The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
DETAILED ACTION
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on October 27, 2025 has been entered.
Response to Arguments
On page 7 of the Remarks, the applicant states that “The Claims have been amended without prejudice to address the rejections under 35 U.S.C. 112.” Applicant’s arguments with respect to the claim (i.e., “the claims have been amended in a manner that moots the previous rejections of record”) have been considered. No other arguments are present. The examiner respectfully disagrees that the amendments overcome the prior art previously applied. As there are no specific arguments to rebut, see the rejections that follow, including new rejections under 35 USC 112.
It is noted that 37 C.F.R. 1.111(b) states “In order to be entitled to reconsideration or further examination, the applicant or patent owner must reply to the Office action. The reply by the applicant or patent owner must be reduced to a writing which distinctly and specifically points out the supposed errors in the examiner’s action and must reply to every ground of objection and rejection in the prior Office action. The reply must present arguments pointing out the specific distinctions believed to render the claims, including any newly presented claims, patentable over any applied references… A general allegation that the claims define a patentable invention without specifically pointing out how the language of the claims patentably distinguishes them from the references does not comply with the requirements of this section.”
Claim Objections
Claim 25 is objected to because of the following informalities:
Claim 25 is objected to because it should state “by collecting new electrical parameter values” in line 2, in the same way that claim 29 was amended, thereby providing consistency within the claims.
Appropriate correction is required.
Claim Rejections - 35 USC § 112
First Paragraph
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 9 and 10 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 9 recites “wherein the preconditioning electrical current therapy is in an amount sufficient to increase ATP production in cells of the myocardial tissue.” Firstly, the specification fails to describe what is “an amount” sufficient to increase ATP production. Secondly, the specification fails to describe anything regarding ATP production specific to myocardial tissue. ATP is discussed in the following areas of the specification (with paragraphs being cited from US PGPUB 2021/0138241, representative of the originally filed disclosure, emphasis added):
[0002] “The present disclosure relates to a method and apparatus for treating biological tissue using electrical current. For example, aspects of the present disclosure relate to a method and apparatus for treating and preconditioning damaged myocardial tissue, for influencing the behavior of stem cells, for increasing production of insulin by pancreatic tissue, for increasing production of glucagon and other small molecule products of the pancreas, for increasing cellular production of ATP, for reinvigorating aging cells and for preventing and treating cancer by applying an electrical current, which can be anodal or biphasic, to the appropriate tissue and cells.”
[0008] “Depolarization in areas other than heart and nerve tissue is poorly appreciated as in the Beta cell in the pancreas where depolarization initiates the secretion of insulin. This occurs in two phases. An initial phase lasts 5 minutes and is initiated by closure of ATP-sensitive potassium channels. When the pancreas sees a glucose molecule, electrons get stripped from it and get passed down the electron transport chain thereby converting ADT to ATP. This is seen by the cell and the ATP-sensitive potassium channels close causing the depolarization of the Beta cell.”
[0025] “According to an exemplary embodiment, placing anodal currents on the outside of cells increases the membrane potential, and, as first recognized by the present inventor, such an effect may last for a number of hours. The application of anodal currents also gives rise to an increased production of adenosine tri-phosphate (ATP) which is further used for the work of the cell.”
[0028] “The application of anodal, biphasic or cathodal also current increases the membrane potential thereby producing more ATP. Such an application of electrical current therapy can have many implications from a therapeutic standpoint. Firstly, diabetes may be ameliorated by applying current to the pancreas…”
[0032] “As an example, a number of types of cell cultures in Petri dishes, including mature and immature fibrocytes, were subjected to pacing across the Petri dishes. The cells were found to line up along the lines of electrical flux and to divide and differentiate more rapidly. Furthermore, the membrane potential of the cells increased and lasted for several hours. ATP levels were found to be increased due to the anodal component of the waveforms…”
[0034] “For some reason, human small vessel cell cultures cannot be stimulated in this pharmacologically to grow blood vessels and, as a result, cannot be used to improve tissues intended for transplant. Thus, using anodal, biphasic or cathodal current to produce ATP to increase metabolism artificially and to augment cellular functions can bypass the block in the usual pathway of stimuli and produce the desired result by an alternate route, allowing this technique of improving transplant viability to be extended to human tissue as well.”
