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Difference in the Diastolic Left Ventricular Wall Motion Velocities Between Aortic and Mitral Regurgitation by Pulsed Tissue Doppler Imaging
Difference in the Diastolic Left Ventricular Wall Motion Velocities Between Aortic and Mitral Regurgitation by Pulsed Tissue Doppler Imaging Miho Abe, MD, Takashi Oki, MD, Tomotsugu Tabata, MD, Arata Iuchi, MD, and Susumu Ito, MD, Tokushima, Japan
We evaluated the difference in the diastolic left ventricular (LV) wall motion velocity between chronic isolated aortic and mitral regurgitation (AR and MR, respectively) by recording subendocardial motion velocity patterns at the middle site of the LV posterior wall in the parasternal (along the short axis) and apical (along the long axis) long-axis views of the left ventricle with pulsed tissue Doppler imaging. We studied 33 patients with AR and 35 with MR, showing moderate to severe regurgitation, and 34 healthy controls (C). The enddiastolic LV dimension along the short axis was greater in the AR and MR groups than in the C group, and that along the long axis was greater in the AR group than in the MR and C groups. There were no significant differences in percent LV fractional shortening along the short axis among the 3 groups, whereas that along the long axis was significantly smaller in the AR group than in the MR and C groups. The peak early diastolic wall motion velocity (Ew) and the time to Ew from the
A ortic regurgitation (AR) and mitral regurgitation (MR) are characterized by left ventricular (LV) dilation caused by diastolic LV volume overload. However, because the regurgitant modes differ between the 2 disease conditions, changes in the LV shape and compensatory LV hypertrophic patterns are also different.1-9 Generally, AR has a tendency to cause ellipsoidal dilation of the LV cavity along the long axis, whereas MR leads to spherical dilation of the LV cavity along the short axis.1,3-7 On the other hand,
From The Second Department of Internal Medicine, School of Medicine, The University of Tokushima. Reprint requests: Takashi Oki, MD, The Second Department of Internal Medicine, School of Medicine, The University of Tokushima, 2-50 Kuramoto-cho, Tokushima 770-8503, Japan. Copyright © 1999 by the American Society of Echocardiography. 0894-7317/98/$8.00 + 0 27/1/94692
aortic component of the second heart sound (S2Ew) along the long axis were significantly lower and longer, respectively, in patients with AR than in the 2 other groups. The Ew and S2-Ew along both the short and long axes were significantly higher and shorter, respectively, in patients with MR than in the 2 other groups. The peak early diastolic velocity of the transmitral flow correlated positively with Ew along the short axis in all patients with AR and correlated positively with Ews along the long and short axes in all patients with MR. In conclusion, early diastolic LV filling was associated with expansion of the LV wall along the short axis but with decreased excursion along the long axis in patients with AR, whereas that in patients with MR was associated with expansion of the LV wall along both the long and short axes. Pulsed tissue Doppler imaging was useful for evaluation of diastolic LV function along the long and short axes in patients with diastolic LV volume overload. (J Am Soc Echocardiogr 1999;12:15-21.)
many studies have reported abnormalities in regional LV wall motion in both patients with AR and MR,4,6-9 and they have referred mainly to the systolic LV function. However, no detailed study exists on the difference in the diastolic LV function along the long and short axes.Taking advantage of the difference in the characteristics of Doppler signals between ventricular wall and blood flow, a tissue Doppler imaging method has recently been developed in which large Doppler signals obtained from the ventricular wall can be selectively displayed as a color or pulsed Doppler image by eliminating small Doppler signals produced by the blood flow.10-15 The purpose of our study was to evaluate the differences in diastolic LV dysfunction between patients with chronic AR and MR by measuring regional motion velocities of the LV wall along the long and short axes by pulsed tissue Doppler imaging. 15
16 Abe et al
Figure 1 Method for recording motion velocity patterns of the LV posterior wall by pulsed tissue Doppler imaging in the parasternal long-axis view of the LV (top, left) and apical long-axis view of the LV (top, right), and measurement of variables obtained from the wall motion velocity (bottom). Open circles indicate sample volumes. T, transducer; RV, right ventricle; LV, left ventricle; Ao, ascending aorta; LA, left atrium; Sw, systolic wave of the wall motion velocity; Ew, peak early diastolic wall motion velocity; Aw, peak atrial systolic wall motion velocity; S2-Ew, time interval from the aortic component of the second heart sound to the Ew; P-Aw, time interval from the onset of the electrocardiographic P wave to the Aw; ECG, electrocardiogram; PCG, phonocardiogram.
METHODS Study Population Of the 650 consecutive patients who underwent cardiac catheterization and coronary angiography for examination of the cardiac abnormalities at our institute between 1995 and 1997, 33 patients with chronic AR (age range 44 to 86 years, mean age 66 ± 12 years) and 35 patients with chronic MR (age range 35 to 85 years, mean age 65 ± 17 years), defined as greater than 3+ by Sellers’16 classification from left ventriculography, were selected. Patients with significant mitral or aortic stenosis, moderate to severe regurgitation or stenosis of other valves, New York Heart Association functional class III or more, or a history of congestive
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heart failure were excluded. Thirty-four age-matched healthy subjects (age range 38 to 82 years, mean age 60 ± 10 years) were selected as control subjects.These patients were examined with chest radiography, phonocardiography, routine echocardiography, and cardiac catheterization (including coronary angiography) for evaluation of chest pain, palpitations, dyspnea, or heart murmur on auscultation, but showed no evidence of significant organic cardiovascular disease. The underlying diseases in the patients with AR were of arteriosclerotic origin in 14 patients, aortic valve prolapse in 11 patients, annuloaortic ectasia in 5 patients, and aortic bicuspid valve in 3 patients.The underlying diseases in the patients with MR were mitral valve prolapse in 16 patients, ruptured chordae tendineae in 15 patients, and infective endocarditis in 4 patients. Diagnosis of these diseases had been made at least 6 months before this study.All patients were in sinus rhythm without first-degree atrioventricular block and were well compensated at rest. All patients were examined by serial echocardiography and cardiac catheterization including coronary angiography. No significant coronary stenoses were observed by coronary angiography, and no regional LV wall asynergy was detected by left ventriculography. Severity of the regurgitation was determined by aortography and left ventriculography in the AR and MR patients, respectively, according to the Sellers classification.16 LV ejection fraction was calculated by the biplane area-length method from left ventriculography data. The objective of the examinations was explained to each subject and informed consent was obtained.
