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(Circulation. 1999;99:254-261.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Doppler Estimation of Left Ventricular Filling Pressures in Patients With Hypertrophic Cardiomyopathy
From the Department of Medicine, Section of Cardiology, Baylor College of Medicine at Houston, Tex.
Correspondence and reprint requests to Sherif F. Nagueh, MD, Section of Cardiology, Baylor College of Medicine, SM1246, 6550 Fannin, Houston, TX 77030. E-mail sherifn{at}bcm.tmc.edu
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Abstract |
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Background—Conventional Doppler parameters are unreliable for estimating left ventricular (LV) filling pressures in hypertrophic cardiomyopathy (HCM). This study was undertaken to evaluate flow propagation velocity by color M-mode and early diastolic annular velocity (Ea) by tissue Doppler 2 new indices of LV relaxation, combined with mitral E velocity for estimation of filling pressures in HCM.
Methods and Results—Thirty-five HCM patients (52±15 years) underwent LV catheterization simultaneously with 2-dimensional and Doppler echocardiography. Pulsed Doppler echocardiography of mitral and pulmonary venous flows was obtained along with flow propagation velocity and Ea. LV preA pressure had weak or no relations with mitral, pulmonary venous velocities and atrial volumes. In contrast, preA pressure related strongly to E velocity/flow propagation velocity (r=0.67; SEE=4) and E/Ea (r=0.76; SEE=3.4). In 17 patients with repeat measurements, preA pressure changes were well detected by measuring E velocity/flow propagation velocity (r=0.68; P=0.01) or E/Ea (r=0.8; P<0.001). PreA pressure estimation with these 2 methods was tested prospectively in 17 additional HCM patients with good results (E velocity/flow propagation velocity, r=0.76; E/Ea, r=0.82).
Conclusions—LV filling pressures can be estimated with reasonable accuracy in HCM patients by measuring E velocity/flow propagation velocity or E/Ea. These ratios also track changes in filling pressures.
Key Words: echocardiography • pressure • ultrasonics, Doppler • hypertrophy • cardiomyopathy
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Hypertrophic cardiomyopathy (HCM) is a genetic disease that frequently presents with dyspnea.1 Although left ventricular outflow tract (LVOT) obstruction is not always there, diastolic dysfunction is almost universally present. Thus, a noninvasive method for determination of LV filling pressures in HCM is highly desirable. Although echocardiography has been successfully used to estimate filling pressures in a variety of cardiac disorders,2 3 4 5 6 7 8 9 10 11 current methods are unreliable with normal systolic function,12 particularly in HCM.13 These results are related in part to the impaired relaxation-dominant influence on mitral inflow that overshadows the effects of increased filling pressures. Thus, mitral peak velocity of early filling (E velocity) combined with a load-independent index of relaxation may improve Doppler estimation of filling pressures. There are currently 2 relaxation indices that appear less preload-dependent: early flow propagation velocity14 15 16 by color M-mode and early diastolic annular velocity (Ea) by tissue Doppler (TD).17 18 19 These indices may correct for the influence of relaxation on mitral E velocity. We20 and others21 have noted that mitral E velocity/flow propagation velocity relates well to filling pressures. Similarly, we showed recently that E/Ea predicts filling pressures well throughout a wide range of systolic performance.18 It is currently unknown whether E velocity/flow propagation velocity or E/Ea can be applied in HCM. Our purpose was, therefore, to determine the role of these new noninvasive relaxation parameters in estimating filling pressures in HCM patients.
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Methods |
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The protocol was approved by the institutional review boards of Methodist Hospital and Baylor College of Medicine, and all patients gave written informed consent before participation. The group was composed of 35 HCM patients enrolled for ethanol septal reduction therapy.22 Patients had asymmetrical septal hypertrophy with septal thickness
1.5 cm, and
septum/posterior wall thickness 1.3. They were all dyspneic, and most
were in NYHA functional class III or IV. Inclusion criteria were normal
sinus rhythm, absence of mitral stenosis or prosthetic
mitral valve, and adequate Doppler measurements. All had
simultaneous Doppler (including color M-mode and TD)
and LV pressure measurements.
