Ex Parte Ross et al

Patent Trial and Appeal Board

Mar 13, 2017

11017237 (P.T.A.B. Mar. 13, 2017)

United States Patent and Trademark Office
UNITED STATES DEPARTMENT OF COMMERCE
United States Patent and Trademark Office
Address: COMMISSIONER FOR PATENTS
P.O.Box 1450
Alexandria, Virginia 22313-1450
www.uspto.gov
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
11/017,237 12/20/2004 Jeffrey Ross 115.0191US01 (03-197) 3232
62058 7590 03/15/2017
PAULY, DEVRIES SMITH & DEFFNER, L.L.C.
Suite 900
121 South 8th Street
MINNEAPOLIS, MN 55402-2481
EXAMINER
KAHELIN, MICHAEL WILLIAM
ART UNIT PAPER NUMBER
3762
NOTIFICATION DATE DELIVERY MODE
03/15/2017 ELECTRONIC
Please find below and/or attached an Office communication concerning this application or proceeding.
The time period for reply, if any, is set in the attached communication.
Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the
following e-mail address(es):
docketing@pdsdlaw.com
kds@pdsdlaw.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte JEFFREY ROSS and RODNEY W. SALO1
Appeal 2014-002633
Application 11/017,237
Technology Center 3600
Before FRANCISCO C. PRATS, JOHN G. NEW, and
JOHN E. SCHNEIDER, Administrative Patent Judges.
NEW, Administrative Patent Judge.
DECISION ON APPEAL
appellants state the real party-in-interest is Cardiac Pacemakers, Inc. App.
Br. 2.
Appeal 2014-002633
Application 11/017,237
SUMMARY
Appellants file this appeal under 35 U.S.C. § 134(a) from the
Examiner’s Final Rejection of claims 17-27, 37^13, and 45. Specifically,
claims 17-19, 22, 23, 27, 37, 38^442 stand rejected as unpatentable under 35
U.S.C. § 103(a) as being obvious over the combination of Lindemans et al.
(US 6,385,491 Bl, May 7, 2002) (“Lindemans”) and Badylak et al. (US
4,902,508, February 20, 1990) (“Badylak”).
Claims 17-27, 37-38, and 42^14 stand rejected as unpatentable under
35 U.S.C. § 103(a) as being obvious over the combination of Lindemans,
Badylak, and Michal et al, US 7,294,334 Bl, November 13, 2007)
(“Michal”).
Claim 45 stands rejected as unpatentable under 35 U.S.C. § 103(a) as
being obvious over the combination of Lindemans, Badylak, and Aldrich
(US 2002/0147479 Al, October 10, 2002) (“Aldrich”).
Claims 17-27, 37, 38, and 42-44 also stand rejected under as
unpatentable 35 U.S.C. § 103(a) as being obvious over the combination of
Freyman et al. (US 2005/0013870 Al, January 20, 2005) (“Freyman”) and
Badylak.
2 Claim 44 has been canceled (See, e.g., Amended Claims, filed April 9,
2013). Furthermore, neither the Examiner nor Appellants address the
rejection of claim 45. We attribute this to an error on both the Examiner’s
and Appellants’ part; we therefore do not address claim 44 and consider
claim 45 to be argued together with the rest of the claims.
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Claim 45 stands rejected as unpatentable under 35 U.S.C. § 103(a) as
being obvious over the combination of Freyman, Badylak, and Aldrich (US
2002/0147479 Al, October 10, 2002) (“Aldrich”).3’4
We have jurisdiction under 35 U.S.C. § 6(b)
We AFFIRM.
NATURE OF THE CLAIMED INVENTION
Appellants’ invention is directed to methods and devices useful for
cardiac repair. Abstract.
3 Claims 17-27, 37^13, and 45 were also rejected under 35 U.S.C. § 112,
first paragraph, as lacking written descriptive support. Final Act. 2.
Appellants do not address this rejection in their Appeal Brief, nor does the
record demonstrate that the Examiner has ever withdrawn this rejection. We
consequently summarily affirm the Examiner’s rejection of the claims on
this ground. See 37 C.F.R. § 41.67(c)(vii) (“Any arguments or authorities
not included in the brief... will be refused consideration by the Board”); see
also MPEP § 1205.02 (“If a ground of rejection stated by the examiner is not
addressed in the appellant’s brief, appellant has waived any challenge to that
ground of rejection and the Board may summarily sustain it, unless the
examiner subsequently withdrew the rejection in the examiner’s answer.”).
