HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Gerald D. Buckberg Bernd Jung Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Buckberg, G. D. Articles by Ballester-Rodes, M. Search for Related Content PubMed PubMed Citation Articles by Buckberg, G. D. Articles by Ballester-Rodes, M. Related Collections Cardiac - physiology Cardiac - other

Eur J Cardiothorac Surg 2006;29:S165-S177
© 2006 Elsevier Science NL

MRI myocardial motion and fiber tracking: a confirmation of knowledge from different imaging modalities

^a Option on Bioengineering, California Institute of Technology, Pasadena, CA, USA
^b Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
^c Department of Surgery, Division of Cardiothoracic Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, 62-258 CHS, Los Angeles, CA 90095-1741, USA
^d Department of Diagnostic Radiology, University Hospital Freiburg, Germany
^e Hospital de Mataro, Barcelona, Spain

Received 22 February 2006; accepted 27 February 2006.

^_* Corresponding author. Tel.: +1 310 206 1027; fax: +1 310 825 5895. (Email: gbuckberg{at}mednet.ucla.edu).

	Abstract

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

 
Objective: A helical configuration underlies the anatomy of cardiac structure, and a structure/function relationship is needed to determine if the ventricular myocardial band model defines this spatial relationship. This report explores how studies of velocity-encoded phase contrast magnetic resonance imaging (MRI) for myocardial motion and fiber tracking algorithms that imply fiber orientations can (a) quantify regional myocardial wall motion of the entire heart, (b) determine if these motion of implied fiber orientation link with the helical heart model, and (c) reveal if this new knowledge correlates with imaging information from other different imaging modalities. Methods: Accumulated left ventricular motion patterns that accurately differentiate radial (i.e. contraction and expansion), rotational (i.e. twisting and untwisting), and longitudinal (i.e. lengthening and shortening) motion components are correlated with structure/function data achieved by sonomicrometer crystals, echocardiography, corrosion casts, and MUGA recordings. Results: Acceleration fiber tracking to determine fiber orientation and cardiac motion during the ejection and rapid filling phases of the cardiac cycle corresponded to maximal force displayed by ultrasonic crystals placed into the angulation of the presumed functional units of the descending and ascending segments of the apical loop of the helical ventricular myocardial band, and motion by echocardiographic recordings. These integrated findings imply a favourable interaction of MRI with the myocyte orientation of the helical ventricular myocardial band. Conclusions: These composite findings indicate that phase contrast MRI techniques for high temporal resolution velocity mapping during cardiac motion and myocardial fiber tracking confirm other technologies, and centralize the capacity of MRI to link other imaging methods together relative to a single helical structural model. The close agreement amongst a spectrum of imaging studies provide a very powerful integration that transcends a single look; the same thing is observed by each component of global technology, thereby implying that the helical ventricular band is the structural basis for these functional changes.

Key Words: MRI myocardial motion • Fiber tracking • Helical ventricular myocardial band • Echocardiography • Sonomicrometer crystals • Radionuclide ventriculography • Corrosion casts • Isovolumic contraction

	1. Introduction

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

 
Phasic myocardial action involves a form–function relationship. The underpinning of this interaction requires testing fiber orientation against a structural model, that generates these normal sequential motions, followed by secondary correlation with data from other imaging modalities. The importance of this interaction is clarified by recognizing the direct cardiac vision and magnetic resonance imaging show that the classical functions for ejection and filling are a twisting motion for ejection and reciprocal twisting for rapid filling (see Video 1 in http://www.ejcts.ctsnetjournals.org/cgi/content/full/27/2/202/DC1) rather than the constriction and passive filling described by Harvey [1], as learned by most students.

The dynamics of cardiac action become evident from MRI recordings [2], a tool that also implies structural fiber orientation by generating acceleration fiber tracking [3]. These MRI recordings demonstrate the rotational motions of twisting and longitudinal motion that underlie the narrowing, shortening, lengthening, and widening motions performed by the normal ventricular chamber [4]. Each dominant motion component responsible for cardiac mechanics during isometric contraction, systole during ejection, the isovolumetric phase for rapid filling, and diastole must evolve myocardial fiber orientation exerts its dynamic action on left ventricular performance. There must be a clear structural basis for what we see, thereby creating the structure/function relationship.

This report will define results from analysis of normal myocardial motion by means of functional magnetic resonance imaging (MRI) in the context of dominate motion components during different phases of the cardiac cycle and myocardial fiber tracking, and compare these findings with other phasic measurements of cardiac activity made by ultrasonic sonomicrometer crystals [5], echocardiography, radionuclide ventriculography tracings [6], and determine if a structure/function relationship can be linked to spatial orientation of the helical ventricular myocardial band [7].

These results will demonstrate a close relationship between MRI resolution of myocardial motion and fiber tracking with these other technologies during each phase of the cardiac cycle. The integration of these techniques with the helical heart ventricular band model identifies structural reasons for the sequential dynamics responsible for global functional events, that include (a) ‘cocking’ of the heart during isometric contraction, (b) ‘co-contraction’ during shortening during ejection, and (c) a muscular reason for reciprocal twisting and lengthening during the isovolumetric contraction (IVC) during rapid ventricular filling, a phase previously thought of as IVR or isovolumetric relaxation.

