| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Qingdao University Medical College Hospital, Qingdao, China; 2Cardiovascular Research Group, Department of Cardiac Sciences and Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada; and 3Department of Bioengineering, Imperial College of Science, Technology and Medicine, London, United Kingdom
Submitted 1 March 2004 ; accepted in final form 18 November 2004
 |
ABSTRACT |
|---|
 TOP ABSTRACT MATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXGRANTSREFERENCES |
|---|
)] and, by the second, end-systolic volume (VLVES). We used wave-intensity analysis (WIA) to measure the total energy transported by the backward expansion wave (IW–) during LV relaxation in an attempt to reconcile these mechanisms. In six anesthetized, open-chest dogs, we measured aortic, LV (PLV), LA (PLA), and pericardial pressures and LV volume by orthogonal ultrasonic crystals. Mitral velocity was measured by Doppler echocardiography, and aortic velocity was measured by an ultrasonic flow probe. Heart rate was controlled by pacing, VLVES by volume loading, and by isoproterenol or esmolol administration. IW– was found to be inversely related to and VLVES. Our measure of DS, the energy remaining after mitral valve opening, IW–DS, was also found to be inversely related to and VLVES and was 
10% of the total "aspirating" energy generated by LV relaxation (i.e., IW–). The size of the Doppler (early filling) E wave depended on IW–DS in addition to IW+, the energy associated with LA decompression. We conclude that the energy of the backward-going wave generated by the LV during relaxation depends on both the rate at which elastance decreases (i.e., ) and VLVES. WIA provides a new approach for assessing DS and reconciles those two previously proposed mechanisms. The E wave depends on DS in addition to LA decompression.
diastole; hemodynamics; mitral valve; ventricles
Wiggers implied that the relaxing LV generates an "aspirating force" from the moment LV pressure begins to decrease. Accordingly, as elaborated upon below, the first effect of a relaxation-generated aspirating force must be to decelerate the mass represented by the stroke volume. Relaxation continues through isovolumic relaxation and only the energy remaining when the mitral valve opens can augment diastolic filling. The second proposed mechanism of DS is represented by Bloom (4, 5) and Brecher (7–9) and a number of later investigators including ourselves (1, 2, 16, 17, 22–24), who related DS to negative LV pressure (PLV) and the sigmoidal nature of the diastolic LV transmural pressure-volume (P-V) relation. As LV transmural pressure (PLVTM) is negative at small volumes, this explanation implies that the LV will tend to refill itself until transmural pressure (PTM) is zero and that the smaller the LV end-systolic volume (VLVES), the greater the DS.
Because of its ability to identify and measure upstream and downstream events and their interaction, we used wave-intensity analysis (WIA) (27, 39, 40), as we have done with respect to other hemodynamic problems (20, 21, 45). WIA provides information regarding the direction, intensity, and type of waves present at any given moment and location in a blood vessel. Because it is a time-domain analysis, wave intensity can be related temporally to hemodynamic parameters and beat-to-beat analyses can be performed (28, 39). WIA is based on the concept that "waves" [i.e., propagated disturbances (35)] that travel through the vasculature are manifested by changes in pressure and velocity (40). The energy that is transported by a wave can be quantified by measuring the changes in pressure and velocity across the wavefront (35). Waves can be either forward (i.e., in the direction of net blood flow) or backward going in direction and either compression or expansion in type. Thus there are four possible combinations: forward compression, backward compression, forward expansion, and backward expansion waves. Compression waves have a "pushing" effect and increase pressure. Forward-going compression waves increase pressure and increase velocity, whereas backward-going compression waves increase pressure and decrease velocity (in the forward direction). Expansion waves have a "pulling" effect and decrease pressure (43). Forward-going expansion waves decrease pressure and decrease velocity, whereas backward-going expansion waves decrease pressure and increase velocity (in the forward direction).