Echocardiographic Studies
Patients were imaged in supine position with the Acuson XP-128
ultrasound system equipped with a multifrequency transducer and TD.
From the apical view, the pulsed Doppler sample volume was placed
at mitral valve annulus then at tips, and 5 to 10 cardiac cycles were
recorded at each site during normal respiration. The cursor was
placed between LV outflow and mitral inflow to record isovolumic
relaxation time (IVRT).4 Pulmonary venous (PV)
flow was recorded from the right vein with color Doppler
guidance. With the use of color Doppler
echocardiography, the M-mode cursor was positioned
within the center of the mitral inflow stream, and M-mode
recording of the early flow propagation velocity into the LV
was obtained. Baseline shift was performed as needed to obtain a
distinct color border of the propagation velocity that extended into
the distal portion of the LV cavity.14 20 The TD program
was set to pulsed-wave mode (-30 to 30 cm/s), with gain adjusted to
minimize background noise. From the 4-chamber view, a 5-mm sample
volume was placed at the lateral border of the mitral
annulus17 18 and 5 to 10 cycles were recorded. Studies
were stored on 1/2-in VHS videotape for later playback and
analysis.
Echocardiographic Analysis
All measurements were made by an observer blinded to
hemodynamic data on an off-line analysis
station (Digisonics EC500) with 2-dimensional and Doppler
measurement software. Left atrial23 and LV volumes were
derived with the discs method. Mitral inflow was measured and traces
were obtained for the following: peak velocity of early (E) and late
(A) filling, acceleration time of E (AT-E), deceleration times of E
(DT-E) and A (DT-A), and atrial filling fraction
(AFF).4 11 IVRT was measured as previously
described.4 6 PV inflow was analyzed for peak
velocity and velocity time integral (VTI) of systolic (S),
diastolic (D), and atrial reversal waves (Ar; Figure 1
). Systolic filling fraction
(SFF) was calculated as follows: S-VTI/total forward flow
VTI.2 6 Mitral A velocity duration at the annulus and Ar
duration were measured. Subsequently, Ar-A duration was
derived.5 6 The flow propagation velocity (cm/s) was
measured as the slope of the linear component of the color border
produced by propagation of E velocity into the LV, past the mitral
valve tips14 20 (Figure 1). Mitral E velocity/flow
propagation velocity was calculated.20 21 The following
measurements were made from TD tracings (Figure 1): early (Ea)
and late (Aa) diastolic annular velocities, Ea/Aa, and
mitral E/Ea ratios.18
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Pressure Measurements
A 7F pigtail catheter was used for LV pressure measurements.
Medex transducers (fluid column length, 1.88 in; observed natural
frequency, 105 Hz) were balanced before acquisition of
hemodynamic data with zero level at mid axillary line.
Baseline pressure measurements were acquired before coronary
angiography, and none of the patients had ventriculography. LV
diastolic pressures measured were as follows: minimal
pressure, preA, and end diastolic pressure (LVEDP; Figure 1B
). PreA pressure was taken before the pressure increase due to
atrial contraction, and LVEDP was determined before the rise in
systolic pressure (at end-expiration with the average of 3
cycles). After septal infarction, patients received meperidine
hydrochloride (Demerol) or morphine. Seventeen patients in normal sinus
rhythm had repeat measurements of filling pressures
simultaneous with Doppler
echocardiography.
Test Population
The equations derived to estimate filling pressures were tested
in 17 consecutive patients (9 of them women, 47±18 years; age range,
19 to 74 years). Doppler and pressure data were obtained
simultaneously. Patients studied had the same inclusion and
exclusion criteria as the initial group. Doppler measurements and
calculations were made without knowledge of
hemodynamics.
