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Am J Physiol Heart Circ Physiol 291: H1210-H1215, 2006. First published April 7, 2006; doi:10.1152/ajpheart.01339.2005
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Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole: model-based prediction with in vivo validation

Matt M. Riordan2 and Sándor J. Kovács1,2

1Department of Internal Medicine, Cardiovascular Biophysics Laboratory, Cardiovascular Division, Washington University School of Medicine; and 2Department of Biomedical Engineering, School of Engineering and Applied Science, Washington University, St. Louis, Missouri

Submitted 19 December 2005 ; accepted in final form 30 March 2006


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 GRANTS
 REFERENCES
 
Previous studies in healthy humans have established that the ({approx}850 ml) volume enclosed by the pericardial sac is nearly constant over the cardiac cycle, exhibiting a transient {approx}5% decrease ({approx}40 ml) from end diastole to end systole. This volume decrease manifests as a "crescent" at the ventricular free wall level when short-axis MRI images of the epicardial surface acquired at end systole and end diastole are superimposed. On the basis of the (near) constant-volume property of the four-chambered heart, the volume decrease ("crescent effect") must be restored during subsequent early diastolic filling via the left atrial conduit volume. Therefore, volume conservation-based modeling predicts that pulmonary venous (PV) Doppler D-wave volume must be causally related to the radial displacement of the epicardium ({Delta}) (i.e., magnitude of "crescent effect" in the radial direction). We measured {Delta} from M-mode echocardiographic images and measured D-wave velocity-time integral (VTI) from Doppler PV flow of the right superior PV in 11 subjects with catheterization-determined normal physiology. In accordance with model prediction, high correlation was observed between {Delta} and D-wave VTI (r = 0.86) and early D-wave VTI measured to peak D-wave velocity (r = 0.84). Furthermore, selected subjects with various pathological conditions had values of {Delta} that differed significantly. These observations demonstrate the volume conservation-based causal relationship between radial pericardial displacement of the left ventricle and the PV D-wave-generated filling volume in healthy subjects as well as the potential role of the M-mode echo-derived radial epicardial displacement index {Delta} as a regional (radial) parameter of diastolic function.

constant-volume heart; left atrial conduit volume

TELEOLOGICAL AND PHYSIOLOGICAL arguments applied to the fetal environment have proposed, and several cardiac MRI-based studies (8, 13, 16–18) have concluded, that the four-chambered, adult human heart is very nearly a constant-volume pump. In a more recent study (4) using high-resolution MRI cine loops, the investigators measured the cross-sectional area of the pericardium from the ventricular apex through the superior-posterior wall of the left atrium (LA) over the course of the cardiac cycle and found that the volume enclosed by the pericardial sac does indeed deviate slightly from the constant-volume state. The maximum variation was found to occur at end systole in most subjects, when the volume enclosed by the pericardium was ~5% lower than at end diastole. However, this decrement of volume was consistently recovered by the end of the following diastolic period.

In a later study (24), these investigators, again using MRI, sought to determine the mechanisms responsible for the {approx}5% decrease in the volume of the pericardial sac at end systole and its recovery by end diastole. They discovered that the change in longitudinal pericardial cross-sectional area (from the apex to mediastinum) in the four-chamber view was negligible (due to pericardial attachment to immobile anatomic structures) (1), whereas the change in pericardial cross-sectional area in a short-axis ventricular slice was ~12%. These findings, which are corroborated by other investigators (8), indicate that the {approx}5% deviation in pericardial volume must be accounted for by radial rather than longitudinal epicardial displacements. Indeed, when short-axis MRI slices of the left ventricle (LV) and right ventricle (RV) just below the mitral valve plane at end systole and end diastole were superimposed, this ~12% change in short-axis pericardial cross-sectional area was observed to be primarily localized to the LV rather than evenly distributed between both ventricles (8, 24); whereas RV radial motion due to interventricular coupling and torsion was observed, it was found that RV cross-sectional area remained relatively constant from end systole to end diastole (8). On closer examination, the radial epicardial displacement of the LV at end diastole usually assumed the form of a crescent of somewhat variable orientation, but most often along the postero-lateral wall (Fig. 1). Displacement of the septal epicardial (i.e., RV septal surface) wall was also sometimes observed. Because no significant variation in pericardial cross-sectional area was found above the plane of the A-V valves, it was concluded that the "crescent effect"—manifesting as radial pericardial displacement, most often along the postero-lateral free wall of the LV during diastolic filling—is the primary mechanism accounting for restoration of the approximate {approx}5% volume loss of the pericardial sac by end systole.