[0035] “Further, electrical current therapy can be promoted to up-regulate functioning of suppressor oncogenes to suppress cancer growth … This is but one of the cellular functions which can be stimulated back to normal by exposing cells to anodal current, creating ATP at virtually no cost to the cell, repairing the cell, increasing its resistance to becoming cancerous, and likely even causing regression of existing tumors.”
As illustrated above, increased ATP production is not taught in any relation to the disclosed embodiments pertaining to the myocardium, nor is there any discussion of what is “an amount sufficient to increase ATP production”. The underlined portions above illustrate discussion of tissue other than the heart. The bold portion above illustrates the only aspect that provides any insight into any mechanism that actually produces the desired result of increased ATP production (i.e., the use of anodal signals). Therefore, any prior art that utilizes anodal signals is sufficient to read on the subject matter of claim 9.
Claim 10 recites “wherein the preconditioning electrical current therapy is in an amount sufficient to increase mobility of stem cells in the myocardial tissue...” Firstly, the specification fails to describe what is “an amount” sufficient to mobility of stem cells. Secondly, the specification fails to describe anything regarding stem cell mobility specific to myocardial tissue. Stem cells are discussed in the following areas of the specification (with paragraphs being cited from US PGPUB 2021/0138241, representative of the originally filed disclosure, emphasis added):
[0002] “The present disclosure relates to a method and apparatus for treating biological tissue using electrical current. For example, aspects of the present disclosure relate to a method and apparatus for treating and preconditioning damaged myocardial tissue, for influencing the behavior of stem cells, for increasing production of insulin by pancreatic tissue, for increasing production of glucagon and other small molecule products of the pancreas, for increasing cellular production of ATP, for reinvigorating aging cells and for preventing and treating cancer by applying an electrical current, which can be anodal or biphasic, to the appropriate tissue and cells.”
[0020] As first recognized by the present inventor, pacing with an anodal component has definite usefulness. For instance, pacing stem cells in a petri-dish with an anodal or biphasic current pulse results in the cells being lined up along the lines of electrical flux as well as those cells multiplying and being differentiated rapidly. Pacing stem cells with anodal currents, for example, cause the stem cells to migrate towards the anodal potential. Thus, electrical current therapy may be used to improve stem cell alignment and aid in long-term healing of damaged tissue since the stem cells applied to the damaged tissue are applied with better alignment, and since the stem cells multiply and differentiate more quickly as a result of the electrical current therapy.
[0031] Anodal polarity increases the membrane potential of the heart cells so that when the cells do depolarize, they do so from a more electronegative level, more sodium channels become available, the action potential is more vigorous and travels faster, and more calcium exchanges for the sodium enhancing contractility. Further, the improved cardiac function with the biphasic waveform appears to result from more than just improving hemodynamics. For instance, there seems to be an additional mechanism influencing the functioning of the small numbers of naturally present stem cells in the body. The function of these cells appears to be that they are delivered to damaged areas in the body in an attempt to repair them.
Regarding paragraph 31 above, it is noted that this paragraph does not discuss mobility of stem cells within the heart as being changed, but simply “an additional mechanism influencing functionality”, which is not specific and for which this mechanism is not clearly described. Furthermore, this paragraph fails to discuss what is considered “an amount sufficient” to alter stem cell mobility in any way. As clearly illustrated in paragraph 31, the use of an anodal polarity signal is what is described as providing the results claimed in claim 10. Therefore, any prior art that utilizes anodal signals is sufficient to read on the subject matter of claim 10.
Second Paragraph
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 9, 10, 23 and 31 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 9 is rejected because, as described in the rejection under 35 USC 112(a) above, the specification fails to describe what is meant by “an amount sufficient to increase ATP production” within any type of cell, let alone within myocardial tissue. As such, claim 9 is indefinite.
Claim 10 is rejected because, as described in the rejection under 35 USC 112(a) above, the specification fails to describe what is meant by “an amount sufficient to increase mobility of stem cells” within any type of cell, let alone within myocardial tissue. As such, claim 10 is indefinite.