Statistical Analysis
Linear regression analysis was used to correlate
continuous variables with each other. Agreement between
Doppler-estimated and catheter-measured pressures was evaluated by
plotting the difference against the mean value of the 2 measurements
(Bland-Altman plots). We estimated a correlation coefficient between
Doppler parameters and LV diastolic
pressures of 
0.6 to 0.7, with a power of 0.9 at 
=0.05.
Accordingly, our sample size of 35 was adequate to detect such a
relation (calculated sample size of 25 at r=0.6).
Significance was set at P<0.05.
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Results |
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Mean age was 52±15 years (range, 24 to 83 years; 19 men, heart rate 71±9 bpm; range, 52 to 86 bpm). All but 4 had a LVOT gradient due to systolic anterior motion of the mitral valve at rest (56±29 mm Hg; range, 15 to 120 mm Hg). They all had hyperdynamic ventricles, but none had severe mitral regurgitation. Satisfactory mitral inflow signals and mitral annulus TD recordings were obtained in 35 patients, flow propagation velocity in 31, and PV flow in 23.
Correlation of Filling Pressures with Doppler Parameters
Table 1 summarizes the LV
pressures and Doppler parameters for the study group. A
preA pressure of 14±5 mm Hg (range, 4 to 30 mm Hg) did not
correlate with any of the left atrial volumes. Significant weak
correlations were present with mitral E velocity (r=0.4;
P=0.02) and E/A ratio (r=0.33; P=0.04;
Table 2) with no relations to other
transmitral flow parameters (Figure 2). None of the PV velocities or VTIs
including SFF related significantly with preA pressure (Figure 2). Despite the poor relations of conventional Doppler
indices with preA pressure, all had cutoff thresholds beyond which they
were specific for pressure >15 mm Hg (specificity of E/A 1.1
and SFF 
40% of 83% to a specificity of 92% for IVRT 70 ms). Ar-A
duration (PV atrial reversal velocity duration minus mitral A
duration) exhibited a significant relation with LVEDP
(r=0.53, P<0.01; Figure 3). Applying a previous
equation9 from our laboratory to predict preA
pressure in non-HCM patients resulted in a weak relation
(r=0.35, P=0.03). Likewise, a previous
equation4 derived in our laboratory to estimate LVEDP
in non-HCM patients demonstrated no relation with the measured LVEDP
(r=0.14).
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Flow propagation velocity had no significant relation to preA pressure
but related significantly to LV minimal pressure (r=-0.5,
P<0.01, Figure 4). E
velocity/flow propagation velocity demonstrated a strong relation with
preA pressure (r=0.67; SEE=4 mm Hg; P=0.02;
Figure 5). Ea demonstrated a weak
relation with preA pressure (r=-0.35, P=0.01)
and a strong relation with LV minimal pressure (r=-0.73,
P<0.001, Figure 4). Ea also had a significant
inverse correlation with the LV end systolic volume
(r=-0.55, P=0.02). E/Ea related well to preA
pressure (r=0.76; SEE=3.4 mm Hg; P<0.001;
Figure 6). PreA pressure could be
estimated with E velocity/flow propagation velocity as follows:
4.5+[5.28x(E velocity/propagation velocity)], and E/Ea could be
estimated as 3.2+[1.1x(E/Ea)]. The mean difference between the
Doppler estimate and catheter measurement was 0±3.9 mm Hg
(range, -9 to 8 mm Hg) when E velocity/flow propagation velocity
was used, and 0±3.3 mm Hg (range, -8 to 6.8 mm Hg) with
E/Ea (Bland-Altman plots in Figures 5 and 6). The
correlation between the new derived indices and preA pressure was
further examined in 11 patients with E/A <1 and DT >250 ms
(severely impaired relaxation); E velocity/flow propagation velocity
and E/Ea still related well to preA pressure (r=0.62 and
0.72, respectively).