Thus, according to WIA, blood in the cardiovascular system is accelerated or decelerated by forward- or backward-going compression or expansion waves (28). At the beginning of systolic ejection, the LV generates a compression wave that accelerates stroke volume and, after the LV begins to relax, an expansion wave that decelerates stroke volume, reducing aortic flow to zero and causing the aortic valve to close. During isovolumic relaxation, the falling ventricular pressure generates self-cancelling forward and backward expansion waves. When the mitral valve opens, the backward expansion wave, which continues until PLV reaches a minimum, propagates into the atrium and initiates diastolic filling. Only the fraction of the total energy of this expansion wave that remains at the opening of the mitral valve can augment diastolic filling.
Therefore, the purpose of this study was to measure the total "aspirating energy" (i.e., IW–; see below) associated with LV relaxation and to test the hypothesis that IW– depends on both the rate at which elastance decreases [as measured by the exponential time constant of LV relaxation ()] and the completeness of LV emptying (as measured by VLVES). In addition, we measured the fraction of IW– expended in decelerating the stroke volume at the end of systolic ejection, the fraction associated with isovolumic relaxation, and the fraction available to accelerate mitral inflow. Finally, we studied the acceleration phase of the Doppler E wave and related its magnitude to its possible causes [i.e., the "push" from the decompressing left atrium (LA) and/or the "pull" from the relaxing LV, a.k.a. DS].
Glossary
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXGRANTSREFERENCES |
|---|
90 min and, after a 30-min equilibration period, collection of the data required 2 h.
Experimental protocol.
The rationale of our protocol was to acquire a "three-dimensional" matrix of data by systematically manipulating three independent variables [PLVED (as a means of changing VLVES), HR, and ] through wide ranges. Starting at PLVED = 10 mmHg, HR was increased continuously from 90 to 130 beats/min. We then gave esmolol (0.1 mg/kg LV bolus) and repeated the HR manipulation. Next, after allowing several minutes for recovery, we gave isoproterenol (0.3 µg/kg LV bolus) and repeated the HR manipulation again. PLVEDs of 15, 20, and 25 mmHg were achieved by infusing volume (an albumin-Ringer lactate solution). At each volume level, we recorded a series of transmural P-V loops during blood withdrawal and/or constriction of the posterior vena cava. At each level of PLVED, the same HR and esmolol-isoproterenol interventions were performed. This provided a range of at the control and extreme values of both VLVES and HR, thus describing a matrix of data in terms of the independent variables (i.e., HR, , and PLVED). Between each intervention, enough time was allowed for hemodynamic stability to be reestablished. Data were recorded using a computer system (Sonometrics; Ontario, Canada); each data-acquisition period lasted 2 min.
Data processing and analysis. The digitized data were analyzed (CVSOFT, Odessa Computer System; Calgary, Alberta, Canada); hemodynamic values were obtained by averaging the data obtained during steady-state recording intervals that spanned at least three expiratory cycles.
ED was defined as the relative minimum in PLV that followed the A wave. End-ejection (i.e., ES) was defined by the incisura in the PAo waveform. PLVTM equalled (PLV – PPeric). VLV was modelled as a modified general ellipsoid using the following formula: VLV = (
/6)·DAP·DSL·DLA. VLVES was normalized by the LV V0 for each dog [i.e., VLVES (%) = (VLVES / V0)·100]. V0 (the zero-pressure intercept of the end-diastolic P-V relationship) was estimated by first collecting a series of PLVTM and VLV data points and then characterizing the plot with two logarithmic curves (one for each of the positive and negative portions of the PLVTM-VLV relation) (37). was determined by fitting the data from minimum dPLV/dt to mitral valve opening to the following equation: P(t) = PA·e–t/ + PB, where t is the time from minimum dPLV/dt, PA is PLV at that instant, and PB is PLV when t = 
.
To determine the degree to which relaxation was complete at the time of mitral valve opening, we expressed that value of PLV as a fraction of the difference between the asymptotic value (PB) and the end-systolic value.
