Eur J Cardiothorac Surg 2005;27:202-209
© 2005 Elsevier Science NL
Architecture must document functional evidence to explain the living rhythm
Gerald D. Buckberga,b,*
a Department of Cardiothoracic Surgery, David Geffen School of Medicine at UCLA, Box 951741, 62-258 CHS, Los Angeles, CA 90095-1741, USA
b Options in Bioengineering, California Institute of Technology, 1200 East California Boulevard, Mail Code 230-87, Pasadena, CA 91125, USA
Received 11 August 2004;
received in revised form 1 September 2004;
accepted 5 October 2004.
* Tel.: +1 310 206 1027; fax: +1 310 825 5895. (E-mail: gbuckberg{at}mednet.ucla.edu).
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Abstract
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The central theme of surgical procedures is to interact structure and function. Two reviews of architecture by Torrent-Guasp and Lunkenheimer provide anatomic observations, and then only deduce, rather than test and verify functional relationships. Lunkenheimer previously showed the reciprocal helical configuration of the connective tissue scaffold, a weave-like network that may be the lattice for the descending and ascending segments of Torrent-Guasp's apical loop formed from the helical band. Lunkenheimer stresses cardiac development from a blood vessel, and exposes the need to disregard heart formation by a band that develops between the pulmonary artery and aorta. Torrent-Guasp's band-like concept is confirmed by MRI and sonomicrometer measurements, together with early systolic filling by ongoing, unopposed contraction of the ascending segment of the apical loop. This muscular component contradicts conventional concepts that elastic recoil causes rapid ventricular filling. However, direct physiologic measurements show that Torrrent-Guasp's physiologic timing sequence must be revised. While presumption is an important first step, proof of the marriage of structure and function happens only with measurement, a critical step before surgical action.
Key Words: Ventricular myocardial band • Connective tissue scaffold • MRI and sonomicrometer testing • Cardiac embryology
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1. Introduction
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The benchmark of surgical methods is creation of corrective procedures that alter structure to improve function. The keystone of our educational progress is understanding that (a) disease disrupts the natural or normal form relationship and thus causes adverse function, (b) corrective operations must restore the structure/function relationship, (c) critical evaluation of geometric results by recording functional improvement that (d) provide a data-driven reason to change surgical actions. This central physiologic theme requires observing the living form, while simultaneously recording valid measurements of contractile and rhythm pattern, and then rebuilding structure to restore functional recovery. This surgical outlook differs from approaches of the anatomist or pathologist, who observes the dead, and then deduces how non-viable part observations may explain living action. Life is movement, not conjecture.
The structure/function search is vital to surgeons as pointed out by Lunkenheimer. Action is our success credo, not the presumptions of others. The cardiac surgical world has just been exposed to recent papers in this European Journal by Torrent-Guasp [1] and Lunkenheimer [2], who called these papers reviews, with an objective to improve current structure and function understanding. However, neither manuscript contains accepted physiologic measurements to confirm their conclusions, nor do they address the functional inconsistencies that relate to any form-related hypothesis.
While a summary of classic teaching accompanies each paper, these looks at the past do not validate truth in every conventional thought. Leonardo Da Vinci said "the experiment is the mother of science, it is useless to conduct an argument by mere quotations from authorities: that does not prove cleverness. It only suggests a good memory" [3]. This report includes cardiac similarities that relate to this concept. Growth in physiologic thinking stems from advancing today's knowledge, a goal improved by using current imaging systems that avoid distortion to improve functional understanding. My Editorial objective is to (a) point out discrepancies between Torrent-Guasp and Lunkenheimer, (b) link their similarities, (c) address the weakness of presenting assumptions without supporting functional data, (d) summarize a novel set of observations in living hearts that may broaden our appreciation of normal structure and function, and (e) suggest how understanding normality can improve understanding of how to deal with changes of intraventricular size and mass in congestive heart failure.
