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Ventricular untwisting: a temporal link between left ventricular relaxation and suction

Yuichi Notomi, Zoran B. Popovi, Hirotsugu Yamada, Don W. Wallick, Maureen G. Martin, Stephanie J. Oryszak, Takahiro Shiota, Neil L. Greenberg, and James D. Thomas

Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio

Submitted 23 August 2007 ; accepted in final form 19 November 2007

	ABSTRACT

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Left ventricular (LV) untwisting starts early during the isovolumic relaxation phase and proceeds throughout the early filling phase, releasing elastic energy stored by the preceding systolic deformation. Data relating untwisting, relaxation, and intraventricular pressure gradients (IVPG), which represent another manifestation of elastic recoil, are sparse. To understand the interaction between LV mechanics and inflow during early diastole, Doppler tissue images (DTI), catheter-derived pressures (apical and basal LV, left atrial, and aortic), and LV volume data were obtained at baseline, during varying pacing modes, and during dobutamine and esmolol infusion in seven closed-chest anesthetized dogs. LV torsion and torsional rate profiles were analyzed from DTI data sets (apical and basal short-axis images) with high temporal resolution (6.5 ± 0.7 ms). Repeated-measures regression models showed moderately strong correlation of peak LV twisting with peak LV untwisting rate (r = 0.74), as well as correlations of peak LV untwisting rate with the time constant of LV pressure decay (tau, r = –0.66) and IVPG (r = 0.76, P < 0.0001 for all). In a multivariate analysis, peak LV untwisting rate was an independent predictor of tau and IVPG (P < 0.0001, for both). The start of LV untwisting coincided with the beginning of relaxation and preceded suction-aided filling resulting from elastic recoil. Untwisting rate may be a useful marker of diastolic function or even serve as a therapeutic target for improving diastolic function.

diastole; relaxation; suction; torsion

LV systolic torsional (twisting) deformation is one mechanism by which potential energy is stored during ejection, to be later released during diastole and contribute to the creation of suction. In systole, as the base and apex of the heart rotate in the opposite direction and generate twisting of the heart muscle, part of the energy used in contraction is stored within extracellular collagen matrix (31) and compressed titin within the myocytes (11). During relaxation, this energy is promptly released and manifested by LV untwisting. About 40% of the LV untwisting occurs during isovolumic relaxation (25) (21), and its rate correlates with the time constant of LV pressure decay (tau) (10). Untwisting that occurs during filling can continue to release elastic energy after mitral valve opening, facilitating filling further. We therefore hypothesized that LV untwisting rate is reflective of relaxation and that it is related to LV pressure decline before and after mitral valve opening, creating IVPG. We therefore sought to investigate this in a closed-chest animal model under conditions of altered inotropy and electrical activation, which are known to modify LV torsional behavior (5, 28).

	METHODS

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Animal Preparation

The study was approved by the Institutional Animal Research committee (ARC#07393) and is in compliance with the Guide for the Care and Use of Laboratory Animals published by the National Institutes of Health. Seven adult mongrel dogs (weighing: 25–32 kg) were anesthetized with thiopental sodium (25 mg/kg) and isoflurane (1%), intubated, and mechanically ventilated using room air. Steerable electrophysiology catheters were inserted from the right and left jugular veins for pacing the right atrial appendage and right ventricular apex. To pace various LV sites, a 64-channel basket-type electrode mapping catheter (n = 4, model 8075; EP Technologies) or a steerable electrophysiology catheter (n = 3) was inserted through the right carotid artery, which also served as an arterial pressure-monitoring site. A conductance catheter was placed in the LV through the left femoral artery to obtain the LV volume signal. A triple-sensor Millar catheter (40 mm, distal to middle; and 20 mm, middle to proximal; Millar Instruments) was inserted in the LV transseptally from the left femoral vein to measure pressure at the LV apex and base and the left atrium. Thus the experiment was undertaken in a fully closed-chest manner. After these preparations, the animal was allowed to stabilize for at least 20 min. All data were collected with the dog in the left decubitus position. If heart rate exceeded 90 beats/min, an infusion of a bradycardic agent (UL-FS49; Boehringer-Ingelheim, Ridgefield, CT), was started with right atrial backup pacing at the rate of 90 beats/min, with the goal to avoid excessive shortening of diastole.

