Clinical investigation
Assessment of mitral annular dynamics during diastole by Doppler tissue imaging: Comparison with mitral Doppler inflow in subjects without heart disease and in patients with left ventricular hypertrophy

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Abstract

The purpose of this study was to determine the normal pattern and magnitude of mitral annular velocities in diastole by Doppler tissue imaging (DTI) and to assess whether this is altered in patients with left ventricular hypertrophy. Mitral annulus velocities were measured by DTI. Peak and time-velocity integral were measured from the DTI tracings and the timing of the velocities in relation to electrocardiogram. DTI was compared with M-mode echo of the annulus and mitral inflow Doppler velocities. Integrated annular velocities by DTI correlated with the annular displacement. Early diastolic velocities decreased with age and in patients with left ventricular hypertrophy. In the hypertrophy group, early diastolic velocities were significantly lower than normal even after correcting for age. Patients with left ventricular hypertrophy also showed a delay in peak early diastolic mitral annular velocity (5.5 ± 21 msec after the E wave). In conclusion, mitral annular velocity in diastole is readily recorded by DTI. The magnitude and the pattern of these velocities are significantly altered by age and by left ventricular hypertrophy. This method provides a new insight into diastolic filling events and may prove useful in detecting abnormal diastolic function.

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    Citation Excerpt :

    In patients with LV hypertrophy and dilated cardiomyopathy, R-pE’ was delayed more than those age-matched subjects. [4,16,31] Furthermore, in patients with LV hypertrophy and dilated cardiomyopathy, R-pE’ adversely preceded peak E. [4,31] In our study, we found that during LV early diastole, the R-pE showed no significant changes, but R-pE’ was delayed, and thus the resultant EDTD (i.e., the time difference of R-pE and R-pE’) was significantly decreased in patients with HF compared with normal controls. When LV relaxation is impaired, LV filling is compensated by augmenting LA contraction. [32]

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Supported in part by the Fondo de Inversiones Sanitarias, Spain, the Uehara Memorial Foundation, Tokyo, Japan, Grant-in-Aid 930133380 from the American Heart Association, and an equipment grant from Acuson, Inc., Mountain View, Calif.

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