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Progressive intraventricular drop of early diastolic flow velocity reflects impaired active ventricular diastolic function in hypertensive heart disease: Comparative study between early diastolic and atrial contraction phases
Progressive Intraventricular Drop of Early Diastolic Flow Velocity Reflects Impaired Active Ventricular Diastolic Function in Hypertensive Heart Disease: Comparative Study Between Early Diastolic and Atrial Contraction Phases Kazuhiro Yanaamoto, MDr Tohru Masuyama, MD, Yasuji Doi, MD, Hiroya Kondo, MD, Johji Naito, MD, Toshiaki Mano, MD, Reiko Nagano, MD, Masatsugu Hori, MD, and Takenobu Kamada, MD, Suita, Japan
Left ventricular (LV) diastolic function in the early diastolic phase includes both active and passive processes, but in the atrial contraction phase it includes only passive processes. To elucidate the relation between the intraventricular dispersion of the flow velocity in diastole and LV diastolic process, 31 normal volunteers and 12 patients with hypertensive heart disease were studied. In these subjects the flow velocity pattern at the mitral tip was recorded simultaneously with regional flow velocity patterns 1, 2, or 3 cm from the mitral tip toward the apex, respectively, with multigate pulsed Doppler echocardiography from the apical long-axis view with the guidance of Doppler color-
flow imaging. Although the ratio of regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase decreased from the mitral tip to the apex to the same degree in the normal vohmteers and patients with hypertensive heart disease, there was a significant difference in the intraventricular dispersion of the early diastolic flow velocity between the two groups. These results suggest that the progressive intraventricular drop of the flow velocity in the early diastolic phase in patients with hypertensive heart disease may reflect the impairment of active rather than passive LV diastolic function. (J AM SOC ECHOCARDIOGR1995;8:654-8.)
W e recently showed that early diastolic flow velocity drops more largely from the mitral tip toward the apex in the left vcntricle in patients with left ventricular (LV) diastolic dysfunction than in normal subjects, irrespective o f the flow velocity pattern at the mitral t i p ) LV diastolic function in the early diastolic phase includes both active and passive processes. 2 The active process o f LV diastolic function is influenced by LV relaxation and LV elastic recoil, and the passive process is influenced by LV compliance. Thus it is not clear from the results of our previous study
which process the intraventricular dispersion o f the early diastolic flow velocity reflects. In contrast to the early diastolic phase, LV diastolic function in the atrial contraction phase includes only passive processes. 2 From this point o f view, we analyzed the intraventricular dispersion o f the flow velocity in the early diastolic and atrial contraction phases to elucidate the relation between the intraventricular dispersion of the flow velocity in diastole and the LV diastolic process.
From the First Department of Medicine, Osaka UniversitySchool of Medicine. Supported in part by research grants from the Ministry of Health and Welfare of Japan and Research Fellowships of the Japanese Society for the Promotion of Science for Young Scientists. ~Research Fellow of the Japanese Society for the Promotion of Science. Reprint requests: Tohru Masuyama,MD, the First Department of Medicine, Osaka UniversitySchool of Medicine, 2-2 Yamadaoka, Suita 565, Japan. Copyright 9 1995 by the American Societyof Echocardiography. 0894-7317/95 $5.00 + 0 27/4/62187 654
METHODS
This study conforms to the guiding principles of the institutional Ethics Committee of Osaka University School of Medicine on Human Research. All patients gave informed consent for participation in this study protocol. The study population consisted of 31 normal volunteers (mean age 52 + 11 years; range 25 to 70 years) and 12 patients with hypertensive heart disease (mean age 53 _+13 years; range 31 to 68 years) who had presumed LV diastolic dysfunction but normal systolic function. All the normal volunteers had no cardiac complaint, negative car-