M-mode Echocardiography M-mode LV echocardiograms were recorded from the parasternal approach, and the maximal left atrial dimension at end-systole, end-diastolic and end-systolic LV dimensions along the short axis (S-Dd and S-Ds, respectively), end-diastolic ventricular septal thickness (VSth), and enddiastolic LV posterior wall thickness (PWT) were measured. From the parameters obtained, the percent LV fractional shortening along the short axis (S-%FS) and the mean LV wall thickness (mLVth) were calculated with the following equations: S-%FS = [(S-Dd – S-Ds) / S-Dd] × 100 (%) mLVth = (VSth + PWT) / 2 (mm) On the M-mode LV echocardiograms recorded from the apical approach, the end-diastolic and end-systolic LV dimensions along the long axis (L-Dd and L-Ds, respectively) were measured, and the percent LV fractional shortening along the long axis (L-%FS) was calculated with the following equation:
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L-%FS = [(L-Dd – L-Ds) / L-Dd] × 100 (%) The ratio of the end-diastolic LV dimension along the long-to-short axis (L/S-Dd) was also calculated.
Transmitral Flow Velocity A sample volume was set at the mitral valve orifice in the long-axis view of the LV, or the 4-chamber view was recorded from the cardiac apex, and transmitral flow velocity patterns were recorded with a commercially available 2.5MHz probe (model SSA-380A,Toshiba Corporation,Tokyo, Japan). From the patterns obtained, the peak early diastolic velocity (E), peak atrial systolic velocity (A), and their ratio (A/E) were determined.
Pulsed Tissue Doppler Imaging In the parasternal and apical long-axis views of the LV, sample volumes were set at the endocardial portions of the middle sites of the LV posterior wall, and the wall motion velocities at each site were recorded by the pulsed Doppler method with a 3.75-MHz probe (Toshiba SSA-380A) (Figure 1, top). The spectral pulsed Doppler signal filters were adjusted to obtain a Nyquist limit of 30 and 40 cm/s to eliminate the signals produced by transmitral flow. To prevent the sample volume from falling outside the endocardial portion of the LV posterior wall during cardiac cycles, the sample volume was set to 5 mm × 8 mm. From the patterns obtained, the peak early diastolic wall motion velocity (Ew), the peak atrial systolic wall motion velocity (Aw), the time interval from the aortic component of the second heart sound to the peak of the Ew (S2-Ew), and the time interval from the onset of the electrocardiographic P wave to the peak of the Aw (P-Aw) were measured (Figure 1, bottom). The wall motion velocity patterns, electrocardiogram, and phonocardiogram were simultaneously recorded with a strip chart recorder at a paper speed of 100 mm/s.
Statistical Analysis Values are expressed as means ± SD. Mean values in different patient groups were compared by analyses of variance (ANOVA) and the Scheffé test. Linear regression coefficients were obtained to show the degree of correlation among variables. A P value less than .05 was considered statistically significant.
RESULTS Patient Characteristics No significant differences were found in the age, heart rate, and systolic blood pressure among the AR, MR, and C groups (Table 1).The diastolic blood pressure was significantly lower in the AR group than in
Abe et al 17
Table 1 Clinical, M-mode echocardiographic, and left ventriculographic variables Variable
Age (y) HR (bpm) SBP (mm Hg) DBP (mm Hg) mLVth (mm) LAD (cm) S-Dd (cm) S-FS (%) L-Dd (cm) L-FS (%) L/S-Dd EF (%)
C group (n = 34)
60 63 130 68 9.5 3.3 4.6 39 7.3 25 1.8 68
± ± ± ± ± ± ± ± ± ± ± ±
10 6 14 12 1.3 0.4 0.3 8 0.5 6 0.3 10
AR group (n = 33)
64 61 136 56 12 3.6 6.0 36 8.2 16 1.4 63
± ± ± ± ± ± ± ± ± ± ± ±
12 10 10 14‡ 3.0† 0.6 0.5‡ 7 1.2* 3‡ 0.1‡ 7
MR group (n = 35)
65 67 128 73 8.9 4.7 6.1 44 7.5 22 1.2 64
± ± ± ± ± ± ± ± ± ± ± ±
17 12 13 9¶ 0.9¶ 0.8‡¶ 0.5‡ 8*§ 0.8 6¶ 0.1‡ 7
C, Control; AR, aortic regurgitation; MR, mitral regurgitation; HR, heart rate; SBP, systolic blood pressure; DBP, diastolic blood pressure; mLVth, mean left ventricular wall thickness at end diastole; LAD, maximal left atrial dimension at end systole; S-Dd and L-Dd, end-diastolic left ventricular dimension along the short and long axes, respectively; S-Ds and L-Ds, endsystolic left ventricular dimension along the short and long axes, respectively; S-FS and L-FS, percent fractional shortening of the left ventricle along the short and long axes, respectively; L/S-Dd, ratio of the long-toshort axis end-diastolic left ventricular dimension; EF, left ventricular ejection fraction calculated from left ventriculography. *P < .05 vs C group. †P < .01 vs C group. ‡P < .0001 vs C group. §P < .05 vs AR group. P < .01 vs AR group. ¶P < .0001 vs AR group.
the 2 other groups.The mean LV wall thickness was significantly greater in the AR group than in the 2 other groups. The maximal left atrial dimension was significantly greater in the MR group than in the 2 other groups. The end-diastolic LV dimensions along both short and long axes in the AR group were significantly greater than those in the C group, and that along the long axis in the AR group was slightly greater than that in the MR group. On the other hand, end-diastolic LV dimension along the short axis in the MR group was significantly greater than that in the C group.The percent LV fractional shortening along the short axis was significantly greater in the MR group than in the 2 other groups, and that along the long axis in the AR group was significantly lower than that in the 2 other groups.The ratio of the end-diastolic LV dimension along the long-to-short axis was significantly lower in the MR and AR groups than in the C group, and it was significantly greater in the AR group than in the MR group. No significant difference was found in the LV ejection fraction among the 3 groups. Pulsed Doppler Echocardiographic Variables The E of the transmitral flow was significantly greater in the MR group than in the 2 other groups,
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18 Abe et al
Figure 2 Correlations between the transmitral flow and pulsed tissue Doppler imaging variables in patients with aortic regurgitation. S-Ew and L-Ew, peak early diastolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; E, peak early diastolic velocity of the transmitral flow; S-Aw and L-Aw, peak atrial systolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; A, peak atrial systolic velocity of the transmitral flow.