Figure 1
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  		Fig. 1. Idealized schematic of superimposed short-axis slices of left (LV) and right ventricles (RV). Only the epicardial contours at end systole and end diastole at mid-LV level are shown. Echocardiographic M-mode insonification direction (dashed line) is shown as well as orientation of the "crescent effect." Areas enclosed by end-systolic epicardial/pericardial RV and LV boundaries are shaded in gray; same contours in diastole are outlined in black. Note crescent shape swept out by radial displacement of the epicardial surface of the LV lateral free wall. See text for details.

 
During diastole, the only extrapericardial volume entering the left heart is contributed by the pulmonary vein (PV) D-wave, the onset of which is simultaneous with the E-wave. The mechanical suction, equivalent to a simultaneous decrease in pressure and increase in volume (dP/dV < 0), exerted by LV recoil generates the atrioventricular pressure gradient that initiates early rapid filling. Because the mitral valve is open during the E-wave, most of the PV D-wave volume passes through the LA into the LV as the LA conduit volume (LACV) (5). It is part of this E-wave blood volume that is accommodated by the LV "crescent effect" via pericardial displacement to restore the four-chambered heart to its (near) constant-volume physiological state.

The hypothesis that the present study tests is that lateral LV pericardial displacement from end systole to end diastole determines, within obvious geometric constraints/approximations, the volume contributed by the PV D-wave to the LV and thus should be related to this volume. Using M-mode echocardiography and Doppler echocardiographic recordings of flow from the right superior PV, we evaluated whether and the extent to which this relationship is valid. In effect, we sought to elucidate the mechanism of the {approx}5% volume restoration of pericardial sac contents from end systole to end diastole ("crescent effect") by testing the hypothesis that it occurs predominantly via radial displacement of the LV epicardial surface. In addition, we assessed whether pericardial displacement from end systole to end diastole is a potentially useful clinical index of regional (i.e., radial) diastolic function by comparing its value in healthy subjects to its value in a subject with mitral regurgitation, a subject with congenital absence of the pericardium, and a subject with concentric LV hypertrophy (LVH), respectively.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 CONCLUSIONS
 GRANTS
 REFERENCES
 
Modeling. Specifically, PV D-wave volume is given by the product of the effective PV area (in cm2) and velocity-time integral (VTI) of the D-wave (in cm), which we write as:

Formula 1(1)
We also assume that the D-wave of the single PV imaged is characteristic of the other three (unimaged) PVs, because other investigators have reported similar flow patterns in the four PVs (15, 19). We approximate the volume (in cm3) due to the "crescent effect" as the product of the effective crescent area CRarea (in cm2) on the surface of the LV and the radially measured crescent thickness {Delta} (in cm). Accordingly, we write:

Formula 2(2)
Equating the two volumes, as required by the law of conservation of volume, yields the predicted linear relation between D-wave VTI and {Delta} that we seek to test:

Formula 3(3)
where m is CRarea/PVAEff and b accounts for the offset due to nonsimultaneous measurements of Doppler flow velocity and M-mode displacement, our imprecise knowledge of the precise shape of CRarea and its orientation, and related simplifications. Our intent is to experimentally validate Eq. 3. We clarify that our underlying hypothesis concerning the existence of these relationships, based on causality (volume conservation), is intended to be predictive (Eq. 3) rather than accommodative of the data to be analyzed (20).

