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Eur J Cardiothorac Surg 2006;29:S238-S244
© 2006 Elsevier Science NL

Form versus disease: optimizing geometry during 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 8 February 2006.

* Corresponding author. Address: 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).


   Abstract
Top
 Abstract
1. Introduction
 2. The disease and...
 3. Restoration and conical...
 4. Implications with helical...
 5. Conclusions
 References
 
Objective: Dilated cardiomyopathy from many causes results in a change in ventricular geometry, whereby the elliptical chamber becomes more spherical. This may be the unifying geometric concept of heart failure, with similar alteration of spatial configuration in non-ischemic diffuse myocyte disease, ischemic cardiomyopathy with and without scar, and in valvular heart disease. Methods: This change in architecture alters fiber direction and diminishes function, and has been related to alteration of the apical loop of the helical ventricular myocardial band model of cardiac shape. The underlying concept of rebuilding the ventricle by ventricular restoration is suggested to be reconstruction of form, rather than focusing on only the underlying disease. Results: Examples are shown where the Surgical Anterior Ventricular Exclusion (SAVE) or Pacopexy procedure has been successfully applied to each of the above-mentioned diseases, and is suggested for dilated valvular cardiomyopathy. The interaction between rebuilding form and how this procedure restores more normal fiber orientation is discussed, and the possibility of a macroscopic/microscopic marriage between surgically altering the cardiac scaffold by restoration (macro) and cell biology to improve function in a new helical shape is suggested. Conclusions: The implication of these observations is that the surgical objective should become rebuilding ventricular form, rather than restricting restoration procedures to only addressing the disease.

Key Words: Ventricular restoration • Helical ventricular myocardial band • Ischemic cardiomyopathy • Non-ischemic cardiomyopathy • Valvular cardiomyopathy • Ventricular fiber orientation • SAVE • Pacopexy


   1. Introduction
Top
 Abstract
 1. Introduction
2. The disease and...
 3. Restoration and conical...
 4. Implications with helical...
 5. Conclusions
 References
 
The conical pattern of normal cardiac size and shape is well known. The spatial arrangements of this structural pattern are closely linked to the helical ventricular myocardial band, a myocardial fold that separates the surrounding wrap of the basal loop from the oblique fibers that form the apical loop composed of descending and ascending segments with a spiral vortex at the apex. This configuration is shown in Fig. 1a and the implications of this model were discussed at a recent NIH symposium [1].


Figure 1
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  		Fig. 1. (a) Cardiac configuration of the helical myocardial band. Note the transverse fibers of the basal loop and the oblique fibers of the apical loop. The arrows in the right figure show the ~60° angulation in the normal heart. (b) Shows how the dilated heart changes the fiber angulation and the apical loop now has a more horizontal fiber angulation (shown by arrows), as demonstrated by the lower arrows.

 
Size and shape change following dilated cardiomyopathy as the enlarged global ventricle develops a spherical configuration. A postulated geometric component is spherical widening of the apical loop as shown in Fig. 1b, whereby the architecture of oblique apical loop fibers becomes more transverse to more closely resemble the horizontal fiber orientation of the basal loop. Ventricular size progressively increases in spherical dilated hearts to worsen the symptoms of heart failure or cause ventricular fibrillation, which are coequal and predominant reasons for mortality.

Surgical correction of the dilated heart requires changing the spherical configuration architecture into a more normal elliptical form [2,3]. The bioengineering infrastructure for this mechanical change in size and shape is rebuilding more oblique fiber orientation. This anisotropic configuration requires a conical form, whereby the increased deformation responsible for contractile strain improves from the widened base to the helical apex vortex [4]. The pattern of ejection and filling are related to a sequential twisting of the LV to eject and rapid untwisting to suction venous return to rapidly fill [5]. These normal twisting patterns were originally described by Borelli in 1660 and are visible at operation or by MRI recordings.

Basic scientific studies set the precedent for this geometric component by establishing how the normal 15% fiber shortening of isolated muscle strands is changed when an integrated fiber orientation exists within the intact heart. Ejection fraction (EF) is 30% if fiber orientation is transverse, and increases to 60% with oblique fiber direction, as deformation increases during transition from mid wall to apex [6]. This functional pattern displays the transverse and oblique fiber orientation of the basal and apical loops. The stretched dilated heart loses the normal twisting pattern and its apical loop fibers develop more horizontal arrangement (Fig. 1b) to resemble the basal loop configuration.