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2. Discrepancy
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The major difference is that Torrent-Guasp defines a ventricular muscular band that, when wrapped creates a helical heart, comprised of a transverse basal buttress loop that encases an oblique apical loop comprised of descending and ascending segments that form a helix, while Lunkenheimer and Anderson think this band is produced by artifact through deformation by distortion in the heart dissection needed to unfold it. Second, Torrent-Guasp's concept of a band extending from the pulmonary artery to aorta is disputed as a violation of embryologic development, since the heart must arise from a vascular tube, a structure that exists before the truncus arteriosis changes into aorta and pulmonary artery. Third, the principal structural issue between Torrent-Guasp and Lunkenheimer is linked to the cardiac helix, a central theme in the wrapped myocardial band. Unfortunately there is complete absence of the term ‘helix’ from Lunkenheimer's report. This absence is surprising, since Pettigrew described the helical apex from inspecting the cardiac apex, and concept of the internal ventricular helix is a fundamental structural hypothesis over the past 500 years, included the work of Lower, Senec, Krell, Mall, and defined in Robb and Robb's 1942 summation of concepts of 58 anatomists [4]. More recently, Streeter's chapter in the 1979 Handbook of Physiology [5] used the treibwerk of Krell, and helix of Torrent-Guasp to define structure. Lunkenheimer uses the shingles on a roof concept introduced by Streeter, yet questions this work in favor of Jouk who terms his own final model conjectural and based upon the examiner's experience with dissection slide reading.
Only discrete inspection of the report of Jouk [6], who saw multiple helices in his dissections, allows Lunkenheimer to consider, but not state in his report, the importance of this basic structural helical finding. Furthermore, the criss-cross pattern of structure in ventricular cross sections is reported by Greenbaum and Anderson [7] to address a helical pattern of endocardial and epicardial fibers, yet this structure/function relationship is absent from their ‘review’ of Ventricular Architecture and its functional implications. Lunkenheimer poses a descriptive difference that may be confusing to all readers, by introducing the new functional terms of ‘auxotonic and unloading’. These actions stem from his interpretation of force within his unique measuring device, a method that is not conventionally used by other physiologists or investigators.
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3. Similarity
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There is similarity on the concept of dualism, but Torrent-Guasp ascribes this to opposition of forces from obliquely contracting apical loop helical fibers, while Lunkenheimer contrasts contraction from muscular forces and dilation from connective tissue factors. The major problem with both reports is that there is no data presented, or summarized, to justify the major functional conclusions drawn as these anatomists deduce how the living heart moves in relation to the underlying architecture.
An enormous discrepancy between reality and presumption relates to Lunkenheimer's fundamental questioning of the importance of contractility, as he uses the concept of constriction (from muscle) and dilation (from connective tissue) in its stead. This concept of constriction and dilation stems from Harvey's description of compression and dilation, yet visualization during cardiac surgery (Fig. 1, and Online Video 1) shows twisting to eject and forceful reciprocal twisting during ventricular suction to be the correct actions. These twisting motions are evident by MRI (Fig. 2 and Online Video 2), but recognition of this functional reality is absent in Lunkenheimer's report. While the literature is replete with studies of instantaneous tagging MRI measurements of twisting, Lunkenheimer restricts our attention to a series of 10 transverse slices to inspect function that differs between regions, but we must know why this occurs.
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Fig. 2. Dense MRI images showing the intraventricular twisting motion during ejection and filling. Please note the intramyocardial twisting toward the apex in the free LV wall and apex regions. Courtesy of Han Wen PhD at NIH.
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Lunkenheimer focuses proper attention to the spatial relationships, the major orientation of myocytes, and the role of connective tissue in muscle structure. Prior work from his laboratory [8] was unique in showing the elegant connective tissue scaffold, found through creating transpneumonic spreading of connective tissue. The clear-cut reciprocal spiral collagen weaves correlates exactly with the muscular scaffold of Torrent-Guasp's apical helical loop. It is surprising that Lunkenheimer does not recognize that muscle cells must fill the reciprocal connective tissue helix defined by his injections. This spiral harmony blends perfectly with the helical spirals of DNA, the double helix of actin, myosin, tropomyosin, calcium within each cell [9] and within its coil, spatial gradient of myosin regulatory light chain phosphorylation [10], and the conduction system spirals described by Taccardi [11]. Failure to make this correlation does not diminish his creative contribution to spatial collagen scaffolding.
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4. Assumption without data
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Torrent-Guasp cites the four MRI proven actions of compression (narrowing for constriction), ejection (shortening), suction (lengthening) and drainage (widening0, but provides no evidence of how the ventricular myocardial band causes them. Although postulations about his hypotheses are logical, the link between structure and function involves testing presumed concepts. There is now physiologic confirmation that his anatomic evidence of the inner helical loop surrounded by the external buttress are correct, and the ‘systolic ventricular filling’ is supported by the new data, but there must be revision of the suggested timing mechanisms of the structure/function sequence of compression, ejection and suction, as shown in Figs. 5 and 6 of the cardiac cycle.