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Detection of Filling Pressures Changes
Ten patients (10 of 35) developed complete heart block and were
pacemaker-dependent immediately after ethanol-induced septal
infarction; 8 of 35 did not undergo repeated measurements of
pressures. Accordingly, only 17 patients in normal sinus rhythm
underwent repeated simultaneous measurements of LV
pressures with Doppler echocardiography. No
significant relations were present between preA pressure changes
and changes in AT-E, DT-E, DT-A, AFF, and IVRT. Weak but insignificant
relations were noted with changes in A velocity (r=-0.43;
P=0.1), E velocity/A velocity (r=0.44;
P=0.09), and Ea (r=-0.4; P=0.11).
Significant relations were present, however, between preA pressure
changes and E velocity changes (r=0.56; P=0.01),
E velocity/flow propagation velocity (r=0.68;
P=0.01), and E/Ea (r=0.8; SEE=3.6 mm Hg;
P<0.001; Figure 7). Five of
the 6 patients with increases in preA pressure 5 mm Hg had
increments in E/Ea 2. In 1 patient, preA pressure was reduced by
5 mm Hg with diuretics; E/Ea decreased by 6.1, predicting
a pressure reduction of 6 to 7 mm Hg (Bland-Altman plot in Figure 7).
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Test Population
The equations derived with the use of E velocity/flow
propagation velocity and E/Ea in the initial group were tested
prospectively in the test population. Flow propagation velocity was
satisfactorily measured in 11 patients (in 6, the quality of the
2-dimensional traces was not adequate because of patients' supine
position on the catheterization table), whereas Ea was
ascertained in all 17. Estimation of preA pressure was possible with
either method (Figure 8). With the E
velocity/flow propagation velocity, the correlation coefficient was
0.76, and the mean difference between Doppler-estimated and
catheter-measured pressures was –0.5±5 mm Hg. Applying E/Ea,
the correlation coefficient was 0.82 and the mean difference was
–0.7±3 mm Hg between Doppler-estimated and
catheter-measured pressures. When the 52 patients were combined, E/Ea
10 had the best combination of sensitivity (92%) and specificity
(85%) for preA pressure >15 mm Hg (area under receiver
operating characteristic curve=0.91; Figure 9). For E velocity/flow propagation
velocity, a ratio 1.8 had a sensitivity of 79% with a specificity of
77%. A lower ratio (1.6) had a higher sensitivity (95%) with a
lower specificity (54%), whereas a ratio 2 was more specific (88%)
but less sensitive (68%).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrates for the first time the role of 2 new LV relaxation indices, the flow propagation velocity and Ea, in estimation of LV filling pressures in patients with HCM. Conventional mitral inflow and PV velocities had weak or no relation to filling pressures. However, mitral E velocity, corrected for the influence of LV relaxation with the use of either of the 2 new indices, related well to preA pressure. Figure 1
is from a patient with a preA pressure
of 24 mm Hg. E velocity/flow propagation velocity (2.7) predicted
a 19 mm Hg pressure. Likewise, E/Ea (16.7) predicted a 22
mm Hg pressure. Notice that the E/A ratio is <1 and that the DT is
prolonged, findings usually associated with normal filling pressures in
non-HCM patients.
Use of Conventional Doppler in the Estimation of Filling
Pressures in HCM Patients
Mitral and PV velocities are currently used in patients with
systolic dysfunction to estimate LV filling pressures with
reasonable accuracy.2 3 4 5 6 7 8 9 10 11 Recently, Nishimura et
al13 reported that HCM patients present a particular
challenge whereby conventional Doppler parameters (DT-E
and E/A) are poorly predictive of filling pressures. Our findings
further corroborate these observations. In the HCM patients in our
study, among the mitral inflow parameters, only the E
velocity and E/A ratio had significant but weak correlations with
filling pressures. DT-E, DT-A, IVRT, and AFF had no correlation with LV
diastolic pressures. Despite high filling pressures, many
patients had prolonged DT-E, E/A <1, and a high AFF. Because preload
and relaxation both influence mitral E velocity,24 this
poor correlation was present in HCM, in which relaxation is
severely impaired. Atrial volumes have been previously found to relate
to filling pressures.6 Accordingly, they were evaluated;
however, the results were still poor. Because many HCM patients
initially have left atrial hypertension in response to severely
impaired relaxation, atrial dilatation is frequently present
regardless of atrial pressures.
