WO2007021258A1 - Stimulateur cardiaque et procede de stimulation pour traiter l'hypertension - Google Patents

Stimulateur cardiaque et procede de stimulation pour traiter l'hypertension Download PDF

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Publication number
WO2007021258A1
WO2007021258A1 PCT/US2005/028415 US2005028415W WO2007021258A1 WO 2007021258 A1 WO2007021258 A1 WO 2007021258A1 US 2005028415 W US2005028415 W US 2005028415W WO 2007021258 A1 WO2007021258 A1 WO 2007021258A1
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WIPO (PCT)
Prior art keywords
heart
lead
blood pressure
placing
pacing
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PCT/US2005/028415
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English (en)
Inventor
Robert S. Schwartz
Robert Van Tassel
Original Assignee
Schwartz Robert S
Robert Van Tassel
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Publication date
Application filed by Schwartz Robert S, Robert Van Tassel filed Critical Schwartz Robert S
Priority to PCT/US2005/028415 priority Critical patent/WO2007021258A1/fr
Publication of WO2007021258A1 publication Critical patent/WO2007021258A1/fr

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Classifications

    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/362—Heart stimulators
    • A61N1/3627—Heart stimulators for treating a mechanical deficiency of the heart, e.g. congestive heart failure or cardiomyopathy
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/362—Heart stimulators
    • A61N1/365—Heart stimulators controlled by a physiological parameter, e.g. heart potential
    • A61N1/36514—Heart stimulators controlled by a physiological parameter, e.g. heart potential controlled by a physiological quantity other than heart potential, e.g. blood pressure
    • A61N1/36564—Heart stimulators controlled by a physiological parameter, e.g. heart potential controlled by a physiological quantity other than heart potential, e.g. blood pressure controlled by blood pressure
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/362—Heart stimulators
    • A61N1/365—Heart stimulators controlled by a physiological parameter, e.g. heart potential
    • A61N1/368—Heart stimulators controlled by a physiological parameter, e.g. heart potential comprising more than one electrode co-operating with different heart regions
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/362—Heart stimulators
    • A61N1/365—Heart stimulators controlled by a physiological parameter, e.g. heart potential
    • A61N1/368—Heart stimulators controlled by a physiological parameter, e.g. heart potential comprising more than one electrode co-operating with different heart regions
    • A61N1/3684—Heart stimulators controlled by a physiological parameter, e.g. heart potential comprising more than one electrode co-operating with different heart regions for stimulating the heart at multiple sites of the ventricle or the atrium
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/362—Heart stimulators
    • A61N1/365—Heart stimulators controlled by a physiological parameter, e.g. heart potential
    • A61N1/368—Heart stimulators controlled by a physiological parameter, e.g. heart potential comprising more than one electrode co-operating with different heart regions
    • A61N1/3684—Heart stimulators controlled by a physiological parameter, e.g. heart potential comprising more than one electrode co-operating with different heart regions for stimulating the heart at multiple sites of the ventricle or the atrium
    • A61N1/36842—Multi-site stimulation in the same chamber
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/362—Heart stimulators
    • A61N1/365—Heart stimulators controlled by a physiological parameter, e.g. heart potential
    • A61N1/368—Heart stimulators controlled by a physiological parameter, e.g. heart potential comprising more than one electrode co-operating with different heart regions
    • A61N1/3684—Heart stimulators controlled by a physiological parameter, e.g. heart potential comprising more than one electrode co-operating with different heart regions for stimulating the heart at multiple sites of the ventricle or the atrium
    • A61N1/36843—Bi-ventricular stimulation

Definitions

  • the present invention relates generally to stimulating or pacing the human heart and more particularly to a device and method for treating hypertension through a periodic or episodic electrical stimulation of selected portions of the heart at selected times.
  • the device of present invention is a heart muscle stimulator for supplying an electrical stimulation therapy to anatomic structures of the heart for altering blood pressure.
  • the device and method can be used to treat hypertension and other disorders.
  • the invention is disclosed in the context of treating high blood pressure with or without congestive heart failure (CHF).