Patient selection. A sample of 11 normotensive subjects having normal LV ejection fraction (LVEF ≥ 55%) and without ischemia, previous myocardial infarction, wall motion abnormalities on ventriculography, history or evidence of diabetes, cardiomyopathy, valvular disease or insufficiency, renal disease, congestive heart failure, hypertrophy, or other cardiac disease (the normal group) was selected from an existing database (21) of simultaneous (micromanometric) LV pressure and transmitral flow velocity recordings of subjects scheduled for elective diagnostic cardiac catheterization. The study was approved by the Washington University Human Studies Committee, and all subjects provided informed consent for echocardiography and catheterization according to Washington University Human Studies Committee (Institutional Review Board) requirements. The database includes M-mode recordings of LV septal and posterior wall motion just below the level of the mitral annulus and echocardiographic recordings of flow (D-waves) from the right superior PV. For illustrative comparison, three separate subjects, one with slight mitral regurgitation, one with congenital absence of the pericardium, and one with concentric LVH, were also selected from the database. Each of these subjects had normal LVEF. Some subjects in the control group had angiographically documented coronary artery disease, but none had active ongoing ischemia. In addition to the exclusion criteria enumerated above, to be included in the normal group, subjects had to have M-mode and PV flow recordings of sufficient quality such that the contour of the epi/pericardium (from M-mode) and the initiation, peak, and termination of the D-wave (from PV flow) could be identified. The inclusion criterion for the pathophysiological group was that the subject have a good-quality M-mode recording for determination of {Delta}. Selected clinical variables for all control subjects are shown in Table 1.


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  		Table 1. Clinical variables for control group

 
Data acquisition. The methodology employed has been previously described (2, 21, 26). Briefly, immediately before cardiac catheterization, a full two-dimensional Doppler examination is performed by an experienced sonographer using a standard clinical imaging system (Acuson, Mountain View, CA) with a 3-MHz transducer in the catheterization laboratory. With the patient supine, M-mode recordings were obtained at the near mid-LV level in accordance with American Society of Echocardiography criteria (25). PV flow recordings were obtained from apical four-chamber views with the sample volume gated at 2.5 to 5 mm and placed at the orifice to the right superior PV. To minimize artifacts due to misalignment between the imaging beam and direction of PV flow, the insonification direction was aligned along the direction of flow using color Doppler as a guide. The wall filter was set at 50 Hz, the baseline adjusted to take advantage of the full height of the CRT display, and the velocity scale adjusted to exploit the dynamic range of the output without aliasing. Simultaneous limb lead II ECG was displayed on all images. All images were recorded continuously via VHS or magneto-optical disk and subsequently digitized offline via a dedicated custom video capture station.

M-mode image analysis. For each subject, four to ten cardiac cycles of LV lateral wall motion were selected, clipped, and converted to 8-bit grayscale images with Paint Shop Pro 7 (Jasc Software, Minnetonka, MN). Pericardial displacement ({Delta}) from end systole (defined as the time of lowest cross-sectional diameter during the corresponding beat) to end diastole (defined as the time of greatest cross-sectional diameter prior to the R-wave of the following beat) was measured for three cardiac cycles and averaged to further minimize any physiological variation (see Fig. 2). Specifically, respiratory effects cause translation of the heart and cause variable preload effects. Accordingly, if the pericardial displacement for a given cardiac cycle was determined to differ by more than two pixels from the other cardiac cycles for the same subject (except for the subject with congenital absence of the pericardium, due to the magnitude of {Delta}) it was deemed due to respiration and was excluded. Similarly, if the M-mode data were excessively noisy to reliably identify the pericardial contour at end systole and end diastole, the subject was excluded. All values of {Delta} were obtained by measuring the relative displacement of the outer edge of the epicardium, based on pixel intensity, from end systole to end diastole (see figures). To overdetermine {Delta}, the relative displacement of the inner edge of the pericardium (i.e., the epicardial/pericardial interface) was also measured for each subject in this manner.


Figure 2
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  		Fig. 2. Temporal alignment using QRS as a fiducial marker of pulmonary venous (PV) flow and short-axis M-mode (at similar heart rates) of the LV for one representative control subject. A: PV flow pattern from right superior PV, showing S- and D-waves. D-wave contour is approximated as a triangle. Areas of acceleration and deceleration portions comprise D-wave velocity-time integral (VTI). Triangle formed by D-wave acceleration portion is VTIAT. B: M-mode of lateral displacement of pericardium from end systole to end diastole ({Delta}). Note close temporal alignment and agreement between D-wave duration and pericardial displacement duration. See text for details.