4 Claims 17-27, 37^13, and 45 were also rejected under 35 U.S.C. § 112,
second paragraph, as indefinite. Final Act. 2. We understand that the
Examiner agreed that the rejection would be obviated by amending claim 17
to substitute the definite article “the” for the indefinite article “a” in line 15
of claim 17. See Pre-Brief Appeal Conf., Dec. 2, January 15, 2013.
Although the Examiner has not explicitly withdrawn this rejection for the
record, the amendment having been duly made by Appellants (see Amended
Claims, filed April 9, 2013) and acknowledged by the Examiner (see Misc.
Comm., September 25, 2013), we consider the Examiner’s rejection
withdrawn for purposes of this appeal.
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REPRESENTATIVE CLAIM
Claim 17 is representative of the claims on appeal and recites:
17. A method to enhance electrical therapy that modulates
cardiac remodeling, comprising:
introducing to a mammal having damaged cardiac
tissue resulting from myocardial infarction, an
implantable device comprising a sensor to sense a
physiological signal indicative of a predetermined cardiac
condition, one or more electrodes comprising a preformed
delaminated, decellularized extracellular matrix (ECM)
sheet affixed to the surface thereof, the ECM in the
preformed ECM sheet having a three dimensional
microstructure of native ECM, the preformed ECM sheet
formed as a sheet before being applied to the surface,
which preformed ECM sheet includes a plurality of
different molecules present in native ECM including
collagens present in native ECM, and a generator coupled
to the sensor and the one or more electrodes, the generator
adapted to control an electrical therapy;
identifying in the mammal a cardiac region of
damaged tissue resulting from myocardial infarction;
applying the one or more electrodes comprising the
preformed delaminated, decellularized ECM sheet to the
identified cardiac region, and
applying the electrical therapy through the one or
more electrodes comprising the preformed delaminated,
decellularized ECM sheet to the identified cardiac region
effective to reduce cardiac remodeling in the mammal
based on at least the sensed physiological signal.
App. Br. 20 (paragraphing added).
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ISSUES AND ANALYSIS
A. Rejection of claims 17-19, 22, 23, 27, 37, 38, 42, 43, and 45 over
Lindemans and Badylak; Rejection of claims 17-27, 37-38, and 42-
44 over Lindemans, Badylak, and Michal
Issue 1
Claim 17 is representative of the claims subject to both rejections. 37
C.F.R. § 41.37(c)(iv). Appellants argue the Examiner erred in finding the
combined cited prior art references teach or suggest the limitations of
representative claim 17 reciting:
[T]he ECM [extracellular matrix] in the preformed ECM sheet
having a three dimensional microstructure of native ECM, the
preformed ECM sheet formed as a sheet before being applied to
the surface, which preformed ECM sheet includes a plurality of
different molecules present in native ECM including collagens
present in native ECM.
App. Br. 10.
Analysis
Appellants argue that the collagen pad taught by Lindemans differs
from the ECM recited in claim 17 because it is not an ECM sheet including
isolated ECM having a native (i.e., naturally occurring) three-dimensional
microstructure which includes a mixture of molecules including collagens.
App. Br. 10. Appellants contend, rather, that Lindemans teaches collagen
pads that may be prepared by suspending collagen, without mentioning other
molecules in an appropriate solution, pouring the suspension into a metal
cast, with subsequent freezing and drying, after which the freeze dried
sponge is pressed to a thickness of 3 mm between heated plates. Id. (citing
Lindemans col. 7,11. 41-55; see also col. 13,11. 23-32).
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Appellants suggest that the mounting pad taught by Lindemans is
likely only composed of purified collagen. App. Br. 11. Appellants support
this contention by observing that: 1) the description in Lindemans of how
those pads are prepared; 2) the teaching by Lindemans that “collagen” is a
natural biopolymer and the principal structural protein in mammals, but that
other biodegradable, biocompatible materials suitable for use in forming the
pad (citing Lindemans col. 7,11. 13-19); 3) Figure 8 of Lindemans depicts
complete degradation of the control “non-crosslinked” collagen samples and
the crosslinked collagen samples with collagenase after 7-8 hours; 4)
Lindemans teaches that the non-crosslinked sample was rapidly denatured
when placed in vivo (citing Lindemans col. 9,11. 50-59; col. 10,11. 9-17; and
5) the commercial source of the collagen pads (Coletica). Id.