Experimental Protocol and Instruments

To observe the hemodynamic and LV torsional alteration by modulation of electrical sequence and inotropic intervention, the study protocol was designed with the following three parts: pacing (at right ventricle apex, LV at basal septum/lateral wall, and LV apex), infusing dobutamine (at 5 and 10 µg·kg^–1·min^–1), and esmolol (at 50 and 100 µg·kg^–1·min^–1). Data were collected in six stages as follows: 1) first baseline, 2) pacing, 3) second baseline, 4) dobutamine infusion, 5) third baseline (>10 min after the end of previous stage), and 6) esmolol infusion. The hemodynamic data were then collected, with the respirator suspended, for at least 10 cardiac cycles. All signals were amplified, digitized in a 1-ms resolution, and stored on a dedicated recording system (CardioLab; GE Marquette Medical Systems, Milwaukee, WI) for subsequent analysis.

Hemodynamic Data Analysis

LV pressures, their peak time derivatives (dP/dt), time constant of LV pressure decay (tau; shifting asymptote model), and LV volumes were analyzed beat-by-beat using a previously described computer program (24). Intraventricular pressure signal was calculated as the base-to-apex pressure difference and then manually analyzed by searching for its first early diastolic peak (12).

Transthoracic Echocardiography

After completion of a standard comprehensive two-dimensional and spectral/color flow Doppler examination, we collected Doppler tissue image (DTI) data sets in the apical, mid, and basal short-axis planes and apical four-chamber view at each stage with a Vivid 7 (GE Medical Systems) and an M3S probe, along with synchronous recording of the hemodynamic data. The velocity range of DTI was set at 20 cm/s to avoid aliasing. We carefully acquired proper short-axis levels based on anatomic landmarks [basal (mitral valve), midventricular (papillary muscle), and apical (no papillary muscle visible) levels (22)].

DTI Data Set Analysis

LV torsion. In this paper, we define angle-displacement about the central axis of the LV in each short-axis slice as "LV rotation." A net difference of the LV rotation between the apical and basal LV slice is defined as "LV torsion." We used the words "twisting" and "untwisting" to describe the systolic and postsystolic parts of LV torsional deformation, respectively. Counterclockwise rotation/torsion when viewed from the apex is expressed as a positive value. LV rotation and torsion were calculated by a method based on the analysis of two-dimensional color tissue Doppler echocardiography data (22). From these data, we calculated the timing and amplitudes of peak twisting (expressed in degrees), and peak untwisting rate (expressed in rad/s).

LV long- and short-axis function. LV long- and short-axis myocardial motion was assessed by averaging the velocities at the most basal septal and lateral regions in the four-chamber DTI image and by calculating the difference between anterior and posterior velocities in the midventricular short-axis DTI image. From these data, the peak rate and the time-to-peak rate of LV lengthening and short-axis expansion were calculated. All of the calculations of DTI data were averaged for at least three consecutive beats.

For temporal analysis (Figs. 1 and 2), the time sequence was normalized to the percent of systole duration [i.e., onset of QRS of the electrocardiogram, time (t) = 0%, and at aortic valve closure, t = 100%], as previously described (21). End-systole, mitral valve opening (i.e., onset of early filling) and timing of peak early filling were determined from the LV outflow and inflow Doppler flow profiles, whereas timing of IVPG was determined from pressure tracings. If measurements of time intervals are discussed, the values are given in milliseconds as well.

View larger version (50K): [in this window] [in a new window]   Fig. 1. A: averaged left ventricular (LV) torsion and torsional velocity profile altered by electrical activation sequence. The amount of LV torsion is presented as the peak systolic twisting value, whereas the untwisting behavior is shown in the velocity profile (as shown in the dotted-line circle). Blue, light green, green, and purple lines indicate apical, mid, and basal rotation and LV torsion, respectively. RV-p, right ventricle pacing; LVa-p, left ventricular apical pacing; ES, end systole; MO, mitral valve opening; E, timing of peak early filling, derived from averaged data in each stage. Please note the velocity profiles represent from onset of the QRS to early filling phase, not entire cardiac cycle. B: averaged LV torsion and torsional velocity profile altered by inotropic manipulation. Note: dobutamine enhanced untwisting velocity both during isovolumic relaxation (ES to MO) and early filling (i.e., the suction phase, shown by *). Thus untwisting occurs over both phases, releasing elastic energy (see DISCUSSION).

