Ex Parte Ross et alDownload PDFPatent Trial and Appeal BoardMar 13, 201711017237 (P.T.A.B. Mar. 13, 2017) Copy Citation 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. 2 Appeal 2014-002633 Application 11/017,237 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. 3 Appeal 2014-002633 Application 11/017,237 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). 4 Appeal 2014-002633 Application 11/017,237 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). 5 Appeal 2014-002633 Application 11/017,237 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 6 Appeal 2014-002633 Application 11/017,237 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 7 Appeal 2014-002633 Application 11/017,237 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 8 Appeal 2014-002633 Application 11/017,237 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 9 Appeal 2014-002633 Application 11/017,237 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 10 Appeal 2014-002633 Application 11/017,237 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. 11 Appeal 2014-002633 Application 11/017,237 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) 12 Appeal 2014-002633 Application 11/017,237 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 13 Appeal 2014-002633 Application 11/017,237 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 14 Appeal 2014-002633 Application 11/017,237 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. 15 Appeal 2014-002633 Application 11/017,237 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 16 Appeal 2014-002633 Application 11/017,237 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. 17 Appeal 2014-002633 Application 11/017,237 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. 18 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 19 Copy with citationCopy as parenthetical citation