Journal of the American Society of Echocardiography Volume 8 Number 5, Part 1
diovascular history, and normal blood pressures. There were no electrocardiographic or echocardiographic abnormalities in any of the volunteers. On the other hand, all the patients had systemic arterial hypertension as a pathologic condition known to cause LV hypertrophy. In all the patients, wall thickness of the interveutricular septum and LV posterior wall was 12 mm or greater (12 to 16 mm), mean estimated LV mass 3 was 311 _ 103 gm, and LV wall motion abnormality was absent on the two-dimensional echocardiogram. They did not have any signs of heart failure. No attempt was made to withhold or account for medications in the patient group. There were no differences in heart rate, LV end-diastolic and end-systolic dimensions, and percent fractional shortening between the two groups (Table 1). Isovolumic relaxation time was significantly prolonged in the patients with hypertensive heart disease (Table 1). All of these subjects had sinus rhythm and none of these subjects had moderate to severe aortic regurgitation assessed with color Doppler echocardiography. These subjects were included in the previous study. In these subjects the flow velocity pattern at the mitral tip was recorded simultaneously with regional flow velocity patterns 1, 2, or 3 cm from the mitral tip toward the apex, respectively, with multigate pulsed Doppler echocardiography (EUB-565A; Hitachi Medical Corp., Tokyo, Japan) from the apical long-axis view) Because Doppler colorflow imaging was used to obtain the main mitral inflow stream and the ultrasound beam was aligned as parallel to the flow as possible, the Doppler angle was negligible and no angle correction was made in any subject. The mitral flow velocity pattern at the mitral tip and the regional flow velocity patterns 1, 2, and 3 cm from the mitral tip toward the apex were traced to obtain regional peak early diastolic flow velocities and regional peak flow velocities at atrial contraction. Values are expressed as mean _+ SD. The statistical significance of the difference in the data between the two groups or between the different diastolic phases was tested with an analysis of variance and Scheffe's F test. The statistical significance of the difference in the data among the different points in one group was tested with a paired t test. Bivariate correlations between variables were performed with simple least-squares linear regression analysis. Results were considered significant at p < 0.05. All of these calculations were performed with the STATVIEW II (Abacus Inc., Berkeley, Calif.) statistical program.
~S~TS T h e peak mitral and regional flow velocities in early diastole and at atrial contraction in each g r o u p were s h o w n in Table 2. In the atrial contraction phase, although the absolute mitral and regional peak flow velocities were higher in the patients with hypertensive heart disease than in n o r m a l volunteers at any
Yamamoto
Table 1
e t al.
655
Characteristics of subjects studied Normal volunteers
H e a r t rate ( b e a t s / m i n ) LVEDD (mm) LVESD (mm) FS (%) I V R T (msec)
66 46 28 41 71
-+ 11 _+4 +4 + 5 + 8
HHD 70 50 29 42 89
-+ 10 +- 9 + 8 + 7 + 10"
Data are means + SD. HHD, Patients with hypertensive heart disease; LVEDD, left ventficular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; FS, fractional shortening; IVRT, isovolumic relaxation time. *p < 0.001 versus normal volunteers.