View larger version (33K): [in this window] [in a new window]   Fig. 2. Averaged LV long- and short-axis velocity and torsional rate profiles at baseline (A) and after being altered by electrical activation sequence and inotropic manipulation (B). Red, orange, and purple lines indicate long-axis, short-axis, and torsional velocity profile in a cardiac cycle. Note: untwisting was observed during isovolumic relaxation and early filling, and the relengthening and expansion occurs subsequently, similar to the baseline and dobutamine stages shown in Fig. 1B.

All data are presented as averages ± SD. Because the experimental design was conceived as a three-part study, we applied repeated-measures analysis of variance to separately assess the impact on LV function parameters by changes in electrical activation pattern and contractility. To assess the relationship between LV peak untwisting rate, tau, and IVPG (Fig. 3), we first controlled for between-animal variability by expressing data as the percent of each baseline value. Next, we applied a repeated-measures regression model:

where Y is the dependent variable (i.e., IVPG or peak untwisting rate), C is a constant, X is a covariate (such as tau, –dP/dt, twisting, or peak untwisting rate), D_i (with i = 1... n – 1) are dummy variables that code for individual animals, and Error is a randomly distributed error term. The goodness-of-fit was assessed by the within-subject correlation coefficient:

where SS_cov and SS_res stand for sum of squares attributed to covariate or to residuals, respectively (4). Multiple linear regression was used to determine the effect of heart rate, end-systolic volume, ejection fraction, peak LV systolic pressure, maximum and minimum dP/dt, and tau on peak LV systolic twisting and untwisting rate, minimum dP/dt, tau, and IVPG. Furthermore, we used stepwise multiple linear regression to determine the potential independent predictors of tau and IVPG. While selecting potential predictors, we assumed that independent variables should precede dependent ones in a time domain (e.g., contraction parameters should precede dP/dt_min, and isovolumic relaxation time should precede IVPG).

View larger version (14K): [in this window] [in a new window]   Fig. 3. Relationship between systolic peak torsion (Torsion) and peak untwisting velocity (Untwisting), peak untwisting velocity and relaxation time constant (tau), and peak untwisting velocity and intraventricular pressure gradient (IVPG). Each legend mark indicates an individual dog. Dotted lines denote simple linear regression line in the each dog. Statistical analysis of overall correlation of the relationship in individual dogs was performed by repeated-measure regression model (correlation, r, P value, and the bold lines on each graph). In each graph, data are normalized with 100, representing the baseline condition.

	RESULTS

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Hemodynamic and DTI recordings were accomplished in the closed-chest setting in all seven dogs (all 7 dogs had pacing stages collected while 5 dogs additionally had dobutamine and esmolol stages collected). DTI was taken at 154 ± 16 frames/s (i.e., 6.5 ± 0.7-ms interval) in the study. The average effects of pacing and inotropic interventions are detailed in Table 1 and 2 (heart rate, volume, and torsion parameters and pressure-derived parameters). Maximum LV twist and peak untwisting rate were obtained from the LV torsion and torsional velocity profiles analyzed in each stage as shown in Fig. 1, A (pacing stage) and B (dobutamine and esmolol stages).

View larger version (17K): [in this window] [in a new window]   Fig. 4. Pressure-Volume (PV), pressure-torsion (PT), torsion-volume (TV) relationships. Baseline stage data in all 7 dogs were averaged for each graph with data (mean ± SD) shown at time intervals corresponding to 10% of the systolic ejection time. Pressure and LV torsion were normalized by the maximum value, and the LV volume was normalized by the stroke volume. MC/MO, mitral valve closure/opening; AO/AC, aortic valve opening/closure; Pk-E/En-E, peak/end of early filling. Red, light blue, and blue lines depict systole, isovolumic relaxation, and early filling phase, respectively.

	DISCUSSION

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Relaxation, Untwisting, Ventricular Shape, and Suction

During relaxation, untwisting occurs because of a combination of a decrease in muscle tension and release of energy from previously distorted extra (31)- and intracellular (13) elastic structures. Thus two factors that modify torsion-untwisting relationships are relaxation rate and the mechanical characteristics of elastic elements. In a normal ventricle, as we demonstrate here, relaxation and untwisting are closely related. However, delayed untwisting despite normal or increased LV torsion or apical rotation has been observed in states associated with worsened relaxation such as chronically pressure overloaded heart (30) and aging (23). On the other hand, changes in elastic elements were demonstrated in tachycardia-induced cardiomyopathy, where altered expression of titin, a major elastic component in cardiac muscle cells, was observed in parallel with decreased IVPG and decreased LV untwisting even after controlling for the amount of systolic shortening (2).

