CLINICAL RESEARCH
Diastolic mitral annular velocityduring the development of heart failure
Hiroshi Hasegawa, MD, PhD*,
William C. Little, MD*,*,
Michiya Ohno, MD, PhD*,
Steffen Brucks, MD*,
Atsushi Morimoto, MD, PhD*,
Heng-Jie Cheng, MD, PhD* and
Che-Ping Cheng, MD, PhD*
* Cardiology Section, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA
Manuscript received November 4, 2002;
revised manuscript received January 14, 2003,
accepted January 24, 2003.
* Reprint requests and correspondence: Dr. William C. Little, Cardiology Section, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157-1045, USA.
wlittle{at}wfubmc.edu
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Abstract
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OBJECTIVES: We sought to investigate the mechanism of reduced diastolic mitral annular velocity with diastolic dysfunction, despite elevated left atrial (LA) pressure.
BACKGROUND: The peak rate of left ventricular (LV) early diastolic filling (E) and velocity of the mitral annulus due to long-axis lengthening (EM) are reduced in mild diastolic dysfunction. With more severe dysfunction, E increases in response to increased LA pressures. In contrast, EM decreases, despite increased LA pressure.
METHODS: We studied eight dogs instrumented to measure LA pressure, LV pressure, and internal dimensions during the progressive development of heart failure (HF) produced by rapid pacing.
RESULTS: Early diastolic filling decreased after four days of pacing from 114 ± 32 to 88 ± 22 ml/s (p < 0.05), but with more severe HF, it progressively increased to 155 ± 32 ml/s (p < 0.05). In contrast, EM progressively decreased from 44 ± 12 mm/s during the control period to 24 ± 8 mm/s after four weeks (p < 0.05). Although EM was related to the time constant of LV relaxation (tau) (R2 = 0.85), E was not. The latter occurred coincident with termination of the early diastolic LA to LV pressure gradient during all conditions. In contrast, with increasing HF, EM was progressively delayed after LA to LV pressure crossover by 37 ± 12 ms (p < 0.05). The time from E to EM was related to tau (R2 = 0.97).
CONCLUSIONS: With slowed relaxation during the development of HF, EM is reduced and delayed so that it occurs after early, rapid filling. Thus, with slowed relaxation, EM does not respond to the early diastolic LA to LV pressure gradient, because it occurs when LV pressure is greater than or equal to LA pressure.
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Abbreviations and Acronyms
| | DAP | = anteroposterior dimension | | DLA | = long-axis dimension | | DSL | = septolateral dimension | | dV/dt | = time derivative of left ventricular volume | | E | = peak early diastolic left ventricular filling | | EM | = peak velocity of mitral annulus away from apex during early diastole | | HF | = heart failure | | LA | = left atrial/atrium | | LV | = left ventricle/ventricular | | tau | = time constant |
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The pattern of left ventricular (LV) filling, as determined by Doppler echocardiography, is used to non-invasively evaluate LV diastolic performance (1,2). Recently, the diastolic motion of the mitral annulus, as measured by tissue Doppler imaging, has been used to provide additional information (3–7).
The LV fills in diastole in response to the pressure gradient from the left atrium (LA) to the LV (8). This occurs at two times during the cardiac cycle: early in diastole after mitral valve opening and late in diastole during atrial systole. The peak rate of early diastolic filling (E) is determined by the LA to LV pressure gradient generated as LV pressure falls below LA pressure (8,9).
The normal pattern of LV filling is altered by diastolic dysfunction, such as that which occurs during the development of heart failure (HF) (1,2,5,7,10). With mild diastolic dysfunction, E is reduced due to a slowing of the rate of LV relaxation (1,10). With worsening diastolic dysfunction, E returns to its normal level. This "pseudonormalization" is due to the effect of increasing LA pressure (1,10), which restores the early diastolic LA to LV pressure gradient, despite a slower rate of LV relaxation and increased LV early diastolic pressure. With even more severe dysfunction, the peak E rate may be higher than normal.
The peak velocity of the mitral annulus away from the apex during early diastole (EM), indicating the rate of longitudinal expansion of the LV, is reduced in patients with impaired relaxation. However, in contrast to E, EM is reduced further in patients with pseudonormalized or restricted filling patterns, despite elevated LA pressure (3,5). Nagueh et al. (11) found in experimental animals that when the rate of LV relaxation is reduced, EM measured by tissue Doppler is not influenced by the early diastolic LA to LV pressure gradient. Similarly, Yalcin et al. (12) found that EM was not altered by changes in preload in patients with LV dysfunction. Thus, EM provides a method to distinguish pseudonormal and restricted filling from the normal filling pattern (3,5,6). Furthermore, because E increases in response to an increase in the LA to LV pressure gradient due to an elevation of LA pressure but EM does not, the ratio of E/EM provides a non-invasive index of LA pressure (4,13,14). The mechanism of the failure of EM to respond to an increased LA to LV pressure gradient in the presence of diastolic dysfunction is not known.