The intensity of the wave that travelled backward from the LV was calculated using the following formula: dIW– = –(4c)–1(dP – cdU)2, where is the density of blood (kg/m3), c is the wave speed (m/s), dP is the incremental difference in PLV (1 mmHg = 133 N/m2) during a 5-ms sampling interval, and dU is the difference in mitral velocity (m/s) (40). The intensity of the wave that travelled forward from the LA was calculated using the following formula: dIW+ = (4c)–1(dP + cdU)2. Wave speed was calculated continuously throughout the cardiac cycle using the following equation: c = (ElA/)0.5 (50). [We compared these values to that estimated as c = dP/dU (39), particularly examining the value at the beginning of LV filling when reflections can be expected to be minimal, and found excellent agreement.] Elastance (E) was defined as E = PLV/(VLV – Vd), where Vd is the zero-pressure intercept of the end-systolic P-V relationship, l is length and equalled DLA, and A is area and equalled (/4)(DAP·DSL)2. Because the end-systolic P-V relationship had not been explicitly defined by caval constriction in most dogs, Vd was assumed to be 72% of V0 based on data from a subset of three dogs.
For this study, we adopted the convention that LV inflow velocities (i.e., the mitral E and A waves) should be given positive values and LV outflow velocity (i.e., aortic flow divided by estimated cross-sectional area) should be given a negative value (see Fig. 1).1 Thus the dIW– waveform (W/m2, power per unit cross-sectional area of the backward-going expansion wave) described the instantaneous aspirating power associated with LV relaxation (52). We calculated the total time integral under (i.e., between the waveform and zero) the dIW– waveform [IW– (J/m2), energy per unit cross-sectional area] to calculate the total aspirating energy. To determine the fraction of the total aspirating energy that was expended as hydraulic work to decelerate the aortic column of blood, we plotted the area under the dIW– waveform until ES (dotted area) versus the total IW– and determined the average fraction by linear regression (forced through the origin). Likewise, to determine the fraction of the total aspirating energy that was expended as hydraulic work to accelerate the mitral column, we plotted the area under the dIW– waveform described after the beginning of mitral flow (diagonally hatched area) versus IW– and determined that average fraction. Similarly, we plotted the area under the dIW– waveform during isovolumic relaxation (oppositely hatched area) (of course, this energy could not be converted to hydraulic work because there was no flow) versus IW– and determined that average fraction also. Each of these energies was expressed as an average fraction of the total energy, IW–. To determine the energy due to the passive decompression of the LA, we calculated the area (IW+) under the dIW+ waveform during the E wave (see FCW in Fig. 1, bottom middle). In addition, the time integral of the early filling velocity waveform (i.e., the E wave) during its acceleration phase (EVIACC; i.e., until the peak of the E wave) was measured.
|
c)–1(dP)2]. The net intensity (dIW = dPdU) is zero because the velocity must be zero at the closed valve. This zero net wave intensity is interpreted as the result of equal and opposite intensities of forward- and backward-going waves, as shown in Fig. 1, top middle. Results are expressed as means ± SD. One-way ANOVA was used to compare the variables between different PLVED levels. Linear and nonlinear regression analyses were performed to explore the interaction between different variables. A probability level of P < 0.05 was accepted as significant.
|
RESULTS |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXGRANTSREFERENCES |
|---|
(P = 0.1). EVIACC increased significantly (P < 0.01). dIW– significantly decreased in absolute value when PLVED was elevated (P = 0.02), as did IW– (P = 0.04) and IW–DS (P = 0.04).
|
, and VLVES on IW– demonstrated that and VLVES were the only independent determinants of IW–. Analysis of each dog’s data (Fig. 2) and the pooled data (see Fig. 4A) showed an inverse relationship between %VLVES and IW–: as %VLVES decreased, IW– increased. We used a three-parameter exponential decay equation [IW– = a·eb(%VLVES) + (IW–)] and found that, in the case of each dog’s data, the 95% confidence intervals of b did not include zero, indicating that the exponential term was significant (see Table 2). Similar inverse relationships were found between IW– and : as decreased, IW– increased (Figs. 3 and 4B). In this case as well, we used a similar equation [IW– = a·eb + (IW–)] and also found that, in every experiment, the 95% confidence intervals of b did not include zero, indicating that the exponential term was significant (see Table 2). In addition to the above statistical justification for using a nonlinear regression, we noted that, in the case of a linear regression, extrapolation would suggest that IW– would go through zero and change its sign at high values of or VLVES, which seemed unreasonable, a priori. Conversely, extrapolation of an exponential decay would suggest that IW– would plateau and reach asymptotic levels at high values of and VLVES. It was found that variance could further be reduced (i.e., both coefficients were statistically significant) when both and VLVES were used to predict IW–; this indicated that the combination of and VLVES predicted IW– better than either one alone (Fig. 5A). Note that and VLVES data were distributed quite uniformly (Fig. 5B).
|
|
|
|
|
|
10% of the total time-integrated area of the waveform. However, like IW– and consistent with the constant proportionality demonstrated in Fig. 6, IW–DS varied inversely with and VLVES (Fig. 7).
|
Determinants of E wave acceleration.
