Eur J Cardiothorac Surg 2006;29:S272-S278
© 2006 Elsevier Science NL
The ventricular septum: the lion of right ventricular function, and its impact on right ventricular restoration
Gerald D. Buckberg
a
,
b
,
*
, the RESTORE Group
a Option on Bioengineering, California Institute of Technology, 1200 E. California Blvd., Pasadena, CA 91125, USA
b David Geffen School of Medicine at UCLA, Box 951741, 62-258 CHS, Los Angeles, CA 90095-1741, USA
Received 3 February 2006;
accepted 7 February 2006.
* Corresponding author. Address: David Geffen School of Medicine at UCLA, Division of Cardiothoracic Surgery, 62-258 Center for the Health Sciences, Los Angeles, CA 90095-1701, USA. Tel.: +1 310 206 1027; fax: +1 310 825 5895. (Email: gbuckberg{at}mednet.ucla.edu).
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Abstract
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Objective: To evaluate the structure–function relationships of the right ventricle (RV) and septum and determine if the helical ventricular band model would define fiber orientation for maximal force response. Implications were made for right ventricular function. Methods: The right ventricular free wall and biventricular septum were studied by inserting sonomicrometer crystals at different angulations to determine the maximum response of fiber shortening. These reactions were compared to the lateral left ventricular (LV) wall and further tested by use of positive and negative inotropic drug infusions. Results: The maximum contraction of the free wall was achieved by placing crystals in the transverse orientation angulations, whereas oblique orientation allowed the maximal septal response. Fiber orientation angulation was the same for the LV free wall and septum. These angulations correlate with the MRI-related twisting actions of septal motion needed for ejection and suction for rapid filling. These findings have important impact, because they imply that the septum is ‘lion of right ventricular function,’ since septal twisting is essential when pulmonary vascular resistance is increased. The incidence of postoperative right heart failure due to septal dyssyncrony, with loss of septal twisting action from inadequate myocardial protection, is explored relative to RV free wall and septum function. Furthermore, early studies of right ventricular restoration in patients with RV dysplasia and RV failure after chronic pulmonary insufficiency following repair of Tetralogy of Fallot are described, with predominant attention directed toward rebuilding normal septal architecture and function. Conclusions: This experimental and clinical overview indicates that the septum is ‘the lion of right ventricular function,’ and implies that the use of this knowledge can become an important guideline for planning novel surgical geometric interventions after RV failure.
Key Words: RV structure/function • RV free wall • Septal function • Helical ventricular myocardial band • Sonomicrometer crystals • Right ventricular restoration
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1. Introduction
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Left ventricular (LV) restoration has been the predominant clinical focus of surgical ventricular reconstruction, and LV rebuilding is based upon the returning of spherical dilated chamber into its natural elliptical form. The principal importance of the right ventricle (RV) has been related to determination of preoperative right ventricular failure, an event that is considered to be a contraindication to LV rebuilding. This adverse decision tree is linked to (a) recognition that treatment options for postoperative RV failure are less favorable than those for left ventricular decompensation, and more importantly (b) limitations of conventional knowledge about geometric determinants of RV performance. This conceptual RV structure/function dilemma has also limited evolution of better RV treatment strategies.
The physiologic remedies of RV failure are directed toward alleviating symptoms of failure rather than correcting the form-related components that underlie dysfunction. The ventricular septum separates the left and right ventricular chambers, and is the central component of this form–function relationship. The current enigma of the septal role in defining cardiac function was initially described in 1865 [1], when the anatomist Hegar indicated that ‘cardiac anatomy and function will be uncertain until the structure and function of the crossed angles of fibers in the septum are defined.’ This report will amplify the septum's central role in determining right ventricular function by presenting novel data that define the septal structure–function relationships.
Prior unavailability of recognition of structural barriers to addressing right ventricular dysfunction underlie the limitation of pulmonary valve implantation alone to correct functional abnormalities and arrhythmias when treating patients with right ventricular outflow obstruction (RVOTO) after developing right heart following pulmonary insufficiency following Tetralogy of Fallot repair [2]. This observation of recognition of a ventricular component introduces the potential evolution of a ‘valve–ventricle approach’ to address chronic right heart failure. Genesis of this new decision tree requires deeper knowledge of the impact of anatomic fiber orientation of the right ventricular architecture (free wall and septum) on resultant performance. Application of this information may generate novel right ventricular surgical restoration strategies to parallel those now used to reshape and resize the left ventricle.