Table 2 Pulsed Doppler echocardiographic variables Variable
E (cm/s) A (cm/s) A/E
C group (n = 34)
AR group (n = 33)
MR group (n = 35)
65 ± 18 70 ± 18 1.3 ± 0.3
53 ± 16* 70 ± 16 1.6 ± 0.7
106 ± 20†‡ 80 ± 28 0.7 ± 0.3†‡
C, Control; AR, aortic regurgitation; MR, mitral regurgitation; E, peak early diastolic transmitral flow velocity; A, peak atrial systolic transmitral flow velocity. *P < .05 vs C group. †P < .0001 vs C group. ‡P < .0001 vs AR group.
and it was significantly lower in the AR group than in the C group (Table 2). However, no significant difference existed in the A of the transmitral flow among the 3 groups. The peak ratio of the atrial/early diastolic velocity was significantly lower in the MR group than in the 2 other groups. LV Posterior Wall Motion Velocity Variables The Ew along the short axis was significantly greater in the MR group than in the 2 other groups, but the difference between the AR and C groups was not significant (Table 3).The Ew along the long axis was significantly lower in the AR group than in the 2 other groups, and it was significantly greater in the MR
group than in the 2 other groups. The time interval from the aortic component of the S2 to Ew along the short axis was significantly shorter in the MR group than in the 2 other groups, but the difference between the AR and C groups was not significant. The time interval from the aortic component of the S2 to Ew along the long axis was significantly longer in the AR group than in the 2 other groups, and it was significantly shorter in the MR group than in the 2 other groups. The Aw along the short axis was significantly greater in the MR group than in the 2 other groups, but the difference between the AR and C groups was not significant. No significant difference was found in the Aw along the long axis among the 3 groups. No significant differences existed in the time interval from the onset of the electrocardiographic P wave to the Aw along both the short and long axes among the 3 groups. Relationships Between the Transmitral Flow and LV Wall Motion Velocities The E of the transmitral flow was positively correlated with the Ew along the short axis (y = 0.15x + 3.9, r = 0.54, P < .01) and long axis (y = 0.11x + 5.1, r = 0.51, P < .01) in the C group. In addition, the A of the
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Figure 3 Correlations between the transmitral flow and pulsed tissue Doppler imaging variables in patients with mitral regurgitation. S-Ew and L-Ew, peak early diastolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; E, peak early diastolic velocity of the transmitral flow; S-Aw and L-Aw, peak atrial systolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; A, peak atrial systolic velocity of the transmitral flow.
transmitral flow also was positively correlated with the Aw along the short axis (y = 0.09x + 1.7, r = 0.61, P < .001) and long axis (y = 0.08x + 4.2, r = 0.63, P < .001). In the AR group, the E of the transmitral flow was closely positively correlated with the Ew along the short axis, but was not significantly correlated with that along the long axis (Figure 2). On the other hand, the A of the transmitral flow was positively correlated with the Aw along both the short and long axes. In the MR group the E of the transmitral flow was roughly positively correlated with the Ew along both the short and long axes (Figure 3), and the A of the transmitral flow was positively correlated with the Aw along both the short and long axes.
DISCUSSION In patients with AR the LV is filled by regurgitant flow from the aorta and transmitral flow from the left atrium during diastole.Therefore the systolic LV work is overloaded because all blood volume in the LV cavity stored during diastole is ejected to the
Table 3 Left ventricular posterior wall motion velocity variables Variable
S-Ew (cm/s) L-Ew (cm/s) S-S2-Ew (ms) L-S2-Ew (ms) S-Aw (cm/s) L-Aw (cm/s) S-P-Aw (ms) L-P-Aw (ms)
C group (n = 34)
12.5 13.4 142 144 6.3 9.5 139 128
± ± ± ± ± ± ± ±
3.5 3.8 9 11 1.6 1.9 18 11
AR group (n = 33)
12.3 9.1 136 152 6.1 9.2 135 133
± ± ± ± ± ± ± ±
3.0 1.9‡ 20 35* 0.7 3.5 16 15
MR group (n = 35)
14.9 15.5 114 125 8.8 9.5 136 131
± ± ± ± ± ± ± ±
4.6†§ 4.7* 16†§ 18‡§ 2.7†§ 3.5 10 20
C, Control; AR, aortic regurgitation; MR, mitral regurgitation; S-Ew and L-Ew, peak early diastolic motion velocity of the left ventricular posterior wall along the short and long axes, respectively; S-S2-Ew and L-S2-Ew, time interval from the aortic component of the second heart sound to the Ew along the short and long axes, respectively; S-Aw and L-Aw, peak atrial systolic motion velocity of the LV posterior wall along the short and long axes, respectively; S-P-Aw and L-P-Aw, time interval from the onset of the electrocardiographic P wave to the Aw along the short and long axes, respectively. *P < .05 vs C group; †P < .01 vs C group. ‡P < .0001 vs C group. §P < .01 vs AR group; P < .0001 vs AR group.