Furthermore, Appellants argue, because Lindemans teaches the
process of preparing the mounting pad as suspending collagen in a solution,
pouring the solution into a cast, and pressing the resulting dried material at
80 degrees Celsius to a thickness of 3 mm, the resulting three-dimensional
structure is highly unlikely to have a native microstructure. App. Br. 12.
Finally, Appellants argue the ECM material taught by Badylak is for
alio-, auto-, or heterovascular grafts. App. Br. 14. Appellants assert that
neither Lindemans nor Badylak mention infarction, remodeling, or pacing,
and that providing “the predictable results of ensuring biocompatibility with
excellent mechanical characteristics in ECM scaffold” is not a proper reason
for combining unless there is a reason for which one of ordinary skill in the
art would use the material disclosed in Badylak for vascular grafts, which
need tensile strength, because it provides better biocompatibility with
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excellent characteristics for the purpose of Lindemans, which is to support
electrodes. Id.
The Examiner responds that although there may be differences in the
preparation methods taught by Lindemans and Appellants’ disclosed ECM,
the claims as written require only that the ECM to have a native three
dimensional microstructure. Ans. 3. The Examiner finds the claim term
“native” has not been explicitly defined by Appellants’ Specification, nor do
the claims limit the native three-dimensional micro structure to require the
same preparation methods argued by Appellants. Id. The Examiner
therefore finds that the scope of claim 17 embraces any native, naturally
occurring, ECM, that has a three-dimensional micro structure. Id. The
Examiner finds Lindemans teaches a native ECM in the form of a collagen
ECM, and that such an ECM will have some form of a microstructure prior
to implantation. Id. The Examiner therefore finds Lindemans teaches a
microstructure is native and three-dimensional. Id.
We are not persuaded by Appellants’ arguments. Lindemans teaches:
In one embodiment of the present invention, mounting pad 33 is
constructed and formed from collagen, but may alternatively be
fashioned from any suitable biodegradable, biostable, pliant
material (more about which we say below). It is a particular
advantage of the collagen embodiment of the mounting pad of
the present invention that when mounting pad 33 is formed from
an appropriate collagenous material, mounting pad 33 dissolves
or otherwise dissociates over time following implantation within
the human body.
Lindemans. Col. 6,11. 39—47. Lindemans further teaches that: “Mounting
pad 33 is most preferably formed of a collagenous material that maintains its
structural integrity long enough to permit the post-operative defibrillation
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function of lead 1 to be carried out” and that: “[cjollagen is a natural
biopolymer material well suited for use in forming the biodegradable,
biocompatible, electrode mounting pad of the present invention. Collagen is
the principal structural protein in mammals, constituting approximately one-
third of the total body protein.” Id. at col. 6,11. 52-55; 62-66. Lindemans
also teaches:
Other biodegradable, biocompatible materials suitable for
use in forming the electrode mounting pad of the present
invention include natural materials and their corresponding
synthetic equivalents or derivatives, such as albumin, silk,
poly(L)lysin, fibrin, elastin, hyaluronic acid preparations, and
salts and derivatives thereof such as those described in U.S. Pat.
No. 5,128,326, glycos-amino-glycans, polysaccharrides, keratin,
chondroitin sulfates, dermatan sulfate, keratan sulfate, heparan,
heparan sulfate, heparin substitutes, heparin, heparin substitutes,
cellulose and its derivatives, starch, gelatin, dextrans and their
derivatives, chitin, chitosan, and combinations or mixtures of, or
the products of reactions involving, the foregoing.
Still other natural and synthetic biodegradable,
biocompatible materials suitable for use in forming the electrode
mounting pad of the present invention include, but are not limited
to, aliphatic polyesters, polyamides, polyesteramides,
polyorthoesters, polyanhydrides, polyphosphazenes,
Poly(glycolic acid), Poly(L-lactic acid), Poly(DL-lactic acid),
Poly(p-dioxanone), Poly(E-caprolactone), Poly(3-
hydroxypropionic acid), Poly(3- hydroxybutyric acid), Poly(a-
malic acid), Poly(P-malic acid), Poly(serine ester).
