricular free wall thickness were measured in all patients and normal subjects as recommended by the American Society of Echocardiography. In the eight patients with severe SAM, four additional measurements were made: the time from the onset of the QRS complex to (1) initial onset of SAM; (‘2) initial SAM-septal contact; (3) end of SAM-septal contact; and (4) end of SAM. In the five patients with mild/moderate SAM, three additional measurements were made: the time from the onset of the QRS complex to (1) initial onset of SAM; (2) peak of SAM; and (3) end of SAM. The excursion time of SAM was measured from the onset of SAM to the initial SAM-septal contact (in severe SAM patients) or to the peak of SAM (in mild/moderate SAM
Volume 122 Numbor 6
Table
Relation
between LVOT
Doppler
and SAh4 in HCM
1673
I. M-mode echocardiography of SAM and Doppler characteristics
Peak velocity (cm/set) Doppler acceleration (cmhec’) Doppler deceleration (cm/sec2) SAM excursion (cmhec) SAM regression (cmhec) Ejection time (msec)
Severe SAM (n = 8)
Mild/Moderate SAM (n = 5)
No SAM (n = 7)
Control (n = IO)
A wave 127 t 35s B wave 121 + 46 1798 * 8003
125 t 51s
93 k 25s
51 It 7
859 + 259*
717 -+ 166
570 + 193
1325 -+ 755s
893 t 522$
533 k 155s
292 f 45
305 +I 12t
271 + 25
15 + 6a
652
17 -t- 7a
8+2
325 + 54t
310 + 36’
SAM, Systolic anterior motion of the mitral valve. *p < 0.03, tp < 0.01, $p < 0.001, §p < 0.0001 compared “p < 0.01 compared with mild/moderate group, values
with control. expressed as Mean
patients). The excursion rate of SAM was calculated by dividing the amplitude of the SAM by the excursion time. The regression time of SAM was measured from the end of the SAM-septal contact (in severe SAM patients) or the peak of SAM (in mild/moderate patients) to the end of SAM. The regression rate of SAM was calculated by dividing the amplitude of the SAM by the regression time (Fig. 1, right panel). Doppler echocardiography. All Doppler echocardiographic studies were performed immediately after each M-mode study. Recordings were obtained with the patients/subjects at rest from the apical long-axis approach. The sample volume of pulsed Doppler was carefully moved step by step from the apical level toward the SAM-septal contact level. Doppler spectrums of each area were recorded on the strip chart. To overcome the movement of the heart that may make the position of the sample volume unsteady at the exact anatomic location, we performed a continuous strip-chart recording, especially when the sample volume was positioned between the ventricular septum and the maximal anterior apposition of the mitral valve (Fig. 2). For patients with no SAM or in normal subjects, the equivalent SAMseptal contact area Doppler spectrum was obtained by placing the sample volume at 1 to 2 cm proximal to the aortic valve near the ventricular septum. Timing of the Doppler spectrum was measured from the onset of the QRS complex to: (1) the initial onset of Doppler; (2) the peak of Doppler; and (3) the end of Doppler. Acceleration time was measured from the onset of ejection to the time of peak flow velocity. Average acceleration was calculated by dividing peak flow velocity by acceleration time. Deceleration time was measured from the time of peak flow velocity to the end of Doppler. Average deceleration was calculated by dividing peak flow velocity by deceleration time (Fig. 1, left lower panel). In patients with severe SAM, average acceleration was calculated by dividing A wave peak velocity by A wave acceleration time, and average deceleration was calculated by dividing B wave
+ SD.
peak velocity by B wave deceleration time (Fig. 1, left upTiming of the Doppler spectrum in severe SAM patients was measured from the onset of the QRS complex to: (1) the initial onset of the A wave; (2) the peak of the A wave; (3) the end of the A wave or the onset of the B wave; (4) the peak of the B wave; and (5) the end of the B wave. The presenting of a biphasic Doppler spectrum in severe SAM patients will be discussed later.
per panel).
Temporal relationship between Doppler flow events and SAM. To minimize the differences in physiologic state,
identical R-R cycles (i.e., cycle lengths to within 10 msec of each other) of M-mode and Doppler echocardiograms were measured in three cycles each in the same patient. All data of time were corrected for heart rate with the square root of the R-R interval to normalize for patient variability. Statistics. Analysis was performed by means of t tests. Comparison was performed using Pearson’s correlation coefficient. Values are means k standard deviations. RESULTS Doppler waveform of the LVOT outflow contact level in patients with hypertrophic athy and normal subjects (Table I)
at SAM-septal cardiomyop-
Pulsed Doppler waveform. The Doppler spectrum of the maximal anterior mitral valve apposition level can be obtained approximately by means of simultaneous two-dimensional imaging. Movement of the heart relative to the Doppler sample volume precludes exact anatomic localization in a given case. However, a continuous strip-chart recording could help to identify the local specific Doppler waveform. A unique biphasic DoppIer waveform can be obtained at the SAM-septal contact area in all patients with severe SAM. There were two peak flow velocities of the A wave and B wave, which were different from those of patients with mild/moderate SAM (Fig. 3).
1674
December 1991 American Heart Journal
Lin et al.
3. Pulsed Doppler flow patterns of the left ventricular outflow tract in patients with severe SAM (upper panel) and moderate SAM (lower panel). Two Doppler echograms are matched for the cycle length. Note that a biphasic pattern (A and B wave) and a higher acceleration in a patient with severe SAM can be discerned. Fig.
mild/moderate SAM (125 t 51 cmlsec), but was sipnificantly higher than that of the no SAM group (93 + 25 cm/set) (p < 0.05) and normal subjects (51 t- 7 cm/set) (p < 0.0001). However, in patients with severe SAM, flow velocity increased sharply and reached a peak of the A wave at 189 f 43 msec after the initial QRS wave, which was significantly earlier than in patients with mild/moderate SAM (257 + 17 msec) (p < 0.007) or in the no SAM group (238 + 23 msec) (p < 0.019). Therefore acceleration was higher in patients with severe SAM (1798 + 800 cm/set’) than in patients with mild/moderate SAM (859 + 259 cm/sec2) (p < 0.029) or with no SAM (717 + 166 cm/ sec2) (p < 0.004) and in normal subjects (570 * 193 cm/sec2) (p < O.OOOl),as shown in Table I and Fig. 4. The peak flow velocity of the B wave (121 t 46 cm/ set) was not different from that of the A wave. Blood flow deceleration was higher in patients with severe SAM (1325 t 755 cm/se&?) than in patients with no SAM (533 + 155 cm/sec2) (p < 0.018) or in normal subjects (292 i- 45 cm/set’) (p < O.OOOl),but was not different from that of patients with mild/moderate SAM (893 1. 522 cm/set”). Ejection time with pulsed Doppler was significantly longer in patients with severe SAM (325 I 54 msec) than in normal subjects (271 f 25 msec) (p < O.Ol), but was not significantly different from that of patients with mild/moderate SAM (310 * 36 msec) or from that of the no SAM group (305 I 12 msec). Pulsed Doppler waveform in a patient with premature ventricular contraction. A patient with severe SAM with premature ventricular contraction whose Doppler waveform was obtained from the SAM-septal contact area showed postextrasystolic potentiation (Fig. 5). The postextrasystolic beat revealed an increase of outflow acceleration (from 1032 & 177 to 1910 rt 466 cm/sec2, p < 0.006), a more rapid SAM excursion rate (from 12 i 2 to 19 + 4 cm/set, p < 0.03), a prolonged SAM-septal contact (from 87 ri: 12 to 172 +- 28 msec, p < O.OOOl), and increasing midsystolic outflow Doppler signal cessation (from 148 +- 15 to 282 +- 13 msec, p < 0.0001) and ejection period (from 270 ~tr10 to 382 + 11 msec, p < 0.0001). Temporal relation events of SAM
The A wave was generated in early systole and the B wave appeared in mid-systole after a transient cessation of the Doppler flow signal. The A wave constituted a relatively small fraction of the overall forward flow velocity (44 t 14%). The velocity contour of mild/moderate SAM patients was not significantly different from that of the normal subjects and the no SAM group. The peak flow velocity of the A wave in severe SAM patients (127 f 35 cm/set) was not significantly different from that of the patients with
between
Doppler
waveform
and
Severe SAM group. Table II (left column) is a summary of the temporal relations between the Doppler waveform and events of SAM measured after the initial QRS wave. Fig. 6 shows these relationships in a patient with severe SAM recorded at different times and matched for the cycle length. The onset of SAM (106 * 16 msec) and the onset of the Doppler A wave (107 t 20 msec) occurred almost simultaneously. The onset of SAM-septal contact (211 t 33 msec) was statistically similar to the peak
Volum* 122 Number 6
1675
Relation between LVOT Doppler and SAM in HCM
0
f
I
0
1
80VW9
1
mild/mod
I
no
I
control
SAM Fig. 4. Left ventricular outflow accelerations are presented for normal subjects, and for groups with hypertrophic cardiomyopathy having severe SAM, mild/moderate SAM, and no SAM. Patients with severe SAM have a higher acceleration than normal subjects and other hypertrophic cardiomyopathy groups. Table
II. Sequence
and timing
of SAM and Doppler Severe Case
Onset of SAM Onset of A wave Peak A wave Onset of SAMseptal contact End A wave or onset of B wave Peak of B wave End SAMseptal contact End B wave End SAM
SAM
events for all patients
group
Mild/Moderate
No.