aorta of the high-pressure system, resulting in LV dilation and compensatory LV hypertrophy. However,
20 Abe et al
although the LV is overloaded in patients with MR as in patients with AR, the flow to the LV is only from the left atrium during diastole, and the blood in the LV cavity is partially ejected to the left atrium of the low-pressure system during systole.8 Therefore the mode of abnormal LV shape caused by diastolic LV volume overload may be different between patients with AR and MR. Several studies have been conducted on the relationship between morphologic changes in the LV cavity and abnormal LV wall motion in patients with MR and AR.1-9 However, most of the studies were performed by invasive cardiac catheterization and examined the systolic LV function. In patients with AR, regional LV wall motion asynergy is sometimes found at the anterior septum, lateral wall, and the cardiac apex,4,6,9 because of morphologic changes in the LV cavity caused by diastolic volume overload, abnormalities in microvascular blood flow of the coronary artery, small myocardial lesions after rheumatic myocarditis, or metabolic abnormalities of the LV myocardium. Badke et al2 examined morphologic changes in the LV cavity by preparing a model of the LV volume overload. They reported that only the midcavity of the LV is dilated at the acute stage of the volume overload, and the cardiac apex becomes dilated at the chronic stage, resulting in a spherical shape rather than an ellipsoidal shape. Ross et al17 prepared a similar model and demonstrated that sarcomeres are morphologically altered in the LV myocardium. Okada et al3 and Ohi et al5 showed that the LV shape examined by echocardiography and cardiac catheterization is ellipsoidal in patients with AR and spherical in patients with MR. Tissue Doppler imaging, by which regional ventricular wall motion velocity can be measured, has recently been developed, and quantitative evaluation of the wall motion velocities in various heart diseases has become possible.10-15 This method is noninvasive, repeatable, and allows easy evaluation of LV systolic and diastolic function along the short and long axes.18 Several clinical studies have been conducted on diastolic LV function with this method. For example, studies have reported that this method is useful for detection of abnormalities in diastolic LV function along the long axis on the basis of analysis of mitral annular motion velocity.19,20 In addition, research has shown that abnormal LV relaxation can be accurately evaluated with the early diastolic LV wall motion velocity variables, such as Ew and S2 – Ew in our study, along the short axis; such evaluation includes patients with marked elevation of LV enddiastolic pressure.21 In our AR group the Ew along the long axis was
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significantly lower than in the C group, and the E of the transmitral flow was positively correlated with the Ew only along the short axis. However, the Aw, which is passively generated by an atrial kick, was more closely correlated with the A of the transmitral flow along the short axis than along the long axis. Hiro et al6 reported that percent LV fractional shortening along the long axis by left ventriculography is slightly decreased in patients with AR, agreeing with the morphologic characteristics of the LV cavity in the autopsied AR heart reported by Okada et al.3 Gould et al22 found that end-diastolic LV wall stress is greater in the meridional direction than in the circumferential direction in patients with AR.Therefore impaired diastolic LV function in patients with AR is likely to be more severe along the long axis than along the short axis, suggesting that LV dilation during diastole depends on the expansion of LV myocardium along the short axis. On the other hand, the Ew in the MR group was greater than that in the 2 other groups along both the long and short axes. Hiro et al6 and Osbacken et al8 reported that hyperdynamic LV wall motion is commonly observed along the short axis rather than along the long axis during the compensatory stage in patients with MR. However, other studies emphasized that the LV cavity becomes spherical shape in patients with MR, and therefore LV wall motion along the long and short axes contributes to LV filling.3,6 In fact, there were significant positive correlations between early diastolic and atrial systolic variables obtained from the transmitral flow velocity and LV posterior wall motion velocity along both the long and short axes in our subjects with MR. Study Limitations Despite the advantages of evaluating diastolic LV function by tissue Doppler imaging, our analyses still have some limitations. First, we measured the motion velocity only at the endocardial portions of the LV wall and therefore could not calculate the transmyocardial velocity gradient. Consequently, diseaseassociated influences on the motion of the whole heart cannot be ruled out.13,15 However, the motion velocity at the endocardial portion generally is significantly higher than that at the epicardial portion. Furthermore, the goal of our study was not to obtain absolute values of the various parameters in patients with different conditions, but to assess the differences in the parameters derived from pulsed tissue Doppler imaging among the patient groups and the C group.Therefore in this study the determination of the motion velocity only at the endocardial portions has no clinical impact.
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Second, since regional LV wall motion velocity is measured by the above method, evaluation of global LV function with the variable of only the LV posterior wall is not appropriate in patients with regional LV asynergy. In patients with AR, direction of regurgitant jet is considered to affect LV wall motion. In this study, however, patients with markedly deviated regurgitant jet had been excluded, and regurgitant jet had reached the region near the cardiac apex beyond the papillary muscles in most patients. Third, tissue Doppler imaging has intrinsic technical limitations. As in routine echocardiographic examination, it cannot accurately reflect wall motion velocity if the direction of the beam is parallel to the wall motion (eg, for the upper medial and upper lateral walls).We measured wall motion velocity at the middle site of the LV posterior wall that is perpendicular to the beam in both the parasternal and apical 2-dimensional long-axis views of the LV. Because motion velocity in the ventricular septum is easily affected by motion of the whole heart or the right ventricle, and therefore the velocity measured by the parasternal approach is low, it is often difficult to evaluate accurately the wall motion characteristics of the ventricular septum.
