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MRI-determined left ventricular "crescent effect": a consequence of the slight deviation of contents of the pericardial sack from the constant-volume state

¹Department of Biomedical Engineering, Washington University, and ²Cardiovascular Biophysics Laboratory and Cardiovascular Magnetic Resonance Laboratories, Cardiovascular Division, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri

Submitted 23 July 2004 ; accepted in final form 11 October 2004

	ABSTRACT

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During one cardiac cycle, the volume encompassed by the pericardial sack in healthy subjects remains nearly constant, with a transient ±5% decrease in volume at end systole. This "constant-volume" attribute defines a constraint that the longitudinal versus radial pericardial contour dimension relationship must obey. Using cardiac MRI, we determined the extent to which the constant-volume attribute is valid from four-chamber slices (two-dimensional) compared with three-dimensional volumetric data. We also compared the relative percentage of longitudinal versus radial (short-axis) change in cross-sectional area (dimension) of the pericardial contour, thereby assessing the fate of the ±5% end-systolic volume decrease. We analyzed images from 10 normal volunteers and 1 subject with congenital absence of the pericardium, obtained using a 1.5-T MR scanner. Short-axis cine loop stacks covering the entire heart were acquired, as were single four-chamber cine loops. In the short-axis and four-chamber slices, relative to midventricular end-diastolic location, end-systolic pericardial (left ventricular epicardial) displacement was observed to be radial and maximized at end systole. Longitudinal (apex to mediastinum) pericardial contour dimension change and pericardial area change on the four-chamber slice were negligible throughout the cardiac cycle. We conclude that the ±5% end-systolic decrease in the volume encompassed by the pericardial sack is primarily accounted for by a "crescent effect" on short-axis views, manifesting as a nonisotropic radial diminution of the pericardial/epicardial contour of the left ventricle. This systolic drop in cardiac volume occurs primarily at the ventricular level and is made up during the subsequent diastole when blood crosses the pericardium in the pulmonary venous Doppler D wave during early rapid left ventricular filling.

constant-volume heart; cardiac magnetic resonance imaging; diastolic function

However, analysis of the essentially constant-volume attribute of the heart has never been extended to elucidating the kinematic mechanism and volumetric fate of the observed 5% change in the total volume encompassed by the pericardial sack (3). Temporally, the volume decrease occurs during systole, with a total 5% reduction at end systole, and is regained by the next end diastole. Viewed from a kinematic perspective, if the four-chambered heart were a perfect constant-volume pump, the change in pericardial volume should be 0%. The observed 5% volumetric change can be viewed as a 5% "ejection fraction" of the passive pericardial sack, driven by ventricular contraction. Conservation of mass and volume of muscle tissue and blood (considered incompressible) requires that the 5% end-systolic volume decrease be compensated for by global epicardial wall motion. A comparison of two-dimensional (2-D) and three-dimensional (3-D) measurements of MRI images of the heart and pericardial sack contour demonstrates that the 5% pericardial sack volume change is not isotropic. We assessed regional epicardial heart wall displacement in an effort to track the fate of the 5% change in pericardial sack volume over the course of a cardiac cycle.

We selected three planes for analysis: the standard four-chamber slice and two short-axis slices, one immediately below the most apical excursion of the mitral valve plane in the ventricles (hereinafter referred to as the "short-axis ventricular slice") and a second immediately above the most basal excursion of the mitral valve plane in the atria (hereinafter referred to as the "short-axis atrial slice"). These three slices allowed us to obtain both longitudinal and radial information regarding the epicardial contour while considering separately the atria and ventricles, which exhibit a well-established reciprocal filling relationship.

	METHODS

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After appropriate institutional informed consent was obtained, 10 normal healthy volunteers and 1 patient with congenital absence of the pericardium were scanned using a 1.5-T Philips Gyroscan (Release 8.1) as previously described (3). Briefly, for each study, a balanced fast-field echo (bFFE) short-axis cine stack (18–20, 9-mm-thick slices; zero gap) was obtained, spanning the full pericardial range from the ventricular apex to the left atrial superior-posterior wall. The image slices were obtained during 10-s end-expiratory breath holds, each containing 20 phases triggered from the ECG R wave and covering the entire cardiac cycle. Four-chamber bFFE cine loops were also obtained, each containing 20–28 phases triggered from the ECG R wave. Data were transferred to a remote Sun Microsystems Ultra Sparc 2 workstation running Philips EasyVision image-analysis software (Release 5.1). All image analysis was performed off-line using eFilm 1.5.3 (eFilm Medical; Toronto, Ontario, Canada), Paint Shop Pro 7 (Jasc Software; Minnetonka, MN), Scion Image (Scion; Frederick, MD), EasyVision, and Matlab 6.1 (Release 12.1, MathWorks; Natick, MA).