We found that ventricular untwisting preceded and was a strong predictor of IVPG, which is manifested in part by apical pressure decline. An obvious manner in which untwisting can affect LV suction is through a change of LV shape. As opposed to depolarization, repolarization, and therefore relaxation, progresses from epi- toward endocardial layers with little or no basoapical gradient (32). Because subepicardial fibers are predominantly responsible for twisting, it is no surprise that the first motion detectable during relaxation is untwisting (1). This is closely followed by a change of orientation of myocardial sheets that becomes less perpendicular toward the long axis and that in turn leads to sub-endocardial radial thinning (1, 27). This initial, discreet, and very early change facilitates a continuous apical LV pressure drop during the diastolic suction phase. The importance of this apical relaxation to LV suction was noted by Davis et al. (9) and Steine et al. (29).

Finally, we have shown that untwisting precedes not only peak IVPG development but also long-axis LV lengthening and short-axis expansion. Previous studies indicated that early long-axis relengthening is an important manifestation of restoring forces. However, its relatively late appearance that is almost coincidental with radial expansion argues against this. Thus long- and short-axis expansion seem to proceed predominantly as reflections of LV filling and not as a result of restoring forces.

Clinical and Research Implication

Despite the identification of numerous molecular mechanisms that have the potential to alter myocyte contraction/relaxation, their interaction and quantitative clinical impact on relaxation remains unclear. Although strain analysis shows important information on regional deformation, there is little information available during isovolumic relaxation when myocyte relengthening begins (26). LV twisting/untwisting profile may provide further insight into the behavior at the myocyte level and help connect basic and clinical observations. By use of DTI, serial assessment of LV torsional deformation may assist in the early detection of disease and monitoring of the response to therapeutic interventions.

Limitations

The current study is limited to demonstrate the correlations between, and temporal successions of, isovolumic pressure decay, LV untwisting, and IVPG and does not address the cause-and-effect relationships between these phenomena. Inherently, multiple components of the contributing physiological variables are highly interdependent. An investigation to selectively clarify the interdependence or to integrate the observed data with mechanistic model analysis remains to be addressed by a future study.

Although the conductance signal has been validated against a variety of methods, (14, 15) it is certainly subject to its own error. The advantage of high temporal resolution of the conductance catheter and disadvantage of image-quality dependence of echocardiography to measuring LV volume should be addressed also.

Although all hemodynamic and echocardiographic data were acquired at virtually the same time (<1 min), they were analyzed off-line and synchronized by aligning the QRS of the electrocardiogram. Ideally, all measurements should be simultaneous, but we took care to maintain constant hemodynamic conditions during acquisition.

Although the current Doppler method possesses higher temporal resolution than conventional magnetic resonance imaging (MRI) tissue tagging imaging, LV torsional behavior was analyzed from multiple aligned two-dimensional DTI data sets, not true three-dimensional data, which MRI provides. However, we have shown that this DTI method agrees very well with MRI (22), and the superior frame rate allows us to better elucidate the brief events during IVR. On the other hand, transmural variation in torsion has been reported by MRI analysis (6, 17), but the DTI method calculates the LV rotation/torsion value averaged throughout ventricular thickness. Analysis of this transmural variation in torsion would affect the results obtained from the current study or reveal more important findings. Additionally, IVPG is related to, but not identical with, rigorous definition of suction (19); however, Nikolic et al. (20), using pressure sensors located in the base and apex of the left ventricle, demonstrated that IVPG originates through and reflects the force of elastic recoil/suction. Finally, IVPG may underestimate a total suction effect, since it does not include pressure drop across the mitral valve. In the isovolumic period, the suction generated by the restoring force in the LV wall contributes to both IVPG and the pressure drop across the mitral valve. Because mitral valve impedance varies, the fractions of the suction force that goes in the pressure drop across the mitral valve and in IVPG may vary. On the other hand, incorporating atrial pressures, especially in a setting of even mildly restrictive mitral orifice (often seen in a variety of heart diseases), may severely overestimate suction force.