We hypothesized that in the presence of severe diastolic dysfunction, with slowed LV relaxation, EM does not occur during rapid, early filling. Instead EM is delayed and predominately caused by rearrangement of the LV after rapid filling has been nearly completed. If this is correct, EM is insensitive to changes in LA pressure and the transmitral pressure gradient because it occurs after equilibration of LA and LV pressures. Furthermore, the delay in EM may reflect the degree of slowing of LV relaxation.
This study was undertaken to test these hypotheses by evaluating long-axis lengthening, LV filling (determined from the time derivative of left ventricular volume [dV/dt]), and LA and LV pressures in dogs during the development of progressive diastolic dysfunction associated with HF produced by rapid pacing (10).
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Methods
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Instrumentation.
Eight healthy mongrel dogs weighing between 23 and 35 kg were instrumented. Observations of LV filling dynamics (but not long-axis lengthening) from five of these animals were included in a previous report (10). Anesthesia was induced with xylazine (2.0 mg/kg intramuscularly) and sodium pentobarbital (6 mg/kg intravenously) and maintained with halothane (1% to 2%). The pericardium was opened through a left thoracotomy. Micromanometer pressure transducers (Konigsberg Instruments, Pasadena, California) and polyvinyl catheters for transducer calibration (1.1 mm internal diameter) were inserted into the LV through the LV apical stab wound and into the LA through the LA appendage. The LV transducer was snugly placed on the endocardial surface of the apex and sutured in place. Hydraulic occluded cuffs were placed around the vena cavae.
Three pairs of ultrasonic crystals (5 MHz) were implanted in the endocardium of the LV to measure the anteroposterior (DAP), septolateral (DSL), and base–apex or long-axis (DLA) dimensions (15). The crystals used to measure DLA were placed at the apex and on the septal side of the mitral annulus. A pacing lead was attached to the right ventricle or right atrium and connected to a programmable pacemaker (model 8329, Medtronic Inc., Minneapolis, Minnesota) implanted subcutaneously. All wires and tubing were exteriorized through the posterior neck.
Data collection.
Studies were begun after full recovery from instrumentation (10 to 14 days after surgery). The LV and LA catheters were connected to pressure transducers (Statham p23Db, Gould, Valley View, Ohio) calibrated with a mercury manometer. The signal from the micromanometer was adjusted to match that of the catheter. The LA micromanometer was adjusted to match LA and LV pressures at the end of long periods of diastasis.
The analog signals were digitized at 200 Hz. Each data acquisition period lasted for 12 s, spanning several respiratory cycles.
Experimental protocol.
Data were recorded with conscious, unsedated animals standing quietly. Control data were acquired after full recovery from the surgical instrumentation before initiating pacing. Pacing was then started at 200 to 230 beats/min to produce HF (16). To record data, we turned off the pacemaker transiently after four days of pacing and then after approximately one, two, three, and four weeks of pacing. Before we acquired data, the animals were allowed to stabilize for 30 min with the pacer turned off. After the data were recorded, the pacing was reinstituted.
The dependence of filling parameters on load was assessed in five of the animals, using transient caval occlusions before and after HF (16).
Postmortem evaluation.
At the conclusion of the studies, the animals were euthanized with an overdose of pentobarbital, and the hearts were examined to confirm the proper positioning of instrumentation.
Data processing and analysis.
As previously described (16,17), LV volume was calculated as a modified general ellipsoid. The rate of LV relaxation was analyzed by determining the exponential time constant (tau) of the isovolumic fall of LV pressure using the equation:  as we have previously described (15).
Ventricular filling patterns were measured using the time derivative of LV volume (dV/dt) and of each of the three LV diameters (dDAP/dt, dDSL/dt, and dDLA/dt). The characteristics of the filling patterns were evaluated by determining the maximal rates of E or lengthening in each of the three dimensions (EAP, ESL, EM).