Finally, it is fair to state that yet other natural and
synthetic biodegradable, biocompatible materials, whether
existing presently or in future, will find application and
suitability in forming a biodegradable, biocompatible electrode
mounting pad of the present invention.
Lindemans col. 7,11. 13—41. We quote extensively from Lindemans to
emphasize that, contrary to Appellants’ arguments, which are based
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principally on selected embodiments, Lindemans teaches a wide variety of
naturally occurring (i.e., native) and complex chemical matrices, including
“a plurality of different molecules present in native ECM including
collagens present in native ECM” and exhibiting “a three dimensional
microstructure of native ECM, the preformed ECM sheet formed as a sheet”
(i.e., a pad). We consequently conclude that a person of ordinary skill in the
art, upon apprehending the teachings and suggestions of Lindemans, would
realize that Lindemans teaches the disputed limitation of claim 17.
Finally, we are not persuaded by Appellants’ argument that the
combination of Lindemans and Badylak is improper. Appellants appear to
argue that the references constitute non-analogous art and the Examiner
erred because a person of ordinary skill would have no reason to combine
them. See App. Br. 14. We disagree.
Two separate tests define the scope of analogous prior art: (1)
whether the art is from the same field of endeavor, regardless of
the problem addressed and, (2) if the reference is not within the
field of the inventor's endeavor, whether the reference still is
reasonably pertinent to the particular problem with which the
inventor is involved.
In re Bigio, 381 F.3d 1320, 1325 (Fed. Cir. 2004). We agree with
Appellants that Badylak is not directed to the field of cardiac pacemakers, as
is Lindemans. However, Badylak teaches delaminated collagenous tissue
(i.e., an extracellular matrix) as a mechanical and structural support for
vascular grafts. We conclude that a person of ordinary skill in the art,
understanding the teachings of Badylak and Lindemans would be motivated
to combine the teachings of the references to address the particular problem
of providing a collagen-based ECM for the structural support of
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microelectrodes and which is biodegradable and dissolves over time in
human body fluids.
Issue 2
Appellants argue the Examiner erred in finding the combined cited
prior art teaches or suggests the limitation of claim 17 reciting “applying the
electrical therapy through the one or more electrodes comprising the
preformed delaminated, decellularized ECM sheet to the identified cardiac
region effective to reduce cardiac remodeling in the mammal based on at
least the sensed physiological signal.” App. Br. 12-13.
Analysis
Appellants dispute the Examiner’s finding that the
pacemaker/defibrillator disclosed by Lindemans modulates cardiac
remodeling insofar as cardiac rhythm management provides proper electro­
mechanical function and prevents/reduces cardiomyopathy, which is a form
of cardiac remodeling. App. Br. 12 (citing Final Act. 4). Appellants
likewise dispute the Examiner’s finding that the method taught by
Lindemans would necessarily also treat infarcted tissue because it is
damaged cardiac tissue and because pacing electrodes are used to treat
infarcted tissue. Id. at 12-13 (citing Final Act. 5). Appellants further argue
the Examiner erroneously found the pacemaker/defibrillator taught by
Lindemans modulates cardiac remodeling as evidenced by Heynen et al. (US
6,507,756 Bl, January 14, 2003) (“Heynen”), and that any pacing is
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considered a form of passive prevention and reduction of cardiac
remodeling. Id. at 13 (citing Final Act. 13; Heynen col. 5,11. 49-51).
Appellants point out that the claim term “remodeling” is a term of art
and refers to progressive change of ventricular shape and size. App. Br. 13
(citing, e.g., Spec 2-3). Appellants assert that Lindemans is silent with
respect to infarction or remodeling and that the “temporary postoperative
pacing of the heart” to improve “cardiac function by the cessation of atrial
fibrillation” taught by Lindemans is different than electrical therapy to
modulate cardiac remodeling. Id. (citing Final Act. 4). Appellants therefore
contend that Lindemans does not provide any teaching by which
“conventional pacing methods” necessarily modulate the progressive change
of ventricular shape and size. Id.
With respect to the Examiner’s finding that “that any pacing is
considered a form of passive prevention and reduction of cardiac
remodeling,” Appellants contend that such a finding is an improper use of
official notice. App. Br. 13 (quoting Final Act. 13). Appellants further
contend that the Examiner’s finding is not cured by Heynen, because
Heynen provides a method and apparatus that “may aid in the remodeling
process” by alleviating pacing-induced stress of a patient’s heart by
programming a relative long starting or initial AV delay that is decremented
to a relatively short AV delay over a given time interval. Id. In other words,
Appellants argue, the teachings of Heynen allow for gradual cardiac
remodeling, rather than reducing cardiac remodeling, as recited in claim 17.