In conclusion, ventricular untwisting provides a temporal link between ventricular relaxation and suction-aided filling and shows a strong association with both of these phenomena. The echocardiographic approach used here should facilitate assessment of LV torsional deformation and may bring new, valuable, information about diastolic relaxation and suction to heart failure patients. (Table 5).

	GRANTS

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Y. Notomi is funded through a postdoctoral fellowship grant of the Ohio Valley affiliate of the American Heart Association (0325237B), and the current study is a part of the grant. This study was also supported in part by the National Space Biomedical Research Institute through National Aeronautics and Space Administration Grant NCC 9-58 (Houston, TX) and the Department of Defense (United States Army Medical Research and Material Command Grant No. 02360007; Ft. Detrick, MD). This work is also supported in part by the National Institutes of Health, National Center for Research Resources, General Clinical Research Center Grant MO1 RR-018390.

	FOOTNOTES

 

Address for reprint requests and other correspondence: J. D. Thomas, Dept. of Cardiovascular Medicine/F15, The Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195 (e-mail: thomasj{at}ccf.org)

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. Ashikaga H, Criscione JC, Omens JH, Covell JW, Ingels NB Jr. Transmural left ventricular mechanics underlying torsional recoil during relaxation. Am J Physiol Heart Circ Physiol 286: H640–H647, 2004.[Abstract/Free Full Text]
2. Bell SP, Nyland L, Tischler MD, McNabb M, Granzier H, LeWinter MM. Alterations in the determinants of diastolic suction during pacing tachycardia. Circ Res 87: 235–240, 2000.[Abstract/Free Full Text]
3. Beyar R, Yin FC, Hausknecht M, Weisfeldt ML, Kass DA. Dependence of left ventricular twist-radial shortening relations on cardiac cycle phase. Am J Physiol Heart Circ Physiol 257: H1119–H1126, 1989.[Abstract/Free Full Text]
4. Bland JM, Altman DG. Calculating correlation coefficients with repeated observations: part 1–correlation within subjects. Br Med J 310: 446, 1995.[Free Full Text]
5. Buchalter MB, Rademakers FE, Weiss JL, Rogers WJ, Weisfeldt ML, Shapiro EP. Rotational deformation of the canine left ventricle measured by magnetic resonance tagging: effects of catecholamines, ischaemia, and pacing. Cardiovasc Res 28: 629–635, 1994.[Abstract/Free Full Text]
6. Buchalter MB, Weiss JL, Rogers WJ, Zerhouni EA, Weisfeldt ML, Beyar R, Shapiro EP. Noninvasive quantification of left ventricular rotational deformation in normal humans using magnetic resonance imaging myocardial tagging. Circulation 81: 1236–1244, 1990.[Abstract/Free Full Text]
7. Courtois M, Kovacs SJ Jr, Ludbrook PA. Transmitral pressure-flow velocity relation Importance of regional pressure gradients in the left ventricle during diastole. Circulation 78: 661–671, 1988.[Abstract/Free Full Text]
8. Courtois M, Kovacs SJ, Ludbrook PA. Physiological early diastolic intraventricular pressure gradient is lost during acute myocardial ischemia. Circulation 81: 1688–1696, 1990.[Abstract/Free Full Text]
9. Davis KL, Mehlhorn U, Schertel ER, Geissler HJ, Trevas D, Laine GA, Allen SJ. Variation in tau, the time constant for isovolumic relaxation, along the left ventricular base-to-apex axis. Basic Res Cardiol 94: 41–48, 1999.[CrossRef][Web of Science][Medline]
10. Dong SJ, Hees PS, Siu CO, Weiss JL, Shapiro EP. MRI assessment of LV relaxation by untwisting rate: a new isovolumic phase measure of tau. Am J Physiol Heart Circ Physiol 281: H2002–H2009, 2001.[Abstract/Free Full Text]
11. Granzier H, Wu Y, Siegfried L, LeWinter M. Titin: physiological function and role in cardiomyopathy and failure. Heart Fail Rev 10: 211–223, 2005.[CrossRef][Web of Science][Medline]
12. Greenberg NL, Vandervoort PM, Firstenberg MS, Garcia MJ, Thomas JD. Estimation of diastolic intraventricular pressure gradients by Doppler M-mode echocardiography. Am J Physiol Heart Circ Physiol 280: H2507–H2515, 2001.[Abstract/Free Full Text]
13. Helmes M, Trombitas K, Granzier H. Titin develops restoring force in rat cardiac myocytes. Circ Res 79: 619–626, 1996.[Abstract/Free Full Text]