The close agreement amongst a spectrum of imaging studies provides a very powerful integration that transcends a single look by any one imaging modality, since each component of global technology sees the same thing. These findings imply that the helical ventricular band is the infrastructure for the global functional changes observed by MRI and other technologies.

	2. Methods

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

 
The background for the MRI tissue phase mapping of acceleration velocity to characterize motion and myocardial fiber tracking is defined in the prior two reports [2,3]. MRI velocity studies were done in healthy volunteers, where there was no hemodynamic monitoring of intravascular pressures. For hemodynamic comparison, phasic records of ultrasonic crystal recordings were reviewed that displayed the standard motion findings in these four phases of isometric contraction, ejection, rapid filling in the isovolumic phase, and mid-diastole [5], together with data obtained by echocardiography (methods described below) and recently reported radionuclide ventriculography findings by Ballester-Rodes et al. [6]. There is also correlation of MRI-described motion with morphologic data about how the trabecular arrangements of spiral ventricular fibers compress underlying blood, and how ventricular musculature effects blood flow, using corrosion cast analyses [8].

The spatial structure of the helical ventricular myocardial band was employed to determine if the MRI and the other functional tests had correlation to this configuration (Fig. 1 ). Unfolding of this band configuration shows that the heart comprises two loops that include a wrap around basal loop composed of a right and left ventricular segment that contains transverse fibers and acts like a buttress that surrounds the underlying oblique apical loop. The apical loop has a helical configuration and is constructed from the oblique fibers of the descending and ascending segments that have a crisscross fiber orientation arrangement that forms a vortex at the left ventricular apex.

View larger version (57K): [in this window] [in a new window]   Fig. 1. Progressive unwrapping of helical ventricular myocardial band. Note (a) the intact, (b) detachment of the right ventricle free wall or transverse orientation of the left and right basal segments, together with the obliquely oriented fibers of the ascending segment of the apical loop, (c) the genu adjacent to the septum separates right and left ventricles and shows the helical configuration is clearer, composed of superimposed descending and ascending segments of the apical loop, (d) detaching the aorta to show the unwrapped ascending segment of the apical loop, and further exposing the underlying descending segment, and (e) the myocardial band, showing the fold at junction between basal and apical loops, and displaying the completely unwrapped heart.

We systematically describe our observations of cardiac motion using transesophageal echocardiography (TEE) in humans. Various imaging modes including strain-, tissue velocity-, m-mode and two-dimensional echocardiography have been utilized in standard TEE views to validate the motion in the helical heart. Left ventricular velocities and motion are measured in reference to transducer at the apex of the sector scan.

This echocardiographic approach defined the four phases of motion including narrowing, shortening, lengthening, and widening during the cardiac cycle, to complement information gained from other imaging techniques like MRI (twisting), radionuclide ventriculography (endocardial motion on ventricular blood pool), and sonomicrometer crystals that show only regional shortening between pairs of crystals, but cannot distinguish quantify twisting, transmural thickening, shortening or lengthening of the chamber. The interaction of this broad spectrum of imaging methods may improve understanding of how the underlying model of cardiac structure determines the sequences of cardiac motion they measure.

	3. Results

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

 
3.1 MRI measurements
(Appendix A) demonstrate the basal slice with rapid velocity information in TPM data (temporal resolution of 13.8 ms) of the twisting motion throughout the cardiac cycle, together with color-coded maps of tangential motion. These motions resulted from underlying contraction of the myocardial segments, and the motion behavior of the LV in basal, as well as the mid-ventricular and apical slice positions in terms of the contraction/expansion, rotation (clockwise/counter-clockwise), and lengthening/shortening movement that was followed throughout the cardiac cycle. Fig. 2 displays the breakdown of the twisting motions during the isometric, ejection, isovolumic phase before rapid filling and diastolic phases of the cardiac cycle. The initiation of these timed MRI data records, recorded at 72 frames/min, was 13.8 ms after the QRS. This slight delay in determining initiation of twisting and study of the shorter intervals was subsequently blended with the echocardiographic data, allowing more immediate recordings, obtained at >250 frame rates/s, allowing instantaneous measurement of the sequential narrowing, shortening, lengthening and widening motions throughout the cardiac cycle.

View larger version (96K): [in this window] [in a new window]   Fig. 2. Sequences of tangential motion recorded simultaneously from the apex and base. Note the twisting patterns that include clockwise (marker to right) and counter-clockwise (marker to left) movements characterized by a counter-clockwise motion during isometric contraction, and the twist during systole (apex and base in different directions). All motions are described in the text.

View larger version (27K): [in this window] [in a new window]   Fig. 3. Differences between normalized mean values for tracing velocity motion each 13.8 s for 12 volunteer subjects, with recorded variance (above), and data from one subject with exact time scales shown below. Values above the zero line indicate thickening for contraction and below the line expansion (widening) ms time to the end of thickening is used in the text as a 320 ms time frame for the end of systole, but site will vary somewhat, depending on heart rates in different subjects.