SAM
Case
1
2
3
4
5
6
7
8
85
115
108
106
81
113
110
131
Mean
k SD
106 + 16
84
131
110
107
77
109
102
134
107 -t 20
170
267
191
181
121
171
180
230
189 + 43
234
270
232
195
170
211
179
200
211 + 33
215
365
245
222
143
235
279
290
249 + 65
288
439
323
365
211
292
325
410
332 f
311
364
389
366
270
387
347
320
357 T!Z 48
423
500
430
499
311
405
379
510
432 -+ 69
409
504
446
483
346
462
417
540
451 + 61
All values are in milliseconds. Abbreviations as in Table I.
with SAM
12 Onset
of
SAM Onset of Doppler Peak of Doppler Peak SAM
group
No. 3
4
5
Mean
f SD
120
106
82
85
115
102 * 17
109
109
89
106
107
104 I 8
271
241
237
272
264
257 + 17
299
230
245
283
310
273 t 35
-
73
End of Doppler End SAM
383
438
388
391
471
414 1?I 39
397
413
395
442
432
416 * 21
1676
Lin et al.
December 1993 American Heart Journal
5. M-mode and Doppler echograms of a patient with severe SAM with premature ventricular contraction (PVC). Note post-PVC beat (arrow) shows an increase of outflow acceleration, more rapid excursion rate of SAM, prolonged SAM-septal contact, and increasing midsystolic Doppler flow signal cessation. Fig.
of the A wave (189 + 43 msec). After a transient cessation of blood flow, a second flow wave (B wave) was generated promptly after the A wave at 249 t 65 msec. It reached peak velocity at 332 f 73 msec and ended at 432 f 69 msec. The end of SAM-septal contact (357 +- 48 msec) and the end of SAM (451 + 61 msec) were statistically similar to the peak of the B wave (332 t 73 msec) and the end of the B wave (432 f 69 msec), respectively. Mild/moderate SAM group. The sequence and timing of events after the initial QRS wave are shown in Table II (right column). The onset of SAM (102 + 17 msec) was almost simultaneous with the onset of Doppler (104 * 8 msec). The timing peak of Doppler after the initial QRS wave (257 t 17 msec) was statistically similar to the peak of SAM (273 +- 35 msec). The end of SAM (416 + 21 msec) and the end of Doppler (414 & 39 msec) occurred almost simul-
taneously. Fig. 7 shows these relationships between the events of SAM and hhe Doppler waveform of a patient with moderate SAM recorded at different times and matched for cycle length. Relation of SAM generation and resolution Doppler. The sequence and relationship
to LVOT
between Doppler and SAM events were similar in both severe and mild/moderate SAM groups. Thus the data for all 13 patients in Table II have been grouped together (Table III and Fig. 8), based on the events of SAM generation and resolution. SAM generation. The term of SAM generation is defined from the onset of SAM to the peak of SAM (either the onset of SAM-septal contact in the severe group or the peak of SAM in the mild/moderate group). The corresponding Doppler signal is defined from the onset of Doppler to the peak of Doppler (either the peak of the A wave in the severe group or the
Volume 122 Number 6
Relation between LVOT Doppler and SAM in HCM
1677
Fig. 6. The relationships between the events of SAM and the left ventricular outflow tract Doppler in a patient with severe SAM recorded at different times and matched for the cycle length. Note the correspondence of the onset of SAM and the onset of the Doppler A wave, the peak of the A wave and the onset of SAM-septal contact, and the end of SAM and the end of the Doppler B wave.
Fig. 7. The relationships between the events of SAM and the left ventricular outflow tract Doppler in a patient with moderate SAM recorded at different times and matched for the cycle length. Note the correspondence of the onset of SAM and the onset of Doppler, the peak of SAM and the peak of Doppler, and the end of SAM and the end of Doppler.
peak of Doppler in the mild/moderate group). In all patients with SAM, timing either between the onset of SAM and the onset of Doppler or the peak of SAM and the peak of Doppler was statistically similar. A correlation existed between the onset of Doppler and the onset of SAM (r = 0.834, p < 0.0001) (Fig. 9, upper panel) and there was also a correlation between
the timing of the peak of Doppler and the peak of SAM (r = 0.836, p < 0.0001) (Fig. 9, lower panel). Thus the generation time of Doppler and SAM corresponded. The excursion rate of anterior motion of the mitral valve (Table I) was higher in patients with severe SAM (15 + 6 cm/set) than in the mild/moderate group (6 ? 2 cm/set) (p < 0.01). In all patients
1678
December 1991 American Heart Journal
Lin et al. Onset
Onset Doppler
t
-
0
I
’
50
I
’
100
Offset
Peak
Peak Doppler
I.
I
’
200
150
I
250
msec after
End
Offset
m
1
’
300
End
I
’
350
1
’
400
I
-
450
I
500
R wave
8. The sequence of events, with the echocardiographic events on top and Doppler events underneath. Time intervals displayed are the means for all 13 patients with systolic anterior motion (SAM) of the mitral valve. Fig.
III. Grouped data of sequence and timing of SAM generation/resolution all 13 patients with SAM
Table
SAM Onset of SAM Onset of Doppler Peak of Doppler Peak of SAM
generation
(msec)
and corresponding Doppler events for SAM
104 106 215 235
++ Ii +
16 16 49 45
Offset of Doppler Offset of SAM End of Doppler End of SAM
resolution
(msecl 303 325 425 437
t t IIZ t
68 59 58 51
All values are Means + SD. Abbreviations as in Table I.
with SAM, the excursion rate of SAM correlated with the outflow acceleration (r = 0.828, p < 0.0001) (Fig. 10). The correlation of these two perpendicular motions may indicate, the cause-and-effect relationship of LVOT blood flow acceleration and SAM. SAM resolution. The term of SAM resolution is defined from the offset of SAM (either the end of SAM-septal contact in the severe group or the peak of SAM in the mild/moderate group) to the end of SAM. The corresponding Doppler signal is defined from the offset of Doppler (either the peak of the B wave in the severe group or the peak of Doppler in the mild/moderate group) to the end of Doppler. In all patients with SAM, timing either between the offset of SAM and the offset of Doppler or the end of SAM and the end of Doppler was statistically similar. The timing of the offset of SAM showed a correlation with the offset of Doppler (r = 0.795, p < 0.001) (Fig. 11,
upper panel). A correlation also appeared between the end of Doppler and the end of SAM (r = 0.859, p < 0.0001) (Fig. 11, lower panel). Thus the timing of termination of SAM and Doppler corresponded (Fig. 8). The regression rate of SAM (Table I) was higher in patients with severe SAM (17 f 7 cm/set) than in patients with mild/moderate SAM (8 rt 2 cm/set). In all patients with SAM, the blood flow deceleration showed a correlation with the regression rate of SAM (r = 0.668, p < 0.013) (Fig. 12). This result showed a close relationship between the resolution of SAM and blood flow deceleration. DISCUSSION
Analysis of the pulsed Doppler spectrum obtained at the maximal SAM-septal apposition can more actually realize the localized blood flow in relation to SAM. The unique biphasic Doppler waveform ob-
Volume 122 Number 6
Relation
between LVOT
r=O.BU
Doppler
and SAM in HCM
1679
P-co.oool
y~19.930+0.83119x 90-. 70-t 60
. 90
1 110
100 OMSEf
.