Abe et al 21
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normal volumes and function in chronic aortic regurgitation by quantitative shape analysis—an early maker of left ventricular decompensation [abstract]. J Am Coll Cardiol 1997;29 (Suppl):26A. Osbacken MD, Bove AA, Spann JF. Left ventricular regional wall motion and velocity of shortening in chronic mitral and aortic regurgitation. Am J Cardiol 1981;47:1005-9. Jhonson AD, Alpert JS, Francis GS, Vieweg VR, Ockene I, Hagan AD. Assessment of left ventricular function in severe aortic regurgitation. Circulation 1976;54:975-9. Sutherland GR, Stewart MJ, Groundestroem KWE, Moran CM, Fleming A, Guell-Peris FJ, et al. Color Doppler myocardial imaging: a new technique for the assessment of myocardial function. J Am Soc Echocardiogr 1994;7:441-58. McDicken WM, Sutherland GR, Moram CM, Gordon LN. Color Doppler velocity imaging of the myocardium. Ultrasound Med Biol 1992;18:651-4. Fleming AD, McDicken WM, Sutherland GR, Hokins PR. Assessment of color Doppler tissue imaging using test-phantoms. Ultrasound Med Biol 1994;20:937-51. Miyatake K, Yamagishi M, Tanaka N, Uematsu A, Yamazaki N, Mine Y, et al. New method for evaluating left ventricular wall motion by color-coded tissue Doppler imaging in vitro and in vivo studies. J Am Coll Cardiol 1995;25:717-24. Palka P, Lange A, Fleming AD, Sutherland GR, Fenn LN, McDicken WN. Doppler tissue imaging myocardial wall motion velocities in normal subjects. J Am Soc Echocardiogr 1995;8:659-68. Donovan CL, Armstrong WF, Bach DS. Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects. Am Heart J 1995;130:100-4. Sellers RD, Levy MJ, Anplatz K, Lellenhei CW. Retrograde angiography in acquired cardiac disease technique indication and interpretation of 700 cases. Am J Cardiol 1964;14:43751. Ross J Jr, Sonnenblick EH, Tayar RR, Spotnits HM, Covell JW. Diastolic geometry and sarcomere lengths in the chronically dilated canine left ventricle. Circ Res 1971;28:49-61. Oki T, Tabata T, Yamada H, Wakatsuki T, Mishiro Y, Abe M, et al. Left ventricular diastolic properties of hypertensive patients measured by pulsed tissue Doppler imaging. J Am Soc Echocardiogr 1998;11:1106-12. Gulati VK, Katz WE, Follansbee WP, Gorcsan J III. Mitral annular descent velocity by tissue Doppler echocardiography as an index of global left ventricular function. Am J Cardiol 1996;77:979-84. Rodriguez L, Garcia M, Ares M, Griffin BP, Nakatani S, Thomas JD. Assessment of mitral annular dynamic during diastole by Doppler tissue imaging: comparison with mitral Doppler inflow in subjects without heart disease and in patients with left ventricular hypertrophy. Am Heart J 1996; 131:982-7. Oki T, Tabata T, Yamada H, Wakatsuki T, Shinohara H, Nishikado A, et al. Clinical application of pulsed Doppler tissue imaging for assessing abnormal left ventricular relaxation. Am J Cardiol 1997;79:921-8. Gould LK, Lipscomb K, Hamilton GW, Kennedy JW. Relation of left ventricular shape, function and wall stress in man. Am J Cardiol 1974;34:627-34.
We evaluated the difference in the diastolic left ventricular (LV) wall motion velocity between chronic isolated aortic and mitral regurgitation (AR and MR, respectively) by recording subendocardial motion velocity patterns at the middle site of the LV posterior wall in the parasternal (along the short axis) and apical (along the long axis) long-axis views of the left ventricle with pulsed tissue Doppler imaging. We studied 33 patients with AR and 35 with MR, showing moderate to severe regurgitation, and 34 healthy controls (C). The enddiastolic LV dimension along the short axis was greater in the AR and MR groups than in the C group, and that along the long axis was greater in the AR group than in the MR and C groups. There were no significant differences in percent LV fractional shortening along the short axis among the 3 groups, whereas that along the long axis was significantly smaller in the AR group than in the MR and C groups. The peak early diastolic wall motion velocity (Ew) and the time to Ew from the
A ortic regurgitation (AR) and mitral regurgitation (MR) are characterized by left ventricular (LV) dilation caused by diastolic LV volume overload. However, because the regurgitant modes differ between the 2 disease conditions, changes in the LV shape and compensatory LV hypertrophic patterns are also different.1-9 Generally, AR has a tendency to cause ellipsoidal dilation of the LV cavity along the long axis, whereas MR leads to spherical dilation of the LV cavity along the short axis.1,3-7 On the other hand,
From The Second Department of Internal Medicine, School of Medicine, The University of Tokushima. Reprint requests: Takashi Oki, MD, The Second Department of Internal Medicine, School of Medicine, The University of Tokushima, 2-50 Kuramoto-cho, Tokushima 770-8503, Japan. Copyright © 1999 by the American Society of Echocardiography. 0894-7317/98/$8.00 + 0 27/1/94692
aortic component of the second heart sound (S2Ew) along the long axis were significantly lower and longer, respectively, in patients with AR than in the 2 other groups. The Ew and S2-Ew along both the short and long axes were significantly higher and shorter, respectively, in patients with MR than in the 2 other groups. The peak early diastolic velocity of the transmitral flow correlated positively with Ew along the short axis in all patients with AR and correlated positively with Ews along the long and short axes in all patients with MR. In conclusion, early diastolic LV filling was associated with expansion of the LV wall along the short axis but with decreased excursion along the long axis in patients with AR, whereas that in patients with MR was associated with expansion of the LV wall along both the long and short axes. Pulsed tissue Doppler imaging was useful for evaluation of diastolic LV function along the long and short axes in patients with diastolic LV volume overload. (J Am Soc Echocardiogr 1999;12:15-21.)
many studies have reported abnormalities in regional LV wall motion in both patients with AR and MR,4,6-9 and they have referred mainly to the systolic LV function. However, no detailed study exists on the difference in the diastolic LV function along the long and short axes.Taking advantage of the difference in the characteristics of Doppler signals between ventricular wall and blood flow, a tissue Doppler imaging method has recently been developed in which large Doppler signals obtained from the ventricular wall can be selectively displayed as a color or pulsed Doppler image by eliminating small Doppler signals produced by the blood flow.10-15 The purpose of our study was to evaluate the differences in diastolic LV dysfunction between patients with chronic AR and MR by measuring regional motion velocities of the LV wall along the long and short axes by pulsed tissue Doppler imaging. 15
16 Abe et al
Figure 1 Method for recording motion velocity patterns of the LV posterior wall by pulsed tissue Doppler imaging in the parasternal long-axis view of the LV (top, left) and apical long-axis view of the LV (top, right), and measurement of variables obtained from the wall motion velocity (bottom). Open circles indicate sample volumes. T, transducer; RV, right ventricle; LV, left ventricle; Ao, ascending aorta; LA, left atrium; Sw, systolic wave of the wall motion velocity; Ew, peak early diastolic wall motion velocity; Aw, peak atrial systolic wall motion velocity; S2-Ew, time interval from the aortic component of the second heart sound to the Ew; P-Aw, time interval from the onset of the electrocardiographic P wave to the Aw; ECG, electrocardiogram; PCG, phonocardiogram.