View larger version (34K): [in this window] [in a new window]   Fig. 4. Radial (contraction), tangential (twisting), and longitudinal velocities. See text for description.

Tangential motion (twisting) is displayed in Fig. 4b, and shows that initially, all segments move counter-clockwise during the isometric phase. However, throughout systole (the time frame the radial tracing velocities are above the zero line), the basal slice develops a clockwise motion, while the apex continues a counter-clockwise motion. These MRI components thereby compliment the twisting motion seen in Video 1 in http://www.ejcts.ctsnetjournals.org/cgi/content/full/27/2/202/DC1 and Fig. 2. Apical and mid-wall regions’ tangential motion begins to reverse direction during the later phases of systole at the isovolumic interval just before rapid filling. Consequently, there was initiation of a reversal toward a clockwise motion during the ongoing thickening that is evident by contraction shown in Fig. 4a, demonstrating values above the zero line.

The longitudinal velocity of shortening exists in the base and mid-wall, as values are above the zero line, during this systolic phase that extends to 320 ms. There is negligible apical motion during this systolic time frame, thus codifying movement of the base toward the apex during systole. This downward motion of the base toward the apex is further amplified by the echo tracings described below.

Mean radial velocity of expansion (lack of contraction) occurs after the 320 ms time frame, accompanied by a reversal of the tangential (twisting) velocity, so that the base proceeds clockwise and apex counter-clockwise, and the longitudinal velocities display lengthening (values below the zero baseline), with two distinct peaks appearing during subsequent diastole. Fig. 5 displays the radial velocity of thickening owing to contraction, and documents ongoing thickness during and just beyond the isovolumetric phase at the end of systole. The temporal axis was normalized to end systole in order to avoid temporal jitter owing to different heart rates.

View larger version (28K): [in this window] [in a new window]   Fig. 5. Comparison between radial velocities (above) and muscle thickening (below) and the line shows end systole (ES). Note thickening remains for a time interval after radial velocity goes below the zero line to indicate expansion (widening).

Fig. 6 shows three-dimensional identification of acceleration tracks at these four different cardiac frames, and displays a smooth coverage of the entire LV for the cardiac frame during isovolumetric contraction (IVC) (a). The oblique angulation, from base to apex, shown during mid-systole (b) conforms to the oblique fiber orientation of the descending segment of the helical myocardial band (Fig. 7 ), the angulation of the ultrasonic crystals used previously to show maximum force of shortening during ejection (Fig. 8 ), and the spiral trabeculae that compress blood within the LV cavity in corrosion casts, prepared by Gorodkov et al. [8] (Fig. 9 ).

View larger version (112K): [in this window] [in a new window]   Fig. 6. Pixelwise arrow plots of the in-plane velocity component in a basal short-axis view for a healthy volunteer: cardiac frames for acceleration tracking during (a) IVC, (b) mid-systole, (c) IVR, and (d) mid-diastole. The large arrows represent the mean velocities in eight left ventricular angular areas of equal size for better visualization. Bottom: global radial, tangential and longitudinal velocities illustrating the dominant motional behavior over the cardiac cycle. The small circles indicate the temporal location of the arrow plots within the cardiac cycle.

View larger version (68K): [in this window] [in a new window]   Fig. 7. Unfolded segments of the helical heart showing the two segments of the basal and apical loops.

View larger version (44K): [in this window] [in a new window]   Fig. 8. Sites of placement of sonomicrometer crystals in the descending and ascending segments of the apical loop. The heart model and the sites used experimentally in the intact heart are shown in the upper and lower images. The oblique angulation for maximal force of shortening is shown, with the solid line in the descending segment and hatched line in the ascending segment. The solid and hatched lines in the tracings show the beginning and end of shortening in the descending and ascending segments. Note (a) earlier start in descending segment, (b) co-contracton during ejection, and (c) ongoing ascending shortening after descending shortening ends during the negative dP/dt of the LV pressure tracing.

View larger version (62K): [in this window] [in a new window]   Fig. 9. Comparison of fiber orientation in corrosion casts (left), descending segment of myocardial band (middle) and in-plane velocity component of acceleration tracts by MRI analysis (right).

View larger version (82K): [in this window] [in a new window]   Fig. 10. Comparison, during the isovolumic phase before the rapid filling of (a) structure in ascending segment of myocardial band (left) and (b) in-plane velocity component of acceleration tracts by MRI analysis during tissue phase mapping (right).

View larger version (77K): [in this window] [in a new window]   Fig. 11. Comparison of fiber orientation during diastole of myocardial band (left), and acceleration fiber tracking by MRI analysis during tissue phase mapping (right).

View larger version (62K): [in this window] [in a new window]   Fig. 12. (a) Esophageal four-chamber view with strain imaging of the basal lateral wall shows positive strain generated during the isometric contraction period without longitudinal shortening. (b) Strain imaging of the upper septum adjacent to mitral annulus. Arrow shows strain during the isometric contraction period that exists without longitudinal shortening.