I 120
130
6 140
SAM (mno)
r.0.636
p.zo.ooo1
y - 0.92312 + 0.9104Gx I 206
I 300 PEAKSAY
8 400
(mm)
Fig. 9. Correlation between the timings of the onset of SAM and the onset of Doppler (upper panel), and the peak of SAM and the peak of Doppler (lower panel) in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve.
tained in this study has been mentioned by others20*21; however, no further interpretations were done. In this study, this biphasic Doppler flow pattern was obtained in all patients with severe SAM by careful step-by-step positioning of the sample volume and by performing a continuous strip-chart recording to overcome the movement of the heart. The first Doppler wave-the A wave-was generated at the same time as the mitral valve anterior motion. A sudden midsystolic transient outflow Doppler signal cessation between two peak flow velocities was most likely caused by impedance of the blood flow by the anterior motion of the mitral valve, because its occurrence corresponded to the timing of the SAMseptal contact. Although the B wave appeared after blood flow was impeded by SAM, the blood was possibly still flowing through the orifice along both lateral margins of the mitral valve, because the anteriorly moving mitral valve assumes a unique cowl-like configuration with mitral septal contact centrally and a preserved orifice along each lateral margin.7 In the present study, a correlation was found to exist between LVOT outflow Doppler and SAM in
patients with HCM, suggesting a cause-and-effect relationship. We examined the temporal relationship between SAM and the Doppler waveform in patients with severe and mild/moderate SAM. As a group, the timing of SAM generation and resolution showed a correlation with the Doppler events (Fig. 8). Although the LVOT blood flow velocity when SAM began was low, the acceleration of the LVOT blood outflow was higher than normal (Fig. 4), and this acceleration correlated with the excursion rate of the mitral valve anterior motion (Fig. 10). A basic knowledge of fluid dynamics in a tapering flow field22l 23 reveals that the instantaneous “Bernoulli pressure drop” in the early ejection phase of a pulsatile flow is mostly accounted for by the local acceleration effect. At peak flow in the latter phase, only the convective acceleration effects are responsible for measured pressure drop. Thus this early systolic high outflow acceleration is an important factor in producing the pressure drop and in drawing the mitral valve anteriorly. Hypercontractile ventricles and rapid ejection have been postulated by hemodynamic12 and angiographic studies24y 25 in patients with HCM. These ex-
1660
December
Lin et al.
American
1491
Heart Journal
. ZCQ! 200
0 I 0
10
20
300
400
1 500
OFFSET SAY (mrs)
1 30
SAM EXCURSION RATE (cmisec)
10. Correlation between the left ventricular outflow acceleration and the excursion rate of SAM in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve. Fig.
traordinarily hyperdynamic ventricles may produce a rapid acceleration of the exiting blood flo~.~” Our study indicated the same findings-that the patient with severe SAM had a higher outflow acceleration than the others (Fig. 4). The result of the Bernoulli pressure drop due to a high acceleration blood outflow produced by hypercontractile ventricles can explain why some patients27T 28 and animals in an experimental study2g without asymmetric septal hypertrophy also may manifest SAM phenomenon in a hypercontractile cardiac state. This high blood flow acceleration effect may also be clearly shown in a patient with severe SAM with premature ventricular contractions (Fig. 5) whose postextrasystolic potentiation of the ventricular contractility produced a higher outflow acceleration and resulted in a more rapid SAM excursion rate, prolonging SAM-septal contact, and increasing midsystolic Doppler flow signal cessation and the ejection period. Hemodynamic studies12* 25~26 have shown that the majority of flow (at least 70 % ) is unusually rapid in patients with HCM and is completed earlier in systole than in normal individuals. These authors suggest that most of the stroke volume is in fact expelled before obstruction commences. “Outflow obstruction,” as traditionally defined by the presence of an abnormal intraventricular pressure gradient and SAM of the mitral valve, does not impede the left ventricular outflow in HCM.i2 In the present study, acceleration of the LVOT blood flow was significantly higher in the group with severe SAM than in the control and the other HCM groups. The available systolic ejection period, as determined from the Doppler waveform, tended to be longer in the group with severe SAM than in the others. Since the
300
400
500
600
END SAM (nw.c)
11. Correlation between the timing of the offset of SAM and the offset of Doppler (upper panel), and the end of SAM and the end of Doppler (lower panel) in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve.
Fig.
prolonged systolic ejection period and increased midsystolic Doppler flow signal cessation after the ectopic beat-indicating more severe obstruction-is observed in spite of increased blood flow ejection, it is likely that a certain amount of blood is in fact impeded in its ejection by the anterior motion of the mitral valve. The mechanism of maintaining anterior motion of the mitral valve in late systole when the aortic flow velocity is low or negligible is debatable.18 However, in our study a higher than normal blood flow velocity (B wave) appeared through the course of SAM-septal contact until it started to decelerate when the offset of SAM-septal contact began. The discrepancy of this result with those of others studies is possibly due to the different flow patterns of the aorta and the LVOT. The difference has been demonstrated by the low aortic flow velocity in mid and late systole compared with the high LVOT velocity waveform shown in mid to late systole.16, 2o It is not known whether the B wave takes part in maintaining the SAM-septal contact or not. Although the B wave velocity (121 cm/set) is higher than normal, it seems insufficient to produce a pressure drop by convective acceleration to maintain
the SAM-septal
contact. Nevertheless,
the
Volumb 122 Numbrr 6
Relation
between LVOT
Doppler
and SAM in HCM
1661
.
3000 r-0.666
pco.013
y = 266.40 + 65.765x
0 1 0
I 20
1 10 SAM REGRESSION
1 30
RATE (cmhc)
Fig. 12. Correlation between the left ventricular outflow deceleration and the regression rate of SAM in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve.