METHODS Study Population Of the 650 consecutive patients who underwent cardiac catheterization and coronary angiography for examination of the cardiac abnormalities at our institute between 1995 and 1997, 33 patients with chronic AR (age range 44 to 86 years, mean age 66 ± 12 years) and 35 patients with chronic MR (age range 35 to 85 years, mean age 65 ± 17 years), defined as greater than 3+ by Sellers’16 classification from left ventriculography, were selected. Patients with significant mitral or aortic stenosis, moderate to severe regurgitation or stenosis of other valves, New York Heart Association functional class III or more, or a history of congestive
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heart failure were excluded. Thirty-four age-matched healthy subjects (age range 38 to 82 years, mean age 60 ± 10 years) were selected as control subjects.These patients were examined with chest radiography, phonocardiography, routine echocardiography, and cardiac catheterization (including coronary angiography) for evaluation of chest pain, palpitations, dyspnea, or heart murmur on auscultation, but showed no evidence of significant organic cardiovascular disease. The underlying diseases in the patients with AR were of arteriosclerotic origin in 14 patients, aortic valve prolapse in 11 patients, annuloaortic ectasia in 5 patients, and aortic bicuspid valve in 3 patients.The underlying diseases in the patients with MR were mitral valve prolapse in 16 patients, ruptured chordae tendineae in 15 patients, and infective endocarditis in 4 patients. Diagnosis of these diseases had been made at least 6 months before this study.All patients were in sinus rhythm without first-degree atrioventricular block and were well compensated at rest. All patients were examined by serial echocardiography and cardiac catheterization including coronary angiography. No significant coronary stenoses were observed by coronary angiography, and no regional LV wall asynergy was detected by left ventriculography. Severity of the regurgitation was determined by aortography and left ventriculography in the AR and MR patients, respectively, according to the Sellers classification.16 LV ejection fraction was calculated by the biplane area-length method from left ventriculography data. The objective of the examinations was explained to each subject and informed consent was obtained.
M-mode Echocardiography M-mode LV echocardiograms were recorded from the parasternal approach, and the maximal left atrial dimension at end-systole, end-diastolic and end-systolic LV dimensions along the short axis (S-Dd and S-Ds, respectively), end-diastolic ventricular septal thickness (VSth), and enddiastolic LV posterior wall thickness (PWT) were measured. From the parameters obtained, the percent LV fractional shortening along the short axis (S-%FS) and the mean LV wall thickness (mLVth) were calculated with the following equations: S-%FS = [(S-Dd – S-Ds) / S-Dd] × 100 (%) mLVth = (VSth + PWT) / 2 (mm) On the M-mode LV echocardiograms recorded from the apical approach, the end-diastolic and end-systolic LV dimensions along the long axis (L-Dd and L-Ds, respectively) were measured, and the percent LV fractional shortening along the long axis (L-%FS) was calculated with the following equation:
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L-%FS = [(L-Dd – L-Ds) / L-Dd] × 100 (%) The ratio of the end-diastolic LV dimension along the long-to-short axis (L/S-Dd) was also calculated.
Transmitral Flow Velocity A sample volume was set at the mitral valve orifice in the long-axis view of the LV, or the 4-chamber view was recorded from the cardiac apex, and transmitral flow velocity patterns were recorded with a commercially available 2.5MHz probe (model SSA-380A,Toshiba Corporation,Tokyo, Japan). From the patterns obtained, the peak early diastolic velocity (E), peak atrial systolic velocity (A), and their ratio (A/E) were determined.
Pulsed Tissue Doppler Imaging In the parasternal and apical long-axis views of the LV, sample volumes were set at the endocardial portions of the middle sites of the LV posterior wall, and the wall motion velocities at each site were recorded by the pulsed Doppler method with a 3.75-MHz probe (Toshiba SSA-380A) (Figure 1, top). The spectral pulsed Doppler signal filters were adjusted to obtain a Nyquist limit of 30 and 40 cm/s to eliminate the signals produced by transmitral flow. To prevent the sample volume from falling outside the endocardial portion of the LV posterior wall during cardiac cycles, the sample volume was set to 5 mm × 8 mm. From the patterns obtained, the peak early diastolic wall motion velocity (Ew), the peak atrial systolic wall motion velocity (Aw), the time interval from the aortic component of the second heart sound to the peak of the Ew (S2-Ew), and the time interval from the onset of the electrocardiographic P wave to the peak of the Aw (P-Aw) were measured (Figure 1, bottom). The wall motion velocity patterns, electrocardiogram, and phonocardiogram were simultaneously recorded with a strip chart recorder at a paper speed of 100 mm/s.
Statistical Analysis Values are expressed as means ± SD. Mean values in different patient groups were compared by analyses of variance (ANOVA) and the Scheffé test. Linear regression coefficients were obtained to show the degree of correlation among variables. A P value less than .05 was considered statistically significant.
RESULTS Patient Characteristics No significant differences were found in the age, heart rate, and systolic blood pressure among the AR, MR, and C groups (Table 1).The diastolic blood pressure was significantly lower in the AR group than in
Abe et al 17
Table 1 Clinical, M-mode echocardiographic, and left ventriculographic variables Variable
Age (y) HR (bpm) SBP (mm Hg) DBP (mm Hg) mLVth (mm) LAD (cm) S-Dd (cm) S-FS (%) L-Dd (cm) L-FS (%) L/S-Dd EF (%)
C group (n = 34)
60 63 130 68 9.5 3.3 4.6 39 7.3 25 1.8 68
± ± ± ± ± ± ± ± ± ± ± ±
10 6 14 12 1.3 0.4 0.3 8 0.5 6 0.3 10
AR group (n = 33)
64 61 136 56 12 3.6 6.0 36 8.2 16 1.4 63
± ± ± ± ± ± ± ± ± ± ± ±
12 10 10 14‡ 3.0† 0.6 0.5‡ 7 1.2* 3‡ 0.1‡ 7
MR group (n = 35)
65 67 128 73 8.9 4.7 6.1 44 7.5 22 1.2 64
± ± ± ± ± ± ± ± ± ± ± ±
17 12 13 9¶ 0.9¶ 0.8‡¶ 0.5‡ 8*§ 0.8 6¶ 0.1‡ 7
C, Control; AR, aortic regurgitation; MR, mitral regurgitation; HR, heart rate; SBP, systolic blood pressure; DBP, diastolic blood pressure; mLVth, mean left ventricular wall thickness at end diastole; LAD, maximal left atrial dimension at end systole; S-Dd and L-Dd, end-diastolic left ventricular dimension along the short and long axes, respectively; S-Ds and L-Ds, endsystolic left ventricular dimension along the short and long axes, respectively; S-FS and L-FS, percent fractional shortening of the left ventricle along the short and long axes, respectively; L/S-Dd, ratio of the long-toshort axis end-diastolic left ventricular dimension; EF, left ventricular ejection fraction calculated from left ventriculography. *P < .05 vs C group. †P < .01 vs C group. ‡P < .0001 vs C group. §P < .05 vs AR group. P < .01 vs AR group. ¶P < .0001 vs AR group.