  • CHF congestive heart failure
  • Hypertension is a very common medical condition, with increasing prevalence with older age groups.
  • the most common form of the disorder is termed 'essential hypertension', and it is a condition that may result from a mismatch between the heart output and the resistance of the major blood vessels.
  • Untreated or poorly controlled hypertension can result in CHF.
  • CHF is a common disease with a large number of clinical associations.
  • the invention is expected to be a significant advance in the treatment of hypertension and CHF, and other medical complications of hypertension including but not limited to kidney failure, atherosclerosis and vascular disease, heart attack, and stroke.
  • the method and device can be used to treat other diseases and the selected indications that are used as examples and should be considered illustrative and not limiting.
  • a CHF patient undergoing chronic resynchronization therapy will be taking appropriate drugs such as ACE inhibitors, Angiotensin receptor blockers, diuretics, beta blockers, digoxin, other inotropes, and antiarrhythmics.
  • appropriate drugs such as ACE inhibitors, Angiotensin receptor blockers, diuretics, beta blockers, digoxin, other inotropes, and antiarrhythmics.
  • device based therapies include pacemaker type stimulators for non-cardiac structures for treating hypertension as taught by U.S. Patent 6,073,048 to Kieval which discloses a device that delivers stimulation to arterial baroreceptors to lower systemic blood pressure indirectly through neurogenically mediated pathways.
  • the present invention attempts to induce a controlled and temporary "lack of coordination" between mechanical and electrical activities of parts of the heart. This will lower blood pressure (BP) through changing the energy and power coupling between the heart and the major blood vessels.
  • BP blood pressure
  • the present invention acts to promote or cause myocardial dyssynchronization which has the beneficial clinical effect of reducing observed blood pressure through alteration of the activation profile of the heart in both spatial and temporal dimensions.
  • This therapy also alters the resulting ejection profile as observed in the time domain or alternatively spatial across the anatomic structures of the heart. The result of this therapy is to reduce pretreatment blood pressure to a clinically beneficial post treatment value.
  • the preferred stimulation regime occurs episodically or periodically and it may be invoked on demand or on a chronological basis.
  • the therapy is applied for a relatively short time to reduce blood pressure and then the therapy stops and the pacing device reverts to its normal pacing regime. It is expected that the pacing therapy when coupled to systemic administration of drugs will "amplify" the effect of the drug, so that less drug need be administered. Data is presented to support the therapy in conjunction with any of several known pacing lead configurations with the dual ventricular configuration being preferred.
  • Figure IA is a VOO pacing configuration used in an experiment
  • Figure IB is a data graph of blood pressure reduction at three pacing rates as measured in connection with an experiment
  • Figure 2A is a VOO pacing configuration used in an experiment
  • Figure 2B is a data graph of blood pressure reduction at three pacing rates
  • Figure 3A is a DOO pacing configuration used in an experiment
  • Figure 3B is a data graph of blood pressure reduction at three pacing rates
  • Figure 4A is a biventricular DOO pacing configuration used in an experiment
  • Figure 4B is a data graph of blood pressure reduction at three pacing rates
  • Figure 5 A is a DOO pacing configuration used in an experiment
  • Figure 5B is a data graph of blood pressure reduction at three pacing rates
  • Figure 6A is a multisite VOO pacing configuration used in an experiment
  • Figure 6B is a data graph of blood pressure reduction at three pacing rates
  • Figure 7 A is a multisite VOO pacing configuration used in an experiment
  • Figure 7B is a data graph of blood pressure reduction at three pacing rates
  • FIG. 8 is a diagram showing an exemplary and illustrative heart stimulator capable of carrying out the invention.
  • Figure 9 is a diagram comparing drug therapy with the inventive therapy.
  • Figure 10 is a diagram showing how the inventive stimulation can be combined into a hybrid stimulator /drug therapy; and, Figure 11 is a diagram summarizing the representative pacing configurations. Description Of the Invention Definitions
  • Dyssynchrony is inducing a cardiac ejection cycle where the normal spatial contraction sequence is altered, either within a chamber or across multiple cardiac chambers. It may also refer to changes in contraction within a chamber or across multiple chambers in time. This means that the ejection of blood may for example be delayed, or prolonged.