B wave flow could possibly be present as a drag force to maintain SAM-septal contact until the blood velocity starts to decelerate. In all patients with SAM, the timing of the SAM resolution showed a correlation with Doppler events (Fig. 8) and the regression rate of SAM corresponded with the Doppler deceleration (r = 0.668, p < 0.013). These findings suggest a rapid decrease in the pressure drop, and the blood flow velocity produced mitral valve regression. The mechanism of SAM is still debatable, nor can our study make any conclusion; however, we offer some new findings to suggest that high left ventricular outflow acceleration in early systole may produce the Venturi effect and may result in mitral valve anterior motion. At mid-systole, the SAM-septal contact is maintained, either by the suction effect of continued pressure drop or by the drag force, resulting in left ventricular outflow obstruction. At late systole, the pressure drop and the blood flow deceleration produce mitral valve regression. REFERENCES
1. Wigle ED, Adelman AG, Silver MD. Pathophysiological
considerations in muscular subaortic stenosis. In: Wolstenholme GEW, O’Connor M, eds. Hypertrophic obstructive cardiomyopathy. CIBA Foundation Study Group No. 37. London: J & A Churchill, Ltd, 1971:63-76. 2. Henry WL, Clark CE, Gri5th JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructiveasymmetricseptalhypertrophy.Am JCardiol1975;35:337-
45. 3. Rodger JC. Motion of mitral apparatus in hvpertronhic
cardiomyopathy with obstruction. -Br Heart J 1976;3&732-7. 4. Kina JF. DeMaria AN. Reis RL. Bolton MR. Dunn MI. Mason DT. Echocardiographic assessment of idiopathic hypertrophic subaortic stenosis. Chest 1973;64:723-31. 5. Nagata S, Nimura Y, Beppu S, Park YD, Sakakibara H. Mechanism of systolic anterior motion of mitral valve and site of intraventricular pressure gradient in hypertrophic obstructive cardiomyopathy. Br Heart J 1983;49:234-43. ”
I
6. Shah PM, Taylor RD, Wong M. Abnormal mitral valve coaptation in hypertrophic obstructive cardiomyopathy: proposed role in systolic anterior motion of mitral valve. Am J Cardiol 1981;48:258-62. 7. Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. AM HEARTJ 1987;113:633-44. 8. Cape EG, Simons D, Jimoh A, Weyman AE, Yoganathan AP, Levine RA. Chordal geometry determines the shape and extent of systolic anterior mitral motion: in vitro studies. J Am Co11 Cardiol 1989;13:1438-48. 9. Kikami T, Hashimoto M, Kudo T, Sugawara T, Sakamoto S, Yasuda H. Mitral valve and its ring in hypertrophic cardiomyopathy, a mechanism creating surplus mitral leaflet involved in systolic anterior motion. Jpn Circ J 1988;52:597-603. 10. Moro E, TenCate FJ, Leonard JJ, Hugenholtz PG, Roelandt J. Genesis of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an anatomical or dynamic event? Eur Heart J 1987;8:1312-21. 11. Pollick C, Morgan CD, Gilbert BW, Rakowski H, Wigle ED. Muscular subaortic stenosis: the temporal relationship between systolic anterior motion of the anterior mitral leaflet and the pressure gradient. Circulation 1982;66:1087-94. 12. Murgo JP, Alter BR, Dorethy JF, Altobelli SA, McGranahan GM Jr, Dunne TE. Dynamics of left ventricular ejection in obstructive and nonobstructive hypertrophic cardiomyopathy. J Clin Invest 1980;66:1369-82. 13. Spirit0 P, Maron BJ. Patterns of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: assessment by two-dimensional echocardiography. Am J Cardiol 1984; 543039-46. 14. Maron BJ, Gottdiener JS, Arce J, Rosing DR, Wesley YE, Epstein SE. Dynamic subaortic obstruction in hypertrophic cardiomyopathy: analysis by pulsed Doppler echocardiography. J Am Co11 Cardiol 1985;6:1-15. 15. Gardin JM, Dabestani A, Glasgow GA, Butman S, Burn CS, Henry WL. Echocardiographic and Doppler flow observations in obstructed and nonobstructed hypertrophic cardiomyopathy. Am J Cardiol 1985;56:614-21. 16. Yock PG, Hatle L, Popp R. Patterns and timing of Dopplerdetected intracavitary and aortic flow in hypertrophic cardiomyopathy. J Am Co11 Cardiol 1986;8:1047-58. 17. Bryg RJ, Pearson AC, Williams GA, Labovitz AJ. Left ventricular systolic and diastolic flow abnormalities determined by Doppler echocardiography in obstructive hypertrophic cardiomyopathy. Am J Cardiol 1987;59:925-31. 18. Levine RA, Weyman AE. Dynamic subaortic obstruction in
1682
19.
20.
21.
22.
23.
24.
Lin et al. hypertrophic cardiomyopathy: criteria and controversy. J Ant Co11 Cardiol 1985;6:16-8. Gilbert BW, Pollick C, Adelman AG, Wigle ED. Hypertrophit cardiomyopathy: subclassification by M-mode echocardiography. Am J Cardiol 1980;45:861-72. Hatle L, Angelsen B. Pulsed and continuous wave Doppler II) diagnosis and assessment of various heart lesion. In: Hatle L. Angelsen B, eds. Doppler ultrasound in cardiology. 2nd ed. Philadelnhia: Lea & Febiger. 198520516. Kertes PJ, Darkin LM, Hunt D. Regional left ventricular Doppler velocity profiles in hypertrophic cardiomyopathy [Abstract]. Circulation 1987;76(suppl IV):IV-96. Pasipoularides A, Murgo JP, Miller JW, Craig WE. Nonobstructive left ventricular ejection pressure gradients in man Circ Res 1987;61:220-7. Pasipoularides A, Murgo JP, Bird JJ, Craig WE. Fluid dynamics of aortic stenosis: mechanisms for the presence of subvalvular pressure gradients. Am J Physiol 1984;H542-50. Siegel RJ, Criley JM. Comparison of ventricular emptying with and without a pressure gradient in patients with hypertrophic cardiomyopathy. Br Heart J 1985;53:283-91.
December 1991 American Heart Journal
25. Sugrue IlLI, McKenna WJ- Dickie S. Myers MJ, 1,avender .JI”. Oakley CM, Goodwin JF. Relation between left ventricular gradient and relative stroke volume ejected in early and late systole in hypertrophic cardiomyopathy; assessment with ra dionuclide cineangiography. Br Heart J 1984;52:602-9. ED, Barclay S.4, Davis AL, Mannering D, Mehta N. 26. Bennett Ascending aortic blood velocity and acceleration using Doppler ultrasound in the assessment of left ventricular function. Circ Res 1984;18:632-8. 27. Come PC, Bulkley BH, Goodman ZD, Hutchins GM, Pitt B, Fortuin NJ. Hypercontractile cardiac states simulating hypertrophic cardiomyopathy. Circulation 1977;55:901-8. MN. Seeal BL. Parrv WR. Svstolic anterior 28. Mintz GS. Kotler motion of the mitral valve in the absence of asymmetric septal hypertrophy. Circulation 1978;57:266-63. 29. Sakurai S. Tanaka H. Yoshimura H, Nakao S, Tahara M. Production of’ systolic anterior motion of the mitral valve in dogs. Circulation 1985;71:805-12.
Chung-Sheng Lin, MD, Kuo-Shuen Chen, MD, Ming-Cheng Lin, MD, Men-Chin Fu, MD, and Shu-Mei Tang, BS. Taichung, Taiwan, Republic
Since echocardiographic recording of systolic anterior motion (SAM) of the mitral valve in patients with hypertrophic cardiomyopathy (HCM) was observed, several mechanisms have been proposed to explain this motion, l-i0 but the Venturi theory1 has been most widely accepted. This hypothesis states that rapid ejection in the early phase of systole through a narrowed left ventricular outflow tract (LVOT) produces a high-velocity stream above the mitral valve that, according to Bernoulli’s equation, decreases the pressure above the valve, drawing it anteriorly. However, despite recent studies using From the Departmentof Internal Medicine, Chung Shari Medical and Dental College Hospital. Received for publication Jan. ‘7, 1991; accepted May 1, 1991. Reprint requests: Chung-Sheng Lin, MD, 23 Sec. 1, Taichung Kang Rd., Taichung, Taiwan 40334, Republic of China. 4/l/32948
of China
hemodynamic monitoring,“, l2 two-dimensional echocardiography,2-7F galo, l3 and Doppler echocardiography,14-17 several questions are still unanswered regarding the relationship between velocities in the LVOT, the pattern of flow in the ascending aorta, and SAM of the mitral valve.18 Previous Doppler studies in patients with HCM concentrated on analyzing the Doppler aortic flow to correlate the events of SAM. However, Doppler aortic studies fail to explain many of the observed features of SAM.18 In this study, we analyzed the pulsed Doppler obtained at the maximal mitral-septal apposition to gain further insight into the relationship of SAM and Doppler and to attempt to fmd the mechanism of SAM. METHODS Patient
secutive
selection.
patients
with
Echocardiographic studies of 20 conHCM were evaluated. All patients 1671
1672
December 1991 American Heart Journal
Lin et al.
.
I
D=+ Mild/Mod
SAM
-
SAMER=+
Fig. 2. Method of pulsed Doppler echocardiographic examination. The sample volume was placed at the region between the maximal anterior apposition of the mitral valve and the interventricular septum from the apical long-axis view. LA, Left atrium; LV, left ventricle; RV, right ventricle; Ao, aorta.