the 2 other groups.The mean LV wall thickness was significantly greater in the AR group than in the 2 other groups. The maximal left atrial dimension was significantly greater in the MR group than in the 2 other groups. The end-diastolic LV dimensions along both short and long axes in the AR group were significantly greater than those in the C group, and that along the long axis in the AR group was slightly greater than that in the MR group. On the other hand, end-diastolic LV dimension along the short axis in the MR group was significantly greater than that in the C group.The percent LV fractional shortening along the short axis was significantly greater in the MR group than in the 2 other groups, and that along the long axis in the AR group was significantly lower than that in the 2 other groups.The ratio of the end-diastolic LV dimension along the long-to-short axis was significantly lower in the MR and AR groups than in the C group, and it was significantly greater in the AR group than in the MR group. No significant difference was found in the LV ejection fraction among the 3 groups. Pulsed Doppler Echocardiographic Variables The E of the transmitral flow was significantly greater in the MR group than in the 2 other groups,
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18 Abe et al
Figure 2 Correlations between the transmitral flow and pulsed tissue Doppler imaging variables in patients with aortic regurgitation. S-Ew and L-Ew, peak early diastolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; E, peak early diastolic velocity of the transmitral flow; S-Aw and L-Aw, peak atrial systolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; A, peak atrial systolic velocity of the transmitral flow.
Table 2 Pulsed Doppler echocardiographic variables Variable
E (cm/s) A (cm/s) A/E
C group (n = 34)
AR group (n = 33)
MR group (n = 35)
65 ± 18 70 ± 18 1.3 ± 0.3
53 ± 16* 70 ± 16 1.6 ± 0.7
106 ± 20†‡ 80 ± 28 0.7 ± 0.3†‡
C, Control; AR, aortic regurgitation; MR, mitral regurgitation; E, peak early diastolic transmitral flow velocity; A, peak atrial systolic transmitral flow velocity. *P < .05 vs C group. †P < .0001 vs C group. ‡P < .0001 vs AR group.
and it was significantly lower in the AR group than in the C group (Table 2). However, no significant difference existed in the A of the transmitral flow among the 3 groups. The peak ratio of the atrial/early diastolic velocity was significantly lower in the MR group than in the 2 other groups. LV Posterior Wall Motion Velocity Variables The Ew along the short axis was significantly greater in the MR group than in the 2 other groups, but the difference between the AR and C groups was not significant (Table 3).The Ew along the long axis was significantly lower in the AR group than in the 2 other groups, and it was significantly greater in the MR
group than in the 2 other groups. The time interval from the aortic component of the S2 to Ew along the short axis was significantly shorter in the MR group than in the 2 other groups, but the difference between the AR and C groups was not significant. The time interval from the aortic component of the S2 to Ew along the long axis was significantly longer in the AR group than in the 2 other groups, and it was significantly shorter in the MR group than in the 2 other groups. The Aw along the short axis was significantly greater in the MR group than in the 2 other groups, but the difference between the AR and C groups was not significant. No significant difference was found in the Aw along the long axis among the 3 groups. No significant differences existed in the time interval from the onset of the electrocardiographic P wave to the Aw along both the short and long axes among the 3 groups. Relationships Between the Transmitral Flow and LV Wall Motion Velocities The E of the transmitral flow was positively correlated with the Ew along the short axis (y = 0.15x + 3.9, r = 0.54, P < .01) and long axis (y = 0.11x + 5.1, r = 0.51, P < .01) in the C group. In addition, the A of the
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Abe et al 19
Figure 3 Correlations between the transmitral flow and pulsed tissue Doppler imaging variables in patients with mitral regurgitation. S-Ew and L-Ew, peak early diastolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; E, peak early diastolic velocity of the transmitral flow; S-Aw and L-Aw, peak atrial systolic motion velocity of the left ventricular posterior wall along the short and long axis, respectively; A, peak atrial systolic velocity of the transmitral flow.
transmitral flow also was positively correlated with the Aw along the short axis (y = 0.09x + 1.7, r = 0.61, P < .001) and long axis (y = 0.08x + 4.2, r = 0.63, P < .001). In the AR group, the E of the transmitral flow was closely positively correlated with the Ew along the short axis, but was not significantly correlated with that along the long axis (Figure 2). On the other hand, the A of the transmitral flow was positively correlated with the Aw along both the short and long axes. In the MR group the E of the transmitral flow was roughly positively correlated with the Ew along both the short and long axes (Figure 3), and the A of the transmitral flow was positively correlated with the Aw along both the short and long axes.
DISCUSSION In patients with AR the LV is filled by regurgitant flow from the aorta and transmitral flow from the left atrium during diastole.Therefore the systolic LV work is overloaded because all blood volume in the LV cavity stored during diastole is ejected to the
Table 3 Left ventricular posterior wall motion velocity variables Variable
S-Ew (cm/s) L-Ew (cm/s) S-S2-Ew (ms) L-S2-Ew (ms) S-Aw (cm/s) L-Aw (cm/s) S-P-Aw (ms) L-P-Aw (ms)
C group (n = 34)
12.5 13.4 142 144 6.3 9.5 139 128
± ± ± ± ± ± ± ±
3.5 3.8 9 11 1.6 1.9 18 11
AR group (n = 33)
12.3 9.1 136 152 6.1 9.2 135 133
± ± ± ± ± ± ± ±
3.0 1.9‡ 20 35* 0.7 3.5 16 15
MR group (n = 35)
14.9 15.5 114 125 8.8 9.5 136 131
± ± ± ± ± ± ± ±
4.6†§ 4.7* 16†§ 18‡§ 2.7†§ 3.5 10 20
C, Control; AR, aortic regurgitation; MR, mitral regurgitation; S-Ew and L-Ew, peak early diastolic motion velocity of the left ventricular posterior wall along the short and long axes, respectively; S-S2-Ew and L-S2-Ew, time interval from the aortic component of the second heart sound to the Ew along the short and long axes, respectively; S-Aw and L-Aw, peak atrial systolic motion velocity of the LV posterior wall along the short and long axes, respectively; S-P-Aw and L-P-Aw, time interval from the onset of the electrocardiographic P wave to the Aw along the short and long axes, respectively. *P < .05 vs C group; †P < .01 vs C group. ‡P < .0001 vs C group. §P < .01 vs AR group; P < .0001 vs AR group.