Id. Furthermore, Appellants argue, Heynen provides a specific type of
pacing that may aid in the remodeling process. Id.
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Appellants also adduce several references as evidence that some
conventional pacing therapies cause or worsen adverse ventricular
remodeling.5 App. Br. 13. Consequently, Appellants argue, a person of
ordinary skill in the art would not understand that conventional pacing
would modulate adverse cardiac remodeling, e.g., after myocardial
infarction. Id. at 14.
The Examiner agrees that Lindemans is silent with respect to
modulating cardiac remodeling. Ans. 3. However, the Examiner finds that
Heynen explicitly teaches that conventional pacing provides for passive
prevention of cardiac remodeling in that the conventional pacing, as
disclosed by Lindemans, will entrain the heart to the proper AV delay and
which aids in cardiac remodeling. Id. at 4. The Examiner therefore finds the
teachings of Heynen supports the Examiner’s finding that conventional
pacing aids in cardiac remodeling of the heart by providing the heart with
proper contraction through pacing therapy. Id. The Examiner finds the cited
prior art teaches that cardiac remodeling is reduced in the sense that adverse
remodeling, cardiomyopathy, is reduced and positive remodeling is
promoted. Id. The Examiner finds this interpretation is consistent with
5 Citing, e.g., J.-B. Thambo et al., Detrimental Ventricular Remodeling in
Patients With Congenital Complete Heart Block and Chronic Right
Ventricular Apical Pacing, 110 Circulation 3766-72 (2004); G. F.
Tomaselli, Pacing-Induced Remodeling of the Ventricle: Fire in the Matrix,
21 J. Cardiovasc. Electrophysiol. 1150-52 (2010); L. F. Tops et al., The
Effects of Right Ventricular Apical Pacing on Ventricular Function and
Dyssynchrony: Implications for Therapy, 54 J. Am. College Cardiol. 764-
76 (2009); M. F. M. van Oosterhout, Remodeling by Ventricular Pacing in
Hypertrophying Dog Hearts, 49 Cardiovasc. Res. 771-78 (2001)
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Appellants’ usage of cardiac remodeling as treating an adverse condition
that is sought to be reduced/prevented. Id.
Appellants reply that the teachings of Heynen allow for gradual
cardiac remodeling (i.e., the pacing in Heynen promotes cardiac remodeling)
rather than reducing cardiac remodeling as recited in claim 17. Reply Br. 4.
Therefore, Appellants argue, Heynen teaches away from the use of pacing to
reduce cardiac remodeling. Id. Furthermore, Appellants argue, a person of
ordinary skill in the art, even considering the teachings of Heynen, would
not consider the use of conventional pacing to reduce cardiac remodeling
because some conventional pacing therapies cause or worsen adverse
ventricular remodeling. Id.
We are not persuaded by Appellants’ arguments. Appellants’
Specification discusses the claim term “cardiac remodeling” as follows:
After [cardiac ischemic] injury, the heart lacks the ability to
effectively regenerate cardiomyocytes to replace the injured cells
of the myocardium. Each injured area eventually becomes a
fibrous scar that is nonconductive and non-contractile.
Consequently, the overall contractility of the myocardium is
weakened, resulting in decreased cardiac output. As a
physiological compensatory mechanism that acts to increase the
cardiac output, the LV [left ventricle] diastolic filling pressure
increases as the pulmonary and venous blood volume increases.
This increases the LV preload, including the stress on the LV
wall before the LV contracts to eject blood. The increase of the
LV preload leads to progressive change of the L V shape and size,
a process referred to as remodeling. Remodeling is initiated in
response to a redistribution of cardiac stress and strain caused by
the impairment of contractile function in the injured tissue as
well as in nearby and/or interspersed viable myocardial tissue
with lessened contractility due to the infarct. The remodeling
starts with expansion of the region of the injured tissue and
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progresses to a chronic, global expansion in the size and change
in the shape of the entire LV.