level, the ratio o f regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase decreased progressively from the mitral tip to the apex to the same degree in the two groups (Figures 1 and 2). T h e ratio o f regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase did not correlate with the peak mitral flow velocity at atrial contraction in the subjects studied 1, 2, or 3 cm from the mitral tip ( r = 0.08 [difference n o t significant]; r = 0.03 [difference n o t significant]; and r = 0.19 [difference n o t significant], respectively). Thus the intraventricular dispersion o f the flow velocity in the atrial contraction phase was n o t related to the peak mitral pressure gradient between the left atrium and left ventricle during atrial contraction as expressed by the peak mitral flow velocity at atrial contraction. T h e r e was a significant difference in the intraventricular dispersion o f the early diastolic flow velocity between the two groups (Figures 1 and 2). A l t h o u g h the peak early diastolic flow velocity was maintained from the mitral tip toward the apex in n o r m a l volunteers, it d r o p p e d progressively in the patients with hypertensive heart disease. As a result, in the patients with hypertensive heart disease the ratio o f regional peak flow velocity/mitral peak flow velocity in the early diastolic phase was significantly lower 3 cm f r o m the mitral tip c o m p a r e d with the normal volunteers. Thus the intraventricular drop o f the flow velocity in the early diastolic phase was m o r e progressive in the patients with hypertensive heart discase than in the n o r m a l volunteers. T h e patients with hypertensive heart disease had a lower value for the ratio o f m i t r a l peak early diastolic flow velocity/mitral peak flow velocity at atrial contraction c o m p a r e d with n o r m a l volunteers (0.9 +_0.4 versus 1.2 _+0.4; p = 0.05). T h e r e were n o significant relations between the intravcntricular dispersion o f the flow velocities and the ratio o f mitral peak early diastolic flow velocity/mitral peak flow velocity at atrial contraction. T h e r e was no significant difference
656
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F i g u r e 1 Representative recordings of diastolic flow velocity patterns at mitral tip and 1, 2, and 3 cm from mitral tip to apex in normal volunteer (Normal, left panel) and patient with hypertensive heart disease (HHD, r~qht panel). (A, Peak flow velocity at atrial contraction at each site; E, peak early diastolic flow velocity at each site, ECG, electrocardiogram; PCG, phonocardiogram; s, second.) Table 2 Peak early diastolic flow velocities and peak flow velocities at atrial contraction at the mitral tip and 1, 2, and 3 cm from the mitral tip to the apex in normal volunteers and patients with hypertensive heart disease
Peak early diastolic flow velocity (E) Mitral I ( c m / s e c )
E at 1 cm (cm/sec) E at 2 cm (cm/sec) E at 3 cm (cm/sec) Peak flow velocity at atrial contraction (A) Mitral A (cm/sec) A at 1 cm (cm/sec) A at 2 cm (cm/sec) A at 3 cm (cm/sec)
Normal volunteers
HHD
57 + 13
57 + 16
57 + 13 53 + 11 52 -+.12
54 + 14 59 -+ 13 36 + 14"
52 + 12 44 + 12 37 + 13 30 + 9
70 + 16" 60 + 15" 52 + 141" 43*
Data are means -+ SD. HHDj patients with hypertensive heart disease; E, peak early diastolic flow velodty at each site; A, peak flow velocity at atrial contraction at each site. *p < 0,001 versus normal voiunteers. ~'p < 0.005 versus normal volunteers.
in d e c e l e r a t i o n time o f mitral early diastolic flow velocity b e t w e e n t h e t w o groups.
DISCUSSION This s t u d y s h o w e d t h a t the intraventricular dispersion o f the flow velocity in t h e atrial c o n t r a c t i o n phase was n o t significantly different b e t w e e n the
n o r m a l volunteers a n d the patients w i t h hypertensive h e a r t disease, a l t h o u g h the intraventricular dispersion in the early diastolic phase was significantly different. W e previously s h o w e d t h a t early diastolic flow velocity d r o p s m o r e largely from the mitral tip tow a r d t h e apex in the left ventricle in patients w i t h LV diastolic dysfunction t h a n in n o r m a l volunteers.~ LV diastolic fimction in the atrial c o n t r a c t i o n phase includes o n l y the passive process in c o n t r a s t to the fact
Journal o f the American Society o f Echocardiography Volume 8 N u m b e r 5, Part 1
Y a m a m o t o et al.
Early diastolic phase
657
Atrial contraction phase
+
(%) 100 ............ ~.
100
8O
4.
+++
++
80 ++
\.
60.
60.
40.