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Fig. 5. The onset of a helical structure from the stream functions (red curves) plotted for the 3D displacement vector field acquired using the DENSE method in a human subject. Courtesy of Han Wen PhD at NIH, Nikoo Saber PhD and Morteza Gharib PhD at Caltech.
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Lunkenheimer and Anderson are correct that the heart develops from a vascular tube, and we must learn if and how this tube can (a) correctly define the validity of how Torrent-Guasp's concept of the ventricular myocardial fold develops to (b) ultimately become a transverse basal loop and oblique helical apical loop. Torrent-Guasp's evolution concept is misleading if one assumes the myocardial band develops between the pulmonary artery and aorta, since the earliest cardiac configuration involves the four segments of an atrium, ventricle, bulbus cordis and truncus arteriosis. It is now clear that within the cardiac muscular tube, the ventricle has greater preferential growth than the bulbus cordis. This differential growth may cause the twist in the endocardial tube that accounts for the myocardial fold, as shown in the images of Manner [12] (Fig. 3 and Online Video 3) and suggested by Buckberg [13] (Fig. 4). The recent report by Manner [14] also defines the early helix formation of the chick embryo, again codifying a central architectural part of cardiac anatomy, and setting the stage for the twisting functional action of cardiac fibers that exists in species ranging from the zebra fish [15] (140Å) to the adult healthy patient.
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Fig. 3. Sequential preferential enlargement of ventricle (v), and bulbo conus (c) in chick embryo, simultaneously defining the cardiac twist to fold the right side of the ventricle (r) over the left (l) side, and move the atrium (a) cephlad toward its ultimate position.
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Lunkenheimer and Anderson's principal objection to the unfolding of the heart by Torrent-Guasp is distortion of tissue planes in the syncytial heart by manual dissection. Besides the traditional use of this separation method by anatomists for 500 years, the living proof must relate to how the structural results of unfolded and then refolded anatomy matches viable function. The ventricular myocardial band physiology was tested by MRI and sonomicrometer methods with efforts to offset problems with tissue invasion.
Clearly, Lunkenheimer accepts the deformation resulting from (a) his fiber strand peel-off (SGOT) stripping method [16], (b) the fibers cut in the dissected fetus by Jouk [6], (c) the hemorrhage and laceration he reports is imposed by inserting a 2.7mm needle into the heart wall to create a ‘large ventricular hole in the muscle whose underlying muscle must be analyzed’, as well as (d) cutting nerve connections of the muscle within the force probe that is used to gauge tensile force of fibers contained within this major ventricular hole his device created. Lunkenheimer and Anderson's comparison of this ventricular defect caused by a large force probe to a surgical suture placement, reflects the fundamental differences between an anatomist and his understanding gap into clinical methods used in the live patient. In contrast, surgeons place small needles into the ventricular chamber, a hemodynamic measuring event that does not deform the ventricular chamber volume as we evaluate our pressure target. Furthermore, the reader needs precedent for Lunkenheimer's correlating transmural function measurements from fibers existing within ventricular walls penetrated by his massive needle insertion sites. Personal records using data from 1986 studies must be supported by confirmation by others to avoid bias.
Lunkenheimer's observation of segmental gradients in velocity of contraction, variations in time course of activity, and oblique ventricular fibers is well known, but how does the underlying structure account for observed ventricular action? More importantly, the concept of a ventricular wall composed of functional ‘self controlled’ wedge shaped units is proposed, but no evidence is provided to document these units, organize the time scale for ventricular activity (i.e. excitation contraction coupling), or define what this novel entity of self control means for rhythmic cardiac activity.
Similarly, Torrent-Guasp must show why there is a delay in shortening from endocardial contraction, which he deems responsible for ejection, since this muscle is adjacent to, and stimulated first by the Purkinje system. Conversely, there must be a reason why earlier compression during the pre-ejection phase is caused by the basal loop, which is farthest from the conduction system. Matching of excitation and contraction is a vital component of understanding the structure–function relationship.
The concept of systolic ventricular filling as a contractile event is thought by Lunkenheimer to reflect a basic misunderstanding of basic mechanisms of contraction. He ascribes this event to be related to rapid recoil of the connective tissue. Others think titin [17], a protein myofilament, causes these restoring forces. However, neither collagen nor protein has evidence of the rapid repeated oxygen uptake needed for rapid untwisting. Such oxygen uptake is possible in contracting muscle, a mechanism suggested by Torrent-Guasp. Evidence will be provided to show ongoing fiber shortening during this 120ms duration of the isovolumetric period during which the ventricular pressure drops to 85% of its diastolic value.