Because the position of the LV apex remains fixed during diastole, DLA reflects the motion of the mitral annulus (18). We compared EM measured from dDAP/t to the peak velocity of the septal mitral annulus by using tissue Doppler imaging (Sonus 5500, Agilent Technology, Palo Alto, California) with the transducer placed at the apex.
Statistical analysis.
Changes in the variables during the development of HF were assessed using repeated-measures analysis of variance. If significant differences were present, comparisons to control values were performed using Dunnett’s test. We assessed the relationship of E and EM to the peak LA to LV pressure gradient by determining the slopes of their linear regression during caval occlusions before and after HF (4 weeks of pacing). The correlations of variables during the development of HF were assessed by linear regression of the mean values at each time period. A p value <0.05 was accepted as significant. Data are expressed as the mean value ± SD.
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Results
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Using tissue Doppler imaging, EM measured from the maximum early diastolic dDLA/dt was similar to the peak early diastolic velocity of the septal mitral annulus (R2 = 0.98, SEE = 6.8 mm/s, y = 0.8x + 18 mm/s).
Rapid pacing produced a progressive deterioration in LV diastolic and systolic performance (Table 1). An example of the relationships between E and EM to the peak LA to LV pressure gradient before and after HF is shown in Figure 1. For the group, the slope relating E to the peak LA to LV pressure gradient was similar both before (25.3 ± 10.8 ml/s per mm Hg) and after HF (20.3 ± 5.8 ml/s per mm Hg, p = NS). In contrast, EM was much less sensitive to the pressure gradient after HF (3.0 ± 1.9 vs. 11.6 ± 9.4 mm/s per mm Hg, p < 0.01).
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Figure 1 Plots of the peak left ventricar (LV) filling rate (E) and peak rate of longitudinal expansion (EM) to the peak early diastolic left atrial (LA) to LV pressure gradient during transient caval occlusions before and after heart failure (HF) was produced by four weeks of rapid pacing. Under normal conditions, both E and EM are strongly related to the pressure gradient, indicated by the slopes of the linear regression lines. The dependence of E on the pressure gradient is not altered by HF. In contrast, the dependence of EM on the pressure gradient is markedly reduced after HF.
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Under normal conditions, all three LV dimensions and LV volume increased simultaneously during rapid early diastolic filling (Fig. 2). With the development of HF, the early diastolic lengthening of DLA was progressively delayed. So with severe HF, the expansion of DLA occurred after termination of the early diastolic LA to LV pressure gradient and after most of the early diastolic increase in LV volume and expansion of the two short axes (DSL and DLA) had occurred.
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Figure 2 Analog recordings in a conscious animal before (normal) and after producing progressive heart failure (HF) with four weeks of rapid pacing. Shown are left atrial (LA) and left ventricular (LV) pressures (PLA/PLV), LV volume (VLV), and three LV internal dimensions: anteroposterior (DAP), septolateral (DSL), and long axis (DLA). Under normal conditions, the increase in LV volume during early diastolic filling occurs as all three dimensions expand symmetrically. Most of the increase in LV volume and expansion occurs before the crossover of PLV and PLA (dotted line). In contrast, after HF, the expansion of the long axis is delayed (arrows), occurring after PLA is greater than or equal to PLV, and most of the early diastolic increase in LV volume and expansion of the short-axis dimensions (DSL and DAP) is complete.
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The peak rate of E and the peak expansion rate of the anteroposterior (EAP) and septolateral (ESL) dimensions initially declined in response to a decrease in the early diastolic LA to LV pressure gradient and subsequently increased as the LA to LV pressure gradient increased with worsening HF (Figs. 3 and 4). In contrast, EM progressively declined, despite the increasing pressure gradient during the development of HF. Although E, EAP, and ESL were positively correlated with the peak LA to LV pressure gradient, EM was negatively correlated (Fig. 4).
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Figure 3 Analog recordings of left ventricular (LV) and left atrial (LA) pressures (P), the rate of change of LV volume (dV/dt), and the long-axis dimensions of the LV (dDLA/dt) during the progressive development of pacing-induced heart failure (HF) in a conscious animal. The peak diastolic filling rate (E) declined with mild HF (four days) but progressively increased with more severe HF. In contrast, the peak expansion rate of DLA (EM) progressively declined with increasing HF. Under all circumstances, E coincided with the crossover of LA and LV pressures (dotted line). In contrast, the peak long-axis lengthening (EM) was progressively delayed, relative to E and LA/LV pressure crossover, with increasingly severe HF. Thus, starting after four days of pacing, EM occurred when LV pressure  LA pressure.