Claim 23 is rejected because it is unclear what is considered “sufficient to increase the amount of available sodium channels to increase the action potential to increase the amount of calcium-sodium exchanges to enhance contractility of the damages myocardial tissue”. Paragraph 31 of the PGPUB of the instant application states “Anodal polarity increases the membrane potential of the heart cells so that when the cells do depolarize, they do so from a more electronegative level, more sodium channels become available, the action potential is more vigorous and travels faster, and more calcium exchanges for the sodium enhancing contractility.” Therefore, any anodal polarity is considered sufficient for this purpose, and any prior art that teaches the use of anodal signals reads on claim 23.
Claim 31 is rejected because “the damaged cardiac tissue” in line 2 lacks antecedent basis.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claims 1, 3 and 32 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Prystowsky et al. (US Patent No. 4,554,922).
Regarding claims 1 and 32, Prystowsky discloses programming circuitry (see programmable stimulator 60 in Figure 8) that has pre-programmed parameters to generate precondition electrical current therapy (see Figure 7 and column 5, lines 33-60) for myocardial tissue (see electrodes attached to the heart in Figure 8, and column 5, line 61 through column 6, line 28), the preconditioning electrical current therapy having a set predetermined waveform (see Figure 7 and column 5, lines 33-60, which discuss the variables associated with the predetermined waveform(s) that may be applied). Prystowsky teaches an embodiment in which “instead of delivering Sc after each beat 30, the spontaneous electrical activity of the heart can be sensed and whenever response 40 occurs and is sensed, Sc can be delivered in the refractory period of response 40 to prevent the subsequent tachycardia or fibrillation precipitated by the trigger 40” (see column 5, lines 27-32), which reads on “sensing an electrical parameter of myocardial tissue in the patient’s heart with an electrical sensor”, and “responsive to sensing the electrical parameters, making a determination if preconditioning electrical current therapy is necessary based on the sensed electrical parameter”. This also reads on the limitation of “analyzing the electrical parameter over time to evaluated a trend in the electrical parameter” because the trend being analyzed over time here is whether or not the there is little to no electrical activity. For instance, when electrical activity of the heart (i.e., the top graph of Figure 6) remains flat between peaks 30 and 32, the trend of no activity is sensed and there is no need for Sc to be delivered. As such, this also reads on “responsive to determining that preconditioning electrical current therapy is necessary, administering the preconditioning electrical current therapy to the myocardial tissue” since Prystowsky teaches “whenever response 40 occurs and is sensed, Sc can be delivered” (see column 5, lines 27-32). Specific to “administering the preconditioning electrical therapy to the myocardial tissue”, it is noted that delivery of the electrical energy to the heart as taught and illustrated in the disclosure of Prystowsky, the electrical energy will inherently propagate within the heart muscle, including to the myocardial tissue, even if it is deemed that Figure 8 illustrates electrodes on the pericardium.
Regarding claim 3, it is noted that Sc is taught as “an inhibiting electrical stimuli” (see column 2, lines 21-24, lines 39-43 and lines 52-60). As such, these stimuli do not trigger a new re-polarization and actually inhibit such a response, which means that they do not cause depolarization (i.e., they are applied in an amount below a depolarization threshold of the myocardial tissue).
Claims 1, 3-6, 22-23, 25-26, 32 and 34 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Mower (US Patent No. 6,411,845).