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2. Background
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The right ventricle has traditionally received less consideration than the left ventricle, since it contains a ‘thin free wall’ and delivers the same cardiac output as the thick-walled left ventricle, but into a pulmonary vascular resistance bed that is one-sixth of systemic vascular resistance. Attention to the right ventricle gains importance when postoperative RV failure supervenes because of treatment limitations imposed by incomplete understanding of form function relationships. Dell’Italia [3], in 1991, observed that the ventricular septum is the central theme to both ventricles, since it binds them together with spiral muscle bundles that encircle them in a complex interlacing fashion to form a highly interdependent functional unit that exists despite their markedly different muscle mass and chamber geometry.
The RV free wall and septum are the two architectural components of the right ventricle, and the underlying theme of treatment relates to the concept that fiber orientation determines ejection. In a Petri dish, only 15% muscle fiber shortening follows sarcomere stimulation, but the intact heart has connected fibers with a varying angular orientation that defines resultant function. Rushmer et al. [4], in 1952, reported that ejection fraction is approximately 30% after only transverse or circumferential muscle contraction, and Ingels [5], Sallin [6], and Arts et al. [7] showed that ejection fraction increases to 60% if there is oblique fiber orientation. Fiber orientation configuration within these two cardiac components identified by Rushmer et al. [4], Greenbaum et al. [8], Streeter, Lunkenheimer et al. [9], and Torrent-Guasp et al. [10] showed that a predominantly transverse orientation exists in the RV free wall, while the septal component contains a right-angle cross-striation of oblique longitudinal fibers that are directed toward and away from the conical apical tip. These elements are shown in Fig. 1
, and this report will show how right ventricular function was tested in these fiber angulations.
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Fig. 1. Comparison of ejection fraction in isolated ventricular muscle fibers that have 15% fiber shortening. The changes in ejection fraction are shown with (a) transverse wrap, 30% ejection fraction, to simulate RV free wall transverse muscle and (b) 60% in the septum, with spiral architecture (from helix formed by descending and ascending segments of apical loop, hatched and solid lines) to demonstrate how fiber angulation alters function, which was only 15% when muscle strips are in Petri dish.
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The helical ventricular myocardial band model of Torrent-Guasp was studied [10] and its spatial configuration shows that the heart is composed of two interconnected loops. The basal loop is transverse and wraps around the right and left ventricles. The band contains a central myocardial fold that changes fiber direction to an oblique direction and then creates a helix that involves an apical loop comprised of descending and ascending segments that form the apical vortex The RV free wall predominantly contains the transverse basal loop that surrounds the septum, which is comprised of oblique fibers of the apical loop (Figs. 2 and 3
). The most important aspect of this model is that the septum does not have a predominant right or left ventricular side, rather the septum is the central structure between left- and right-sided cavities that is comprised of the same fiber elements that form the free left ventricular wall.
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Fig. 2. Fiber orientation relationship of the septum, composed of oblique fibers that arise from the descending and ascending segments of the apical loop, surrounded by the transverse muscle orientation of the basal loop that comprises the free right ventricular wall. Note the conical arrangement of the septum muscle and the basal loop wrap, forming the RV cavity.
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Fig. 3. Unfolding of the heart model to show (a) the intact ventricle; (b) detachment of the pulmonary artery to begin unfolding the basal segment (note underlying obliquely oriented descending and ascending segment of septum); (c) complete unfolding of basal loop of the right ventricle with the genu, posteriorly, separated from the left ventricular segment of the basal loop (note transverse fiber orientation of free wall). Note the basal loop that surrounds the obliquely oriented fibers within the descending and ascending segments of the apical loop is responsible for septal motion. The rope-like model conforms to this anatomic unwinding.
