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Transcript
European Journal of Cardio-thoracic Surgery 29S (2006) S238—S244
www.elsevier.com/locate/ejcts
Form versus disease: optimizing geometry during
ventricular restoration§
Gerald D. Buckberg a,b,* and 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
Abstract
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.
# 2006 Elsevier B.V. All rights reserved.
Keywords: Ventricular restoration; Helical ventricular myocardial band; Ischemic cardiomyopathy; Non-ischemic cardiomyopathy; Valvular cardiomyopathy;
Ventricular fiber orientation; SAVE; Pacopexy
1. Introduction
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].
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
§
Read at 10th RESTORE meeting in San Francisco, California. April 9, 2005.
* 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.
E-mail address: [email protected].
1010-7940/$ — see front matter # 2006 Elsevier B.V. All rights reserved.
doi:10.1016/j.ejcts.2006.02.015
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
G.D. Buckberg / European Journal of Cardio-thoracic Surgery 29S (2006) S238—S244
S239
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 608 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.
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
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).
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
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).
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 preoperative 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 preoperative 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.
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G.D. Buckberg / European Journal of Cardio-thoracic Surgery 29S (2006) S238—S244
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) prerestoration 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.
Suma and his team led the novel surgical approach to sitespecific 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% fiveyear 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
2.4. Restoration in non-ischemic disease without scar
3.1. Ischemic disease with 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.
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 postoperative ventriculograms display a smaller, but spherical,
chamber.
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.
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.
G.D. Buckberg / European Journal of Cardio-thoracic Surgery 29S (2006) S238—S244
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 nonischemic 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.
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
S241
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 preoperative 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.
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.
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.
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.
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G.D. Buckberg / European Journal of Cardio-thoracic Surgery 29S (2006) S238—S244
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 nonischemic 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
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.
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.
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
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
G.D. Buckberg / European Journal of Cardio-thoracic Surgery 29S (2006) S238—S244
[2]
[3]
[4]
[5]
[6]
[7]
[8]
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’.
[9]
[10]
[11]
[12]
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.
[13]
[14]
5. Conclusions
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.
[15]
[16]
[17]
[18]
[19]
[20]
[21]
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