As illustrated in Fig. 1, bottom middle, a FCW began just after PLV reached its nadir, when mitral velocity was continuing to increase. The energy (IW+) of this FCW, which would tend to force blood into the LV, was attributed to the passive emptying of a stretched LA. Blood is also drawn into the LV by the remaining aspirating energy (IW–DS). Thus, to determine the relative contributions of this LA push and LV pull, we applied multiple linear regression, considering EVIACC to be the dependent variable and IW+ and IW–DS to be independent variables (Fig. 8). Both IW+ and IW–DS predicted EVIACC in that they both reduced variance statistically significantly. These results suggest that early diastolic filling (as measured by EVIACC) was determined by both the passive push of the LA (as measured by IW+) and the active pull of the LV (as measured by IW–DS). A 1-cm increase in EVIACC was associated with a 0.08 J/m2 increase in IW+ and a 1.7 J/m2 increase in IW–DS. Thus the LV expends 20 times more energy to accelerate the mitral flow than the LA.
|
|
DISCUSSION |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXGRANTSREFERENCES |
|---|
). This demonstration fulfills Wiggers’ anticipation that decreasing PLV, per se, is capable of generating an aspirating force (52) and is consistent with the interpretation of those investigators who have emphasized the significance of the rate of relaxation as a determinant of DS (11, 12, 30, 38, 47). The total energy of that expansion wave (IW–) and the energy remaining after the mitral valve opens (IW–DS) were also demonstrated to be inversely related to the completeness of LV emptying (i.e., VLVES). This demonstration is consistent with that body of work that relates DS to LV V0 (1, 2, 4, 5, 7–10, 16, 17, 22–24, 37, 44, 48). Thus analysis of the energy of the backward-going, LV-generated, expansion wave seems to reconcile the two apparently unrelated mechanisms of DS that had been proposed previously. As the backward-going expansion wave generated by the relaxing LV began at the moment PLV and E began to decline, its onset coincided with the beginning of Wiggers’ "phase of reduced ejection" (51), an instant substantially later than the peak of the calcium transient (25). dIW– then increased rapidly (in absolute value) and reached a peak near the time when dPLV/dt reached its largest negative value. dIW (net intensity, a.k.a. dPdU) is equal to the sum of dIW+ and dIW–, and its sign (positive or negative) indicates whether the forward or backward wave is dominant at that instant. In Fig. 1, bottom middle, note that dIW began to increase when the mitral valve opened and declined to zero when dPLV/dt equalled zero (36). This implies that the backward-going expansion wave was no longer dominant after PLV reached its minimum value, thus corresponding precisely to Katz’s conclusion that the LV tends to fill itself until the nadir in PLV (12, 30, 38, 47). Katz analyzed the early phase of diastolic filling and concluded that the fact that PLV decreased during early filling meant that the LV was filling itself. Because LV E (i.e., the slope of a line drawn from the origin to a point on the P-V loop) decreased continuously during this period, he inferred that the LV was relaxing faster than it could be filled and, so, was responsible for its own filling (30).
Figures 2 and 4A demonstrate the dependence of dIW– on VLVES, and it is important to note that, despite the vigorous volume loading in this experimental protocol, most values of VLVES were less than V0 (see Table 1). This implies that these hearts usually emptied to volumes that were less than their V0 and suggests that the V0 mechanism may be an important factor in LV filling under a wide range of loading conditions. However, it should be noted that our protocol did not include the study of ventricles made markedly hypovolemic except by increasing contractility.