SAMRR=+ Fig.
1. Scheme
showing
(A) and deceleration
calculation
of flow acceleration
(D), SAM excursion rate (SAMER), rate (SAMRR) in patients with severe
and SAM regression SAM (upper panel) and mild/moderate SAM (lower panel). VI and Vs are peak Doppler flow velocities of A wave and B wave, respectively. SAM, Systolic anterior motion of the mitral valve.
showed diagnostic quality Doppler and M-mode echocardiographic studies. Ten normal subjects without any heart disease were selected for control studies. All patients and normal subjects were in normal sinus rhythm. HCM was diagnosed by characteristic clinical findings and the demonstration of left ventricular hypertrophy without cavity dilatation or any known cause of hypertrophy. All patients with HCM demonstrated a ventricular septal thickness of more than 15 mm and a diastolic septal-to-left ventricular free wall ratio of at least 1.5 below the level of the mitral valve on an M-mode echocardiogram. The magnitude of SAM was classified using a modification of the classification proposed by Gilbert et al.lg The SAM was defined as mild if the minimal mitral-septal distance was greater than 10 mm, as moderate SAM if this distance was 10 mm or less but with no mitral-septal contact, and as severe SAM if there was either brief or prolonged mitral-septal contact. Among 20 patients with HCM, eight
patients were classified in the severe SAM group, five patients were classified in the mild/moderate SAM group, and seven patients were classified in the no SAM group. Ultrasound system. All echocardiographic studies were performed using a phased-array echocardiographic color Doppler system (Hewlett-Packard Co., Medical Products Group, Andover, Mass.). The pulsed Doppler examination of this system is performed under simultaneous guidance of a two-dimensional color Doppler image. A 2.5 MHz transducer was used in this study. Echocardiograms of this study were recorded on the strip charts at paper speeds of 50 to 100 mm/set. M-mode echocardiography. M-mode echocardiograms were obtained with the patients and normal subjects in the supine position. Ventricular septal and left ventricular free wall thickness were measured in all patients and normal subjects as recommended by the American Society of Echocardiography. In the eight patients with severe SAM, four additional measurements were made: the time from the onset of the QRS complex to (1) initial onset of SAM; (‘2) initial SAM-septal contact; (3) end of SAM-septal contact; and (4) end of SAM. In the five patients with mild/moderate SAM, three additional measurements were made: the time from the onset of the QRS complex to (1) initial onset of SAM; (2) peak of SAM; and (3) end of SAM. The excursion time of SAM was measured from the onset of SAM to the initial SAM-septal contact (in severe SAM patients) or to the peak of SAM (in mild/moderate SAM
Volume 122 Numbor 6
Table
Relation
between LVOT
Doppler
and SAh4 in HCM
1673
I. M-mode echocardiography of SAM and Doppler characteristics
Peak velocity (cm/set) Doppler acceleration (cmhec’) Doppler deceleration (cm/sec2) SAM excursion (cmhec) SAM regression (cmhec) Ejection time (msec)
Severe SAM (n = 8)
Mild/Moderate SAM (n = 5)
No SAM (n = 7)
Control (n = IO)
A wave 127 t 35s B wave 121 + 46 1798 * 8003
125 t 51s
93 k 25s
51 It 7
859 + 259*
717 -+ 166
570 + 193
1325 -+ 755s
893 t 522$
533 k 155s
292 f 45
305 +I 12t
271 + 25
15 + 6a
652
17 -t- 7a
8+2
325 + 54t
310 + 36’
SAM, Systolic anterior motion of the mitral valve. *p < 0.03, tp < 0.01, $p < 0.001, §p < 0.0001 compared “p < 0.01 compared with mild/moderate group, values
with control. expressed as Mean
patients). The excursion rate of SAM was calculated by dividing the amplitude of the SAM by the excursion time. The regression time of SAM was measured from the end of the SAM-septal contact (in severe SAM patients) or the peak of SAM (in mild/moderate patients) to the end of SAM. The regression rate of SAM was calculated by dividing the amplitude of the SAM by the regression time (Fig. 1, right panel). Doppler echocardiography. All Doppler echocardiographic studies were performed immediately after each M-mode study. Recordings were obtained with the patients/subjects at rest from the apical long-axis approach. The sample volume of pulsed Doppler was carefully moved step by step from the apical level toward the SAM-septal contact level. Doppler spectrums of each area were recorded on the strip chart. To overcome the movement of the heart that may make the position of the sample volume unsteady at the exact anatomic location, we performed a continuous strip-chart recording, especially when the sample volume was positioned between the ventricular septum and the maximal anterior apposition of the mitral valve (Fig. 2). For patients with no SAM or in normal subjects, the equivalent SAMseptal contact area Doppler spectrum was obtained by placing the sample volume at 1 to 2 cm proximal to the aortic valve near the ventricular septum. Timing of the Doppler spectrum was measured from the onset of the QRS complex to: (1) the initial onset of Doppler; (2) the peak of Doppler; and (3) the end of Doppler. Acceleration time was measured from the onset of ejection to the time of peak flow velocity. Average acceleration was calculated by dividing peak flow velocity by acceleration time. Deceleration time was measured from the time of peak flow velocity to the end of Doppler. Average deceleration was calculated by dividing peak flow velocity by deceleration time (Fig. 1, left lower panel). In patients with severe SAM, average acceleration was calculated by dividing A wave peak velocity by A wave acceleration time, and average deceleration was calculated by dividing B wave
+ SD.
peak velocity by B wave deceleration time (Fig. 1, left upTiming of the Doppler spectrum in severe SAM patients was measured from the onset of the QRS complex to: (1) the initial onset of the A wave; (2) the peak of the A wave; (3) the end of the A wave or the onset of the B wave; (4) the peak of the B wave; and (5) the end of the B wave. The presenting of a biphasic Doppler spectrum in severe SAM patients will be discussed later.
per panel).
Temporal relationship between Doppler flow events and SAM. To minimize the differences in physiologic state,
identical R-R cycles (i.e., cycle lengths to within 10 msec of each other) of M-mode and Doppler echocardiograms were measured in three cycles each in the same patient. All data of time were corrected for heart rate with the square root of the R-R interval to normalize for patient variability. Statistics. Analysis was performed by means of t tests. Comparison was performed using Pearson’s correlation coefficient. Values are means k standard deviations. RESULTS Doppler waveform of the LVOT outflow contact level in patients with hypertrophic athy and normal subjects (Table I)
at SAM-septal cardiomyop-
Pulsed Doppler waveform. The Doppler spectrum of the maximal anterior mitral valve apposition level can be obtained approximately by means of simultaneous two-dimensional imaging. Movement of the heart relative to the Doppler sample volume precludes exact anatomic localization in a given case. However, a continuous strip-chart recording could help to identify the local specific Doppler waveform. A unique biphasic DoppIer waveform can be obtained at the SAM-septal contact area in all patients with severe SAM. There were two peak flow velocities of the A wave and B wave, which were different from those of patients with mild/moderate SAM (Fig. 3).
1674
December 1991 American Heart Journal
Lin et al.