The PV systolic and diastolic velocities also related poorly to filling pressures, with SFF having no relation to the LV diastolic pressures measured in the present study. A similar observation was recently made by Yamamoto et al12 in non-HCM patients with normal ejection fractions (r=-0.29). In our series, a number of the patients with high filling pressures had a SFF >50%. The following may explain why the SFF remains normal in the presence of elevated filling pressures in patients with HCM. The PV systolic and diastolic antegrade flows occur in response to pressure gradients between the PV and the left atrium and are modulated by left atrial compliance and relaxation, in addition to LV relaxation and systolic function.3 In HCM patients during systole, a relatively higher pressure gradient (compared with diastole) is established between the PV and the left atrium, in part because of a normal (or increased) mitral annular descent that occurs with the hyperdynamic LV function and possibly also a hyperdynamic function and relaxation of the atrium, thus preserving systolic (S1 and S2) antegrade flow. In contrast, during diastole a relatively lower pressure gradient between the veins and the left atrium occurs because of the markedly prolonged LV relaxation, which leads to reduced atrial emptying in early diastole and, consequently, reduced PV diastolic antegrade flow.
The Ar-A duration was the only variable that had a relation to
LVEDP. However, the correlation was still weak and with large spread
(SEE=6 to 7 mm Hg). This may be related in part to the presence
of only a few patients with LVEDP <15 mm Hg and Ar-A duration
0. Accordingly, it is possible that if we had had a larger number of
HCM patients, the relation between Ar-A and LVEDP could have been
improved. In summary, the mitral and PV flow variables are helpful
only if they show patterns consistent with high filling
pressures. However, these conventional parameters are not
sensitive in patients with HCM.
Application of the New LV Relaxation Indices in HCM
Patients
Transmitral flow follows the development of an
atrioventricular pressure gradient. This gradient is
determined by the left atrial V wave and the LV minimal
pressure. In early diastole, the ventricular
pressure normally decreases rapidly before the mitral valve opens,
creating a positive pressure gradient, whereas in HCM it does so at a
slower rate. This is related to contraction load (due to LVOT
obstruction) delaying LV relaxation.25 Also, the disparity
between the myocardial mass and capillary density and the inadequate
vasodilator reserve are contributing factors.25 However,
the energy stored during systole provides restoring forces that allow
HCM patients to develop low diastolic pressures rapidly and
to "suck" blood from the atrium. In HCM, these forces can be
greater than those in healthy subjects given the small
end-systolic volumes that are frequently present in HCM
patients with small and hyperdynamic hearts. Thus, some HCM patients
can have normal filling pressures.13 Given the complex
interactions between these variables in HCM, we explored 2
relatively load-independent LV relaxation indices, flow propagation
velocity and Ea. The propagation velocity relates inversely with
14 15 16 and LV minimal
pressure.14 15 We demonstrated its relation to LV minimal
pressure in HCM patients. E velocity/flow propagation velocity has
related well to LV filling pressures in previous investigations, in
sinus rhythm21 and in atrial fibrillation.20
The correlations in both studies were similar to the one in the
present investigation (r=0.821
and r=0.6520 ). The higher correlation
observed in a previous study21 may be related to the
inclusion of patients with systolic dysfunction, in which the
mitral E velocity alone relates better to filling pressures. In the
present study, acute changes in preA pressure did not alter the
propagation velocity, further demonstrating the insensitivity of this
index to preload. In contrast, these preload changes produced similar
directional changes in mitral E velocity. The propagation velocity
corrected for the influence of LV relaxation on the E velocity and,
thus, unmasked the pressure changes.