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Figure 4 The peak early diastolic left ventricular (LV) filling rate (E) and peak lengthening rate of the LV anteroposterior dimension (EAP) and septolateral dimension (ESL) were closely related to the peak early diastolic left atrial (LA) to LV pressure gradient during the development of heart failure (HF). In contrast, the peak long-axis lengthening rate (EM) progressively declined, despite the increase in the LA to LV pressure gradient during the development of HF.
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Under normal conditions, the peak rate of LV volume increase (dV/dt) and the peak expansion rate of all three LV diameters (EAP, ESL, EM) occurred simultaneously, coincident with the crossover of LA and LV pressures (Fig. 3). During worsening HF, E, EAP, and ESL continued to occur at the same time as the crossover of LA and LV pressures (Figs. 3 and 5) , but the occurrence of EM was progressively delayed so that it occurred 37 ± 12 ms (p < 0.05) after LA/LV pressure crossover in severe HF (Fig. 5).
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Figure 5 During the development of heart failure (HF), the peak early diastolic left ventricular (LV) filling rate (E) and peak lengthening rate of the LV anteroposterior dimension (EAP) and septolateral dimension (ESL) occurred nearly simultaneously with the crossover of LV and left atrial (LA) pressures. In contrast, the peak long-axis lengthening rate (EM) occurred progressively later during the development of HF.
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As LV relaxation slowed during the development of HF (manifest as a longer time constant), EM decreased and was correlated with tau (R2 = 0.85, p < 0.01). In contrast, E did not correlate with tau (Fig. 6).
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Figure 6 The peak early diastolic left ventricular (LV) filling rate (E) was not related to the time constant of LV pressure fall. In contrast, the peak long-axis lengthening rate (EM) and the time from E to EM were closely related to the time constant.
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Discussion
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Our study examined the effect of progressive diastolic dysfunction produced by rapid pacing on the dynamics of LV filling and the motion of the mitral annulus determined from long-axis lengthening. The peak rate of LV filling, E decreased with mild diastolic dysfunction but progressively increased in response to elevations in LA pressure and the early diastolic LA to LV pressure gradient. This results in E returning to normal levels (pseudonormalization) and ultimately exceeding normal (restrictive filling) in severe HF. In contrast, the peak rate of long-axis lengthening (EM) progressively declined with worsening HF, despite the increases in LA pressure and the LA to LV pressure gradient. Thus, E had a biphasic response to worsening HF and did not reflect LA pressure or the rate of LV relaxation (5). In contrast, EM progressively decreased, despite the increasing LA to LV pressure gradient with worsening HF. Thus, EM (but not E) accurately reflected the progressive slowing of LV relaxation as HF developed.
Why does E respond to increases in the LA to LV pressure gradient during HF, but EM does not? The LV fills in response to the LA to LV pressure gradient, generated as LV relaxation causes early diastolic LV pressure to fall below LA pressure. Normally, this pressure gradient does not just exist from the LA to the LV inflow tract. Instead, rapid LV relaxation produces a progressive pressure gradient that extends all the way to the LV apex (19). This progressive pressure gradient is apparent on color Doppler M-mode echocardiography as a rapid velocity of flow propagation toward the apex (20). The pressure gradient from the inflow tract to the apex is increased when LV relaxation is enhanced (21). In contrast, the inflow tract to apex pressure gradient and rapid flow propagation are lost when LV relaxation is slowed (22). Thus, in the presence of impaired relaxation, there is a delay from the time blood enters the LV inflow tract until filling of the apex. Consistent with this concept, we observed that under normal conditions, the peak inflow (E) and the peak lengthening of the long axis (EM) occurred nearly simultaneously. However, during the progressive development of HF, EM occurred after E. The peak rate of E and peak rate of expansion of the two short axes (DSL and DAP) occurred coincident with the equilibration of LA and LV pressure under normal conditions and with progressive HF (Figs. 2, 3, and 5). After LA and LV pressures equalize, there is no longer a pressure gradient to further accelerate flow into the LV. With continued filling, LV pressure then exceeds LA pressure, decelerating and stopping early filling (23). Under normal conditions, the peak long-axis lengthening (EM) also occurs nearly coincident with the crossover of LA and LV pressures. However, with slowing of the rate of LV relaxation (i.e., longer tau), EM is delayed so that it occurs in severe HF up to 37 ± 12 ms after the crossover of LA and LV pressures and after LV filling (dV/dt) has almost ceased (Figs. 2, 3, and 5). Thus, under these circumstances, EM is occurring when LV pressure is greater than or equal to LA pressure.