View larger version (82K): [in this window] [in a new window]   Fig. 13. (a) Esophageal four-chamber view with m-mode through upper septum (adjacent to mitral annulus). Arrows show slight upward septal displacement during the isovolumetric contraction period. (b) Transgastric long-axis two-chamber view of left atrium and left ventricle. m-Mode image at the level of the mitral annulus shows initiation of constriction of the mitral annulus during isometric contraction period (arrow).

View larger version (63K): [in this window] [in a new window]   Fig. 14. (a) Sequential motion of endocardium by radionuclide ventriculography at the initiation of the cardiac cycle. Motion activity is shown by the development of a lighter color, and motion starts on the right side. (b) The sequential motion (lighter shade) forms a wrap around the central darker shade that proceeds from right to left, with persistent absence of motion in the center, where septal endocardium is adjacent to the ventricular blood pool. (c) Sequential motion during ejection displaying lighter color showing movement in the central region where septum endocardium is adjacent to the ventricular blood pool, with disappearance of motions in the right and left outer areas that were activated earlier in the cardiac cycle.

View larger version (69K): [in this window] [in a new window]   Fig. 15. Esophageal four-chamber view m-mode of the long axis of the left ventricle showing shortening of left ventricle in the ejection period (bold arrows) and lengthening of left ventricle in the relaxation period (light arrows).

View larger version (51K): [in this window] [in a new window]   Fig. 16. (a) Esophageal four-chamber view with TVI of the upper septum (adjacent to mitral annulus) demonstrating shortening during ejection. (b) TVI of the left ventricle at the lateral mitral annulus. TVI imaging (a and b) during the isovolumic ‘relaxation’ phase showing upward directed velocities and displacement of the upper septum and of left ventricle at the lateral mitral annulus, respectively. There is strain in the lateral wall during this ‘relaxation’ phase, signifying ‘contraction’. E' and A' refer to early and late diastolic tissue velocities during left ventricular filling.

View larger version (65K): [in this window] [in a new window]   Fig. 17. Sonomicrometer recording during the isovolumic phase before rapid filling, showing, on the heart, the ascending segment (solid line) and posterior basal segment (hatched bar) to define site of crystal placement. The hatched lines in the hemodynamic tracing during this isovolumic phase show ongoing shortening of the apical loop (ascending segment), because crystals come closer together. Simultaneously, the base widens (upswing of crystals) indicating the crystals are further apart.

	4. Discussion

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

The characteristic global movements documented by TPM velocity recordings during the cardiac cycle have traditionally been evident by echocardiography and ventriculogram, and include narrowing during the isometric phase of contraction, shortening during ejection, lengthening during the isovolumetric phase of rapid lengthening in preparation for rapid filling, and widening as passive ventricular filling occurs. Patterning of these findings with other imaging modalities, by using the model of the helical ventricular myocardial band gave insight into the structural reasons for global and regional motion dynamics defined by these imaging tools.

The tangential motions of twisting during TPM velocity recordings with also evident in the whole heart in Video 1 in http://www.ejcts.ctsnetjournals.org/cgi/content/full/27/2/202/DC1 and have been observed by tagging MRI studies [4]. The movements include counter-clockwise twisting during the isometric phase, torsion during ejection characterized by clockwise twisting of the base and counter-clockwise twisting of the apex, a reversal of this pattern in the apex during the isovolumetric phase before rapid ventricular filling, and continuance of this into early diastole. Similar reciprocal twisting of the walls was also previously reported by the DENSE studies of MRI motion obtained at the NIH by Wen (see Video 2 in http://www.ejcts.ctsnetjournals.org/cgi/content/full/27/2/202/DC1). These motions are related to actions of the underlying muscle, and correlation between these MRI measurements and motion by other collective imaging modalities was closely interfaced with the spatial structure of the myocardial band.

Isolated focus was not the purpose of this study although clear correlation of phases of individual TPM measurements with DTI measurements was evident, such as the brief small biphasic wave during isovolumetric relaxation. Rather, the intent was to try to match sequential TPM measurements and myocardial fiber tracking during the aforementioned four phases of cardiac movement during the cardiac cycle, together with associated twisting movements to determine if a structure/function relationship existed in relationship to the myocardial band.

4.1 Isometric contraction
The counter-clockwise twisting during the early isovolumetric phase of systole was reported by Lorenz et al. [4], and the correlation with other functional measurements defined a muscular cause of this movement. Narrowing of the chamber was evident by the TMP radial velocities of thickening, as well as by constriction of the mitral ring by echocardiogram [14]. This phase exists before ejection has been termed as ‘cocking’ of the chamber and before the downward motion during ventricular systole [15].