14. Kass DA, Yamazaki T, Burkhoff D, Maughan WL, Sagawa K. Determination of left ventricular end-systolic pressure-volume relationships by the conductance (volume) catheter technique. Circulation 73: 586–595, 1986.[Abstract/Free Full Text]
15. Lankford EB, Kass DA, Maughan WL, Shoukas AA. Does volume catheter parallel conductance vary during a cardiac cycle? Am J Physiol Heart Circ Physiol 258: H1933–H1942, 1990.[Abstract/Free Full Text]
16. Little WC. Diastolic dysfunction beyond distensibility: adverse effects of ventricular dilatation. Circulation 112: 2888–2890, 2005.[Free Full Text]
17. Moore CC, Lugo-Olivieri CH, McVeigh ER, Zerhouni EA. Three-dimensional systolic strain patterns in the normal human left ventricle: characterization with tagged MR imaging. Radiology 214: 453–466, 2000.[Abstract/Free Full Text]
18. Nakatani S, Firstenberg MS, Greenberg NL, Vandervoort PM, Smedira NG, McCarthy PM, Thomas JD. Mitral inertance in humans: critical factor in Doppler estimation of transvalvular pressure gradients. Am J Physiol Heart Circ Physiol 280: H1340–H1345, 2001.[Abstract/Free Full Text]
19. Nikolic S, Yellin EL, Tamura K, Vetter H, Tamura T, Meisner JS, Frater RW. Passive properties of canine left ventricle: diastolic stiffness and restoring forces. Circ Res 62: 1210–1222, 1988.[Abstract/Free Full Text]
20. Nikolic SD, Feneley MP, Pajaro OE, Rankin JS, Yellin EL. Origin of regional pressure gradients in the left ventricle during early diastole. Am J Physiol Heart Circ Physiol 268: H550–H557, 1995.[Abstract/Free Full Text]
21. Notomi Y, Martin-Miklovic MG, Oryszak SJ, Shiota T, Deserranno D, Popovic ZB, Garcia MJ, Greenberg NL, Thomas JD. Enhanced ventricular untwisting during exercise: a mechanistic manifestation of elastic recoil described by Doppler tissue imaging. Circulation 113: 2524–2533, 2006.[Abstract/Free Full Text]
22. Notomi Y, Setser RM, Shiota T, Martin-Miklovic MG, Weaver JA, Popovic ZB, Yamada H, Greenberg NL, White RD, Thomas JD. Assessment of left ventricular torsional deformation by Doppler tissue imaging: validation study with tagged magnetic resonance imaging. Circulation 111: 1141–1147, 2005.[Abstract/Free Full Text]
23. Oxenham H, Sharpe N. Cardiovascular aging and heart failure. Eur J Heart Fail 5: 427–434, 2003.[Abstract/Free Full Text]
24. Popovic ZB, Mowrey KA, Zhang Y, Zhuang S, Tabata T, Wallick DW, Grimm RA, Thomas JD, Mazgalev TN. Slow rate during AF improves ventricular performance by reducing sensitivity to cycle length irregularity. Am J Physiol Heart Circ Physiol 283: H2706–H2713, 2002.[Abstract/Free Full Text]
25. Rademakers FE, Buchalter MB, Rogers WJ, Zerhouni EA, Weisfeldt ML, Weiss JL, Shapiro EP. Dissociation between left ventricular untwisting and filling. Accentuation by catecholamines. Circulation 85: 1572–1581, 1992.[Abstract/Free Full Text]
26. Rodriguez EK, Hunter WC, Royce MJ, Leppo MK, Douglas AS, Weisman HF. A method to reconstruct myocardial sarcomere lengths and orientations at transmural sites in beating canine hearts. Am J Physiol Heart Circ Physiol 263: H293–H306, 1992.[Abstract/Free Full Text]
27. Rosen BD, Gerber BL, Edvardsen T, Castillo E, Amado LC, Nasir K, Kraitchman DL, Osman NF, Bluemke DA, Lima JA. Late systolic onset of regional LV relaxation demonstrated in three-dimensional space by MRI tissue tagging. Am J Physiol Heart Circ Physiol 287: H1740–H1746, 2004.[Abstract/Free Full Text]
28. Sorger JM, Wyman BT, Faris OP, Hunter WC, McVeigh ER. Torsion of the left ventricle during pacing with MRI tagging. J Cardiovasc Magn Reson 5: 521–530, 2003.[CrossRef][Web of Science][Medline]
29. Steine K, Stugaard M, Smiseth OA. Mechanisms of retarded apical filling in acute ischemic left ventricular failure. Circulation 99: 2048–2054, 1999.[Abstract/Free Full Text]
30. Stuber M, Scheidegger MB, Fischer SE, Nagel E, Steinemann F, Hess OM, 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]
31. Waldman LK, Nosan D, Villarreal F, Covell JW. Relation between transmural deformation and local myofiber direction in canine left ventricle. Circ Res 63: 550–562, 1988.[Abstract/Free Full Text]
32. Yan GX, Antzelevitch C. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. Circulation 98: 1928–1936, 1998.[Abstract/Free Full Text]