Several diseases alter ventricular shape towards the spherical contour, and this report will analyze if surgical treatment options should be focused only toward correcting the responsible disease versus supplemental reconstruction of the abnormal form responsible for abnormal function.


   2. The disease and the ventricle
Top
 Abstract
 1. Introduction
 2. The disease and...
3. Restoration and conical...
 4. Implications with helical...
 5. Conclusions
 References
 
Enlarged ventricular size with the spherical shape becomes a unifying theme of dilated cardiomyopathy. The underlying pathologic processes responsible for spherical configuration range from (a) ischemic disease causing an extensive post-myocardial infarction scar leading to secondary stretch of compensatory remote fibers within unscarred muscle, or global stretch from multiple small scars, but without a large asynergic region, (b) non-ischemic disease causing distention stretch from volume loading following mitral or aortic valve incompetence, or (c) non-ischemic cardiomyopathy destroying segments of regional myocardial fibers with secondary distention of remaining hypertrophied and thicker viable muscle. Consequently, the spherical chamber shape becomes the common architectural event following any disease that causes global stretch (Fig. 2 ).


Figure 2
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  		Fig. 2. Comparison between the normal elliptical shape (above) and the common spherical shape (below) that provides a unified form to ischemic (left) and non-ischemic cardiomyopathy (right).

 
2.1 Ischemic disease
Current surgical treatment of dilated cardiomyopathy addresses the disease-related causative factor. The specific disease generating elements are evident, so that surgical rebuilding efforts naturally focus upon excluding them during the operative procedure. For example, ventricular restoration in ischemic disease is linked toward recognizing the borders of discrete extensive scar. The scar perimeter then becomes the junction between scar and surrounding normal muscle. This junction then becomes the positioning site for subsequent patch insertion. However, selection of this structural position does not (a) recognize the importance of ventricular chamber size, (b) take into account that compensating remote muscle progressively stretches during the process of cardiac enlargement, and (c) consider that long-term prognosis worsens following restoration if pre-operative end systolic volume index is >100–120 ml/m2 [7]. Follow-up studies in large hearts with extensive scar show that post-reconstruction LV volumes remain high, since scar rim patch attachment leaves a large residual volume of dilated remote muscle. Conversely, dilated hypokinetic left ventricles without scar do not currently undergo reconstruction, since coronary artery bypass grafting (CABG) remains the only treatment. Despite successful revascularization, post-operative volumes may remain high and may progressively increase [8], when ventricular geometry is not approached at the initial procedure.

2.2 Valve disease
Valve replacement or repair alone is done in dilated hearts caused by mitral or aortic valve insufficiency, without consideration of ventricular restoration. There is no visible myocyte pathology in dilated heats with valvular disease so that ventricular rebuilding is not a current decision making consideration. Although valve competence is successfully restored by replacement or repair procedures when pre-operative ejection fraction is <40%, a progressively downward death trajectory exists during late follow-up in ischemic and non-ischemic disease [9]. The mortality factors of progressive heart failure or sudden death from arrhythmias account for the discrepancy between ‘fixing the valve and losing the patient’; a symptom complex (CHF and sudden death) that precisely mirrors mortality factors after ischemic dilated cardiomyopathy.

2.3 Non-ischemic disease
Non-ischemic cardiomyopathy from direct muscular involvement may stem from inflammation, sarcoidosis, idiopathic, or other causes. Surgical restoration approaches have been virtually abandoned because partial left ventriculectomy (PLV) has led to early failure [10]. The responsible mechanism may relate to the prior incorrect assumption that this was a homogeneous global disease. This consideration led to initiation of surgical approaches that only exclude the lateral ventricular wall, with the assumption that a non-homogeneous component was absent. Recent data defines that non-ischemic cardiomyopathy is a non-homogeneous disease that predominantly affects the septum and lateral wall in 66% of patients, but had variability in distribution [11]. Consequently, prior failure is likely related to excluding the wrong lateral wall segment, especially if it was the only healthy part.

Unfortunately, it was not possible to previously recognize that the underlying pathology may be site specific. Improved diagnosis is now available by use of tagged MRI studies [12], and intraoperative echocardiograpic testing so that (a) pre-restoration identification of predominant disease regions septum or lateral wall is possible and (b) novel surgical protocols evolved to use site specificity to determine how to rebuild ventricular form.