 
PV flow image analysis. For each subject in the control group, several displays containing two to four cardiac cycles of Doppler PV flow were selected, clipped, and converted to 8-bit grayscale images with Paint Shop Pro 7 as for the M-mode images. D-wave acceleration time, deceleration time, duration, and peak amplitude were measured for three D-waves. The velocity-time integral of the entire right superior PV D-wave (VTI) and velocity-time integral of the acceleration portion of the D-wave (VTIAT) were calculated from the geometric measurements previously listed and averaged over at least three beats. Both VTI measurements were obtained by approximating the acceleration and deceleration portions of the D-wave as triangles (see Fig. 2 and Table 2), which has slight limitations (12). Only PV flow images without excessive noise were analyzed to ensure reliability of D-wave measurements.


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  		Table 2. M-mode and pulmonary venous flow data for control group

 

   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 CONCLUSIONS
 GRANTS
 REFERENCES
 
For the control group, both D-wave VTI and VTIAT were highly correlated with pericardial displacement {Delta} (r = 0.86 and r = 0.84, respectively) as measured via M-mode from the outer edge of the pericardium (Fig. 3). To determine whether our results depended on whether {Delta} was measured from the outer versus inner aspect of the pericardium, {Delta} was also measured from the inner edge of the pericardium. Results showed excellent agreement and high correlation with {Delta} measured from the outer edge ({Delta}inner = 0.86{Delta}outer + 0.10, r = 0.91). Indeed, all but three subjects had values of {Delta}inner and {Delta}outer that differed by <5%, and only one subject had values that differed by >8%, which was the main source of variation between {Delta}inner and {Delta}outer. Because interobserver variation (among 3 observers) for determining {Delta} was somewhat less for {Delta} measured from the outer edge of the pericardium, the reported values use this method.


Figure 3
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  		Fig. 3. PV flow volume (as VTI)-to-epicardial radial displacement ({Delta}) relation. D-wave VTI (solid circles) and VTIAT (open circles) as functions of pericardial displacement, {Delta}. Least squares linear regressions: VTI = 4.50{Delta} + 2.62 (r = 0.86) and VTIAT = 3.32{Delta} + 0.57 (r = 0.84). See text for details.

 
The parameter {Delta} for each of the selected pathophysiological examples was either substantially greater or less than the values of {Delta} observed in the healthy (control) subjects (Fig. 4). Intraobserver variation was assessed by twice measuring pericardial displacement (outer edge) and right superior PV D-wave attributes, including D-wave acceleration time, deceleration time, and peak velocity for 10 subjects. The coefficients of variation (3) for pericardial displacement, D-wave acceleration time, D-wave deceleration time, D-wave peak velocity, D-wave VTI, and VTIAT were 3, 4, 4, 3, 7, and 6%, respectively.


Figure 4
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  		Fig. 4. M-mode tracings with simultaneous ECG for selected subjects illustrating variability of {Delta} in the presence of pathology, determined by averaging pericardial displacement over 3 cardiac cycles. Vertical distance (in mm) between outer edge of pericardium at end systole and end diastole (temporally coinciding with R-wave) determines {Delta}. Scale is same as in Fig. 2B (tick marks on ordinate = 20 mm). A: representative normal subject ({Delta} = 6.4 mm). B: subject with congenital absence of pericardium ({Delta} = 20.9 mm). C: subject with mild mitral regurgitation ({Delta} = 10.1 mm). D: subject with concentric LV hypertrophy ({Delta} = 3.9 mm). See text for details.

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
CONCLUSIONS
 GRANTS
 REFERENCES
 