The mechanisms of this ‘cocking’ action are suggested by (a) a sequential shortening of the right, then the left segments of the basal loop by ultrasonic crystals, and (b) evidence of endocardial motion by radionuclide ventriculography that begins in the right segment and proceeds to the left segment of the basal loop of the myocardial band [6,16]. These motions suggest that the heart is pulled in a counter-clockwise direction by the right to left sequence of movement. A similar motion of the base, whereby the right segment pulled the left in a counter-clockwise movement was also reported in 1961 [17] by Coghlan who used simultaneous pressure derivative analysis of all chambers and great vessels. Furthermore, preliminary strain recordings by DENSE MRI methodology (see Video 4 in http://www.ejcts.ctsnetjournals.org/cgi/content/full/27/2/202/DC1) show sequential development of strain in the base of the heart before a spiral motion toward the apex. The counter-clockwise twisting, coupled with simultaneous narrowing of the mitral annulus during the isometric phase provided a muscular cause that is related to sequential movement of the basal loop. This motion explains the 28% compression of the mitral annulus in man during the pre-ejection phase on two-dimensional echocardiography previously reported by Ormiston et al. [14].

There is no longitudinal motion of ventricular shortening during this isometric interval, as the septum and lateral wall do not move downward toward the apex, so that the recorded endocardial shortening by sonomicrometer crystals does not contain the transmural component needed to generate global shortening. This longitudinal motion would be evident by echocardiogram and MRI but did not occur. Simultaneously, demonstration of positive strain in the septum by echocardiography, clarified the validity of endocardial shortening findings by sonomicrometer crystals.

The m-mode echocardiogram showed the septum slightly lengthened during this isometric phase. The upward motion of the septum during isometric contraction seems, at first, to reflect a paradoxical movement because the endocardium of the apical loop is simultaneously contracting and would be expected to shorten. However, the absence of shortening by echocardiogram and ongoing circumferential compression by the contracting basal loop implies that only the endocardial region of the septum is shortening, rather than the full wall. The apical loop narrows during its compression by a basal loop contraction, signifying that the basal loop is the dominant force, despite sonomicrometer evidence of descending segment (endocardial) contraction in the septum and the free wall and septum. The incompletely contracting septum is raised cephalad during the isometric phase of systole, and is associated with billowing of the closed mitral valve into the atrium.

4.2 Ejection
The phase of ejection is documented by thickening and shortening by TMP measurement and was accompanied by clockwise twisting of the base and counter-clockwise twisting of the apex. Longitudinal shortening was documented by echocardiogram and co-contraction of both the descending and ascending segments of the apical loop of the ventricular band was confirmed by ultrasonic crystal recordings.

The crystals were placed in a crisscross manner to obtain the maximal force of shortening, and the change of the slope during ejection implies that the counterforce of ascending shortening in a different or upward direction during co-contraction may explain the less steep slope of the sonomicrometer crystal tracing during this phase of ejection, as seen in Fig. 8.

Reciprocal twisting of the ventricle occurs during longitudinal shortening during ejection, and co-contraction of the ascending and descending segments of the apical segment of the myocardial band maximize the rate of shortening. Studies by Gorodkov et al. [8] document how the oblique spiral architecture compresses the corrosion cast (reflecting blood within the LV cavity), and we suspect the predominant power resides in the descending segment (Fig. 7) which becomes dominant during this ejection time period, despite epicardial ascending segment shortening and thickening.

4.3 Isovolumetric phase before rapid filling
The isovolumetric phase initiates before rapid filling (preciously considered isovolumic relaxation (IVR)), and the apex performs a clockwise rotation, whereas basal and mid-ventricular locations show early expansion in the anteroseptal and anterior regions with simultaneous (mild) clockwise rotation. The initiation of these clockwise movements occurs while radial velocity demonstrates ongoing contraction (Fig. 4a–c), so that the beginning of clockwise motion precedes the start of the lengthening motion. The descending segment stops shortening, but ascending segment shortening continues (Fig. 8).

Contraction itself seems to be responsible for this twisting motion, because systole exists and strain is observed in the septum and lateral wall by echocardiogram during the lengthening motion that occurs prior to rapid ventricular filling. The concept of systolic ventricular filling was previously suggested [18,7,19] and differs from prior suggestions that stored potential energy [20] from preceding systole (which is still occurring), collagen [21,22], of titin [22] can explain the tangential twisting motion that exists before rapid filling. The mitral valve opens during this lengthening time frame that the heart undergoes reciprocal twisting [13], and perhaps the active rapid reciprocal twisting of the apex will uncross the papillary muscles to open the valve leaflets.

The reciprocal clockwise shortening and twisting of the ascending segment [18] produces an upward cardiac lengthening on echocardiography (that also shows strain during this phase), and reflects the epicardial ascending segments predominating action during ongoing lengthening; no contraction occurs in the endocardium (descending segment) or basal loop segments during this interval. The unbridled ascending segment reciprocally twists to set the frame work for suction as LV pressure falls below atrial pressure to allow rapid filling.