aorta of the high-pressure system, resulting in LV dilation and compensatory LV hypertrophy. However,
20 Abe et al
although the LV is overloaded in patients with MR as in patients with AR, the flow to the LV is only from the left atrium during diastole, and the blood in the LV cavity is partially ejected to the left atrium of the low-pressure system during systole.8 Therefore the mode of abnormal LV shape caused by diastolic LV volume overload may be different between patients with AR and MR. Several studies have been conducted on the relationship between morphologic changes in the LV cavity and abnormal LV wall motion in patients with MR and AR.1-9 However, most of the studies were performed by invasive cardiac catheterization and examined the systolic LV function. In patients with AR, regional LV wall motion asynergy is sometimes found at the anterior septum, lateral wall, and the cardiac apex,4,6,9 because of morphologic changes in the LV cavity caused by diastolic volume overload, abnormalities in microvascular blood flow of the coronary artery, small myocardial lesions after rheumatic myocarditis, or metabolic abnormalities of the LV myocardium. Badke et al2 examined morphologic changes in the LV cavity by preparing a model of the LV volume overload. They reported that only the midcavity of the LV is dilated at the acute stage of the volume overload, and the cardiac apex becomes dilated at the chronic stage, resulting in a spherical shape rather than an ellipsoidal shape. Ross et al17 prepared a similar model and demonstrated that sarcomeres are morphologically altered in the LV myocardium. Okada et al3 and Ohi et al5 showed that the LV shape examined by echocardiography and cardiac catheterization is ellipsoidal in patients with AR and spherical in patients with MR. Tissue Doppler imaging, by which regional ventricular wall motion velocity can be measured, has recently been developed, and quantitative evaluation of the wall motion velocities in various heart diseases has become possible.10-15 This method is noninvasive, repeatable, and allows easy evaluation of LV systolic and diastolic function along the short and long axes.18 Several clinical studies have been conducted on diastolic LV function with this method. For example, studies have reported that this method is useful for detection of abnormalities in diastolic LV function along the long axis on the basis of analysis of mitral annular motion velocity.19,20 In addition, research has shown that abnormal LV relaxation can be accurately evaluated with the early diastolic LV wall motion velocity variables, such as Ew and S2 – Ew in our study, along the short axis; such evaluation includes patients with marked elevation of LV enddiastolic pressure.21 In our AR group the Ew along the long axis was
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significantly lower than in the C group, and the E of the transmitral flow was positively correlated with the Ew only along the short axis. However, the Aw, which is passively generated by an atrial kick, was more closely correlated with the A of the transmitral flow along the short axis than along the long axis. Hiro et al6 reported that percent LV fractional shortening along the long axis by left ventriculography is slightly decreased in patients with AR, agreeing with the morphologic characteristics of the LV cavity in the autopsied AR heart reported by Okada et al.3 Gould et al22 found that end-diastolic LV wall stress is greater in the meridional direction than in the circumferential direction in patients with AR.Therefore impaired diastolic LV function in patients with AR is likely to be more severe along the long axis than along the short axis, suggesting that LV dilation during diastole depends on the expansion of LV myocardium along the short axis. On the other hand, the Ew in the MR group was greater than that in the 2 other groups along both the long and short axes. Hiro et al6 and Osbacken et al8 reported that hyperdynamic LV wall motion is commonly observed along the short axis rather than along the long axis during the compensatory stage in patients with MR. However, other studies emphasized that the LV cavity becomes spherical shape in patients with MR, and therefore LV wall motion along the long and short axes contributes to LV filling.3,6 In fact, there were significant positive correlations between early diastolic and atrial systolic variables obtained from the transmitral flow velocity and LV posterior wall motion velocity along both the long and short axes in our subjects with MR. Study Limitations Despite the advantages of evaluating diastolic LV function by tissue Doppler imaging, our analyses still have some limitations. First, we measured the motion velocity only at the endocardial portions of the LV wall and therefore could not calculate the transmyocardial velocity gradient. Consequently, diseaseassociated influences on the motion of the whole heart cannot be ruled out.13,15 However, the motion velocity at the endocardial portion generally is significantly higher than that at the epicardial portion. Furthermore, the goal of our study was not to obtain absolute values of the various parameters in patients with different conditions, but to assess the differences in the parameters derived from pulsed tissue Doppler imaging among the patient groups and the C group.Therefore in this study the determination of the motion velocity only at the endocardial portions has no clinical impact.
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Second, since regional LV wall motion velocity is measured by the above method, evaluation of global LV function with the variable of only the LV posterior wall is not appropriate in patients with regional LV asynergy. In patients with AR, direction of regurgitant jet is considered to affect LV wall motion. In this study, however, patients with markedly deviated regurgitant jet had been excluded, and regurgitant jet had reached the region near the cardiac apex beyond the papillary muscles in most patients. Third, tissue Doppler imaging has intrinsic technical limitations. As in routine echocardiographic examination, it cannot accurately reflect wall motion velocity if the direction of the beam is parallel to the wall motion (eg, for the upper medial and upper lateral walls).We measured wall motion velocity at the middle site of the LV posterior wall that is perpendicular to the beam in both the parasternal and apical 2-dimensional long-axis views of the LV. Because motion velocity in the ventricular septum is easily affected by motion of the whole heart or the right ventricle, and therefore the velocity measured by the parasternal approach is low, it is often difficult to evaluate accurately the wall motion characteristics of the ventricular septum.
Abe et al 21
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