For 3-D analyses, the pericardial contour of each slice in the short-axis cine stack was manually traced at each phase, and the segmental volumes were summed to provide an estimate of the volume encompassed by the pericardium at each phase of the cardiac cycle. Three 2-D analyses were performed on the standard four-chamber slice (Fig. 1A), the short-axis atrial slice (Fig. 1B), and the short-axis ventricular slice (Fig. 1C). The pericardial contour of each slice in the appropriate cine loop was traced for a measure of pericardial cross-sectional area at each phase of the cardiac cycle. For the short-axis slices, epicardial chamber contours (including both myocardium and blood pool) were also manually traced.

View larger version (60K): [in this window] [in a new window]   Fig. 1. Typical pericardial traces for calculation of enclosed areas for images from a four-chamber slice (A), short-axis atrial slice (B), and short-axis ventricular slice (C).

Intra- and interobserver variability were computed based on repeat pericardial traces of 15 randomly selected images, consisting of 5 four-chamber images, 5 short-axis atrial images, and 5 short-axis ventricular images. Reported variabilities represent the percent difference between the two measured values.

	RESULTS

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Relevant demographic data of all subjects are provided in Table 1. Evaluation of cardiac volume over time shows a gradual decrease in volume during systole, with a maximum decrease of 5 ± 1%, with recovery of the volume primarily during early diastole (3). The pericardial cross-sectional area measured at the four-chamber slice follows a highly similar pattern, with an average maximum (i.e., end systolic) decrease of 5 ± 2% (Fig. 2A). However, the longitudinal change in dimension from apex to base was 0.03 ± 1.0%, consistent with previous results (5). This indicates negligible longitudinal variation of the contour of the pericardial sack over the course of a cardiac cycle and implies that volumetric changes must be accounted for by radial displacements.

View larger version (14K): [in this window] [in a new window]   Fig. 2. Pericardial area (normalized to end diastole) versus time for the three imaging planes. A: four-chamber slice; B: short-axis ventricular slice; C: short-axis atrial slice. Each symbol represents each subject.

In the short-axis slices, we further examined the epicardial cross-sectional areas of individual chambers (myocardium and blood pool combined). We found an average decrease of 17 ± 7% in the LV and an average decrease of 10 ± 13% in the RV. While the pattern of change in the LV was a fairly smooth curve, the shape of which was highly similar across the sample population, the RV was much more variable between subjects (Fig. 3, A and B). Despite a slight decrease in the average cross-sectional area of the pericardium, the cross-sectional areas of the atria on four-chamber slices increased in size during systole, with the left atrium increasing by 80 ± 37% and the right atrium increasing by 38 ± 26%. In the left atrium, there was a consistent pattern of increase during early systole and relative constancy during late systole, followed by a decrease at early diastole (Fig. 4A). Much greater variation was observed in the right atrium (Fig. 4B).

View larger version (17K): [in this window] [in a new window]   Fig. 3. Individual chamber area (normalized to pericardial end-diastolic area) versus time for the left (A) and right (B) ventricles. Each symbol represents each subject.

View larger version (17K): [in this window] [in a new window]   Fig. 4. Individual chamber area (normalized to pericardial end-diastolic area) versus time for the left (A) and right (B) atria. Each symbol represents each subject.

We evaluated radial wall displacement by superimposing the short-axis epicardial contours at end systole and end diastole. Results are shown in Fig. 5. Inspection of ventricular contours shows that epicardial wall motion is significantly related to displacement of the interventricular septum, but the specific effects vary widely from subject to subject. It should be noted that in some cases there is more RV wall motion than is accounted for by area change alone. Comparison of epicardial contours of the LVs and RVs also indicates bulk rotation of the chambers, a well-established consequence of torsion (15).