There is no counterforce or co-shortening from the descending segment during this time interval of reciprocal twisting. Simultaneous widening of the base of the heart is evident by expansion on TMP velocity recordings, and greater distance between paired sonomicrometer crystals in the basal segments [5,2]. Such expansion prepares the ventricular cavity for rapid filling that occurs when suction is generated by the twisting ascending segment muscular contractile effort.

We had suspected [18,23] that although the active contraction of the descending segment has ceased, this region maintains muscular tone to retain its action as a fulcrum during the lengthening following the clockwise rotation and twist from the ascending segment; this concept is supported by persistent thickness observed by MRI imaging. Left ventricular chamber filling becomes passive after active shortening (crystals) or thickening (MRI) stops in all segments.

These findings of motion by echocardiography, MRI, and sonomicrometer crystals imply that the term isovolumic contraction (IVC) should replace isovolumic relaxation, because thickening, active shortening, and strain occur at a time phase previously thought of as relaxation. These observations thus challenge the concept of systole as contraction and diastole as relaxation, which is considered to begin at the junction of the dichrotic notch of the aortic and left ventricular pressure curves.

Our findings show that a longer systolic interval exits during the period previously called isovolumetric relaxation, and results from ascending segment shortening and twisting motion. The MRI velocity analysis (Fig. 4a–c) indicates a period of ongoing muscular contraction and ventricular compression exists as the twisting for rapid filling develops. Consequently, this muscular phase of prolonged systole, or ventricular systolic filling [19,18] underscores the mechanisms for the deceleration of the LV pressure, negative dP/dt and contractile component of rapid filling, and might expand the understanding of diastolic dysfunction and its potential treatment.

4.4 Diastole
Active contraction by radial velocity has stopped, and longitudinal lengthening is evident by TMP measurement, as well as by echocardiography. However, there is a biphasic wave observed, as with TDI recordings (Fig. 16), as well as an early continuation of the clockwise twisting of the apex and reciprocal twisting of the base to continue torsion. These movements are an active muscular phenomena that augments suction for rapid filling when ventricular pressure falls below atrial pressure. Passive filling from differences in pressures between the atrium and ventricle develops later during the diastolic interval. Shapiro et al. [24] and Rademakers et al. [25] used tagging MRI studies to demonstrate that rapid reciprocal twisting is responsible for 50% of diastolic filling in the normal heart, and becomes augmented to 60% by inotropic drugs to emphasize the muscular aspect of the suction process.

4.5 Fiber orientation
These composite observations from several imaging sources imply that the acquisition of three-directional velocity data over the entire left ventricle provide velocity fields must be related to the myocardial fiber structure. While measured velocity direction may deviate from the structural fiber orientation, this velocity is thought to relate to structural fiber orientation [3]. The implication that more diagonal arrangement of muscle fibers may lead to more efficient cardiac output, is supported by sonomicrometer crystals studies that show the dominant fiber direction of the ascending and descending segments of the ventricular myocardial band exist in this fashion, as shown in Figs. 9 and 10. However, focal crystals are placed upon only the muscle surface, but their motions were considered to reflect movement generated by the overlying cross-striated fibers [5]; the TPM dataset demonstrates this net effect by velocity measurements.

Comparison of velocity-based evaluation with postmortem structural evaluation is needed to determine how generated velocity fibers conform with the structural fiber orientation. An aspect of this interaction is shown in Figs. 9–11, whereby the velocity-based evaluation during both mid-systole, isovolumic phase before rapid filling and mid-diastole show close correlation with corrosion casts used to substitute for cavity blood [8] or helical ventricular myocardial band anatomy. There is similarity between accelerated velocity by MRI, spiral trabeculae of endocardial muscle and myocardial band.

The constraint of deriving structural fiber information from dynamic velocity data is due to limitations from observing that only net effects within each voxel, so that sophisticated dynamic modelling is needed. These data cannot detect resultant force direction from interwoven fiber pathways of different orientation because this velocity acceleration cannot identify such crisscross tissue types that impact this force. This concept of resultant force is, however, also implied by prior ultrasonic crystal measurements [5], whereby the crystals are placed into the angulation of the presumed functional units of the descending and ascending segments of the apical loop of the helical ventricular myocardial band. Correlation of anatomic fiber orientation and the motion characteristics during MRI examination may exist, as suggested in Fig. 8 (ultrasonic crystals) and from Figs. 9 and 10 that correlate TPM velocity acceleration tracts of fiber orientation during systole when the chamber shortens during ejection and lengthens during the isovolumetric phase before rapid filling.

The close interaction of these surrogate MRI parameters during the four phases of motion during the cardiac cycle, together with acceleration velocities for myocardial fiber tracking suggests that these MRI measurements may link with cardiac structure of models like the helical ventricular myocardial band. The correlation of these presumptions with evidence of how the spiral endocardial fibers impacts intracavitary blood by the corrosion cast method [26] expands this interaction, together with support by other imaging modalities like ultrasonic crystals, echocardiography, and radionuclide ventriculography studies.