Consistent with the experimental findings of Nagueh et al. (4) and Firstenberg et al. (24), we found that in the presence of normal LV relaxation, EM is sensitive to changes in the LA to LV pressure gradient. However, with slowed relaxation, the dependence of EM on the pressure gradient is greatly reduced (Fig. 1). We found that when LV relaxation is slowed, EM occurs after LV pressure equals or exceeds LA pressure and is predominantly due to the redistribution of blood that entered the LV earlier in diastole. Thus, with slowed relaxation, EM is much less dependent on the pressure gradient.
Although EM is related to the rate of LV relaxation during the development of HF, we observed no relationship between E and tau (Fig. 6). The delay of EM after E is closely correlated with slowed relaxation. This is consistent with the concept that the delay in the occurrence of EM results from slowed relaxation (22) and suggests that it might provide a non-invasive measure of LV relaxation if it can be measured with adequate temporal resolution.
Clinically, the LV filling pattern is assessed by Doppler measurement of the mitral valve flow velocity, and longitudinal lengthening (EM) by tissue Doppler measurement of mitral annular motion. In this study, we measured EM as the peak rate of lengthening of the long axis (dDLA/dt). Because the position of the apex remains fixed during diastole (18), we found that the EM we measured (peak dDLA/dt) is equivalent to the EM measured by tissue Doppler imaging of the velocity of the mitral annulus away from the apex. We determined E from the derivative of LV volume (dV/dt). This is equivalent to mitral flow. Because the effective mitral orifice is relatively constant during diastole, the pattern of LV filling (dV/dt) we measured is similar to the pattern of diastolic filling assessed clinically by Doppler measurement of mitral valve flow velocity, as we have previously observed (23).
We studied an animal model of progressive systolic and diastolic dysfunction without significant mitral regurgitation produced by rapid pacing (10). This model mimics many of the functional, structural, and neurohormonal features of a dilated cardiomyopathy (16,17). However, we cannot be certain that our findings apply to diastolic dysfunction produced by other conditions.
We conclude that under normal circumstances, the LV expands symmetrically during rapid, early filling. Peak longitudinal expansion (EM) occurs nearly coincident with the peak E in response to a pressure gradient that extends from the LA to LV apex. The synchrony of LV diastolic expansion is altered by the delayed relaxation that is present with pseudonormalized and restricted filling patterns. Early filling is maintained by an elevated LA pressure, despite slowed relaxation; however, in this situation, longitudinal expansion does not occur during rapid, early filling. Instead, it is delayed, occurring after the crossover of LA and LV pressures. The longitudinal expansion of the LV (apparent as EM) is reduced and delayed by slower relaxation and not substantially influenced by LA pressure in the presence of diastolic dysfunction with pseudonormalized and restricted filling patterns. Thus, in contrast to E, EM provides a consistent measure of diastolic dysfunction, despite increases in LA pressure.
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Acknowledgments
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We are grateful for the technical assistance of Mike Cross and the secretarial assistance of Amanda Burnette.
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Footnotes
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This study was supported in part by grants R01-HL53541 and R01-AA12335 from the National Institutes of Health, Bethesda, Maryland, and by grant 9640189N from the American Heart Association.
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S. Masutani, W. C. Little, H. Hasegawa, H.-J. Cheng, and C.-P. Cheng
Restrictive Left Ventricular Filling Pattern Does Not Result From Increased Left Atrial Pressure Alone
Circulation,
March 25, 2008;
117(12):
1550 - 1554.
[Abstract]
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L. Hatle
How to diagnose diastolic heart failure a consensus statement
Eur. Heart J.,
October 2, 2007;
28(20):
2421 - 2423.
[Full Text]
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W. H. Gaasch and W. C. Little
Assessment of Left Ventricular Diastolic Function and Recognition of Diastolic Heart Failure
Circulation,
August 7, 2007;
116(6):
591 - 593.
[Full Text]
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C.-M. Yu, J. E. Sanderson, T. H. Marwick, and J. K. Oh
Tissue Doppler Imaging: A New Prognosticator for Cardiovascular Diseases
J. Am. Coll. Cardiol.,
May 15, 2007;
49(19):
1903 - 1914.
[Abstract]
[Full Text]
[PDF]
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J. Wang, D. S. Khoury, V. Thohan, G. Torre-Amione, and S. F. Nagueh
Global Diastolic Strain Rate for the Assessment of Left Ventricular Relaxation and Filling Pressures
Circulation,
March 20, 2007;
115(11):
1376 - 1383.