2.4 Restoration in non-ischemic disease without scar
PLV, as described by Batista is used with predominant lateral wall involvement [13]. When septal malfunction is the most damaged region, a new procedure termed either Pacopexy, to honor Torrent-Guasp, or Septal Anterior Ventricular Exclusion (SAVE) [11] is employed for patch exclusion of the septum. A conical shape is restored by inserting an oblique patch (Fig. 3 ) between the apex and high septum, just below the aortic valve with subsequent closure of the excluded wall over the patch.


Figure 3
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  		Fig. 3. The non-ischemic ventricle has a spherical configuration pre-operatively. A conical shape is rebuilt following restoration by the SAVE or Pacopexy procedure, an intraventricular patch is placed, with one edge at the apex, near the papillary muscle, and other placed on the septum, just beneath the aorta.

 
Suma and his team led the novel surgical approach to site-specific rebuilding of ventricular form in dilated non-ischemic cardiomyopathy patients. Histopathologic study of approximately 60 septum and lateral wall biopsies/patients displayed similar ~20% fibrosis between segments, but 4–60% variability existed. Early mortality is expected if the 4% scarred lateral wall was excluded and the 60% scarred septum was left in place. These initial observations led to subsequent echocardiograhic intraoperative testing that allows site recognition [13] for decisions about exclusion of either septal or lateral wall. Most importantly, there is not extensive transmural scar, so that each procedure excludes severely hypokinetic rather than akinetic or dyskinetic regions.

Mid-term results from the Cardiovascular Institute and Hayama Heart Center in elective procedures show 71.5% five-year survival for dilated non-ischemic cardiomyopathy. Suma's results specifically address ventricular form without extensive scar, and have become the clinical guideline for novel surgical planning that differs from simply excluding scar. This report shall explore this concept, define expected geometric goals and set the stage for the new clinical procedures reported at the RESTORE meeting.


   3. Restoration and conical architecture
Top
 Abstract
 1. Introduction
 2. The disease and...
 3. Restoration and conical...
4. Implications with helical...
 5. Conclusions
 References
 
3.1 Ischemic disease with scar
Conventional goals during reconstruction of the left ventricle in ischemic disease are directed toward excluding scar. This objective does not account for the secondary stretch of remote muscle, the principal cause of progressive dilation. This remote muscle event explains why initially dyskinetic muscle becomes akinetic, since dynamic wall motion diagnosis compares movement of scar relative to surrounding remote muscle. Progressive loss of contraction of dilated remote muscle makes the scarred area look akinetic because remote compensating region changes adversely without expansion of the infarction scar.

Retention of spherical shape may persist (Fig. 4 ) when patch placement site is limited to the scar rim, since extensively stretched remote muscle stretch is retained. The resultant flatter rather than oblique angulation patch position retains more dilated remote muscle and post-operative ventriculograms display a smaller, but spherical, chamber.


Figure 4
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  		Fig. 4. Left ventriculogram before and after left ventricular restoration. Ventricular volume is reduced by reconstruction, but there is now spherical shape of the post-operative left ventricle.

 
An alternate approach in dilated ischemic cardiomyopathy after anterior infarction, is insertion of an oblique patch between the apex and high septum, just beneath the aortic valve to render a conical form that resembles the shape achieved by Pacopexy or SAVE procedures in non-ischemic cardiomyopathy.

Proximal sutures are placed in non-scarred muscle to keep this obliquely angled patch position (Fig. 5 ) and Isomura et al. [14] will describe recent clinical use of this method. Clinical application of a form-related procedure introduces a technique that does not use the conventional scar-related border decisions. Instead, there is a geometric objective that aims to reconstruct form, instead of making visible disease become the sole guide to decision making.


Figure 5
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  		Fig. 5. Comparison of treatment of the dilated ischemic cardiomyopathy (above) by addressing the disease (lower left) and leaving a spherical shape, or doing the SAVE or Pacopexy (lower right) and rebuilding an elliptical shape. Note that the patch is placed into the septum that does not have scar, and the point of placement is above the scarred region in mid septum.

 
The longer patch covers both scar and the normal septal muscle above the highest point of the septal scar (Fig. 5). There is no dynamic action of the patch, which may become a ‘curtain within the LV chamber’ that is covered by the viable muscle closed over its surface. Creating obliquity by using non-scarred muscle to produce an ellipse was recently reported by Calafiore et al. [15] for septal reshaping following restoration for akinesia and dyskinesia.