View larger version (33K): [in this window] [in a new window]   Fig. 5. Comparison of systolic and diastolic contours for 2 representative normal subjects (subjects NL1 and NL2) and 1 patient with congenital absence of the pericardium (subject NP). Contours from all 3 slices (four-chamber, short-axis atrial, and short-axis ventricular) are shown. Systolic contours are shaded in gray; diastolic contours are outlined in black. Note the "crescent effect" present on free wall of the left ventricle in subject NL1 and on the interventricular septum in subject NL2. Note also the torsional effects on the right ventricle in subject NL1.

	DISCUSSION

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The motion (including slight rotation) of the epicardial surface of the heart, which the pericardial sack adheres to in a way that allows free sliding motion between the two, physically constrains both and generates the 5% observed volume decrease occurring between end diastole and end systole. The unifying theme of studies to date regarding the physiological importance of the constant-volume property of the heart has been the desirability of minimizing the cardiac energy wasted in displacing the lung, liver, and other surrounding tissues (7, 11). Strictly speaking, however, the determinant of surrounding tissue displacement is not volume change but epicardial wall motion. Prior work has focused on volume change as a measure that constrains wall motion, but this may mask physiological subtleties: if one makes the standard assumption that blood and myocardium are incompressible, then it is certainly true that volume change cannot occur without epicardial wall motion, but the converse does not hold. This is evident by the well-established degree of shape change and substantial torsion the LV undergoes during both isovolumic contraction and relaxation (15–17, 19).

Physiological constraints dictate that the volumetric change and compensatory epicardial wall motion cannot be isotropic over the four-chamber heart due to the reciprocal filling arrangement between the atria and ventricles and the established helically woven nature of the myocardial wall (18). To help spatially localize wall movement, we conducted separate analyses of longitudinal motion (using four-chamber images) and radial motion at the atrial and ventricular levels (using the atrial and ventricular sets of short-axis images).

One-dimensional measurements of the four-chamber view at end systole and end diastole showed only a 0.03 ± 1.0% difference in the linear distance between apex and base, indicating essentially zero longitudinal displacement of the epicardial (i.e., pericardial) surface, consistent with other findings (5). As a result, the epicardial displacement responsible for the 5% volume decrease at end systole must be primarily radial in nature. This is easily understood on anatomic grounds, based on the attachment of the pericardium at base and apex to fixed, immobile mediastinal and sternal structures.

While earlier reports (5) have indicated that there is more radial pericardial motion than longitudinal pericardial motion over the course of a cardiac cycle, our high-resolution images allow us to more precisely examine not just pericardial motion but also epicardial motion of the individual cardiac chambers. In considering the radial (short-axis image) analyses, we examined separately short-axis slices from above and below the mitral valve plane. We and others (5) have observed from four-chamber cine loops that epicardial, radially directed wall motion has its largest magnitude in the region traversed by the longitudinal motion of the mitral valve plane. Consequently, we selected for observation the first atrial slice located fully above the mitral valve plane and the first ventricular slice located below the mitral valve plane.

Below the mitral valve plane, the short-axis slice contains only the ventricles. This view is the only one which consistently exhibits significant pericardial displacement, resulting in a 12 ± 4% change in area of the pericardial contour between end diastole and end systole. Furthermore, superimposing the end-systolic and end-diastolic epicardial contours of the RV and LV in this slice shows that the 10% change in cross-sectional area of the pericardial contour is primarily attributable to the LV rather than evenly distributed between the LV and RV (see Fig. 5). Specifically, the ratio of area of the epicardial contour at end systole to end diastole is 0.83 for the LV and 0.90 for the RV. However, in the case of the RV, there is more subject-to-subject variation, and a ratio of unity falls within one standard deviation. As speculated in earlier reports (3, 5), we conclude that contraction of the LV, evidenced by a systolic decrease in epicardial area, is primarily responsible for the observed 5% variation in the 3-D volume encompassed by the pericardial sack.