Spec. 2-3. Appellants’ Specification thus describes remodeling as a
progressive change in the shape and size of the ventricle as part of a
physiological response to an insult to the tissue that results from ischemic
injury causing decreased conductivity. Appellants admit that the claim term
‘“[rjemodeling’ is a term of art,” and their description of cardiac remodeling
is consistent with its general usage in the art. App. Br. 13. For example,
cardiac remodeling is also described as manifesting itself “clinically as
changes in size, shape and function of the heart resulting from cardiac load
or injury, cardiac remodeling is influenced by hemodynamic load,
neurohormonal activation and other factors still under investigation.” J. N.
Cohn et al., Cardiac remodeling—concepts and clinical implications: a
consensus paper from an international forum on cardiac remodeling, 35(3)
J. Amer. Coll. Cardiol. 569-82 (2000). We therefore find that cardiac
remodeling refers to a change in size, shape and function of the heart and,
particularly, the left ventricle.
Heynen is directed to “a method and apparatus for avoiding or
alleviating stress of a patient’s heart induced by programming a relatively
short AV [atrioventricular] delay in comparison to an intrinsic, prolonged
AV delay.” Heynen col. 5,11. 23-26. Specifically, Heynen teaches:
[A] Time-Adaptive AV delay (TA-AV delay) determining
algorithm is started upon implantation of a DDD or DDDR
pacing system in a patient having a CHF/DCM heart. At or about
the time of implantation, the AV delay is initially set at a
relatively long starting or initial AV delay that may be correlated
with any intrinsic AV delay that the patient's heart exhibits.
Thereafter, the TA-AV delay is incrementally decreased or
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decrement over a post-implant Time-Adaptive (TA) period of
time of hours, days or weeks until a programmed, relatively
shorter, AV delay is reached. Then, the programmed, chronic,
AV delay is maintained.
Id. at 11. 27-37. Heynen further teaches:
In this way, the heart gradually adapts to the optimal chronic AV
delay and stress is reduced. This gradual process may aid in the
remodeling process of the CHF/DCM [congestive heart
failure/dilated cardiomyopathy] heart. The process of
remodeling is a gradual adaptation of the muscle cells of the
heart to a new situation of different wall stresses, volume
loading, and/or contraction patterns.
Id. at 11. 49-54.
We interpret these teachings of Heynen to mean that, by chronically
re-entraining the atrioventricular rhythm of the heart beat to an optimal AV
delay, the stress caused by adaptive changes to the ventricular wall by
cardiac remodeling is relieved and, consequently, the process of cardiac
remodeling, which is a response to the stress imposed on the LV wall before
the LV contracts to eject blood, which in turn leads to progressive change of
the LV shape and size, is relieved. See Spec. 2-3. We consequently agree
with the Examiner that a person of ordinary skill would understand that
Heynen teaches relief of the stress imposed on the ventricular wall by
cardiac remodeling and, therefore, “reduce[s] cardiac remodeling in the
mammal,” as recited in representative claim 17. We consequently affirm
both of the Examiner’s rejections that combine Lindemans and Badylak as to
representative claim 17. Other than claims 39-41, discussed below, the
remaining claims subject to these rejections were not argued separately, and
therefore fall with claim 17.
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B. Rejection of claims 39-41
Issue
Appellants argue the Examiner erred by improperly taking official
notice of the claim term “pre-excitation” or the pacemaker operating in VDD
or DDD mode App. Br. 14-15.
Analysis
Appellants point out that, although the Examiner acknowledged that
neither Lindemans nor Badylak teach or suggest the use of pre-excitation
with a pacemaker, or the pacemaker operating in VDD or DDD mode, the
Examiner improperly took official notice that that it would have been
obvious to modify the system as taught by Lindemans in view of Badylak
with the use of a VDD or DDD pacemaker that pre-excites. App. Br. 14.
Appellants contend the Examiner incorrectly found such a modification
would provide the predictable results of providing well known stimulation
timing methods for maximizing hemodynamic benefits for cardiac rhythm
management. Id. at 15.
The Examiner responds that official notice was not taken, but rather,
the Examiner relied upon knowledge commonly known in the art. Ans. 4.
The Examiner finds that Appellants’ Brief is the first time such an argument
has been made by Appellants, and the Examiner therefore cites Shelton et al.