+++
20 Mitral tip = - ~-
lcm
2cm
3cm
Distance from the mitral tip
40. 20 Mitral tip
+++
lcm
3r
Distance from the mitral tip
Normal volunteers Patients with hypertensive heart disease
Figure 2 Ratio of regional peak flow velocity/mitral peak flow velocity in early diastolic phase (left panel) and atrial contraction phase (right panel) of normal volunteers and patients with hypertensive hcart disease. Horizontal bar is distance from mitral tip. Values are expressed as mean _+SD. **p < 0.001 versus normal volunteers; +p < 0.05, ++p< 0.01, and +++p< 0.001 versus mitral tip. that LV diastolic function in the carly diastolic phase includes both active and passive processes. 2 Thus if the impairment of the passive process of LV diastolic function was responsible for the intraventricular drop of the early diastolic flow velocity in the patients, the intraventricular drop in the atrial contraction phase should be more progressive in patients than in norreal volunteers. Thus the progressive intravcntricular drop of the early diastolic flow velocity in the patients is likely to be explained by the impaired active rather than passive process of LV diastolic function. This study also showed that in the normal volunteers the flow velocity was maintained from the mitral tip toward the apex in the early diastolic phase but not in the atrial contraction phase. These findings suggest that the active process of LV diastolic function is, at least partially, responsible for the maintcnancc of the early diastolic flow velocity in the LV cavity in normal volunteers, because LV diastolic function in the atrial contraction phase consists of only the passive process in contrast to the early diastolic phase. 2 These results also support our conclusion that the progressive intraventricular drop of the early diastolic flow may indicate the impairment of the active process of LV diastolic function. The intraventricular dispersion in the atrial contraction phase was not different between the normal volunteers and the patients with hypertensive heart
disease. This may be partially because the intraventricular dispersion in the atrial contraction phase is not sensitive to the impairment of passive process of LV diastolic function. The intravcntricular pressure gradient seems to be smaller in the atrial contraction phase than in the early diastolic phase in the normal condition.4 Thus even if the intraventricular pressure gradient in the atrial contraction phase changes in association with LV diastolic dysfunction, such change may not be large enough to alter the intravcntricular dispersion. Alternatively, changes in the passive process of LV diastolic function in our patients may have been too small to alter the intraventricular dispersion, s'6 The main limitation of this study is the assumption that diastolic dysfunction was present in all the patients with hypertensive heart disease. In this noninvasive study, all the patients studied were not catheterized for ethical reasons and thus the high-fidelity time constant of LV relaxation was not obtained. However, the presence of abnormal diastolic function in patients with systemic arterial hypertension 7"8 has been established by previous studies, particularly in patients with concentric LV hypertrophy. LV hypertrophy, prolonged isovolumic relaxation time, and the low ratio of mitral peak early diastolic flow vclocity/mitral peak flow velocity at atrial contraction were evident in our patients with hypertensive
658
Yamamoto et al.
h e a r t disease, a n d these findings s u p p o r t the presence o f L V diastolic d y s f u n c t i o n in o u r patients w i t h hypertensive h e a r t disease. I n this s t u d y w e d i d n o t analyze the flow p r o p a g a tion velocity o f L V diastolic filling o r the time differences o f the peak early diastolic flow velocity b e t w e e n the mitral tip a n d 1, 2, a n d 3 c m from t h e mitral tip to the apex. As s h o w n in F i g u r e 1, however, flow p r o p a g a t i o n was o b v i o u s l y delayed a n d the time difference s e e m e d to be larger in patients w i t h hypertensive h e a r t disease t h a n in n o r m a l volunteers. I n t e r m s o f flow p r o p a g a t i o n o r a difference in time, c o l o r M - m o d e D o p p l e r i m a g i n g o f L V filling m a y p r o v i d e further i n f o r m a t i o n . 9"]~ I n conclusion, t h e progressive intraventricular d r o p o f the flow velocity in the early diastolic phase in patients w i t h hypertensive h e a r t disease m a y reflect t h e i m p a i r m e n t o f active rather t h a n passive L V diastolic function. C o m p a r i s o n o f the intravcntricular dispersion o f t h e flow velocity in the early diastolic a n d atrial c o n t r a c t i o n phases provides an additional insight to the noninvasivc assessment o f LV diastolic function. REFERENCES
1. Yamamoto K, Masuyama T, Tanouchi J, et al. Intraventricular dispersion of early diastolic filling: a new marker of left ventricular diastolic dysfunction. Am Heart J 1995;129:291-9.