Regarding Claim 1, Mower discloses programming circuitry (see “control circuit logic can activate the multiple site”) that has pre-programmed parameters to generate preconditioning electrical current therapy (see column 7, line 65 through column 8, line 8) for myocardial tissue (see Abstract – “The anodal phase preconditions the myocardium to accept the second phase (cathodal)…”), the preconditioning electrical current therapy having a set predetermined waveform (see claim 10 of Mower, which states that “the first stimulation phase further comprises a series of stimulating pulses of a predetermined amplitude and duration, and a series of rest periods”). Mower teaches sensing an electrical parameter of myocardial tissue in the patient’s heart with an electrical sensor (see column 3, lines 42-53 – “control circuit logic can activate the multiple site(s), biphasic ventricular stimulation upon the occurrence of A-V block in a patient known to be susceptible to multiple random ventricular reentrant foci, or upon the direct or indirect sensing of ventricular fibrillation. For example, direct sensing of ventricular fibrillation can be based on data from multiple ventricular sensing electrodes, and indirect sensing can be based on any of various functional parameters, such as arterial blood pressure, size and/or presence of an R wave, rate of the electrogram deflections, or the probability density function (PDF) of the electrogram“), and responsive to sensing the electrical parameters, making a determination if preconditioning electrical current therapy is necessary based on the sensed electrical parameter (see column 3, lines 42-53 again, for teaching “control circuit logic can activate the multiple site(s), biphasic ventricular stimulation upon the occurrence of A-V block in a patient known to be susceptible to multiple random ventricular reentrant foci, or upon the direct or indirect sensing of ventricular fibrillation”). Mower also teaches analyzing the electrical parameter over time to evaluated a trend in the electrical parameter (see column 3, lines 48-52 where it is taught that “indirect sensing can be based on any of various functional parameters, such as… rate of the electrogram deflections, or the probability density function (PDF) of the electrogram”, noting that both a “rate” and a probability density function are inherently measured “over time” and utilize trends). And Mower also reads on “responsive to determining that preconditioning electrical current therapy is necessary, administering the preconditioning electrical current therapy to the myocardial tissue” (see column 3, lines 42-53 again, for teaching “control circuit logic can activate the multiple site(s), biphasic ventricular stimulation upon the occurrence of A-V block in a patient known to be susceptible to multiple random ventricular reentrant foci, or upon the direct or indirect sensing of ventricular fibrillation”).
Regarding Claim 3, Mower discloses wherein the electrical current therapy is below a depolarization threshold of cells of the tissue “myocardial” (FIGS. 2-5; column 7, lines 43-48 “the magnitude of the anodal phase does not exceed the maximum subthreshold amplitude. The anodal phase serves to precondition the stimulated myocardium, thereby lowering the excitation threshold such that a cathodal stimulation of lesser intensity than normal will produce depolarization leading toe contraction”).
Regarding Claim 4, Mower discloses wherein a signal used in the electrical current therapy includes an anodal signal (see column 3, lines 63-65; “first and second phases of stimulation consist of an anodal pulse (first phase) followed by a cathodal pulse (second phase)”; anodal stimulation 202, 302, 402, or 502; FIGS. 2-5).
Regarding Claim 5, Mower discloses wherein a signal used in the electrical current therapy includes a cathodal signal (see column 3, lines 63-65; “first and second phases of stimulation consist of an anodal pulse (first phase) followed by a cathodal pulse (second phase)”; also see cathodal stimulation 208, 308, 408, or 510; FIGS. 2-5).
Regarding Claim 6, Mower discloses wherein a signal used in the electrical current therapy includes a biphasic signal (see FIGS. 2-5; column 3, lines 38-39; for simultaneous biphasic stimulation, and/or for progressive biphasic stimulation’; column 6, lines 4-5 - “FIGS. 2 through 5 depict a range of biphasic stimulation protocols”).
Regarding claims 9 and 10, Mower teaches “The anodal phase preconditions the myocardium to accept the second phase” (see Abstract). Based on the rejections above under 35 USC 112(a) and 112(b), Mower therefore teaches the conditions necessary to cause the results recited in claims 9 and 10.
Regarding claim 22, Mower discloses applying anodal pulses and also teaches biphasic pacing pulses to the myocardial tissue to increase contractility of the myocardial tissue (see Figs. 2-4; also see column 5, lines 9-13, and column 6, lines 9-55) after administering the preconditioning electrical current therapy. It is noted that the pulses delivered by Mower will be repeatedly applied to the cardiac tissue (e.g., see the last line of claim 1 of Mower, which states “wherein the pacemaker repeatedly provides biphasic stimulation so long as fibrillation is detected“), therefore there will always be a next anodal and/or biphasic pulse that occurs after a first/initial pulse, therefore, Mower reads on this claim.
Regarding claim 23, it is noted that Mower teaches to provide anodal conditioning pulses to the myocardial tissue. Based on the rejections above under 35 USC 112(b), this is sufficient to produce the results as claimed, as there is no clear description as to what is considered “sufficient” other than the use an anodal pulse.
Regarding claim 25, Mower discloses determining the efficacy of the treatment by collecting new parameter values to determine whether further preconditioning electrical current therapy is required, and applying the further preconditioning electrical current therapy if the further electrical current therapy is required (e.g., see the last line of claim 1 of Mower, which states “wherein the pacemaker repeatedly provides biphasic stimulation so long as fibrillation is detected“).