Ea relates inversely to ,26 27 has no relation to
LVEF,18 and identifies patients with a pseudonormal mitral
inflow pattern.18 We extend the aforementioned
observations and show the strong inverse relation between LV minimal
pressure and Ea. In general, the smaller the end systolic
volume, the greater the LV elastic recoil and the lower the LV minimal
pressure and the faster the mitral annuluar basal displacement in early
diastole. Sohn et al27 have shown no Ea
changes with saline infusion or nitroglycerin, although
these interventions induced changes in E velocity and DT-E. We
previously evaluated this index in conjunction with E velocity in
non-HCM patients and found that E/Ea relates well to filling pressures
across a wide range of pressures.18 This investigation
demonstrates that E/Ea can be applied to estimate LV filling pressures
in HCM patients in a similar manner. In general, preA pressure and
pressure changes had higher correlations with E/Ea than with E
velocity/propagation velocity.
Study Limitations
Satisfactory PV velocity recordings were obtained in 23
patients (66%). This success rate is lower than what we experience
routinely in our laboratory and was probably the result of examining
patients in the supine position in the catheterization
laboratory. Although a lateral decubitus position could have provided a
higher yield, imaging in this position is mostly feasible outside the
catheterization laboratory and would have precluded the
simultaneous acquisition of pressure and Doppler data.
Except for Ar-A, it is unlikely that a higher success rate of PV
velocity recordings would have altered the results, given the
poor relation between these velocities and filling pressures. In
contrast, flow propagation velocity and Ea were recorded in the
majority of patients. Annular velocities can be recorded at
multiple corners of the annulus. We measured Ea at the lateral corner
because we previously noted that the lateral annulus Ea is higher and
more reproducible than that of the septal Ea,18
particularly in HCM patients who often have low septal Eas.
Furthermore, our study design included repeat measurements of Ea after
septal infarction, and, therefore, septal velocities then will reflect
more regional than global diastolic function in comparison
to lateral annulus Ea.
There are currently many methods that can be used to measure the early flow propagation velocity. One involves the use of computer analysis to determine either time intervals or slope along the color flow distribution.14 16 Another approach determines the slope of a line connecting 2 points, the point of maximal velocity around the mitral orifice and the point at which this velocity decreases to 70% of its initial value.15 A modified approach used by our group and others involves baseline shift until a distinct color border is obtained and then measurement of the slope of its most linear component past the valve leaflets. At times, blurred wave front signals make it difficult to determine the margin and is a limitation for this methodology. This may explain the better results with E/Ea. Temporal and regional relaxation differences are common in patients with HCM25 and contribute to the diastolic dysfunction, limiting to some degree the application of a single measurement of flow propagation and Ea as parameters of LV relaxation. The 95% confidence limits of the Doppler estimates of filling pressures with either of the 2 new methods were wide and limited the accuracy of an individual estimate (particularly using the flow propagation velocity). Nevertheless, the new methods described in this investigation, which use cutoff values with a high specificity, can provide a good separation between HCM patients with high filling pressures and those with low filling pressures and can detect changes in filling pressures after interventions. Therefore, this new methodology represents a measurable advance in the noninvasive estimation of LV filling pressures in HCM patients.
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Acknowledgments |
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The authors thank Anna Zamora for expert secretarial assistance.
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Footnotes |
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Guest Editor for this article was A. Jamil Tajik, MD, Mayo Clinic, Rochester, Minn.
Received April 22, 1998; revision received August 26, 1998; accepted September 25, 1998.
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27. Sohn D-W, Chai I-H, Lee D-J, Kim H-C, Kim H-S, OH B-H, Lee M-M, Park Y-B, Choi Y-S, Seo J-D, Lee Y-W. Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol. 1997;30:474–480.We evaluated the role of early flow propagation velocity and annular early diastolic velocity (Ea) as parameters of left ventricular relaxation in estimating filling pressures in 35 hypertrophic cardiomyopathy patients. PreA pressure related poorly or not at all with conventional 2-dimensional and Doppler parameters of diastolic function. In contrast, mitral E/early flow propagation velocity and E/Ea related well with preA pressure and accurately tracked pressure changes. These ratios estimated well preA pressure when tested prospectively in 17 additional hypertrophic cardiomyopathy patients.[Abstract]
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