Lunkenheimer focuses upon the critical importance of surgical attention to reduce ventricular radius as we deal with congestive heat failure, the world's leading cause of death. There is, however, a misinterpretation of the surgical literature as (a) the report cited by Batista [18] dealt with only one patient with left heart failure, not hundreds with right heart failure, and (b) the report of Buckberg [19] supports the use of partial left ventriculectomy, provided there is proper site selection to remove the most damaged region. Furthermore, it is not evident how his report of ventricular architecture and its functional implications can allow surgeons to address the organ preserving surgery conveyed by his manuscript title.
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5. Novel observations
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The helical concept of structure has been presumed by anatomists for >500 years, so that a critical study aspect was to determine, in a non-invasive way, if the myocardial torsion, responsible for ejection, occurred in a helical pattern toward the apex. Fig. 5 shows how our use of the recently developed DENSE (Displacement Encoding Stimulated Echo) MRI technique, a non-invasive method, could define a helical pattern of the three-dimensional displacement during the sequence of systole (QRS to end of ejection). The streamlines define a twist around the apex. This observation offers the possibility of inferring fiber orientation and morphology from DENSE MRI data.
A second study, again using the non-invasive DENSE method in Fig. 6a–c and Online Video 4, defined the strain pattern of myocardial contraction, hereby the outer wall of the ventricular base developed strain first, with the impulse going from one side to the other, followed by a sequence of more intense strain defined by a twisting helix from the base to the apex. This coordinated phased pattern of contraction followed the morphology described by Torrent-Guasp, and simultaneously differed from the conventional concept of strain starting from within the heart and moving from endocardium to epicardium.
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Fig. 6. Sequential strain pattern, using the 3D dense vector fields, showing strain starting at the base, extending to the base on the opposite side, and then moving toward the apex in a spiral motion. Courtesy of Han Wen PhD at NIH, Nikoo Saber PhD and Morteza Gharib PhD at Caltech.
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Given this MRI data, coupled with the observation of the twisting nature of cardiac contraction, we must look at how the ventricular myocardial band model of Torrent-Guasp can provide a structural underpinning to MRI evidence of this helical pattern of strain. Our studies used sonomicrometer crystals, placed into the left and right segments of the basal loop, and into the descending and ascending components of the helical apical loop, as well as the wrap around posterior LV wall to correlate the sequence of regional contraction with pressure dimension tracings to determine sequential contraction with the display of LV pressure. Strain was not measured but we (a) found the site of maximal shortening between crystals, and (b) recognized that this isolated segment reflected the major shortening pathway governed by the composite of transmural forces of connected muscle fibers.
Our data supports the anatomic concept of the helical heart surrounded by an external buttress, but demonstrates that the timing mechanisms are different from those Torrent-Guasp deduced from this autopsy observations of the helical and basal loop configuration. The sequential contraction of the basal loop, going from right to left (0.10ms later) was confirmed, but the descending segment of the apical loop contracted at the same time as the right segment of the basal loop (Fig. 7). This observation fits with Purkinje system that is adjacent to the descending segment, and opposes Torrent-Guasp's suggestion of delayed contraction of the descending segment. It also contradicts the statement about abrupt apical dilation, since the descending segment of the apex is contracting to prevent stretch. Consequently, the compression phase (or narrowing) is due to both segments of the basal loop, and the descending segment, a finding that contradicts Torrent-Guasp's deduction. The observed early constriction of the base is reflected by echocardiogram that shows 
25% annular narrowing, an action presumably due to basal loop contraction [20].
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Fig. 7. Sonomicrometer crystal tracings of right and left segments of the basal loop, and descending segment of the apical loop. Note (a) simultaneous shortening of the right segment of the basal loop and descending segment of the apical loop, (b) time delay of 10ms until start of shortening of the left segment of basal loop.
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The sequence of shortening with a sequence going from the descending segment to the posterior segment (0.10ms later) and then to the ascending segment 80ms later is shown in Fig. 8. More importantly, the onset of ejection correlated with the positive dp/dt and corresponded to the onset of contraction of the ascending segment; events that lead to ‘co-contraction’ of both the descending and ascending segment fibers. Such ‘co-contraction’ explains the transmural twisting during ejection, a phenomena codified by tagged MRI images.