3.2 Ischemic disease without scar
Global cardiac dilation during ischemic cardiomyopathy may also exist in a large hypokinetic left ventricle. Multiple areas of small infarction may lead to gradual dilation, so that enlargement develops without the extensive scar that follows acute major coronary artery occlusion. The traditional approach is coronary artery bypass grafting, especially since such hearts display evidence of viability during dopamine infusion or mismatched flow and metabolism following PET scanning. Ventricular size is the keynote to progress after successful revascularization; wall motion score, ejection fraction, and LVESVI improve if initial LVESVI is <75 ml/m2, but progressively deteriorate when pre-operative LVESVI is >75 ml/m2, despite open grafts [8].

The spherical geometry of the globally hypokinetic dilated heart resembles the shape changes noted with extensive scar. Malfunction is related to spherical global shape, and so contractility is not improved by simply restoring blood supply [8]. Consequently, subsequent ventricular architectural issues may need to be addressed, when CABG alone is used to alleviate the underlying ischemia in dilated hypokinetic hearts. Perhaps consideration of vessel and ventricle must enter the decision process.

The surgical problem is restoration for form and not only correction of causative disease. Consequently, the suggested reconstructive procedure excludes marginally scarred muscle rather than the normal muscle above the anterior scar that was previously described (Fig. 5). This more aggressive approach (Fig. 6 ) generates a conical chamber by using the same oblique patch angulation placement technique employed in (a) the prior section with ischemic disease (Fig. 5) and (b) during site selection for non-ischemic disease (Fig. 2). Bockeria et al. [16] summarize early clinical use of reconstructing the LV hypokinetic chamber at the Bakoulev Institute in Moscow.


Figure 6
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  		Fig. 6. Left ventricular restoration in dilated cardiomyopathy in ischemic disease without discrete scar. Note the SAVE or Pacopexy procedure is used to make the spherical chamber become elliptical. A patch is placed between the apex and septum to reconstruct a conical chamber.

 
3.3 Valve disease without scar
Progressive spherical dilation is a hallmark event following prolonged volume loading after chronic aortic or mitral insufficiency. Long-term follow-up shows ~70% late mortality following AVR if <40% pre-operative ejection fraction exists. The downward trajectory for death after aortic insufficiency is steeper than for aortic stenosis because LVESVI is higher pre-operatively. Furthermore, late follow-up studies after aortic valve surgery show that chronic CHF and sudden death cause mortality [17] reproducing the same fatal consequences of dilated hearts after non-ischemic and ischemic disease.

Ventricular architecture in dilated failing hearts with valve incompetence displays the same spherical geometry as observed with ischemia, but the myocardium differs because histology shows only normal muscle with increased collagen. Failure to change the natural time course of progression of heart failure by successful valve replacement suggests a ‘valve and ventricle’ approach should be considered rather than adhering to the conventional restriction that surgical correction should only address the valve disease. Guidelines for successful ‘valve–ventricle approach’ were recently achieved in ischemic disease, where the 50% mortality following CABG and valve repair [18] was improved to 70% survival at 5 years when the ‘triple V’ of correcting the vessel, valve, and ventricle was accomplished [19]. The same spherical ventricular chamber confronted both subsets of ischemic mitral insufficiency patients, but a restoration procedure was needed to rebuild the conical geometry.

There is a unifying central theme of a spherical chamber in many patients with a dilated ventricle with heart failure, yet there is no current category of patients who underwent restoration coupled with valve repair of replacement for non-ischemic valvular disease. A potential answer to this adverse architectural change is described in Fig. 7 that introduces the SAVE or Pacopexy restoration method (found useful in ischemic and diffuse non-ischemic disease) to create a surgical solution. Insight into the value of adding restoration to valve correction is drawn from Batista, who observed best results after ventricular restoration in patients with dilated hearts with valve disease [20]. The same geometric goal may be achieved by Pacopexy or SAVE procedures. The objective is to rebuild the elliptical form, and if this geometric solution provides a successful solution to the current adverse results of addressing only the valve in dilated valvular cardiomyopathy, a novel valve–ventricle approach may evolve.


Figure 7
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  		Fig. 7. Suggested procedure for dilated cardiomyopathy from valvular disease, whereby the dilated spherical left ventricle is made elliptical by rebuilding its form with the SAVE or Pacopexy procedure, using the same patch placement guidelines as described for non-ischemic or ischemic disease.