Closer inspection of LV contraction shows that, in most subjects, the wall motion responsible for its volumetric variation is also radially nonisotropic. In 9 of 10 normal subjects, comparison of the epicardial contours of the LV at end diastole and end systole demonstrate a marked crescent effect (see Fig. 5), wherein a portion of the contours coincides, and, for the remainder of the contours, the diastolic contour expands beyond the systolic contour, creating the appearance of a crescent. Our data showed highly variable orientation of this crescent, with the greatest wall motion occurring primarily along the free LV wall in some subjects but along the interventricular septum in others. Although further study is required, we suggest that the presence of the crescent is related to interventricular coupling, and the variability in orientation reflects individual variation in fiber microstructure and mechanical interventricular coupling during systole. Radial (short-axis) displacement of the LV free wall and overlying pericardium was easily seen on the systolic and diastolic superimposed four-chamber 2-D pericardial traces; this allowed overdetermination of the crescent effect (Fig. 5).

Examination of the RV epicardial contours showed evidence of wall motion related to interventricular coupling and torsion that was not reflected in area changes. In most subjects, there was systolic radial inward motion of the free wall of the RV, which was at least partially offset by radial inward motion of the interventricular septal wall due to contraction of the LV. In approximately one-half of the subjects, this motion was primarily translational in nature; in the other one-half, it appeared to have a significant rotational component (Fig. 5). This suggests that, despite the near constant-volume property of the heart, which should minimize epicardial radial motion, there is actually a small amount of additional radial wall motion along the free wall of the RV representing, in part, bulk displacement of the chamber or through-plane motion of the dynamic RV free wall.

The short-axis slice above the mitral valve plane includes the atria as well as outflow tracts and roots of the great vessels. Although the atria themselves have irregular 3-D geometry and are not fully represented in a single cross-sectional slice, we found no significant variation in the pericardial cross-sectional area at this level. The individual chamber cross-sectional areas, although of limited utility due to the asymmetry of the atria, appear related to the ventricles at least in terms of relative consistency: the cross-sectional areas of both the left atrium and LV appear to follow a highly conserved pattern across the normal subject population, whereas both the right atrium and RV show a great degree of individual variation (Figs. 3, A and B, and 4, A and B).

Analysis of the subject with congenital absence of the pericardium provides a useful comparison to the normal data. This case emphasizes the functional role of the pericardium in maintaining normal motion. The cross-sectional (2-D) four-chamber area varied 10% between end systole and end diastole. Interestingly, as in the normal cases, this variation was due almost entirely to wall motion at the ventricular level. There was a 6% change in the short-axis pericardial area of the atria between end systole and end diastole compared with the 1% change in normal counterparts, and an 18% change in the short-axis pericardial area of the ventricles compared with 12% in normal subjects. Both of these measurements were 1.5 standard deviations from the normal average. Additionally, major differences were noted in chamber variation at the ventricular level: in this case, the variation was distributed equally between the RV and LV instead of being limited essentially entirely to the LV. The change in LV short-axis area was within normal range, but the RV short-axis area changed by 20% compared with only 5% in normal cases. In addition to bulk translation, the LV exhibited an exaggerated crescent effect as described above, sizable in width and located along the free wall of the LV (see Fig. 5). There was significantly more longitudinal variation in this subject; however, some of this variation may be due to lateral displacement of the apex out of the slice plane during systole.

On the basis of our wall motion studies, we suggest that the 5% (40 ml) decrease in the volume encompassed by the pericardial sack during the systolic portion of the cardiac cycle occurs primarily in the location of the LV and is caused primarily (but not solely) by the LV. In evaluating global left heart function, we have previously demonstrated that the Doppler pulmonary vein D wave exists only if the ideal constant-volume state of the heart is disrupted (4). Specifically, systolic deviations of the heart from the constant-volume state are rectified in diastole via the blood flow during the acceleration portion of the pulmonary vein D wave, and the majority of this entering blood travels directly to the LV as the left atrial conduit volume (4). Thus the radial expansion of the ventricles observed in this study during early diastole results from the incoming atrial conduit volume (via the Doppler pulmonary vein D wave), returning the heart to its end-diastolic total blood volume (3). In all subjects studied, this volumetric expansion (due to the left atrial conduit volume via the pulmonary vein D wave) was accommodated by radial expansion of the LV, usually in a nonisotropic fashion, but with large variation in the specific orientation of this expansion (referred to as the crescent effect). The large variation in the macroscopic motion of the LV wall may reflect variation in the microscopic fiber structure between individuals as well as an interaction between the LV and RV during the cardiac cycle. Consequently, pending further study in various patient populations, the crescent effect could potentially be used as an easily imagable index of interventricular coupling in pathologies known to affect it, such as diabetes, left ventricular hypertrophy, and infiltrative diseases. We would also expect it to be useful in the assessment of patients with pericardial disease.