It should be emphasized that we are not attempting to model the mechanics of the LV in this study. We are simply exploring the use of WIA to separate the measured pressure and velocity waveforms into their forward and backward components with no presumptions about the origins of these waves. A number of models of LV filling have been suggested, ranging from one-dimensional parametric models (6, 15, 46) through two-dimensional models (49) to fully three-dimensional models (32). All of these models require prior knowledge about the properties and state of the ventricle to enable the prediction, to different levels of complexity, of the mitral filling pattern. Our work, on the other hand, is primarily descriptive rather than predictive. Of course, the findings do have implications for the modeling of ventricular filling and these have been discussed as appropriate. Similarly, the simultaneous measurement of pressure and velocity in the ventricle is highly invasive and does not lend itself easily to clinical measurements. However, insofar as physiological measurements taken in the open-chested dog are relevant to the human cardiovascular system, the findings of our work do have clinical implications and these will be discussed briefly.
Previously, it was suggested that DS is related to the untwisting of the LV (3, 33, 41), so it is interesting to note that the time course of IW– is similar to that of LV untwisting: both the backward expansion wave and untwisting are largely complete by the time the mitral valve opens (see Fig. 1, bottom). On one hand, this might suggest that neither IW– nor untwisting is as directly related to early mitral filling as had been supposed. On the other hand, with Wiggers’ aspirating force perspective in mind, it might also suggest that both IW– and untwisting are intimately related to the decrease in LV E and to VLVES (33, 41). Furthermore, it might suggest that both IW– and untwisting are related in a major way to the deceleration of the stroke volume and to early mitral filling, the latter, in a perhaps still critically important way, despite the fact that IW–DS is small. Thus, like the earlier authors, we conclude that the relaxation of the "torsional spring" is the likely cause of the decrease in E and the backward-going expansion wave (IW–), 10% of which we equate to DS (IW–DS).
Mitral filling.
We also examined the degree to which DS affects mitral filling. Wiggers acknowledged that the aspirating force would tend to augment mitral filling but emphasized that PLV is nearly at its nadir when the mitral valve opens and, therefore, only a small fraction of that force would be available for diastolic filling (52). (Our data demonstrated that relaxation was 86% complete when the mitral valve opened.) However, our data also demonstrated that there was an association between the size of the E wave and IW–DS in addition to IW+ (see Fig. 7). Although both associations were statistically significant, IW–DS was 20 times greater in magnitude than IW+, suggesting that LV DS is more important than the passive decompression of the LA in determining the size of the E wave. These findings suggest that the role of DS should be evaluated carefully when assessing LV diastolic function in both normal subjects and those with congestive heart failure (29).
Deceleration of aortic flow.
Wiggers’ discussion of the aspirating force (52) would seem to suggest that its first effect is to decelerate, stop, and reverse the column of blood in the aortic outflow tract. Under a variety of loading conditions and with augmented and diminished contractility, we found that a 60% of the total energy of the backward expansion wave is spent in this deceleration.
Limitations. As discussed in our previous study (36), the application of one-dimensional WIA to LV filling is more problematic than it is in the large arteries. However, this concern should be minimal in the plane of the mitral valve. Mitral velocity was measured near the midpoint of the mitral annulus using Doppler echocardiography. This velocity should be representative of the entire cross section in that the velocity profile is blunt in early diastole (31, 34).
So that we could compare the fractions of aspirating energy utilized for stroke volume deceleration and DS, we calculated wave intensity from a single PLV that was measured between the mitral and aortic valves. This violated the wave-intensity principle that pressure and velocity should be recorded from the same cross section. As there are measurable gradients in the LV during diastolic filling (13), our results might be somewhat different quantitatively from those derived from PLVs measured precisely within the mitral orifice, for example. Further experiments are planned to define these differences.
This was an ambitious experimental protocol in which we studied several interventions and measured many parameters in these anesthetized dogs. Probably as a result, the ejection fraction was low and PPeric was higher than we have usually observed and a degree of cardiac depression may have been present in these dogs. It will be important to confirm the most important results of this study in more physiological animal models and/or in human subjects.
With respect to clinical studies, we acknowledge that our measurements were profoundly "invasive" and we do not mean to suggest that our approach is easily adaptable to the clinical laboratory. The ultimate goal of our experimental investigations is to understand the mechanisms that produce the normal and abnormal patterns of mitral and pulmonary venous velocity. With that understanding, we believe that future cardiologists will be able to interpret the clinical patterns more intelligently.
