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Flow propagation velocity is not a simple index of diastolic function in early filling. A comparative study of early diastolic strain rate and strain rate propagation, flow and flow propagation in normal and reduced diastolic function
© Støylen et al; licensee BioMed Central Ltd. 2003
- Received: 6 February 2003
- Accepted: 1 April 2003
- Published: 1 April 2003
Strain Rate Imaging shows the filling phases of the left ventricle to consist of a wave of myocardial stretching, propagating from base to apex. The propagation velocity of the strain rate wave is reduced in delayed relaxation. This study examined the relation between the propagation velocity of strain rate in the myocardium and the propagation velocity of flow during early filling.
12 normal subjects and 13 patients with treated hypertension and normal systolic function were studied. Patients and controls differed significantly in diastolic early mitral flow measurements, peak early diastolic tissue velocity and peak early diastolic strain rate, showing delayed relaxation in the patient group. There were no significant differences in EF or diastolic diameter.
Strain rate propagation velocity was reduced in the patient group while flow propagation velocity was increased. There was a negative correlation (R = -0.57) between strain rate propagation and deceleration time of the mitral flow E-wave (R = -0.51) and between strain rate propagation and flow propagation velocity and there was a positive correlation (R = 0.67) between the ratio between peak mitral flow velocity / strain rate propagation velocity and flow propagation velocity.
The present study shows strain rate propagation to be a measure of filling time, but flow propagation to be a function of both flow velocity and strain rate propagation. Thus flow propagation is not a simple index of diastolic function in delayed relaxation.
- Flow Propagation
- Diastolic Function
- Propagation Velocity
- Early Filling
- Mitral Flow
Strain rate imaging  is a spatial derivation of local velocity gradients: SR = Error!, subtracting translational velocities as well as the effects of adjacent segments (tethering) and giving information about the rate of regional deformation.
As strain rate and strain rate propagation are the main indices of myocardial relaxation, they are considered the primary event, and flow propagation the secondary. The aim of this study was to compare the two measures, to establish the relation between them in normal and moderately reduced function, and to assess the influence of other diastolic measurements on flow propagation.
Subject group characteristics. P values for differences
A specially programmed system FiVe scanner (GE Vingmed Ultrasound, Horten, Norway) with a 2.5 MHz phased array transducer was employed. SRI was processed online on the scanner, and cine-loops of all three standard apical planes were recorded and transferred to a PC computer for analysis in a dedicated software. Frame rate was 70 – 100 FPS and offset length (strain rate sample volume) 5 – 7 mm. Linear propagation velocity of strain rate during early diastole (PVSe) was measured along the front of peak strain rate as shown in Fig 1, in all 6 walls of each ventricle, and averaged for each subject. Peak strain rate during early filling (SRe) was measured in all 16 standard segments  of the left ventricle and averaged for each subject.
P-values for differences between patients and controls are two-tailed probabilities by two-tailed student's T-test. All significant differences were also significant by Wilcoxon's two-sample rank sum test. Relation between flow propagation velocity (dependent) and various variables is by univariate and multiple linear regression. Correlations were by both Pearson's and Spearman's methods. Repeatability of flow propagation measurements was by Bland-Altman statistics.
Diastolic flow and strain rate indices. (SD in parentheses)
The patients show near normal peak mitral flow velocity, near normal, but still reduced E/A ratio compared to controls, and deceleration time of mitral flow velocity and IVR are prolonged in the patient group. Early diastolic annulus velocity and strain rate are reduced in the patient group, showing a moderate diastolic dysfunction. The ratio of mitral flow and annulus velocity, E/Ea was 5,4 in the control group, and 7.4 in the patient group, the difference is significant, but still indicates normal filling pressure in both groups .
In univariate linear regression, only the correlation between strain rate propagation and flow propagation is significant (P = 0.003). No significant relation is found between flow propagation velocity and peak annular early diastolic velocity, left ventricular diastolic diameter, peak early diastolic strain rate, deceleration time of early mitral flow, isovolumic relaxation, HR, EF or age, in either univariate or multivariate analysis. Strain rate propagation velocity is significant in both univariate and multivariate (P = 0.004) analysis. Peak mitral flow velocity is not significant in univariate analysis, only in multivariate (P = 0.017), showing interaction with strain rate propagation velocity (Significance of the interaction: 0.014). Thus, there is a significant correlation between the ratio: peak early mitral flow velocity / strain rate propagation (E/PVSe) and flow propagation velocity, PVFe: R = 0.67, (0.37 – 0.84, p < 0.001, ρ = 0.58, p < 0.002).