The four-chambered heart, or more specifically, the volume of the pericardial sac, deviates from the constant-volume state at end systole because the combined systolic stroke volumes of the LV and RV are not fully restored by the simultaneous apical displacement of the A-V valve planes (with the mitral and tricuspid valves closed) and the blood entering the LA and RA via the PVs and vena cavae, respectively. In particular, the left heart (LA + LV) loses roughly 30% of its end-diastolic volume by end systole (5), demonstrating that the PV S-wave, initiated by LA suction (dP/dV < 0 for the atrium) due to systolic descent of the mitral annulus (and closed mitral valve) and anterior displacement and descent of the roots of the great vessels, aspirates insufficient volume into the LA to fully compensate for LV stroke volume. Subsequently, during early rapid filling, LV suction initiates the gradient that drives blood flow (the D-wave) from the PVs through the LA (volume of which diminishes during the E-wave) and into the LV as the LACV. Thus the D-wave represents inflow into the left heart (and pericardial sac) in the absence of simultaneous outflow (from either the left or right heart) and is crucial in restoring the end-systolic volume decrement of the pericardial sac. It should be noted that, because the E-wave terminates prior to the D-wave, not all of the D-wave volume enters the LV during early rapid filling. Part of the remainder, which is accommodated by the LA, enters the LV during the A-wave and makes a very minor contribution to the radial epicardial displacement of the posterior wall (see Fig. 4). The volume that reenters the PVs during atrial systole (A-wave reversal) after the D-wave constitutes a volumetrically negligible outflow of blood from the left heart (5).

Because the deviation of the pericardial sac from the constant-volume state requires the existence of the LACV, and the LACV comprises most of the D-wave volume, the volume contributed by the D-wave (its VTI multiplied by the effective aggregate PV area) (7), primarily during early rapid filling but also during late atrial filling, should serve as a measurable equivalent of volume entering the LV during diastole by which the "crescent effect" volume is replenished. Moreover, because this entering volume is accommodated by wall-thinning, ascent of the mitral annulus and the preferential expansion of the epicardial/pericardial contour bounding the free wall (the "crescent effect"), it is predictable from volume conservation that the lateral displacement of the epicardial/pericardial surface of the LV from end systole to end diastole should be related (within geometric constraints) to the volume contrib uted to the left heart by the PV D-wave (see derivation in Modeling).

We measured the magnitude of lateral pericardial displacement of the LV posterior wall from end systole to end diastole from M-mode images and found that it correlates highly with the D-wave VTI as well as D-wave VTI measured to peak D-wave velocity from echocardiographic PV flow recordings of the right superior PV. We measured pericardial displacement from both the inner and outer edge of the pericardium, with good agreement. We measured the D-wave VTIAT because it has been shown that the majority of blood volume entering the LV during early filling is achieved by the peak of the E-wave (and the D-wave) due to variation of the effective mitral valve area (6) and aggregate, time-varying PV area (7) during early rapid filling. Furthermore, the D-wave ends after the E-wave ends, which signifies that not all of the volume contributed by the D-wave comprises the LACV.

The acquired data for right superior PV D-wave VTI and VTIAT as functions of pericardial displacement ({Delta}) were plotted in accordance with relations (see Modeling) based on conservation of mass. This can be expressed as:

Formula 4(4)
where Ddur is D-wave duration, D(t) denotes D-wave velocity, APV is the effective aggregate PV area, and Vcrescent effect denotes the volume swept out by the radial motion of the epicardial surface responsible for the "crescent effect." The relationships are shown in Fig. 3.

To illustrate whether pericardial displacement {Delta} measured from M-mode has potential as a clinical index of diastolic function, we compared the average values of {Delta} obtained for the control group with {Delta} in three subjects having established pathophysiological conditions. Pericardial displacement was substantially greater in the subject with mitral regurgitation and more than three times the control group average in the subject with congenital absence of the pericardium. Conversely, pericardial displacement was substantially reduced in the subject with concentric LVH. These selected pathophysiological cases are meant to illustrate the clinical potential of {Delta}, and the observed differences justify additional clinical studies assessing {Delta}. Because M-mode is routinely utilized as part of all echocardiographic examinations and because {Delta} is easily measurable, once validated in future clinical studies, {Delta} has potential as a regional (radial) index of diastolic function.