	5. Conclusions

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

 
MRI myocardial motion and fiber tracking by acceleration velocities in normal volunteers demonstrate a favourable interaction of MRI with echocardiography, sonomicrometer crystals, MUGA records, and LV corrosion casts, thereby implying that myocyte orientation correlates with the helical ventricular myocardial band. This MRI-derived database may be useful to evaluate global and regional systolic and diastolic functions in cardiac pathologic processes.

Of greater importance, the close agreement amongst a spectrum of imaging studies provides a very powerful integration that transcends a single look by any one imaging modality. The integrated global technology of function sees the same thing that evolves from underlying spatial architecture. The collaboration of these different imaging methods provides novel explanations to answer questions posed and unanswered by individual imaging tools. These pooled imaging findings imply that the helical ventricular band is the structural basis for the global functional changes observed by MRI and other technologies.

	Appendix A

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

 
Supplementary data

Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.ejcts.2006.02.064.

	References

Top Abstract 1. Introduction 2. Methods 3. Results 4. Discussion 5. Conclusions Appendix A References

 

1. Harvey W. De Motu Cordis, 1628..
2. Jung B, Markl M, Foll D, Buckberg GD, Hennig J. Investigating myocardial motion by MRI using tissue phase mapping. Eur J Cardiothorac Surg 2006;29S:S150-S157.[Abstract/Free Full Text]
3. Jung B, Kreher B, Markl M, Hennig J. Visualization of tissue velocity data from cardiac wall motion measurements with myocardial fiber tracking: principles and implications for cardiac fiber structures. Eur J Cardiothorac Surg 2006;29S:S159-S164.
4. Lorenz CH, Pastorek JS, Bundy JM. Delineation of normal human left ventricular twist throughout systole by tagged cine. J Cardiovasc Magn Reson 2000;2(2):97-108.[Medline]
5. Castella M, Buckberg GD, Saleh S, Gharib M. Structure/function interface with sequential shortening of basal and apical components of the myocardial band. Eur J Cardiothorac Surg 2005;27(6):980-987.[Abstract/Free Full Text]
6. Ballester-Rodes M, Flotats A, Torrent-Guasp F, Carrio-Gasset I, Ballester-Alomar M, Carreras F, Ferreira A, Narula J. The sequence of regional ventricular motion. Eur J Cardiothorac Surg 2006;29S:S139-S144.[Abstract/Free Full Text]
7. Torrent-Guasp F, Buckberg GD, Clemente C, Cox JL, Coghlan HC, Gharib M. The structure and function of the helical heart and its buttress wrapping. I. The normal macroscopic structure of the heart. Semin Thorac Cardiovasc Surg 2001;13(4):301-319.[Medline]
8. Gorodkov A, Dobrova N, Dubernard JPH, Kiknadze GD, Gatchetchiladze I, Oleinikov V, Kuzmina N, Barat J, Baquey C. Anatomical structures determining blood flow in the heart left ventricle. J Mater Sci 1996;7:153-160.
9. Palka P, Lange A, Fleming AD, Donnelly JE, Dutka DP, Starkey IR, Shaw TR, Sutherland GR, Fox KA. Differences in myocardial velocity gradient measured throughout the cardiac cycle in patients with hypertrophic cardiomyopathy, athletes and patients with left ventricular hypertrophy due to hypertension. J Am Coll Cardiol 1997;30(3):760-768.[Abstract]
10. Dutka DP, Donnelly JE, Palka P, Lange A, Nunez DJ, Nihoyannopoulos P. Echocardiographic characterization of cardiomyopathy in Friedreich's ataxia with tissue Doppler echocardiographically derived myocardial velocity gradients. Circulation 2000;102(11):1276-1282.[Abstract/Free Full Text]
11. Yip G, Abraham T, Belohlavek M, Khandheria BK. Clinical applications of strain rate imaging. J Am Soc Echocardiogr 2003;16(12):1334-1342.[CrossRef][Medline]
12. Voigt JU, Exner B, Schmiedehausen K, Huchzermeyer C, Reulbach U, Nixdorff U, Platsch G, Kuwert T, Daniel WG, Flachskampf FA. Strain-rate imaging during dobutamine stress echocardiography provides objective evidence of inducible ischemia. Circulation 2003;107(16):2120-2126.[Abstract/Free Full Text]
13. Karwatowski SP, Brecker SJ, Yang GZ, Firmin DN, St. John SM, Underwood SR. A comparison of left ventricular myocardial velocity in diastole measured by magnetic resonance and left ventricular filling measured by Doppler echocardiography. Eur Heart J 1996;17(5):795-802.[Abstract/Free Full Text]
14. Ormiston JA, Shah PM, Tei C, Wong M. Size and motion of the mitral valve annulus in man. I. A two-dimentional echocardiographic method and findings in normal subjects. Circulation 1981;64(4):113-120.[Abstract/Free Full Text]
15. Tibayan FA, Lai DT, Timek TA, Dagum P, Liang D, Daughters GT, Ingels NB, Miller DC. Alterations in left ventricular torsion in tachycardia-induced dilated cardiomyopathy. J Thorac Cardiovasc Surg 2002;124(1):43-49.[Abstract/Free Full Text]
16. Ballester-Rodes M, Flotats A, Torrent-Guasp F, Ballester-Alomar M, Carreras F, Ferreira A, Narula J. Base-to-apex ventricular activation: Fourier studies in 29 normal individuals. Eur J Nucl Med Mol Imaging, in press..
17. Coghlan C, Prieto G, Harrison TR. Movement of the heart during the period between the onset of ventricular excitation and the start of left ventricular ejection. Am Heart J 1961;62:65-82.[Medline]
18. Buckberg GD, Clemente C, Cox JL, Coghlan HC, Castella M, Torrent-Guasp F, Gharib M. The structure and function of the helical heart and its buttress wrapping. IV. Concepts of dynamic function from the normal macroscopic helical structure. Semin Thorac Cardiovasc Surg 2001;13(4):342-357.[Medline]
19. Torrent-Guasp F, Kocica MJ, Corno A, Komeda M, Cox J, Flotats A, Ballester-Rodes M, Carreras-Costa F. Systolic ventricular filling. Eur J Cardiothorac Surg 2004;25(3):376-386.[Abstract/Free Full Text]
20. Ingels Jr. NB, Hansen DE, Daughters GT, Stinson EB, Alderman EL, Miller DC. Relation between longitudinal, circumferential, and oblique shortening and torsional deformation in the left ventricle of the transplanted human heart. Circ Res 1989;64(5):915-927.[Abstract/Free Full Text]
21. Lunkenheimer PP, Redmann K, Anderson RH. The architecture of the ventricular mass and its functional implications for organ-preserving surgery. Eur J Cardiothorac Surg 2005;27(2):183-190.[Abstract/Free Full Text]
22. Helmes M, Trombitas K, Granzier H. Titin develops restoring force in rat cardiac myocytes. Circ Res 1996;79(3):619-626.[Abstract/Free Full Text]
23. Buckberg GD, Coghlan HC, Torrent-Guasp F. The structure and function of the helical heart and its buttress wrapping. V. Anatomic and physiologic considerations in the healthy and failing heart. Semin Thorac Cardiovasc Surg 2001;13(4):358-385.[Medline]
24. Shapiro EP, Rademakers FE. Importance of oblique fiber orientation for left ventricular wall deformation. Technol Health Care 1997;5:21-28.[Medline]
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 1992;85(4):1572-1581.[Abstract/Free Full Text]
26. Torrent-Guasp F, Ballester M, Buckberg GD, Carreras F, Flotats A, Carrio I, Ferreira A, Samuels LE, Narula J. Spatial orientation of the ventricular muscle band: physiologic contribution and surgical impolications. J Thorac Cardiovasc Surg 2001;122(2):389-392.[Free Full Text]