3. Pulsed Doppler flow patterns of the left ventricular outflow tract in patients with severe SAM (upper panel) and moderate SAM (lower panel). Two Doppler echograms are matched for the cycle length. Note that a biphasic pattern (A and B wave) and a higher acceleration in a patient with severe SAM can be discerned. Fig.
mild/moderate SAM (125 t 51 cmlsec), but was sipnificantly higher than that of the no SAM group (93 + 25 cm/set) (p < 0.05) and normal subjects (51 t- 7 cm/set) (p < 0.0001). However, in patients with severe SAM, flow velocity increased sharply and reached a peak of the A wave at 189 f 43 msec after the initial QRS wave, which was significantly earlier than in patients with mild/moderate SAM (257 + 17 msec) (p < 0.007) or in the no SAM group (238 + 23 msec) (p < 0.019). Therefore acceleration was higher in patients with severe SAM (1798 + 800 cm/set’) than in patients with mild/moderate SAM (859 + 259 cm/sec2) (p < 0.029) or with no SAM (717 + 166 cm/ sec2) (p < 0.004) and in normal subjects (570 * 193 cm/sec2) (p < O.OOOl),as shown in Table I and Fig. 4. The peak flow velocity of the B wave (121 t 46 cm/ set) was not different from that of the A wave. Blood flow deceleration was higher in patients with severe SAM (1325 t 755 cm/se&?) than in patients with no SAM (533 + 155 cm/sec2) (p < 0.018) or in normal subjects (292 i- 45 cm/set’) (p < O.OOOl),but was not different from that of patients with mild/moderate SAM (893 1. 522 cm/set”). Ejection time with pulsed Doppler was significantly longer in patients with severe SAM (325 I 54 msec) than in normal subjects (271 f 25 msec) (p < O.Ol), but was not significantly different from that of patients with mild/moderate SAM (310 * 36 msec) or from that of the no SAM group (305 I 12 msec). Pulsed Doppler waveform in a patient with premature ventricular contraction. A patient with severe SAM with premature ventricular contraction whose Doppler waveform was obtained from the SAM-septal contact area showed postextrasystolic potentiation (Fig. 5). The postextrasystolic beat revealed an increase of outflow acceleration (from 1032 & 177 to 1910 rt 466 cm/sec2, p < 0.006), a more rapid SAM excursion rate (from 12 i 2 to 19 + 4 cm/set, p < 0.03), a prolonged SAM-septal contact (from 87 ri: 12 to 172 +- 28 msec, p < O.OOOl), and increasing midsystolic outflow Doppler signal cessation (from 148 +- 15 to 282 +- 13 msec, p < 0.0001) and ejection period (from 270 ~tr10 to 382 + 11 msec, p < 0.0001). Temporal relation events of SAM
The A wave was generated in early systole and the B wave appeared in mid-systole after a transient cessation of the Doppler flow signal. The A wave constituted a relatively small fraction of the overall forward flow velocity (44 t 14%). The velocity contour of mild/moderate SAM patients was not significantly different from that of the normal subjects and the no SAM group. The peak flow velocity of the A wave in severe SAM patients (127 f 35 cm/set) was not significantly different from that of the patients with
between
Doppler
waveform
and
Severe SAM group. Table II (left column) is a summary of the temporal relations between the Doppler waveform and events of SAM measured after the initial QRS wave. Fig. 6 shows these relationships in a patient with severe SAM recorded at different times and matched for the cycle length. The onset of SAM (106 * 16 msec) and the onset of the Doppler A wave (107 t 20 msec) occurred almost simultaneously. The onset of SAM-septal contact (211 t 33 msec) was statistically similar to the peak
Volum* 122 Number 6
1675
Relation between LVOT Doppler and SAM in HCM
0
f
I
0
1
80VW9
1
mild/mod
I
no
I
control
SAM Fig. 4. Left ventricular outflow accelerations are presented for normal subjects, and for groups with hypertrophic cardiomyopathy having severe SAM, mild/moderate SAM, and no SAM. Patients with severe SAM have a higher acceleration than normal subjects and other hypertrophic cardiomyopathy groups. Table
II. Sequence
and timing
of SAM and Doppler Severe Case
Onset of SAM Onset of A wave Peak A wave Onset of SAMseptal contact End A wave or onset of B wave Peak of B wave End SAMseptal contact End B wave End SAM
SAM
events for all patients
group
Mild/Moderate
No.
SAM
Case
1
2
3
4
5
6
7
8
85
115
108
106
81
113
110
131
Mean
k SD
106 + 16
84
131
110
107
77
109
102
134
107 -t 20
170
267
191
181
121
171
180
230
189 + 43
234
270
232
195
170
211
179
200
211 + 33
215
365
245
222
143
235
279
290
249 + 65
288
439
323
365
211
292
325
410
332 f
311
364
389
366
270
387
347
320
357 T!Z 48
423
500
430
499
311
405
379
510
432 -+ 69
409
504
446
483
346
462
417
540
451 + 61
All values are in milliseconds. Abbreviations as in Table I.
with SAM
12 Onset
of
SAM Onset of Doppler Peak of Doppler Peak SAM
group
No. 3
4
5
Mean
f SD
120
106
82
85
115
102 * 17
109
109
89
106
107
104 I 8
271
241
237
272
264
257 + 17
299
230
245
283
310
273 t 35
-
73
End of Doppler End SAM
383
438
388
391
471
414 1?I 39
397
413
395
442
432
416 * 21
1676
Lin et al.
December 1993 American Heart Journal
5. M-mode and Doppler echograms of a patient with severe SAM with premature ventricular contraction (PVC). Note post-PVC beat (arrow) shows an increase of outflow acceleration, more rapid excursion rate of SAM, prolonged SAM-septal contact, and increasing midsystolic Doppler flow signal cessation. Fig.
of the A wave (189 + 43 msec). After a transient cessation of blood flow, a second flow wave (B wave) was generated promptly after the A wave at 249 t 65 msec. It reached peak velocity at 332 f 73 msec and ended at 432 f 69 msec. The end of SAM-septal contact (357 +- 48 msec) and the end of SAM (451 + 61 msec) were statistically similar to the peak of the B wave (332 t 73 msec) and the end of the B wave (432 f 69 msec), respectively. Mild/moderate SAM group. The sequence and timing of events after the initial QRS wave are shown in Table II (right column). The onset of SAM (102 + 17 msec) was almost simultaneous with the onset of Doppler (104 * 8 msec). The timing peak of Doppler after the initial QRS wave (257 t 17 msec) was statistically similar to the peak of SAM (273 +- 35 msec). The end of SAM (416 + 21 msec) and the end of Doppler (414 & 39 msec) occurred almost simul-
taneously. Fig. 7 shows these relationships between the events of SAM and hhe Doppler waveform of a patient with moderate SAM recorded at different times and matched for cycle length. Relation of SAM generation and resolution Doppler. The sequence and relationship
to LVOT
between Doppler and SAM events were similar in both severe and mild/moderate SAM groups. Thus the data for all 13 patients in Table II have been grouped together (Table III and Fig. 8), based on the events of SAM generation and resolution. SAM generation. The term of SAM generation is defined from the onset of SAM to the peak of SAM (either the onset of SAM-septal contact in the severe group or the peak of SAM in the mild/moderate group). The corresponding Doppler signal is defined from the onset of Doppler to the peak of Doppler (either the peak of the A wave in the severe group or the
Volume 122 Number 6
Relation between LVOT Doppler and SAM in HCM
1677
Fig. 6. The relationships between the events of SAM and the left ventricular outflow tract Doppler in a patient with severe SAM recorded at different times and matched for the cycle length. Note the correspondence of the onset of SAM and the onset of the Doppler A wave, the peak of the A wave and the onset of SAM-septal contact, and the end of SAM and the end of the Doppler B wave.
Fig. 7. The relationships between the events of SAM and the left ventricular outflow tract Doppler in a patient with moderate SAM recorded at different times and matched for the cycle length. Note the correspondence of the onset of SAM and the onset of Doppler, the peak of SAM and the peak of Doppler, and the end of SAM and the end of Doppler.
peak of Doppler in the mild/moderate group). In all patients with SAM, timing either between the onset of SAM and the onset of Doppler or the peak of SAM and the peak of Doppler was statistically similar. A correlation existed between the onset of Doppler and the onset of SAM (r = 0.834, p < 0.0001) (Fig. 9, upper panel) and there was also a correlation between
the timing of the peak of Doppler and the peak of SAM (r = 0.836, p < 0.0001) (Fig. 9, lower panel). Thus the generation time of Doppler and SAM corresponded. The excursion rate of anterior motion of the mitral valve (Table I) was higher in patients with severe SAM (15 + 6 cm/set) than in the mild/moderate group (6 ? 2 cm/set) (p < 0.01). In all patients
1678
December 1991 American Heart Journal
Lin et al. Onset
Onset Doppler
t
-
0
I
’
50
I
’
100
Offset
Peak
Peak Doppler
I.