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3. Fiber orientation and function
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Fiber orientation defines the extent of ventricular deformation responsible for strain and thickening for blood ejection and suction. Tag images by MRI show the mechanism is through twisting of fibers to eject, followed by untwisting to fill [12] to reflect the ‘wringing a cloth’ functional concept defined in 1681 by Borelli [1]. Free wall contraction causes transverse narrowing and relaxation causes widening of these structures with minimum external wall changes during systole and diastole. Conversely, RV MRI studies confirm that the primary events involving septal muscle are chamber shortening and lengthening caused by twisting and thickening that produce ejection, and untwisting and lengthening for suction filling. Recent functional reports by Klima et al. [13] confirm these predominant septal events.
The impact of these observations relates to how the efficiency of ejection is impacted by the vector forces needed for ejection into the right and left and right sides, since the outflow vascular beds offer different resistances. The oblique orientation of muscle fibers of the LV free wall and septum allows the wringing or twisting required to eject blood into high systemic vascular resistance. In contrast, pulmonary vascular resistance is one-sixth of systemic resistance, so that the compressive force of transverse constriction or bellows like activity is sufficient for ejection under normal conditions.
The safety of this compressive capacity following only free wall contraction is evident clinically, since postoperative septal dysfunction traditionally follows conventional approaches to myocardial protection. Despite septal hypokinesia or akinesia, postoperative right-sided hemodynamics remains normal if pulmonary vascular resistance is low. Consequently, septal malfunction is considered an acceptable and expected complication.
Unfortunately, the twisting capacity of oblique muscle is flawed by septal dysfunction, and right ventricular failure may follow postoperative pulmonary hypertension, because the requisite septal twist required for combating high pulmonary vascular resistance and maintaining cardiac output is unavailable. For these reasons, ‘the septum is the lion of RV function’ [14], because the right ventricle must rely upon this intrinsic twisting function of oblique septal fibers to maintain output against increased pulmonary vascular resistance.
Background for addressing the vital importance of correct fiber orientation for proper function stems from our prior experience with septal malfunction that typically occurs when the oblique structure is made more transverse by left ventricular stretch during LV dilation from ischemic cardiomyopathy. Echocardiographic studies in show dysfunction by its stretch into the RV, together with resumption of normal septal function after LV restoration returns the septum to its central position. A similar dysfunctional septal position was also shown in dilated hearts following mitral insufficiency [15]. This adverse functional septal effect of left-sided stretch was described by Bernheim et al. [16] in 1911, and similarly septal dysfunction occurs after right-sided septal stretch, was described by Dexter in 1956 as a ‘reverse Bernheim effect’ [17] after right-sided stretch after atrial septal defects of volume overload.
The current clinical functional significance of septal dysfunction is linked to functional performance differences that impair right ventricular efficiency when the twisting capacity is impaired by septal stretch. Right ventricular performance is not reduced when the left heart performs properly and pulmonary vascular resistance is low. Despite absent septal motion, a common finding after cardioplegic arrest during cardiac procedures, the normally contracting free wall provides enough compression by transverse circumferential narrowing to maintain normal hemodynamic function.
Conversely, right ventricular failure supervenes following surgical induction of septal akinesia or hypokinesia if there is pulmonary hypertension from raised pulmonary vascular resistance, a hemodynamic event caused either by primary pulmonary arterial vasoconstriction or from a secondary increase due to left ventricular decompensation. Whereas RV function was adequate preoperatively because septal twist was available to properly ensure cardiac output, postbypass imposition of septal dysfunction now causes RV failure because of new loss of the predominant functional capacity of the septum to twist and ensure RV ejection; the right ventricular septal lion is now deficient.
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4. Anatomy and images
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A hallmark surgical concept of understanding this structure–function relationship is that an anatomic picture is worth a thousand words of images; ‘surgeons act upon what they see, not upon what they imagine.’ The aforementioned imaging findings are documentation of cardiac motions without anatomic confirmation of causative events. Our intent is to directly measure the function of the free wall and septal components to demonstrate how fiber orientation contributes to myocyte shortening in these regions [11].