  • Hypertension is defined as blood pressure systolic greater than 130 mmHg and/or diastolic greater than 90 mmHg.
  • Altered Contractility Profile is any disturbance of cardiac contraction that changes the power or energy of the heart. It is best measured by Emax from the end systolic pressure-volume loop relationship across multiple different loading conditions.
  • Pre Treatment Contractility Profile is the spatial and temporal contraction of individual and combined heart chambers prior to treatment. Contractility is best measured by Emax from the end systolic pressure-volume loop relationship across multiple different loading conditions.
  • Altered Ejection Profile is any disturbance of cardiac contraction, either within a chamber or across multiple chambers, that alters the resulting blood pressure as a bolus of blood is ejected from the heart.
  • Pre Treatment Ejection Profile is the spatial and temporal contraction of individual and combined heart chambers prior to treatment.
  • Congestive heart failure is the name given to a spectrum of clinical symptoms. Usually the heart is enlarged and has an inability to sufficiently supply the body's blood pressure and flow needs without generating abnormal intracardiac blood pressures and /or flows. Overview
  • the inventive method is the intentional reduction of a patient's blood pressure though a cardiac stimulation regime that modifies the synchrony between or within the chambers of the heart.
  • pacing level stimuli are applied to the heart trough fixed leads of conventional design. The location of the leads or the timing of the stimuli is selected to alter the ejection profile or the contractility profile of that heartbeat. This modification or modulation of synchrony lowers blood pressure.
  • the preferred device is intended to deliver pacing level stimuli to the heart muscle to treat hypertension.
  • the proposed and preferred device will monitor blood pressure with an indwelling blood pressure sensor and invoke a modulated synchrony therapy that results in blood pressure reduction.
  • Experimental data and computer modeling verify that this therapy may be used alone or in conjunction with drug therapy.
  • a blood pressure (BP) transducer will be exposed to systolic, diastolic, and indeed continuous blood pressures and the device may compute a mean pressure for a beat or several beats of the heart.
  • the BP data may also be used to compute dP/dt and other BP measures.
  • hypertension is taken as a fixed BP threshold. However this threshold may vary as a function of time of day or measured activity. In essence the threshold used to invoke the therapy may itself vary.
  • the modified therapy may be invoked on demand in response to a BP threshold.
  • the therapy may be provided on a periodic (circadian) basis, or even on a beat-by-beat interval, for example skipping one or more beats. It may also be based on the coincidence of a threshold BP occurring simultaneously with measured activity.
  • the therapy may be initiated by the patient or the physician on an acute basis. It is expected that the therapy will not be continuous, but it will be chronic, throughout the lifetime of a hypertensive patient.
  • ACE inhibitors include ACE inhibitors, Angiotensin Receptor blockers (ARB blockers), diuretics, beta receptor blockers, alpha receptor blockers, vasodilators, calcium channel blockers, centrally mediated antihypertensives such as methyl-DOPA, and others.
  • ARB blockers Angiotensin Receptor blockers
  • diuretics include beta receptor blockers, alpha receptor blockers, vasodilators, calcium channel blockers, centrally mediated antihypertensives such as methyl-DOPA, and others.
  • beta receptor blockers include beta receptor blockers, alpha receptor blockers, vasodilators, calcium channel blockers, centrally mediated antihypertensives such as methyl-DOPA, and others.
  • the proposed therapy will enhance the antihypertensive effects of these drugs, allowing them to work more effectively.
  • the therapy can be adjusted to modulate the hypertensive effects of these drugs.
  • blood pressure may be reduced by the administration of a drug that widens the QRS complex by dispersing the electrical-myocardial conduction and contraction that may be additive with the therapy.
  • Candidate drugs include Tricyclic antidepressants, neuroleptics lithium procanimide lidocaine and derivatives, Class I antiarrhyythmics, salbutamol, flecainide, sertindole, propofenone, amiodarone and others.
  • Figure 1 through Figure 7 are intended to show stimulation configurations that can be used to carry out or promote dyssynchrony between and within cardiac chambers to control blood pressure.