I
’
200
150
I
250
msec after
End
Offset
m
1
’
300
End
I
’
350
1
’
400
I
-
450
I
500
R wave
8. The sequence of events, with the echocardiographic events on top and Doppler events underneath. Time intervals displayed are the means for all 13 patients with systolic anterior motion (SAM) of the mitral valve. Fig.
III. Grouped data of sequence and timing of SAM generation/resolution all 13 patients with SAM
Table
SAM Onset of SAM Onset of Doppler Peak of Doppler Peak of SAM
generation
(msec)
and corresponding Doppler events for SAM
104 106 215 235
++ Ii +
16 16 49 45
Offset of Doppler Offset of SAM End of Doppler End of SAM
resolution
(msecl 303 325 425 437
t t IIZ t
68 59 58 51
All values are Means + SD. Abbreviations as in Table I.
with SAM, the excursion rate of SAM correlated with the outflow acceleration (r = 0.828, p < 0.0001) (Fig. 10). The correlation of these two perpendicular motions may indicate, the cause-and-effect relationship of LVOT blood flow acceleration and SAM. SAM resolution. The term of SAM resolution is defined from the offset of SAM (either the end of SAM-septal contact in the severe group or the peak of SAM in the mild/moderate group) to the end of SAM. The corresponding Doppler signal is defined from the offset of Doppler (either the peak of the B wave in the severe group or the peak of Doppler in the mild/moderate group) to the end of Doppler. In all patients with SAM, timing either between the offset of SAM and the offset of Doppler or the end of SAM and the end of Doppler was statistically similar. The timing of the offset of SAM showed a correlation with the offset of Doppler (r = 0.795, p < 0.001) (Fig. 11,
upper panel). A correlation also appeared between the end of Doppler and the end of SAM (r = 0.859, p < 0.0001) (Fig. 11, lower panel). Thus the timing of termination of SAM and Doppler corresponded (Fig. 8). The regression rate of SAM (Table I) was higher in patients with severe SAM (17 f 7 cm/set) than in patients with mild/moderate SAM (8 rt 2 cm/set). In all patients with SAM, the blood flow deceleration showed a correlation with the regression rate of SAM (r = 0.668, p < 0.013) (Fig. 12). This result showed a close relationship between the resolution of SAM and blood flow deceleration. DISCUSSION
Analysis of the pulsed Doppler spectrum obtained at the maximal SAM-septal apposition can more actually realize the localized blood flow in relation to SAM. The unique biphasic Doppler waveform ob-
Volume 122 Number 6
Relation
between LVOT
r=O.BU
Doppler
and SAM in HCM
1679
P-co.oool
y~19.930+0.83119x 90-. 70-t 60
. 90
1 110
100 OMSEf
.
I 120
130
6 140
SAM (mno)
r.0.636
p.zo.ooo1
y - 0.92312 + 0.9104Gx I 206
I 300 PEAKSAY
8 400
(mm)
Fig. 9. Correlation between the timings of the onset of SAM and the onset of Doppler (upper panel), and the peak of SAM and the peak of Doppler (lower panel) in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve.
tained in this study has been mentioned by others20*21; however, no further interpretations were done. In this study, this biphasic Doppler flow pattern was obtained in all patients with severe SAM by careful step-by-step positioning of the sample volume and by performing a continuous strip-chart recording to overcome the movement of the heart. The first Doppler wave-the A wave-was generated at the same time as the mitral valve anterior motion. A sudden midsystolic transient outflow Doppler signal cessation between two peak flow velocities was most likely caused by impedance of the blood flow by the anterior motion of the mitral valve, because its occurrence corresponded to the timing of the SAMseptal contact. Although the B wave appeared after blood flow was impeded by SAM, the blood was possibly still flowing through the orifice along both lateral margins of the mitral valve, because the anteriorly moving mitral valve assumes a unique cowl-like configuration with mitral septal contact centrally and a preserved orifice along each lateral margin.7 In the present study, a correlation was found to exist between LVOT outflow Doppler and SAM in
patients with HCM, suggesting a cause-and-effect relationship. We examined the temporal relationship between SAM and the Doppler waveform in patients with severe and mild/moderate SAM. As a group, the timing of SAM generation and resolution showed a correlation with the Doppler events (Fig. 8). Although the LVOT blood flow velocity when SAM began was low, the acceleration of the LVOT blood outflow was higher than normal (Fig. 4), and this acceleration correlated with the excursion rate of the mitral valve anterior motion (Fig. 10). A basic knowledge of fluid dynamics in a tapering flow field22l 23 reveals that the instantaneous “Bernoulli pressure drop” in the early ejection phase of a pulsatile flow is mostly accounted for by the local acceleration effect. At peak flow in the latter phase, only the convective acceleration effects are responsible for measured pressure drop. Thus this early systolic high outflow acceleration is an important factor in producing the pressure drop and in drawing the mitral valve anteriorly. Hypercontractile ventricles and rapid ejection have been postulated by hemodynamic12 and angiographic studies24y 25 in patients with HCM. These ex-
1660
December
Lin et al.
American
1491
Heart Journal
. ZCQ! 200
0 I 0
10
20
300
400
1 500
OFFSET SAY (mrs)
1 30
SAM EXCURSION RATE (cmisec)
10. Correlation between the left ventricular outflow acceleration and the excursion rate of SAM in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve. Fig.
traordinarily hyperdynamic ventricles may produce a rapid acceleration of the exiting blood flo~.~” Our study indicated the same findings-that the patient with severe SAM had a higher outflow acceleration than the others (Fig. 4). The result of the Bernoulli pressure drop due to a high acceleration blood outflow produced by hypercontractile ventricles can explain why some patients27T 28 and animals in an experimental study2g without asymmetric septal hypertrophy also may manifest SAM phenomenon in a hypercontractile cardiac state. This high blood flow acceleration effect may also be clearly shown in a patient with severe SAM with premature ventricular contractions (Fig. 5) whose postextrasystolic potentiation of the ventricular contractility produced a higher outflow acceleration and resulted in a more rapid SAM excursion rate, prolonging SAM-septal contact, and increasing midsystolic Doppler flow signal cessation and the ejection period. Hemodynamic studies12* 25~26 have shown that the majority of flow (at least 70 % ) is unusually rapid in patients with HCM and is completed earlier in systole than in normal individuals. These authors suggest that most of the stroke volume is in fact expelled before obstruction commences. “Outflow obstruction,” as traditionally defined by the presence of an abnormal intraventricular pressure gradient and SAM of the mitral valve, does not impede the left ventricular outflow in HCM.i2 In the present study, acceleration of the LVOT blood flow was significantly higher in the group with severe SAM than in the control and the other HCM groups. The available systolic ejection period, as determined from the Doppler waveform, tended to be longer in the group with severe SAM than in the others. Since the
300
400
500
600
END SAM (nw.c)
11. Correlation between the timing of the offset of SAM and the offset of Doppler (upper panel), and the end of SAM and the end of Doppler (lower panel) in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve.
Fig.
prolonged systolic ejection period and increased midsystolic Doppler flow signal cessation after the ectopic beat-indicating more severe obstruction-is observed in spite of increased blood flow ejection, it is likely that a certain amount of blood is in fact impeded in its ejection by the anterior motion of the mitral valve. The mechanism of maintaining anterior motion of the mitral valve in late systole when the aortic flow velocity is low or negligible is debatable.18 However, in our study a higher than normal blood flow velocity (B wave) appeared through the course of SAM-septal contact until it started to decelerate when the offset of SAM-septal contact began. The discrepancy of this result with those of others studies is possibly due to the different flow patterns of the aorta and the LVOT. The difference has been demonstrated by the low aortic flow velocity in mid and late systole compared with the high LVOT velocity waveform shown in mid to late systole.16, 2o It is not known whether the B wave takes part in maintaining the SAM-septal contact or not. Although the B wave velocity (121 cm/set) is higher than normal, it seems insufficient to produce a pressure drop by convective acceleration to maintain
the SAM-septal
contact. Nevertheless,
the
Volumb 122 Numbrr 6
Relation
between LVOT
Doppler
and SAM in HCM
1661
.