Limitations. The cine images for this study were acquired during 10-s breath holds and so contain data from multiple heartbeats. However, the breath holds are relatively short, so subjects remain in a physiological steady state, as evidenced by the smoothness and appearance of continuity within each cine loop. An end-expiratory breath hold technique was chosen because of the substantial reduction in blurring (due to respiratory motion) compared with free-breathing scans. Although it was not possible to precisely monitor transpulmonary pressure, patients were equipped with a respiratory monitor, which allowed the technologist to ensure that images were acquired consistently at end expiration. Image slices were acquired with a 9-mm thickness, which could potentially result in partial-volume artifacts; however, this thickness is actually slightly smaller than that reported in many previous MR studies. Further, the individual slices under consideration here have overall large cross-sectional areas (which should minimize the impact of any errors around the boundary) and were acquired in regions where the heart has relatively small epicardial curvature in the long-axis direction. One limitation of our wall motion analyses is that radial (short-axis) measurements of the atria and ventricles were obtained only at one representative plane each (immediately above and below the mitral valve plane). This raises some concerns pertaining to the effect of through-plane motion, which were mitigated by the ability to observe the epicardial displacement in the four-chamber 2-D slices, which further localized the area of LV epicardial radial displacement to the ventricles, below the atrioventricular plane, rather than the pericardial contents (atria and great vessel roots) above the atrioventricular plane. Additionally, because systolic LV shortening is primarily accomplished by apical displacement of the mitral valve plane, we would expect any systemic error to manifest as an overestimation of systolic diameter–meaning that any clear trend to the contrary cannot be explained by systemic error. A final limitation of the atrial measurements is that the exact epicardial boundary is difficult to determine on some of these images and may result in greater errors for these slices. Limitations of the acquisition sequence itself have been discussed previously (3).

In conclusion, the comparison of four-chamber and short-axis 2-D slices suggests that the fate of the 5% decrease in the volume encompassed by the pericardial sack at end systole is primarily generated by the LV through a radial decrease in epicardial cross section. This is achieved in a radially nonisotropic manner such that a crescent is seen in most cases when short-axis end-systolic and end-diastolic epicardial contours are superimposed. There is virtually no change in pericardial sack dimension in the longitudinal (apex to mediastinum) direction from end diastole to end systole. The recovery of the 5% end-systolic volume occuring during early diastole is consistent with our previous findings demonstrating how the left atrial conduit volume (entering via the Doppler pulmonary vein D wave) rectifies the slight systolic deviation of the heart from the constant-volume state. Assessment of this physiological scenario in selected pathological cases is planned.

	GRANTS

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This study was supported in part by the Heartland Affiliate of the American Heart Association (Dallas, TX), the Whitaker Foundation (Arlington, VA), National Institutes of Health Grants HL-54179 and HL-04023, the Alan A. and Edith L. Wolff Charitable Trust (St. Louis, MO), and Philips Medical Systems (Best, The Netherlands).

	ACKNOWLEDGMENTS

 
The authors thank Shelton Caruthers for technical direction, Mary Watkins and Todd Williams for image acquisition, and Amr el Shafei, LaTish McKinney, and Katherine Lehr for subject recruitment.

	FOOTNOTES

 