 
3.4 The macroscopic/microscopic marriage
A further use of the capacity to rebuild a helical surgical scaffold may evolve in the potential ‘macroscopic/microscopic marriage’ that could develop during ‘restoration to construct the cardiac scaffold’ in non-ischemic disease, and the microscopic cell implantation in residual muscle to ‘rebuild functional architecture’. This collaboration of reconstructing the more normal helical architecture by exclusion of more extensive disease (described by Suma in the Pacopexy and SAVE studies [13]) may become coupled with cell implantation into retained remote muscle with marginal, to enhance recovery of retained diseased muscle.

A similar macroscopic/microscopic procedure may also develop in ischemic disease that undergoes restoration when some scar (<25% by gadolinium staining) is retained in remote muscle. The favorable conical form created by restoration may ultimately allow better late improvement of global function if cell implantation is simultaneously accomplished into remote muscle that previously underwent non-transmural infarction, as suggested by De Oliveira et al. [21].


   4. Implications with helical fiber orientation
Top
 Abstract
 1. Introduction
 2. The disease and...
 3. Restoration and conical...
 4. Implications with helical...
5. Conclusions
 References
 
The helical architecture of the normal heart has been confirmed by strain relationships using MRI [22], corrosion casts showing spiral architecture [23], and by sonomicrometry crystals [24]; each pattern reflects the normal oblique fiber orientation that conveys maximum force during ejection and suction. These observations coincide with the helical heart configuration shown in Fig. 1a, and change when dilation alters this architecture (Fig. 1b) because of flattening of the double helical arms of the apical loop.

Prior sonomicrometer crystal recordings document the importance of obliquity to achieve the maximum extent of directional shortening [24]. This functional framework nicely coincides with conceptual determinants of efficiency of ejection fraction, 60% EF is expected with oblique fiber direction, a value that falls 30% EF with transverse or horizontal fiber direction [6]. Although fiber orientation is oblique, recordings from crystal tracings seem to reflect spiral coils within the fibers (or coils within coils) to obtain maximal efficiency [25]. Conversely, reduced shortening develops with a more horizontal position for crystals placement [24].

These shortening patterns closely link with changes in ventricular shape following reconstruction methods that address ‘disease versus form’. The patch position is flatter in ischemic disease when the scar becomes the only marker during ventricular shape rebuilding (Fig. 8 ), and results in a more spherical chamber. Conversely, a more conical chamber is created when form becomes the guideline for patch placement; obliquity now becomes the marker for patch insertion and conceptual goal of the insertion policy. Future comparisons of ventricular function by MRI tagging are needed to define the extent of deformation, and evaluate the validity of this form reconstruction objective.


Figure 8
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  		Fig. 8. Fiber orientation in dilated spherical ventricle (above), whereby the ‘coils within coils’ fiber orientation is more transverse and leads to reduced function. Anticipated changes in fiber orientation are shown below. A spherical form may persist by placing the patch in a flatter (lower left), rather than oblique direction (lower right). This oblique configuration is the desired result of treating ‘form versus disease’.

 

   5. Conclusions
Top
 Abstract
 1. Introduction
 2. The disease and...
 3. Restoration and conical...
 4. Implications with helical...
 5. Conclusions
References
 
Heart failure from dilated cardiomyopathy is associated with a geometric change in the size and shape toward larger volume and conversion from the normal conical to spherical configuration. The sphere becomes a unifying geometric [14] contour that may arise from ischemia, valve insufficiency or myocyte disease. Restoration of the conical contour is possible by decisions that alter ventricular configuration, thus becoming a supplement to correction of the underlying causative factor.

The normal helical configuration is rebuilt by placing an oblique patch from the apex to the high septum to change cardiac form toward an elliptical configuration. Application of this architectural procedure may open new doors to ventricular reconstruction in the spectrum of disease in dilated hearts with ischemic disease with extensive scar or LV hypokinetic function, following chronic aortic of mitral valve incompetence, and in non-ischemic disease with predominant septal pathology. Future testing of these innovative procedures is needed to determine their validation.


   Footnotes
 
{star} Read at 10th RESTORE meeting in San Francisco, California. April 9, 2005.


   References
Top
 Abstract
 1. Introduction
 2. The disease and...
 3. Restoration and conical...
 4. Implications with helical...
 5. Conclusions
 References
 

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