Journal of the AmericanSocietyof Echocardiography September-October 1995
2. Gilbert JC, Glantz SA. Determinants of left ventricular filling and of the diastolic pressure-volume relation. Circ Res 1989;64:827-52. 3. Devereux RB, Reichek N. Echocardiographic determination of left ventricular mass in man: anatomic validation of the methods. Circulation 1977;55:613-8. 4. Courtois M, Kovacs SJ Jr, Ludbrook PA. Transmitral pressure-flow velocity relation: importance of regional pressure gradients in the left ventricle during diastole. Circulation 1988;78:661-71. 5. Van de WerfF, Boel A, Geboers J, et al. Diastolic properties of the left ventricle in normal adults and in patients with third heart sounds. Circulation 1984;69:1070-8. 6. Pasipoularides A, Mirskey I, Hess OT, Grimm J, Krayenbuehl HP. Myocardial relaxation and passive diastolic properties in man. Circulation 1986;74:991-1001. 7. Chenzbraun A, Pinto FJ, Popylisen S, Schnittger I, Popp RL. Filling patterns in left ventricular hypertrophy: a combined acoustic quantification and Doppler study. J Am Coil Cardiol 1994;23:1179-85. 8. Nagano R, Masuyama T, Lee JM, et al. Transthoracic Doppler assessment of pattern of left ventricular dysfunction in hypertensive heart disease: combined analysis of mitral and pulmonary venous flow velocity patterns. J AM Soc ECHOCARDIOGR1994;7:493-505. 9. Brun P, Tribouilloy C, Duval AM, et al. Left ventticular flow propagation during early filling is related to wall relaxation: a color M-mode Doppler analysis. J Am Coil Cardiol 1992; 20:420-32. 10. Stugaard M, Smiseth OA, Rime C, Ihlen H. Intraventricular early diastolic filling during acute myocardial ischemia: assessment by multigated color M-mode Doppler. Circulation 1993;88:2705-13.
Left ventricular (LV) diastolic function in the early diastolic phase includes both active and passive processes, but in the atrial contraction phase it includes only passive processes. To elucidate the relation between the intraventricular dispersion of the flow velocity in diastole and LV diastolic process, 31 normal volunteers and 12 patients with hypertensive heart disease were studied. In these subjects the flow velocity pattern at the mitral tip was recorded simultaneously with regional flow velocity patterns 1, 2, or 3 cm from the mitral tip toward the apex, respectively, with multigate pulsed Doppler echocardiography from the apical long-axis view with the guidance of Doppler color-
flow imaging. Although the ratio of regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase decreased from the mitral tip to the apex to the same degree in the normal vohmteers and patients with hypertensive heart disease, there was a significant difference in the intraventricular dispersion of the early diastolic flow velocity between the two groups. These results suggest that the progressive intraventricular drop of the flow velocity in the early diastolic phase in patients with hypertensive heart disease may reflect the impairment of active rather than passive LV diastolic function. (J AM SOC ECHOCARDIOGR1995;8:654-8.)
W e recently showed that early diastolic flow velocity drops more largely from the mitral tip toward the apex in the left vcntricle in patients with left ventricular (LV) diastolic dysfunction than in normal subjects, irrespective o f the flow velocity pattern at the mitral t i p ) LV diastolic function in the early diastolic phase includes both active and passive processes. 2 The active process o f LV diastolic function is influenced by LV relaxation and LV elastic recoil, and the passive process is influenced by LV compliance. Thus it is not clear from the results of our previous study
which process the intraventricular dispersion o f the early diastolic flow velocity reflects. In contrast to the early diastolic phase, LV diastolic function in the atrial contraction phase includes only passive processes. 2 From this point o f view, we analyzed the intraventricular dispersion o f the flow velocity in the early diastolic and atrial contraction phases to elucidate the relation between the intraventricular dispersion of the flow velocity in diastole and the LV diastolic process.