Sonomicrometer crystals were used and placed onto the free wall and septum. Regional motion was recorded by shortening of crystals, and maximum shortening was considered to reflect the dominant motion of the regional segment and its overlying transmural structure. The free wall is easily assessable, but the septum has not previously been studied. The structure/function goal is documentation of free wall/septal contributions to RV performance in order to create a novel architectural understanding that might improve the surgical evolution of ventricular rebuilding procedures that might improve right ventricular function.
The infrastructure of the recognition of the anatomic approach to documenting the oblique criss-cross fiber configuration of the septum came from several sources including (a) the collagen weave network of reciprocal septal spirals exposed by Lunkenheimer's air inflation studies [9]; (b) Greenbaum et al.'s [8] cross-sections showing criss-cross septal fibers; and (c) the anatomic dissections of the unwrapped heart by Torrent-Guasp [10] (Fig. 3). The hypothesis is that the septum has reciprocally oblique fibers that should display the same functional changes as the LV free wall, because both structures (LV free wall and septum) are formed by the descending and ascending segments of the helical ventricular myocardial band. The only difference is that the septum is hidden from external view, because it is externally surrounded by the attachment of the free wall that attaches to its anterior and inferior surface.
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5. RV free wall
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The impact of fiber orientation on free wall function is shown in Fig. 4
, where maximum shortening of crystals follows their implantation in a transverse direction. Previous studies showed markedly reduced shortening following oblique placement of free wall crystals [11]. The impact of the Torrent-Guasp model on fiber orientation is displayed in Fig. 4, where the RV outflow tract tracings start later are oblique, and match the LV ascending fiber shortening patterns. This information indicates that either the anticipated transverse orientation of free wall fibers is incorrect or we did not uncover the architectural reasons for the observed oblique fiber orientation.
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Fig. 4. Sonomicrometer tracings from the lateral RV wall (shortening earliest), with transverse orientation, and the RV and LV free wall, with oblique angulation (a) begin shortening  80 ms later and (b) start at the same time period.
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The anatomic solution to this dilemma came from the occurrence of oblique aberrant fibers in the outflow tract. This precise configuration was observed by Torrent-Guasp, who describes an oblique fiber component as one that jumps from the oblique ascending segment fibers of the left ventricular apical loop and then covers the transverse fibers of the free wall of the right ventricle (Fig. 5
). This late shortening oblique component may have clinical significance, as observed by Francis Fontan, who suggested that intraoperative pacing of this RV outflow tract region may prematurely narrow this region and impede RV ejection.
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Fig. 5. RV outflow tract is composed of aberrant oblique fibers from the apical loop on the RV surface (upper), and the inner shell also composed of oblique fibers originating from the ascending segment of the apical loop.
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The major contribution of the free wall fibers occurs during the phase of isometric interaction, where they shorten before the septum fully contracts. Wiggers [18], in 1914, found that the isometric phase was unaltered by after loading the right ventricle, because the pulmonary valve did not open during free wall contraction. Conversely, the pre-ejection phase was enhanced by inotropic stimulation to directly affect the circumferential free wall muscle.
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6. RV septum
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The benchmark for matching septal and free wall shortening time frame patterns relates to simultaneous recording of LV free wall records with crystals in the same angulations on the descending and ascending segments of the apical loop, since failure to confirm this commonality would invalidate the hypothesis of this concept.
The natural sequence of shortening of descending and ascending segments of the LV free wall of the apical loop includes an initial shortening that begins in the descending segment, followed 10 ms later by the posterior segment, and 80 ms later by the ascending segment [19]. Ejection occurs by co-contraction of the descending and ascending segments that sequential shortening for the twisting movement [19]. Another sequential end point is the 90 ms time hiatus between the end of descending and completion of ascending segment shortening. Free wall tracings thereby set guidelines for novel recordings from the septal region and will be described below.
The hypothesis that tests the oblique functional yardsticks of septal anatomy requires validation that its architecture mirrors the criss-crossing of fibers of the descending and ascending segments of the apical loop of the helical heart (Fig. 7a). This configuration shows that (a) the underlying septum is hidden by the attachment of the attachment of the RV free wall to the ascending segment; (b) detaching of the free wall from the ascending segment would unravel the septum; and (c) uncover oblique fibers are formed precisely like the LV free wall, which is comprised of oblique overlapping of fibers of the descending and ascending segments of the apical loop. The following experimental steps were taken to confirm this concept.