Limitations. Limitations of transthoracic echocardiography for PV flow recording have been extensively characterized (22, 23). Previous studies using both echocardiography and MRI have indicated that flow through the four PVs into the LA is variable because different PVs reside in different anatomic locations relative to the LV and can exhibit different flow paths (10, 14). However, other studies have reported that the PV flow velocity contour is independent of the vein being imaged and that volume flow is highly correlated with flow velocity in the absence of significant mitral regurgitation (15, 19). While the equations of our experimentally determined relationships between D-wave VTI and VTIAT and pericardial displacement may be influenced somewhat by which PV is imaged in that each PV may deliver a different D-wave volume, the volume conservation-based predictions are not affected. We note that {Delta} and D-wave VTI are relative, rather than absolute, indexes of filling volume and that {Delta} is not sensitive to D-wave velocity contour features but rather to the D-wave VTI (i.e., the volume delivered to the left heart by the D-wave). This is independently supported by the strong correlation observed between {Delta} and right superior PV VTIAT as well as the entire right superior PV D-wave VTI.

Another limitation relates to the quality of M-mode images of pericardial displacement. Although only good-quality M-mode images of beats with discernible and consistent pericardial displacement were selected for analysis, we caution that clear M-mode images are required for accurate determination of {Delta}. Small measurement uncertainties can represent large percentage errors because the pericardial displacements in the control subjects were in the 5- to 9-mm range. However, we note that, depending on image quality and how well the inner and outer edges of the pericardium can be visualized, {Delta} can be determined from either the inner or outer edge of the pericardium, facilitating its measurement.

The orientation of the "crescent" as previously documented via MRI is most often along the LV free wall, but "crescent" orientation cannot be fully assessed by M-mode. Hence our analysis includes those subjects in whom the orientation was such that it could be detected by M-mode. A larger MRI-based study is required to firmly establish "crescent" orientation in a statistical sense. Additionally, we note that while the spatial resolution of MRI is preferable for identifying features such as the epicardial border, the superior temporal resolution of M-mode and its established, relatively low interobserver variability with respect to measurements of LV posterior wall and cavity dimensions (10) justify its use to measure {Delta} in this study. Furthermore, the values of {Delta} reported consist of relative measurements of the displacement of the outer edge of the epicardium from end systole to end diastole (based on pixel intensity). Therefore, the measured values of {Delta} should be reproducible and reasonably accurate.

Although some of the subjects in the control group had evidence of coronary artery disease, none of the subjects had high-grade coronary artery stenoses, active ischemia, or wall motion abnormalities as evidenced by normal LVEF and normal wall motion via ventriculography. Although some of the pathophysiological subjects had abnormalities other than their primary conditions, these primary conditions were the main differentiating feature between them and the control group.


   CONCLUSIONS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
GRANTS
 REFERENCES
 
Maintenance of the constant-volume state (within 95%) of the pericardial sac requires the existence of the LACV, which enters the pericardial sac as the PV D-wave and enters the LV as a component of the E-wave. This entering volume is primarily accommodated by lateral displacement of the pericardial/epicardial contour lining the posterior/lateral wall of the LV in what has been termed the "crescent effect." This implies that the extent of pericardial displacement from end systole to end diastole must be correlated with the VTI of the D-wave. With the use of the conservation of volume-based modeling, the predicted linear relationship between D-wave VTI and {Delta} was experimentally validated (r = 0.86). While {Delta} has a causally derived etiology (D-wave volume), its clinical potential has not been fully exploited. Because it can be easily measured from (good quality) M-mode recordings and appears to have clinical utility in selected pathophysiological cases, it constitutes a novel (radial diastolic function) index that merits additional detailed assessment in clinical studies.


   GRANTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 GRANTS
REFERENCES
 
This study was supported in part by the Heartland Affiliate of the American Heart Association (Dallas, TX); Whitaker Foundation (Rosslyn, VA); National Heart, Lung, and Blood Institute (Bethesda, MD; HL-54179 and HL-04023); Alan A. and Edith L. Wolff Charitable Trust (St. Louis, MO); and Barnes-Jewish Hospital Foundation.


   ACKNOWLEDGMENTS
 
We acknowledge the expert skills of Peggy Brown in echocardiographic data acquisition.


   FOOTNOTES
 

Address for reprint requests and other correspondence: S. J. Kovács, Cardiovascular Biophysics Laboratory, Washington Univ. Medical Center, Box 8086, 660 South Euclid Ave., St. Louis, MO 63110 (e-mail: sjk{at}wuphys.wustl.edu)

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.


   REFERENCES
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 CONCLUSIONS
 GRANTS
 REFERENCES
 

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