3000 r-0.666
pco.013
y = 266.40 + 65.765x
0 1 0
I 20
1 10 SAM REGRESSION
1 30
RATE (cmhc)
Fig. 12. Correlation between the left ventricular outflow deceleration and the regression rate of SAM in all 13 patients with SAM. SAM, Systolic anterior motion of the mitral valve.
B wave flow could possibly be present as a drag force to maintain SAM-septal contact until the blood velocity starts to decelerate. In all patients with SAM, the timing of the SAM resolution showed a correlation with Doppler events (Fig. 8) and the regression rate of SAM corresponded with the Doppler deceleration (r = 0.668, p < 0.013). These findings suggest a rapid decrease in the pressure drop, and the blood flow velocity produced mitral valve regression. The mechanism of SAM is still debatable, nor can our study make any conclusion; however, we offer some new findings to suggest that high left ventricular outflow acceleration in early systole may produce the Venturi effect and may result in mitral valve anterior motion. At mid-systole, the SAM-septal contact is maintained, either by the suction effect of continued pressure drop or by the drag force, resulting in left ventricular outflow obstruction. At late systole, the pressure drop and the blood flow deceleration produce mitral valve regression. REFERENCES
1. Wigle ED, Adelman AG, Silver MD. Pathophysiological
considerations in muscular subaortic stenosis. In: Wolstenholme GEW, O’Connor M, eds. Hypertrophic obstructive cardiomyopathy. CIBA Foundation Study Group No. 37. London: J & A Churchill, Ltd, 1971:63-76. 2. Henry WL, Clark CE, Gri5th JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructiveasymmetricseptalhypertrophy.Am JCardiol1975;35:337-
45. 3. Rodger JC. Motion of mitral apparatus in hvpertronhic
cardiomyopathy with obstruction. -Br Heart J 1976;3&732-7. 4. Kina JF. DeMaria AN. Reis RL. Bolton MR. Dunn MI. Mason DT. Echocardiographic assessment of idiopathic hypertrophic subaortic stenosis. Chest 1973;64:723-31. 5. Nagata S, Nimura Y, Beppu S, Park YD, Sakakibara H. Mechanism of systolic anterior motion of mitral valve and site of intraventricular pressure gradient in hypertrophic obstructive cardiomyopathy. Br Heart J 1983;49:234-43. ”
I
6. Shah PM, Taylor RD, Wong M. Abnormal mitral valve coaptation in hypertrophic obstructive cardiomyopathy: proposed role in systolic anterior motion of mitral valve. Am J Cardiol 1981;48:258-62. 7. Jiang L, Levine RA, King ME, Weyman AE. An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations. AM HEARTJ 1987;113:633-44. 8. Cape EG, Simons D, Jimoh A, Weyman AE, Yoganathan AP, Levine RA. Chordal geometry determines the shape and extent of systolic anterior mitral motion: in vitro studies. J Am Co11 Cardiol 1989;13:1438-48. 9. Kikami T, Hashimoto M, Kudo T, Sugawara T, Sakamoto S, Yasuda H. Mitral valve and its ring in hypertrophic cardiomyopathy, a mechanism creating surplus mitral leaflet involved in systolic anterior motion. Jpn Circ J 1988;52:597-603. 10. Moro E, TenCate FJ, Leonard JJ, Hugenholtz PG, Roelandt J. Genesis of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an anatomical or dynamic event? Eur Heart J 1987;8:1312-21. 11. Pollick C, Morgan CD, Gilbert BW, Rakowski H, Wigle ED. Muscular subaortic stenosis: the temporal relationship between systolic anterior motion of the anterior mitral leaflet and the pressure gradient. Circulation 1982;66:1087-94. 12. Murgo JP, Alter BR, Dorethy JF, Altobelli SA, McGranahan GM Jr, Dunne TE. Dynamics of left ventricular ejection in obstructive and nonobstructive hypertrophic cardiomyopathy. J Clin Invest 1980;66:1369-82. 13. Spirit0 P, Maron BJ. Patterns of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: assessment by two-dimensional echocardiography. Am J Cardiol 1984; 543039-46. 14. Maron BJ, Gottdiener JS, Arce J, Rosing DR, Wesley YE, Epstein SE. Dynamic subaortic obstruction in hypertrophic cardiomyopathy: analysis by pulsed Doppler echocardiography. J Am Co11 Cardiol 1985;6:1-15. 15. Gardin JM, Dabestani A, Glasgow GA, Butman S, Burn CS, Henry WL. Echocardiographic and Doppler flow observations in obstructed and nonobstructed hypertrophic cardiomyopathy. Am J Cardiol 1985;56:614-21. 16. Yock PG, Hatle L, Popp R. Patterns and timing of Dopplerdetected intracavitary and aortic flow in hypertrophic cardiomyopathy. J Am Co11 Cardiol 1986;8:1047-58. 17. Bryg RJ, Pearson AC, Williams GA, Labovitz AJ. Left ventricular systolic and diastolic flow abnormalities determined by Doppler echocardiography in obstructive hypertrophic cardiomyopathy. Am J Cardiol 1987;59:925-31. 18. Levine RA, Weyman AE. Dynamic subaortic obstruction in
1682
19.
20.
21.
22.
23.
24.
Lin et al. hypertrophic cardiomyopathy: criteria and controversy. J Ant Co11 Cardiol 1985;6:16-8. Gilbert BW, Pollick C, Adelman AG, Wigle ED. Hypertrophit cardiomyopathy: subclassification by M-mode echocardiography. Am J Cardiol 1980;45:861-72. Hatle L, Angelsen B. Pulsed and continuous wave Doppler II) diagnosis and assessment of various heart lesion. In: Hatle L. Angelsen B, eds. Doppler ultrasound in cardiology. 2nd ed. Philadelnhia: Lea & Febiger. 198520516. Kertes PJ, Darkin LM, Hunt D. Regional left ventricular Doppler velocity profiles in hypertrophic cardiomyopathy [Abstract]. Circulation 1987;76(suppl IV):IV-96. Pasipoularides A, Murgo JP, Miller JW, Craig WE. Nonobstructive left ventricular ejection pressure gradients in man Circ Res 1987;61:220-7. Pasipoularides A, Murgo JP, Bird JJ, Craig WE. Fluid dynamics of aortic stenosis: mechanisms for the presence of subvalvular pressure gradients. Am J Physiol 1984;H542-50. Siegel RJ, Criley JM. Comparison of ventricular emptying with and without a pressure gradient in patients with hypertrophic cardiomyopathy. Br Heart J 1985;53:283-91.
December 1991 American Heart Journal
25. Sugrue IlLI, McKenna WJ- Dickie S. Myers MJ, 1,avender .JI”. Oakley CM, Goodwin JF. Relation between left ventricular gradient and relative stroke volume ejected in early and late systole in hypertrophic cardiomyopathy; assessment with ra dionuclide cineangiography. Br Heart J 1984;52:602-9. ED, Barclay S.4, Davis AL, Mannering D, Mehta N. 26. Bennett Ascending aortic blood velocity and acceleration using Doppler ultrasound in the assessment of left ventricular function. Circ Res 1984;18:632-8. 27. Come PC, Bulkley BH, Goodman ZD, Hutchins GM, Pitt B, Fortuin NJ. Hypercontractile cardiac states simulating hypertrophic cardiomyopathy. Circulation 1977;55:901-8. MN. Seeal BL. Parrv WR. Svstolic anterior 28. Mintz GS. Kotler motion of the mitral valve in the absence of asymmetric septal hypertrophy. Circulation 1978;57:266-63. 29. Sakurai S. Tanaka H. Yoshimura H, Nakao S, Tahara M. Production of’ systolic anterior motion of the mitral valve in dogs. Circulation 1985;71:805-12.