This article has been cited by other articles:

				J. E. Stelzer, J. R. Patel, J. W. Walker, and R. L. Moss Differential Roles of Cardiac Myosin-Binding Protein C and Cardiac Troponin I in the Myofibrillar Force Responses to Protein Kinase A Phosphorylation Circ. Res., August 31, 2007; 101(5): 503 - 511. [Abstract] [Full Text] [PDF]

				M. Carlsson, M. Ugander, H. Mosen, T. Buhre, and H. Arheden Atrioventricular plane displacement is the major contributor to left ventricular pumping in healthy adults, athletes, and patients with dilated cardiomyopathy Am J Physiol Heart Circ Physiol, March 1, 2007; 292(3): H1452 - H1459. [Abstract] [Full Text] [PDF]

				J. E. Stelzer, S. L. Brickson, M. R. Locher, and R. L. Moss Role of myosin heavy chain composition in the stretch activation response of rat myocardium J. Physiol., February 15, 2007; 579(1): 161 - 173. [Abstract] [Full Text] [PDF]

				J. E. Stelzer, J. R. Patel, and R. L. Moss Protein Kinase A-Mediated Acceleration of the Stretch Activation Response in Murine Skinned Myocardium Is Eliminated by Ablation of cMyBP-C Circ. Res., October 13, 2006; 99(8): 884 - 890. [Abstract] [Full Text] [PDF]

				J. E. Stelzer and R. L. Moss Contributions of Stretch Activation to Length-dependent Contraction in Murine Myocardium J. Gen. Physiol., October 1, 2006; 128(4): 461 - 471. [Abstract] [Full Text] [PDF]

				J. E. Stelzer, J. R. Patel, and R. L. Moss Acceleration of Stretch Activation in Murine Myocardium due to Phosphorylation of Myosin Regulatory Light Chain J. Gen. Physiol., August 28, 2006; 128(3): 261 - 272. [Abstract] [Full Text] [PDF]

				G. D. Buckberg, M. Castella, M. Gharib, and S. Saleh Active myocyte shortening during the 'isovolumetric relaxation' phase of diastole is responsible for ventricular suction; 'systolic ventricular filling' Eur. J. Cardiothorac. Surg., April 1, 2006; 29(Suppl_1): S98 - S106. [Abstract] [Full Text] [PDF]