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Fig. 7. (a) Simultaneous segmental shortening recordings from LV free wall and septum. Note the similar and simultaneous start and end of contraction of the descending segment in the LV free wall and septum (solid line), and the similar and simultaneous start and end of contraction of the ascending segment in the LV free wall and septum (hatched line). (b) Representative example of SS% sequence of the septal ascending and descending segment at baseline, and after administration of dopamine and esmolol. Note the change of time-delay at start of contraction between the descending and ascending segment at baseline, and after dopamine (10 µg/(kg min)) and esmolol (50 mg) administration. Solid line, beginning and end of contraction of the descending segment; hatched line, beginning and end of contraction of the ascending segment.
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The septal component of fiber orientation is displayed in Fig. 6a that guides the logic of this study. The underlying concept is illustrated by the model schematic (Fig. 3) (which also shows the rope-like heart arrangement), and it demonstrates how unwrapping of the RV free wall, by detaching it from the covered septum, shall (a) identify the transverse fiber pattern of the free wall and (b) expose the oblique orientation in the descending (left sided) and ascending (right sided) apical loop segments.
Unfolding a cadaver heart demonstrated how the free wall covers the septum (Fig. 6a), allowing identification of the oblique septal fiber orientation pattern. The oblique septal fiber arrangement in this cadaveric heart precisely matches the same oblique fiber orientation of LV free wall ascending fibers, as the continuation of their fiber tracts is evident (Fig. 6b). Identification of major pathways of fiber angulation by unwrapping in the models and cadaver hearts set the stage for implantation of ultrasonic crystals into the working porcine ventricle.
Fig. 6b displays the oblique orientation of ascending and descending segment crystals of the LV free wall, whereby ascending crystals were placed obliquely in the epicardium and the descending segment crystals were pushed into the LV cavity and withdrawn to obliquely impact on the endocardial surface. Recording from criss-cross crystal orientation displayed the maximum force of segmental shortening, in contrast to diminished shortening when crystals placed a more transverse orientation, as described previously [11].
The final phase of this experimental study is shown in the right-sided image in Fig. 6bC that conveys how the crystals were placed into septum by employing the same LV free wall angular orientation. Exposure of the septum was done via right ventriculotomy during cardiopulmonary bypass in the beating heart to avoid introducing ischemia. The septal right-sided ascending segment crystals were obliquely placed in the same direction as LV free wall ascending segment crystals. The oblique septal descending crystals were inserted across the septum by using the same oblique angle employed during placement of LV free wall descending segment crystals.
Confirmation of maximal shortening was done by comparing these oblique angulations against recordings taken from more transversely placed crystals [14]. Septal findings paralleled free wall observations, as diminished force of shortening followed the more transverse orientation. The free wall was then closed, bypass was discontinued and hemodynamic recordings were made during control settings, followed by positive and negative inotropic stimulation with dopamine and esmolol.
Segmental shortening of the descending and ascending segments of the septum and free wall are shown in Fig. 7a, and these recordings show similar findings like (a) early origin of ascending segment shortening in septum and free wall segments; (b) 80 ms delay in initiation of shortening of the septal and free wall segments; (c) cessation of shortening of septum and free wall descending segments; and (d) 90 ms time delay hiatus for cessation of ascending shortening on he septum and free wall.
The comparability of responses of the septal descending and ascending segments to inotropic agents was also recorded in Fig. 7b [14]. Dopamine produced tachycardia, shortened the time hiatus between shortening of the descending segments, increased the force of shortening, and narrowed the hiatus between cessation of shortening between descending and ascending segments. Conversely, esmolol caused bradycardia, prolonged the hiatus between initiation of shortening between descending and ascending segments, diminished the force of shortening, and prolonged endocardial (descending segment) shortening; the findings exactly paralleled changes in the LV free wall after administration of these agents [19].