Comparison of flow propagation velocity measurements by three methods
Front of aliased velocity
Main aliased velocity
-0.57 (-0.79 – -0.23)
-0.43 (-0.7 – -0.04)
-0.19 (-0.54 – 0.22)
Strain rate propagation is a measure of the rate of chamber expansion as illustrated in fig 1. Deceleration time of early mitral flow is a measure of filling time, and the negative correlation is as expected. Thus, strain rate propagation may be taken as a measure of left ventricular filling dynamics during early diastole.
Flow propagation velocity and strain rate propagation velocity are similar in the control group. While strain rate propagation decreases in the patient group, consistent with delayed relaxation, flow propagation velocity increased. This finding is contrary to previous findings [11, 12, 14, 19–22], and unexpected in view of the reduced strain rate propagation, and the negative correlation between strain rate propagation and flow propagation velocity, is consistent with this finding.
Measurements of propagation velocities have a low precision, as shown by the wide limits of agreements, and the variability given in table 3. This may account for the moderate strength of the correlation found. The actual value of flow propagation velocity depends on the method chosen, as shown in table 3 and fig. 4. In addition, measurements are dependent on scanner settings: Black-to-colour transition depends on the level of low velocity rejection, the aliasing contour on pulse repetition frequency. Comparing different studies is therefore difficult, as shown by the variety of normal values given, and also for methodological reasons, flow propagation velocity has limited value as an index of diastolic function . On the other hand, the low precision of flow propagation cannot explain the significance of the results, as low precision alone will result in random, rather than systematic variation.
Previous studies have all shown reduced flow propagation velocity in reduced diastolic function. However, in many of those studies, there was simultaneous left ventricular dilation [9, 10, 17, 18]. It has been demonstrated that in left ventricular dilation, there is no column propagation, but solely vortex propagation, as the main mechanism for the flow propagation delay [14, 24]. In the present study, there was no left ventricular dilation (except in the one patient commented on), on the contrary, there was a non-significant trend toward a narrowing of the ventricle due to concentric hypertrophy. In addition slower strain rate propagation causes the ventricle to remain narrow for a longer time during early filling. Findings concerning reduced flow propagation in dilated ventricles will thus be irrelevant. However, also in ordinary ageing and in hypertrophic cardiomyopathy, where no dilation is to be expected, there is found delayed flow propagation [21, 22].
The patient group is homogenous, with preserved systolic function and no chamber dilation.
The patient group had delayed relaxation , as evidenced by the prolonged deceleration time and IVR as well as reduced early diastolic mitral annulus velocity by tissue Doppler. The E/A ratio but not the E flow velocity was reduced, but the pattern is more normal than in other studies . There was a significant difference in E/Ea ratio, but it was below the cut off value of 8 in both groups , so there was no indication of pseudonormalised mitral flow, although a difference in filling pressure within the normal range cannot be excluded. The main reason for the high early diastolic flow velocity seems thus to be very moderately reduced diastolic function.
This, however, means that flow propagation velocity is not a simple index of diastolic function, but rather a composite function of more factors, in addition to a low precision. The importance of mitral flow velocity in relation to flow propagation have been found also by others 
The reduced diastolic function in the patient group was due to a combination of age  and hypertension with moderate hypertrophy. This was considered acceptable, in view of the object of the study, the mechanics of filling, not causes of diastolic dysfunction. The function seems to be similar, irrespective of causes , but it still remains a limitation.
Results will have no relevance in dilated ventricles, as they do not concern vortex propagation, nor to regional dysfunction where flow pattern is shown to be more complex due to regional disturbances .
Strain Rate Imaging shows the ventricular deformation during early filling to be a dynamic event that is slowed in subjects with delayed relaxation. The strain rate propagation is the main determinant of the filling rate, and is consistent with filling time.
Flow propagation velocity, in this study, was found to be significantly increased in patients with delayed relaxation, and was shown to be dependent on both strain rate propagation and mitral inflow velocity, and is thus not a simple index of diastolic function. Neither strain rate propagation nor flow propagation velocities do at present show the precision necessary for clinical use.
The study was supported by a grant from the Norwegian Council for Cardiovascular Disease. Björn Olstad, of GE Vingmed Ultrasound, Horten, Norway, programmed the special software for strain rate analysis.
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