This earlier ascending segment contraction contributes to ‘co-contraction’, again contradicting Torrent-Guasp's thought that the descending segment causes ejection and the ascending segment begins contracting at a later time to cause rapid suction. In contrast to Torrent-Guasp's images, the onset of ascending segment contraction does not occur during the descent of left ventricular pressure. Although observed physiology supports the concept of dualism that was introduced by both authors, the mechanism of how this happens is different.
Analysis of Fig. 8 shows that Torrent-Guasp's concept of systolic ventricular filling is fully supported by this sonomicrometer data, as the ascending segment continues to shorten 90ms after shortening stops in the descending segment. The reciprocal oblique fiber orientation allows longitudinal lengthening during its contraction. Such ongoing motion during this hiatus after the descending segment stops is a critical finding, as it introduces the concept that problems in diastolic dysfunction have a muscular origin, and could become managed by altering calcium pathways related to muscular contraction. Furthermore, Lunkenheimer's observation that contractile force of oblique intruding myocardial pathways beyond the end systolic drop in ventricular pressure is correct, but this action may be caused by the same ventricular myocardial band that he considered an artifact. The truth is in the experiment, not the hypothesis.
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6. Distortion by disease
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Ventricular rebuilding has become an area of increasing interest to treat dilated cardiomyopathy, and the geometric findings show that the elliptical, or helical heart form becomes spherical. A geometric background for rebuilding ventricles stems from recent studies of spatial orientation of cardiac fibers that suggest the obliquely orientated fibers of the helical heart become more horizontal when muscle stretches into the spherical form that characterizes the failing ventricle, as shown in Fig. 9 [19,21]. If this concept is correct, the spherical shape will alter fiber orientation and compromise function, as based upon the studies by Salin and Ingels showing how the normal 15% fiber shortening of isolated muscle strands is changed when fiber orientation varies within the intact heart [22,23]. Ejection fraction is 30% if fiber orientation is transverse, and increases to 60% with oblique fiber direction, as deformation increases during transition from midwall to apex [23–25]. This oblique structure is rebuilt during ventricular restoration.
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Fig. 9. Suggested changes in fiber orientation, whereby there is a geometric change in size and shape during ventricular dilation in congestive heart failure: the elliptical heart with a helical fiber orientation becomes spherical and develops a more transverse orientation, as the apex is lost following dilation.
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Lunkenheimer characterized the dilated cardiomyopathy as developing flattened transverse netting, a less advantageous scaffolding for myocytes that exist within this latticework. LeGrice [26] studied the collagen network and showed the radial cleavage planes between epicardium and endocardium created an ordered laminar arrangement of myocytes. Spotnitz [27] found that the cleavage planes become more oblique as the chamber thins and widens, so that the more transverse connective tissue support is consistent with the underlying concept of a spherical chamber in heart failure, a geometry that is made more helical by restoration.
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7. Conclusions
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Lunkenheimer and Torrent-Guasp have made vital anatomic contributions to our understanding of the joining of muscle and collagen into cardiac structure. The elegant demonstration of the double helical coils in Lunkenheimer's past work, fits a collagen scaffold to the helical ventricular band structure described by Torrent-Guasp. Their functional bias, derived from anatomic observations, led each investigator to suggest concepts about how structure explained function. The solution to discrepancies caused by such hypotheses is found by experiments, not through harsh criticism of each other.
Torrent-Guasp, by uncovering the myocardial fold that separated cardiac structure into a basal and apical loop may have set the groundwork for a revolution in our thinking about basic cardiovascular physiology. Lunkenheimer correctly pointed out an error in the embryologic basis, and demonstrated how underlying muscle mass cannot function without interweaving connective tissue.
Concepts about implications of anatomic findings are the source of new studies. We all gain by the exploration of the validity of each hypothesis, whether right or wrong, since the database rather than opinion finds the answer. Torrent-Guasp's correct concept of systolic ventricular filling may have profound applications to clinical management, by opening new myocyte pathways to treatment, and may lead to novel studies of excitation contraction coupling. This knowledge of helical structure can guide us toward innovative ways to restore the ventricular geometry in patients with congestive heart failure, where the normal anatomy is distorted when disease produces a spherical shape to replace the conical chamber.
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L. K. von Segesser
The myocardial band: fiction or fact?
Eur. J. Cardiothorac. Surg.,
February 1, 2005;
27(2):
181 - 182.
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Abstract
1. Introduction