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7. Fiber orientation and right ventricular restoration
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These sonomicrometer experimental studies confirm the commonality of an oblique orientation of septal fiber architecture and establish the importance of the similarity of septal dynamics with those of the LV free wall, since both structures share the same architectural conformation. Crystal shortening only reflects local dimensional changes in the limited region studied, but this action likely underlies the transmural twisting of ventricular movements responsible for ejection and suction. The implications of this knowledge for surgical restoration of the right ventricle stems from the current anatomic data that define the importance of oblique angulations of the descending and ascending segments of septal muscle, as well as from prior reports that functionally show the problems created when the obliquely twisting septum is either injured or retained.
The interaction between septum and free wall was reviewed preciously [20]. The importance of the septum versus the free wall was defined by several studies showing that right ventricular performance was not impaired despite following either cauterizing the entire free wall [21] or replacing the free wall with patch material [22], so long as the septum is intact. Conversely, right ventricular failure became accentuated if the septum was either cauterized, made ischemic by embolization after right coronary artery occlusion, or confronted by pulmonary hypertension [20].
Right ventricular restoration procedures that return septal architecture into a more central position may initially improve the two clinical problems that include (a) right ventricular dysplasia [14,20] or (b) persistence of right heart failure following pulmonary valve insertion to treat right-sided dysfunction after chronic pulmonary insufficiency [23]. The two prerequisites to returning RV performance towards normal by changing septal geometry include (a) maintenance of good septum perfusion and (b) avoidance of septal damage by inadequate intraoperative protection. Our previous report [20] showed that right ventricular function recovered normally in a patient with RV dysplasia after patch replacement of an aneurysmal RV free wall in the beating heart; this positive result simulated the experimental report of patch free wall replacement by Sawatani et al. [22].
Right ventricular dysfunction after chronic pulmonary insufficiency carries several architectural disadvantages that impair right ventricular performance; these include (a) pulmonary insufficiency; (b) a nonfunctional patch on the outflow tract; (c) chronically distended remaining free wall; and (d) displaced septum toward the left side due to volume overload to cause the septal dysfunction as previously described by Dexter [17].
The components of the surgical approach include pulmonary valve replacement, excision of the aneurysm of RV muscle that includes the patch and distended free wall from chronic overloading, imbrication of excessive tissue during RV closure by using with either (a) interrupted sutures to reduce size of the free wall and septum with individual sutures (as previously described for the inferior wall aneurysms [24] or (b) use of a circumferential U-shaped imbrication suture that is connected to the annulus for the purpose of diminishing free wall chamber size and restoring a more normal septal anatomic configuration [23]. This suturing technique places the septum in a mid-line location (as done with left ventricular restoration), and creates a more normal crescent-shaped chamber. The following report by Frigiola et al. [23] will describe implementation of these ‘valve–ventricle’ concepts during treatment of chronic RV dysfunction in RVOTO patients that were initially referred only for pulmonary valve implantation.
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8. Conclusions
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The RV free wall and septum are the architectural components of the right ventricle, and the functional aspects of their anatomic fiber orientation is linked to the transverse fibers of the free wall and the oblique fibers comprising the septum. The correct angulation of these free wall and septal fiber patterns were confirmed by sonomicrometer crystal measurements. The predominantly oblique architecture of septal muscle is similar for the left and right sides of the circulation and governs the twisting cardiac action during ventricular ejection, a necessary component for ejection into a vascular bed with high resistance. This twisting action of oblique fibers differs from the compression that results from shortening of transverse RV free wall fibers. The observations imply that the septum should be considered the ‘lion of right ventricular function.’
Septal dysfunction happens when septal stretch from volume or pressure loading impairs fiber orientation, as the fibers likely develop a more transverse orientation and become dyssynergic. Adherence to rebuilding a normal oblique septal anatomic fiber orientation may govern the operative techniques in procedures that aim to restore septal architecture after RV dysfunction following RVOTO and RV dysplasia. Future testing is needed to determine if these septal form–function relationships will become an important guideline for planning novel surgical geometric interventions after RV failure.
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Appendix A
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Supplementary data
Supplementary data associated with this article can be found, in the online version, at doi:10.1016/j.ejcts.2006.02.011.
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Footnotes
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Read at 10th RESTORE meeting in San Francisco, California, April 9, 2005.
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Top
Abstract
1. Introduction
) and ascending segments (
), or placed perpendicular (
) to maximal segmental shortening position (in A).