In conclusion, the intensity of the backward-going wave generated by the LV during relaxation depends both on the rate at which E decreases (i.e., ) and on the completeness of LV emptying (i.e., VLVES). Wave-intensity analysis provides a new approach for assessing diastolic suction and reconciles those two previously proposed mechanisms. The early filling wave (E wave) depends on DS in addition to the passive decompression of the LA.
|
APPENDIX |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXGRANTSREFERENCES |
|---|
P/V), we suggest that decreasing elastance, per se, caused the backward-going expansion wave. WIA also defined negatively reflected compression and expansion waves (21).
|
|
GRANTS |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXGRANTSREFERENCES |
|---|
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 By this convention, the waves generated by the LV propagating out of the ventricle either into the aorta or the atrium will be seen as backward waves. For the systolic part of the cardiac cycle, this is opposite to the convention that we have adopted in our previous studies of wave intensity measured in the aorta. 
|
REFERENCES |
|---|
|
TOPABSTRACTMATERIALS AND METHODSRESULTSDISCUSSIONAPPENDIXGRANTSREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  J. J. Smolich, J. P. Mynard, and D. J. Penny Ductus arteriosus wave intensity analysis in fetal lambs: midsystolic ductal flow augmentation is due to antegrade pulmonary arterial wave transmission Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2009; 297(4): R1171 - R1179. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. Smolich, J. P. Mynard, and D. J. Penny Dynamic characterization and hemodynamic effects of pulmonary waves in fetal lambs using cardiac extrasystoles and beat-by-beat wave intensity analysis Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2009; 297(2): R428 - R436. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. Zhang, C. S. Chung, L. Shmuylovich, and S. J. Kovacs Is left ventricular volume during diastasis the real equilibrium volume, and what is its relationship to diastolic suction? J Appl Physiol, September 1, 2008; 105(3): 1012 - 1014. [Full Text] [PDF]
|
|
|
|
|
|
J. J. Smolich, J. P. Mynard, and D. J. Penny Simultaneous pulmonary trunk and pulmonary arterial wave intensity analysis in fetal lambs: evidence for cyclical, midsystolic pulmonary vasoconstriction Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2008; 294(5): R1554 - R1562. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. Penny, J. P. Mynard, and J. J. Smolich Aortic wave intensity analysis of ventricular-vascular interaction during incremental dobutamine infusion in adult sheep Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H481 - H489. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Shmuylovich and S. J. Kovacs E-wave deceleration time may not provide an accurate determination of LV chamber stiffness if LV relaxation/viscoelasticity is unknown Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2712 - H2720. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Flewitt, T. N. Hobson, J. Wang Jr., C. R. Johnston, N. G. Shrive, I. Belenkie, K. H. Parker, and J. V. Tyberg Wave intensity analysis of left ventricular filling: application of windkessel theory Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2817 - H2823. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. N. Hobson, J. A. Flewitt, I. Belenkie, and J. V. Tyberg Wave intensity analysis of left atrial mechanics and energetics in anesthetized dogs Am J Physiol Heart Circ Physiol, March 1, 2007; 292(3): H1533 - H1540. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Sun, I. Belenkie, J.-J. Wang, and J. V. Tyberg Assessment of right ventricular diastolic suction in dogs with the use of wave intensity analysis Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H3114 - H3121. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. S. Chung, D. M. Ajo, and S. J. Kovacs Isovolumic pressure-to-early rapid filling decay rate relation: model-based derivation and validation via simultaneous catheterization echocardiography J Appl Physiol, February 1, 2006; 100(2): 528 - 534. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Yotti, J. Bermejo, J. C. Antoranz, M. M. Desco, C. Cortina, J. L. Rojo-Alvarez, C. Allue, L. Martin, M. Moreno, J. A. Serrano, et al. A Noninvasive Method for Assessing Impaired Diastolic Suction in Patients With Dilated Cardiomyopathy Circulation, November 8, 2005; 112(19): 2921 - 2929. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
), isovolumic relaxation (IW–IR; 
), and mitral filling (IW–DS; 
) plotted versus IW– (see 