Address for reprint requests and other correspondence: S. J. Kovács, Cardiovascular Biophysics Laboratory, Washington Univ. Medical Center, Box 8086, 660 S. 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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1. Axel L. Assessment of pericardial disease by magnetic resonance and computed tomography. J Magn Reson Imaging 19: 816–826, 2004.[CrossRef][ISI][Medline]
2. Bowman AW, Caruthers SD, Watkins MP, and Kovács SJ. The effect of diabetes on the constant-volume attribute of the four-chambered heart (Abstract). J Cardiovasc Magn Reson 4: 81, 2002.
3. Bowman AW and Kovács SJ. Assessment and consequences of the constant-volume attribute of the four-chambered heart. Am J Physiol Heart Circ Physiol 285: H2027–H2033, 2003.[Abstract/Free Full Text]
4. Bowman AW and Kovács SJ. Left atrial conduit volume is generated by deviation from the constant-volume state of the left heart: a combined MRI-echocardiographic study. Am J Physiol Heart Circ Physiol 286: H2416–H2424, 2004.[Abstract/Free Full Text]
5. Carlsson M, Cain P, Holmqvist C, Stahlberg F, Lundback S, and Arheden H. Total heart volume variation throughout the cardiac cycle in man. Am J Physiol Heart Circ Physiol 287: H243–H250, 2004.[Abstract/Free Full Text]
6. Fogel MA, Weinberg PM, Fellows KE, and Hoffman EA. Magnetic resonance imaging of constant total heart volume and center of mass in patients with functional single ventricle before and after staged Fontan procedure. Am J Cardiol 72: 1435–1443, 1993.[CrossRef][ISI][Medline]
7. Hamilton W and Rompf H. Movements of the base of the ventricle and the relative constancy of the cardiac volume. Am J Physiol 102: 559–565, 1932.[Free Full Text]
8. Hoffman EA. Constancy of total heart volume: an imaging approach to cardiac mechanics. In: Imaging, Measurements and Analysis of the Heart, edited by Sideman S and Beyar R. New York: Hemisphere, 1991, p. 3–19.
9. Hoffman EA, Ehman RL, Sinak LF, Felmlee J, Chandrasekaran K, Julsrud P, and Ritman E. Law of constant heart volume in humans: a non-invasive assessment via X-ray, CT, MRI, and echo (Abstract). J Am Coll Cardiol 9: 38A, 1987.
10. Hoffman EA and Ritman EL. Invariant total heart volume in the intact thorax. Am J Physiol Heart Circ Physiol 249: H883–H890, 1985.[Abstract/Free Full Text]
11. Hoffman EA and Ritman EL. Heart-lung interaction: effect on regional lung air content and total heart volume. Ann Biomed Eng 15: 241–257, 1987.[ISI][Medline]
12. Hoffman EA and Ritman EL. Intracardiac cycle constancy of total heart volume. Dyn Cardiovasc Im 1: 199–205, 1987.
13. Kroeker CA, Shrive NG, Belenkie I, and Tyberg JV. Pericardium modulates left and right ventricular stroke volumes to compensate for sudden changes in atrial volume. Am J Physiol Heart Circ Physiol 284: H2247–H2254, 2003.[Abstract/Free Full Text]
14. Maruyama Y, Ashikawa K, Isoyama S, Kanatsuka H, Ino-Oka E, and Takishima T. Mechanical interactions between four heart chambers with and without the pericardium in canine hearts. Circ Res 50: 86–100, 1982.[Abstract/Free Full Text]
15. Matter C, Nagel E, Stuber M, Boesiger P, and Hess OM. Assessment of systolic and diastolic LV function by MR myocardial tagging. Basic Res Cardiol 91: 23–28, 1996.[CrossRef][ISI][Medline]
16. Nagel E, Stuber M, Burkhard B, Fischer SE, Scheidegger MB, Boesiger P, and Hess OM. Cardiac rotation and relaxation in patients with aortic valve stenosis. Eur Heart J 21: 582–589, 2000.[Abstract/Free Full Text]
17. Rademakers FE, Buchalter MB, Rogers WJ, Zerhouni EA, Weisfeldt ML, Weiss JL, and Shapiro EP. Dissociation between left ventricular untwisting and filling: accentuation by catecholamines. Circulation 85: 1572–1581, 1992.[Abstract/Free Full Text]
18. Streeter DD Jr and Hanna WT. Engineering mechanics for successive states in canine left ventricular myocardium II. Fiber angle and sarcomere length. Circ Res 33: 656–664, 1973.[Abstract/Free Full Text]
19. Stuber M, Scheidegger MB, Fischer SE, Nagel E, Steinemann F, Hess OM, and Boesiger P. Alterations in the local myocardial motion pattern in patients suffering from pressure overload due to aortic stenosis. Circulation 100: 361–368, 1999.[Abstract/Free Full Text]

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