From the First Department of Medicine, Osaka UniversitySchool of Medicine. Supported in part by research grants from the Ministry of Health and Welfare of Japan and Research Fellowships of the Japanese Society for the Promotion of Science for Young Scientists. ~Research Fellow of the Japanese Society for the Promotion of Science. Reprint requests: Tohru Masuyama,MD, the First Department of Medicine, Osaka UniversitySchool of Medicine, 2-2 Yamadaoka, Suita 565, Japan. Copyright 9 1995 by the American Societyof Echocardiography. 0894-7317/95 $5.00 + 0 27/4/62187 654
METHODS
This study conforms to the guiding principles of the institutional Ethics Committee of Osaka University School of Medicine on Human Research. All patients gave informed consent for participation in this study protocol. The study population consisted of 31 normal volunteers (mean age 52 + 11 years; range 25 to 70 years) and 12 patients with hypertensive heart disease (mean age 53 _+13 years; range 31 to 68 years) who had presumed LV diastolic dysfunction but normal systolic function. All the normal volunteers had no cardiac complaint, negative car-
Journal of the American Society of Echocardiography Volume 8 Number 5, Part 1
diovascular history, and normal blood pressures. There were no electrocardiographic or echocardiographic abnormalities in any of the volunteers. On the other hand, all the patients had systemic arterial hypertension as a pathologic condition known to cause LV hypertrophy. In all the patients, wall thickness of the interveutricular septum and LV posterior wall was 12 mm or greater (12 to 16 mm), mean estimated LV mass 3 was 311 _ 103 gm, and LV wall motion abnormality was absent on the two-dimensional echocardiogram. They did not have any signs of heart failure. No attempt was made to withhold or account for medications in the patient group. There were no differences in heart rate, LV end-diastolic and end-systolic dimensions, and percent fractional shortening between the two groups (Table 1). Isovolumic relaxation time was significantly prolonged in the patients with hypertensive heart disease (Table 1). All of these subjects had sinus rhythm and none of these subjects had moderate to severe aortic regurgitation assessed with color Doppler echocardiography. These subjects were included in the previous study. In these subjects the flow velocity pattern at the mitral tip was recorded simultaneously with regional flow velocity patterns 1, 2, or 3 cm from the mitral tip toward the apex, respectively, with multigate pulsed Doppler echocardiography (EUB-565A; Hitachi Medical Corp., Tokyo, Japan) from the apical long-axis view) Because Doppler colorflow imaging was used to obtain the main mitral inflow stream and the ultrasound beam was aligned as parallel to the flow as possible, the Doppler angle was negligible and no angle correction was made in any subject. The mitral flow velocity pattern at the mitral tip and the regional flow velocity patterns 1, 2, and 3 cm from the mitral tip toward the apex were traced to obtain regional peak early diastolic flow velocities and regional peak flow velocities at atrial contraction. Values are expressed as mean _+ SD. The statistical significance of the difference in the data between the two groups or between the different diastolic phases was tested with an analysis of variance and Scheffe's F test. The statistical significance of the difference in the data among the different points in one group was tested with a paired t test. Bivariate correlations between variables were performed with simple least-squares linear regression analysis. Results were considered significant at p < 0.05. All of these calculations were performed with the STATVIEW II (Abacus Inc., Berkeley, Calif.) statistical program.
~S~TS T h e peak mitral and regional flow velocities in early diastole and at atrial contraction in each g r o u p were s h o w n in Table 2. In the atrial contraction phase, although the absolute mitral and regional peak flow velocities were higher in the patients with hypertensive heart disease than in n o r m a l volunteers at any
Yamamoto
Table 1
e t al.
655
Characteristics of subjects studied Normal volunteers
H e a r t rate ( b e a t s / m i n ) LVEDD (mm) LVESD (mm) FS (%) I V R T (msec)
66 46 28 41 71
-+ 11 _+4 +4 + 5 + 8
HHD 70 50 29 42 89
-+ 10 +- 9 + 8 + 7 + 10"
Data are means + SD. HHD, Patients with hypertensive heart disease; LVEDD, left ventficular end-diastolic diameter; LVESD, left ventricular end-systolic diameter; FS, fractional shortening; IVRT, isovolumic relaxation time. *p < 0.001 versus normal volunteers.