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				D. B. Ennis, T. C. Nguyen, A. Itoh, W. Bothe, D. H. Liang, N. B. Ingels, and D. C. Miller Reduced Systolic Torsion in Chronic "Pure" Mitral Regurgitation Circ Cardiovasc Imaging, March 1, 2009; 2(2): 85 - 92. [Abstract] [Full Text] [PDF]

				W.-J. Kim, B. H. Lee, Y. J. Kim, J. H. Kang, Y. J. Jung, J.-M. Song, D.-H. Kang, and J.-K. Song Apical Rotation Assessed by Speckle-Tracking Echocardiography as an Index of Global Left Ventricular Contractility Circ Cardiovasc Imaging, March 1, 2009; 2(2): 123 - 131. [Abstract] [Full Text] [PDF]

				B. T. Esch and D. E. R. Warburton Left ventricular torsion and recoil: implications for exercise performance and cardiovascular disease J Appl Physiol, February 1, 2009; 106(2): 362 - 369. [Abstract] [Full Text] [PDF]

				M Saito, H Okayama, K Nishimura, A Ogimoto, T Ohtsuka, K Inoue, G Hiasa, T Sumimoto, J Funada, Y Shigematsu, et al. Determinants of left ventricular untwisting behaviour in patients with dilated cardiomyopathy: analysis by two-dimensional speckle tracking Heart, February 1, 2009; 95(4): 290 - 296. [Abstract] [Full Text] [PDF]

				M. L. Geleijnse and B. M. van Dalen Let's twist Eur J Echocardiogr, January 1, 2009; 10(1): 46 - 47. [Full Text] [PDF]

				L. C. Afonso, J. Bernal, J. J. Bax, and T. P. Abraham Echocardiography in hypertrophic cardiomyopathy: the role of conventional and emerging technologies. J. Am. Coll. Cardiol. Img., November 1, 2008; 1(6): 787 - 800. [Abstract] [Full Text] [PDF]

				B. M. van Dalen, K. Caliskan, O. I.I. Soliman, A. Nemes, W. B. Vletter, F. J. ten Cate, and M. L. Geleijnse Left ventricular solid body rotation in non-compaction cardiomyopathy: A potential new objective and quantitative functional diagnostic criterion? Eur J Heart Fail, November 1, 2008; 10(11): 1088 - 1093. [Abstract] [Full Text] [PDF]

				S. Nottin, G. Doucende, I. Schuster-Beck, M. Dauzat, and P. Obert Alteration in left ventricular normal and shear strains evaluated by 2D-strain echocardiography in the athlete's heart J. Physiol., October 1, 2008; 586(19): 4721 - 4733. [Abstract] [Full Text] [PDF]

				E. L. Ritman, A. Pasipoularides, T. Arts, T. Delhaas, P. P. Sengupta, B. K. Khandheria, A. J. Tajik, A. Boussuges, and J. Regnard To the editor: functional imaging(FI) combines imaging datasets and computational fluid dynamics to simulate cardiac flows. J Appl Physiol, September 1, 2008; 105(3): 1015 - 1015. [Full Text] [PDF]

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