[Abstract]
[Full Text]
[PDF]
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G. W. De Keulenaer and D. L. Brutsaert
Systolic and diastolic heart failure: Different phenotypes of the same disease?
Eur J Heart Fail,
February 1, 2007;
9(2):
136 - 143.
[Abstract]
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L. Shmuylovich and S. J. Kovacs
Load-independent index of diastolic filling: model-based derivation with in vivo validation in control and diastolic dysfunction subjects
J Appl Physiol,
July 1, 2006;
101(1):
92 - 101.
[Abstract]
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M. Gharib, E. Rambod, A. Kheradvar, D. J. Sahn, and J. O. Dabiri
Optimal vortex formation as an index of cardiac health
PNAS,
April 18, 2006;
103(16):
6305 - 6308.
[Abstract]
[Full Text]
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J. K. Oh, L. Hatle, A. J. Tajik, and W. C. Little
Diastolic Heart Failure Can Be Diagnosed by Comprehensive Two-Dimensional and Doppler Echocardiography
J. Am. Coll. Cardiol.,
February 7, 2006;
47(3):
500 - 506.
[Abstract]
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Q. Ruan, L. Rao, K. J. Middleton, D. S. Khoury, and S. F. Nagueh
Assessment of left ventricular diastolic function by early diastolic mitral annulus peak acceleration rate: experimental studies and clinical application
J Appl Physiol,
February 1, 2006;
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[Abstract]
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W. C. Little
Diastolic Dysfunction Beyond Distensibility: Adverse Effects of Ventricular Dilatation
Circulation,
November 8, 2005;
112(19):
2888 - 2890.
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J.-W. Ha, J.-R. Cho, J.-M. Kim, J.-A. Ahn, E.-Y. Choi, S.-M. Kang, S.-J. Rim, and N. Chung
Tissue Doppler-Derived Indices Predict Exercise Capacity in Patients With Apical Hypertrophic Cardiomyopathy
Chest,
November 1, 2005;
128(5):
3428 - 3433.
[Abstract]
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J. K. Oh
Echocardiography as a Noninvasive Swan-Ganz Catheter
Circulation,
June 21, 2005;
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A. Diwan, M. McCulloch, G. M. Lawrie, M. J. Reardon, and S. F. Nagueh
Doppler Estimation of Left Ventricular Filling Pressures in Patients With Mitral Valve Disease
Circulation,
June 21, 2005;
111(24):
3281 - 3289.
[Abstract]
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A. E. Weyman
The year in echocardiography
J. Am. Coll. Cardiol.,
February 1, 2005;
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[Full Text]
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M. Filipovic, J. Wang, I. Michaux, P. Hunziker, K. Skarvan, and M. D. Seeberger
Effects of halothane, sevoflurane and propofol on left ventricular diastolic function in humans during spontaneous and mechanical ventilation
Br. J. Anaesth.,
February 1, 2005;
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[Abstract]
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D.-W. Sohn, Y.-J. Kim, Y.-B. Park, and Y.-S. Choi
Clinical validity of measuring time difference between onset of mitral inflow and onset of early diastolic mitral annulus velocity in the evaluation of left ventricular diastolic function
J. Am. Coll. Cardiol.,
June 2, 2004;
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[Abstract]
[Full Text]
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M. Henein and P. O'Callaghan
"From bedside to bench"
J. Am. Coll. Cardiol.,
March 3, 2004;
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928 - 928.
[Full Text]
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W. C. Little
Reply
J. Am. Coll. Cardiol.,
March 3, 2004;
43(5):
928 - 928.
[Full Text]
[PDF]
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A. E. Weyman
The year in echocardiography
J. Am. Coll. Cardiol.,
January 7, 2004;
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[Full Text]
[PDF]
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C. Rivas-Gotz, D. S. Khoury, M. Manolios, L. Rao, H. A. Kopelen, and S. F. Nagueh
Time interval between onset of mitral inflow and onset of early diastolic velocity by tissue Doppler: a novel index of left ventricular relaxation: Experimental studies and clinical application
J. Am. Coll. Cardiol.,
October 15, 2003;
42(8):
1463 - 1470.
[Abstract]
[Full Text]
[PDF]
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J. K. Oh and J. Tajik
The return of cardiac time intervals: The Phoenix is rising
J. Am. Coll. Cardiol.,
October 15, 2003;
42(8):
1471 - 1474.
[Full Text]
[PDF]
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Abstract
Methods