(US 5,527,347, June 18, 1996) (“Shelton”) as evidence supporting the
rejection. Id. The Examiner finds Shelton discloses that pre-excitation is
well known form of treatment for patients suffering cardiomyopathy and that
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DDD pacemakers are also well known for delivering the pre-excitation
pacing therapy. Id. (citing Shelton, e.g., col. 1,11. 35-49, cols. 1-2,11. 63-
31, col. 4,11. 15-31).
We agree with the Examiner. In addition to the teachings of Shelton
relied upon by the Examiner, Heynen also teaches:
Pacing the right ventricular apex before spontaneous atria-
ventricular conduction activates the ventricles is understood to
alter the ventricular septal activation pattern. Since the right
ventricle is caused to contract first, it pulls the septum toward the
right ventricle thereby reducing the LVOT [left ventricular
outflow tract] obstruction. The literature uniformly
acknowledges the potential advantages of synchronized AV
pacing for HOCM [Hypertrophic Obstructive Cardiomyopathy]
patients, stressing the importance of achieving ventricular
capture. Causing “complete ventricular capture” is important to
obtain the above-described septal movement, while selecting the
longest AV delay that results in complete ventricular capture is
important in order to maximize the atrial contribution to
ventricular filling. See, for example, commonly assigned U.S.
Pat. No. 5,507,782, and the literature articles referenced therein.
The delivered pacing pulse should provide “pre-excitation, ” i.e.,
depolarization of the ventricular apex before the septum. This
altered pattern of septal contraction, as well as optimal left
ventricular filling, is generally recognized as being important to
this mode of pacemaker treatment.
Heynen col. 3,11. 10-30 (emphases added). Furthermore, Shelton explicitly
teaches:
[I]n some patients there may also be a benefit to operating the
device in VDD or DVI mode, which provides ventricular pacing
pulses synchronized only to sensed atrial depolarizations or only
delivered to atrial pacing pulses, respectively, depending upon
the specific underlying heart condition of the patient. However,
DDD mode is expected to be the mode most widely used to
practice the present invention.
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Shelton col. 4,11. 24-31. We consequently agree with the Examiner that the
evidence adduced demonstrates that the disputed limitations were well
known in the art at the time of Appellants’ invention, and therefore affirm
the Examiners rejection of claims 19-21.
C. Rejection of claims 17-19, 22-23, 27, 37-38, 42, 43, and 45 over
Freyman and Badylak
Appellants repeat their arguments presented supra with respect to
these claims. We have explained why we are not persuaded by Appellants’
arguments and incorporate that reasoning here by reference.
Furthermore, Freyman teaches a decellularized extracellular matrix
(ECM) of conditioned body tissues and uses thereof. Freyman Title.
Specifically, Freyman teaches:
In response to the need for more efficient and effective
implant materials, the use of extracellular matrix (ECM) as
templates for tissue or organ repair or regeneration has increased.
Although the exact mechanisms through which ECM facilitates
repair or regeneration are not known, the composition and the
organization of the components are considered to be important
factors that influence cell proliferation, gene expression patterns,
and cell differentiation.
ECM is a complex structural entity surrounding and
supporting cells. The extracellular matrix is found within
mammalian tissues and is made up of three major classes of
biomolecules: structural proteins (e.g., collagen and elastin),
specialized proteins (e.g., fibrillin, fibronectin, and laminin), and
proteoglycans (e.g., gly cos aminogly cans). In addition to
providing physical support to cells, the extracellular matrix
affects cell function through mechanical and chemical signals.
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Appeal 2014-002633
Application 11/017,237
Freyman 6-7 (emphases added, internal citations omitted). We
consequently agree with the Examiner that Freyman teaches “a preformed
delaminated, decellularized extracellular matrix (ECM) sheet... the
preformed ECM sheet having a three dimensional microstructure of native
ECM ... which ... includes a plurality of different molecules present in
native ECM including collagens present in native ECM,” as recited in claim
17. We consequently affirm the Examiner’s rejection of the claims.
DECISION
The Examiner’s rejection of claims 17-27, 37^13, and 45 as
unpatentable under 35 U.S.C. § 112, first paragraph (see footnote 3) is
affirmed.
The Examiner’s rejection of claims 17-19, 22-23, 27, 37-38, 42, 43,
and 45 as unpatentable under 35 U.S.C. § 103(a) is affirmed.
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a)(1). See 37 C.F.R.
§ 1.136(a)(l)(iv).
AFFIRMED
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