level, the ratio o f regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase decreased progressively from the mitral tip to the apex to the same degree in the two groups (Figures 1 and 2). T h e ratio o f regional peak flow velocity/mitral peak flow velocity in the atrial contraction phase did not correlate with the peak mitral flow velocity at atrial contraction in the subjects studied 1, 2, or 3 cm from the mitral tip ( r = 0.08 [difference n o t significant]; r = 0.03 [difference n o t significant]; and r = 0.19 [difference n o t significant], respectively). Thus the intraventricular dispersion o f the flow velocity in the atrial contraction phase was n o t related to the peak mitral pressure gradient between the left atrium and left ventricle during atrial contraction as expressed by the peak mitral flow velocity at atrial contraction. T h e r e was a significant difference in the intraventricular dispersion o f the early diastolic flow velocity between the two groups (Figures 1 and 2). A l t h o u g h the peak early diastolic flow velocity was maintained from the mitral tip toward the apex in n o r m a l volunteers, it d r o p p e d progressively in the patients with hypertensive heart disease. As a result, in the patients with hypertensive heart disease the ratio o f regional peak flow velocity/mitral peak flow velocity in the early diastolic phase was significantly lower 3 cm f r o m the mitral tip c o m p a r e d with the normal volunteers. Thus the intraventricular drop o f the flow velocity in the early diastolic phase was m o r e progressive in the patients with hypertensive heart discase than in the n o r m a l volunteers. T h e patients with hypertensive heart disease had a lower value for the ratio o f m i t r a l peak early diastolic flow velocity/mitral peak flow velocity at atrial contraction c o m p a r e d with n o r m a l volunteers (0.9 +_0.4 versus 1.2 _+0.4; p = 0.05). T h e r e were n o significant relations between the intravcntricular dispersion o f the flow velocities and the ratio o f mitral peak early diastolic flow velocity/mitral peak flow velocity at atrial contraction. T h e r e was no significant difference
656
Journal of the American Society of Echocardiography September-October 1995
Yamamoto et al.
F i g u r e 1 Representative recordings of diastolic flow velocity patterns at mitral tip and 1, 2, and 3 cm from mitral tip to apex in normal volunteer (Normal, left panel) and patient with hypertensive heart disease (HHD, r~qht panel). (A, Peak flow velocity at atrial contraction at each site; E, peak early diastolic flow velocity at each site, ECG, electrocardiogram; PCG, phonocardiogram; s, second.) Table 2 Peak early diastolic flow velocities and peak flow velocities at atrial contraction at the mitral tip and 1, 2, and 3 cm from the mitral tip to the apex in normal volunteers and patients with hypertensive heart disease
Peak early diastolic flow velocity (E) Mitral I ( c m / s e c )
E at 1 cm (cm/sec) E at 2 cm (cm/sec) E at 3 cm (cm/sec) Peak flow velocity at atrial contraction (A) Mitral A (cm/sec) A at 1 cm (cm/sec) A at 2 cm (cm/sec) A at 3 cm (cm/sec)
Normal volunteers
HHD
57 + 13
57 + 16
57 + 13 53 + 11 52 -+.12
54 + 14 59 -+ 13 36 + 14"
52 + 12 44 + 12 37 + 13 30 + 9
70 + 16" 60 + 15" 52 + 141" 43*
Data are means -+ SD. HHDj patients with hypertensive heart disease; E, peak early diastolic flow velodty at each site; A, peak flow velocity at atrial contraction at each site. *p < 0,001 versus normal voiunteers. ~'p < 0.005 versus normal volunteers.
in d e c e l e r a t i o n time o f mitral early diastolic flow velocity b e t w e e n t h e t w o groups.
DISCUSSION This s t u d y s h o w e d t h a t the intraventricular dispersion o f the flow velocity in t h e atrial c o n t r a c t i o n phase was n o t significantly different b e t w e e n the
n o r m a l volunteers a n d the patients w i t h hypertensive h e a r t disease, a l t h o u g h the intraventricular dispersion in the early diastolic phase was significantly different. W e previously s h o w e d t h a t early diastolic flow velocity d r o p s m o r e largely from the mitral tip tow a r d t h e apex in the left ventricle in patients w i t h LV diastolic dysfunction t h a n in n o r m a l volunteers.~ LV diastolic fimction in the atrial c o n t r a c t i o n phase includes o n l y the passive process in c o n t r a s t to the fact
Journal o f the American Society o f Echocardiography Volume 8 N u m b e r 5, Part 1
Y a m a m o t o et al.
Early diastolic phase
657
Atrial contraction phase
+
(%) 100 ............ ~.
100
8O
4.
+++
++
80 ++
\.
60.
60.
40.