Regarding claim 26, wherein the sensing step and the administering step occur at the same time in parallel, since Mower teaches that “The control circuit logic can activate the multiple site, biphasic ventricular stimulation upon the occurrence of A-V block in a patient … upon the direct … sensing of ventricular fibrillation. For example, direct sensing of ventricular fibrillation can be based on data from multiple ventricular sensing electrode” (see column 3, lines 46-48). Therefore, this teaches that the stimulation is provided instantaneously upon detection of the issue.
Regarding claim 32, Mower discloses pacing device configured to pace a heart of a patient configured and adapted to execute the method of claim 1 on myocardial tissue of the patient (see claim 1 of Mower).
Regarding claim 34, Mower teaches that “direct sensing of ventricular fibrillation can be based on data from multiple ventricular sensing electrodes” (see column 3, lines 46-48). Also, Mower teaches in the Abstract that “The invention also may be practiced with respect to atria.”
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 21, 24, 31, 35 are rejected under 35 U.S.C. 103 as being unpatentable over Mower in view of Pastore et al. (US Patent Pub. No. 2004/0054381).
Regarding claim 21, Mower teaches sensing rhythm and contraction (“direct sensing of ventricular fibrillation” in column 3, lines 46-47 and “size and/or presence of an R wave, rate of the electrogram deflections, or the probability density function (PDF) of the electrogram” in column 3, lines 50-52).
However, Mower does not teach sensing of membrane potential of the myocardial tissue.
Regarding claims 21 and 35, Pastore teaches a method and apparatus for assessing and treating myocardial wall stress (see Title). “The present invention relates to an apparatus and method for acutely assessing myocardial wall stress at a local site by measuring the action potential duration at the site during systole, referred to herein as an activation-recovery interval” (see paragraph 4). Paragraph 21 provides greater detail, with reference to Figure 1. Pastore teaches to pre-excite stressed site(s) (see paragraph 27).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to utilize the action potential detection scheme of Pastore within the system and methods of Mower in order to identify stressed sections of the heart muscle to provide multi-site pacing, which as stated in paragraphs 8-10 of Pastore would be helpful for patients with some degree of AV block, and Mower explicitly teaches that “the control circuit logic can activate the multiple site, biphasic ventricular stimulation upon the occurrence of A-V block in a patient known to be susceptible to multiple random ventricular reentrant foci, or upon the direct or indirect sensing of ventricular fibrillation” (see column 3, lines 41-44 of Mower).
Regarding claim 24, Pastore teaches that “Pre-excitation may also be applied to stressed regions of the myocardium that have been weakened by ischemia or other causes in order to prevent further dilation and/or promote healing” (see paragraph 27).
Regarding claim 31, Mower discloses applying anodal pulses and also teaches biphasic pacing pulses to the myocardial tissue to increase contractility of the myocardial tissue (see Figs. 2-4; also see column 5, lines 9-13, and column 6, lines 9-55) after administering the preconditioning electrical current therapy. It is noted that the pulses delivered by Mower will be repeatedly applied to the cardiac tissue (e.g., see the last line of claim 1 of Mower, which states “wherein the pacemaker repeatedly provides biphasic stimulation so long as fibrillation is detected“), therefore there will always be a next anodal and/or biphasic pulse that occurs after a first/initial pulse, therefore, Mower reads on this claim. However, Mower does not specifically indicate that the tissue is damaged. However, Pastore teaches that “Pre-excitation may also be applied to stressed regions of the myocardium that have been weakened by ischemia or other causes in order to prevent further dilation and/or promote healing” (see paragraph 27). Therefore, by their combination, the conditioning energy of Mower would be applied to such tissue areas as described by Pastore, when needed.
Claims 27-30, 33 and 36 are rejected under 35 U.S.C. 103 as being unpatentable over Mower in view of Stadler et al. (US Patent Pub. No. 2003/0083702).
Regarding claim 27, Mower teaches that comprising sensing rhythm and contraction (“indirect sensing can be based on any of various functional parameters, such as… size and/or presence of an R wave, rate of the electrogram deflections, or the probability density function (PDF) of the electrogram” in column 3, lines 50-52).
However, Mower does not explicitly mention the PQRS waveform.