+++
20 Mitral tip = - ~-
lcm
2cm
3cm
Distance from the mitral tip
40. 20 Mitral tip
+++
lcm
3r
Distance from the mitral tip
Normal volunteers Patients with hypertensive heart disease
Figure 2 Ratio of regional peak flow velocity/mitral peak flow velocity in early diastolic phase (left panel) and atrial contraction phase (right panel) of normal volunteers and patients with hypertensive hcart disease. Horizontal bar is distance from mitral tip. Values are expressed as mean _+SD. **p < 0.001 versus normal volunteers; +p < 0.05, ++p< 0.01, and +++p< 0.001 versus mitral tip. that LV diastolic function in the carly diastolic phase includes both active and passive processes. 2 Thus if the impairment of the passive process of LV diastolic function was responsible for the intraventricular drop of the early diastolic flow velocity in the patients, the intraventricular drop in the atrial contraction phase should be more progressive in patients than in norreal volunteers. Thus the progressive intravcntricular drop of the early diastolic flow velocity in the patients is likely to be explained by the impaired active rather than passive process of LV diastolic function. This study also showed that in the normal volunteers the flow velocity was maintained from the mitral tip toward the apex in the early diastolic phase but not in the atrial contraction phase. These findings suggest that the active process of LV diastolic function is, at least partially, responsible for the maintcnancc of the early diastolic flow velocity in the LV cavity in normal volunteers, because LV diastolic function in the atrial contraction phase consists of only the passive process in contrast to the early diastolic phase. 2 These results also support our conclusion that the progressive intraventricular drop of the early diastolic flow may indicate the impairment of the active process of LV diastolic function. The intraventricular dispersion in the atrial contraction phase was not different between the normal volunteers and the patients with hypertensive heart
disease. This may be partially because the intraventricular dispersion in the atrial contraction phase is not sensitive to the impairment of passive process of LV diastolic function. The intravcntricular pressure gradient seems to be smaller in the atrial contraction phase than in the early diastolic phase in the normal condition.4 Thus even if the intraventricular pressure gradient in the atrial contraction phase changes in association with LV diastolic dysfunction, such change may not be large enough to alter the intravcntricular dispersion. Alternatively, changes in the passive process of LV diastolic function in our patients may have been too small to alter the intraventricular dispersion, s'6 The main limitation of this study is the assumption that diastolic dysfunction was present in all the patients with hypertensive heart disease. In this noninvasive study, all the patients studied were not catheterized for ethical reasons and thus the high-fidelity time constant of LV relaxation was not obtained. However, the presence of abnormal diastolic function in patients with systemic arterial hypertension 7"8 has been established by previous studies, particularly in patients with concentric LV hypertrophy. LV hypertrophy, prolonged isovolumic relaxation time, and the low ratio of mitral peak early diastolic flow vclocity/mitral peak flow velocity at atrial contraction were evident in our patients with hypertensive
658
Yamamoto et al.
h e a r t disease, a n d these findings s u p p o r t the presence o f L V diastolic d y s f u n c t i o n in o u r patients w i t h hypertensive h e a r t disease. I n this s t u d y w e d i d n o t analyze the flow p r o p a g a tion velocity o f L V diastolic filling o r the time differences o f the peak early diastolic flow velocity b e t w e e n the mitral tip a n d 1, 2, a n d 3 c m from t h e mitral tip to the apex. As s h o w n in F i g u r e 1, however, flow p r o p a g a t i o n was o b v i o u s l y delayed a n d the time difference s e e m e d to be larger in patients w i t h hypertensive h e a r t disease t h a n in n o r m a l volunteers. I n t e r m s o f flow p r o p a g a t i o n o r a difference in time, c o l o r M - m o d e D o p p l e r i m a g i n g o f L V filling m a y p r o v i d e further i n f o r m a t i o n . 9"]~ I n conclusion, t h e progressive intraventricular d r o p o f the flow velocity in the early diastolic phase in patients w i t h hypertensive h e a r t disease m a y reflect t h e i m p a i r m e n t o f active rather t h a n passive L V diastolic function. C o m p a r i s o n o f the intravcntricular dispersion o f t h e flow velocity in the early diastolic a n d atrial c o n t r a c t i o n phases provides an additional insight to the noninvasivc assessment o f LV diastolic function. REFERENCES
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