Stadler teaches that “cardiac IMDs have traditionally employed capabilities of sensing the electrogram of the heart manifested by the cyclic PQRST waveform at one or more locations principally to detect the contraction of the atria as evidenced by a P-wave meeting P-wave detection criteria of an atrial sense amplifier and/or the contraction of the ventricles as evidenced by an R-wave meeting R-wave detection criteria of a ventricular sense amplifier. The timing of detected atrial and ventricular sense events is used to ascertain normal sinus rhythm or the presence of bradycardia, tachycardia or tachyarrhythmia in the monitoring and therapy delivery contexts” (see paragraph 4).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application that Mower’s disclosure of sensing the presence of an R-wave, or measuring the rate of an electrogram deflection would is a sensing of the PQRS waveform, simply specific sections of this waveform, as evidenced by Stadler’s statement that similar individual parameters of this waveform being sensed (i.e., P-wave detection and R-wave detection) are simply sensing an electrogram of this overall PQRS waveform at one (or more) locations.
It is additionally, noted that detecting a rate of deflection entails evaluation over time and also evaluating a trend of the electrogram, thereby reading on the claim.
Specifically with regard to claim 28, it is noted that this claim is the same as claim 1, except for adding that the sensing of the electrical parameter of the myocardial tissue is sensing in “a PQRS waveform”. Therefore, the rejection of claim 1 above is directly applicable to claim 28, and the addition of Stadler as described immediately above for claim 27 fills in the gaps of the rejection of claim 1.
Regarding claim 29, it is noted that Mower teaches to provide anodal conditioning pulses to the myocardial tissue. Based on the rejections above under 35 USC 112(b), this is sufficient to produce the results as claimed, as there is no clear description as to what is considered “sufficient” other than the use an anodal pulse.
Regarding claim 30, wherein the sensing step and the administering step occur at the same time in parallel, since Mower teaches that “The control circuit logic can activate the multiple site, biphasic ventricular stimulation upon the occurrence of A-V block in a patient … upon the direct … sensing of ventricular fibrillation. For example, direct sensing of ventricular fibrillation can be based on data from multiple ventricular sensing electrode” (see column 3, lines 46-48). Therefore, this teaches that the stimulation is provided instantaneously upon detection of the issue.
Regarding claim 33, Mower discloses pacing device configured to pace a heart of a patient configured and adapted to execute the method of claim 1 on myocardial tissue of the patient (see claim 1 of Mower).
Regarding claim 36, Mower teaches that “direct sensing of ventricular fibrillation can be based on data from multiple ventricular sensing electrodes” (see column 3, lines 46-48). Also, Mower teaches in the Abstract that “The invention also may be practiced with respect to atria.”
Claim 37 is rejected under 35 U.S.C. 103 as being unpatentable over Mower in view of Stadler and Pastore.
Mower in combination with Stadler is described above with respect to claim 28. However, while Mower teaches sensing rhythm and contraction (“direct sensing of ventricular fibrillation” in column 3, lines 46-47 and “size and/or presence of an R wave, rate of the electrogram deflections, or the probability density function (PDF) of the electrogram” in column 3, lines 50-52).
However, Mower does not teach sensing of membrane potential of the myocardial tissue.
Pastore teaches a method and apparatus for assessing and treating myocardial wall stress (see Title). “The present invention relates to an apparatus and method for acutely assessing myocardial wall stress at a local site by measuring the action potential duration at the site during systole, referred to herein as an activation-recovery interval” (see paragraph 4). Paragraph 21 provides greater detail, with reference to Figure 1. Pastore teaches to pre-excite stressed site(s) (see paragraph 27).
It would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to utilize the action potential detection scheme of Pastore within the system and methods of Mower in combination with Stadler in order to identify stressed sections of the heart muscle to provide multi-site pacing, which as stated in paragraphs 8-10 of Pastore would be helpful for patients with some degree of AV block, and Mower explicitly teaches that “the control circuit logic can activate the multiple site, biphasic ventricular stimulation upon the occurrence of A-V block in a patient known to be susceptible to multiple random ventricular reentrant foci, or upon the direct or indirect sensing of ventricular fibrillation” (see column 3, lines 41-44 of Mower).
Conclusion
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/JAMES KISH/ Primary Examiner, Art Unit 3792