  • Panel A of each figure shows the lead configuration and panel B shows the measured blood pressure reduction from a control measurement made in the same animal in normal sinus rhythm under otherwise similar conditions.
  • Each panel of the data is taken at progressively higher pacing rates to capture the heart.
  • the pre-treatment activation profile or pret-treatment contractility profile corresponds to the BP in sinus rhythm.
  • the pre-treatment ejection profile corresponds to the BP in sinus rhythm.
  • Figure IA shows a lead 10 located in the apex of the RV coupled to a pacemaker 50 (PM). Capturing the heart at pacing rates of 90, 100, and 110 BPM results in the data shows in the graph of Figure IB. In this figure a reduction of BP by 16 percent is shown with no observable rate dependence.
  • Figure 2A shows a lead 12 located the apex of the LV with a WI pacing configuration operating effectively in a VOO modality with pacemaker 50.
  • the several pacing rates seen the graph of Figure 2B show a -17% BP reduction without rate dependence.
  • Figure 3A shows a DOO modality where the right atrium is paced by lead 14 at a rate above sinus rhythm by pacemaker 50.
  • the LV is paced through lead 12 after a variously short A-V delay preventing normal sinus conduction and contractility.
  • Figure 3B shows that a -8%
  • Figure 4A shows a biventricular modality with VOO pacing of both the RV and the LV through leads 10 and 12. A progressive change was made to the RV-LV pacing interval. The RR interval was above sinus rhythm and scanned as well. No discernable dependence on rate was observed however a large -20% BP reduction was observed as seen in Figure 4B.
  • Figure 5A shows a simple DOO pacing regime carried out in
  • FIG. 5B shows a lead 10 in the LV at a first position and a second lead 12 located in the same chamber along the septum wall.
  • the Lva -Lvb time interval was varied and Figure 6B shows the -17% BP reduction achieved with this protocol.
  • Figure 7A shows an intraventricular anterior-inferior placement of leads 10 and 12. Burst pacing to 300BPM showed a BP reduction of
  • Figure 9 reflects additional computer modeling work was performed to evaluate the effect of modified synchrony pacing or stimulation protocols in comparison to a more conventional drug therapy.
  • Figure 11 is a chart that summarizes the percent reduction based upon pacing configurations used in the experiment.
  • Figure 10 reflects additional computer experimenting showing the value of a combined drug and stimulation therapy.
  • the percent change in BP reduction as a function of pacing increases dramatically. It is expected that combination therapy will be effective as well where the device therapy takes place in a patient with a "background" dose of the antihypertensive drug.
  • Figures 1 through Figure 7 illustrate that any number of conventional stimulation regimes or therapies can be invoked to modify synchrony within or between the heart chambers.
  • the best therapy may vary from patient to patient and some experimentation will be required to tailor a device for a patient. Based on the experiment it appears that the greatest reduction in BP is achieved with RV-LV dyssynchrony stimulation. As seen in Figure 7 A and 7B.
  • Figure 9 shows the relationship between the inventive cardiac stimulation and more traditional pharmacology on the control of blood pressure.
  • Line 100 is the identity line corresponding to no therapy and the pre treatment and post treatment blood pressure is the "same".
  • the pharmacology line 110 shows the control of blood pressure by a drug alone. For example, a patient having a pre treatment pressure of 200 mm of Hg is reduced to about 150 mm of Hg with a hypothetical drug. The linearity of the response however shows that the patient with an acceptable pretreatment BP of 100 mm of Hg would experience a drop to an undesirable BP of approximately 80 mm of Hg with the same drug.
  • This treatment line shows that the systemic and chronic treatment of BP with drug can have an undesirable but concomitant effect on BP.
  • the device therapy is seen on line 120 which offers a BP reduction therapy which is modest and proportional to the need for therapy.
  • the highly nonlinear behaviors of BP reduction with the inventive stimulation regime is of benefit to the patient since it brings a greater percent reduction benefit at the higher more pathologic BP values.
  • the BP reduction occurs quickly with the onset of the stimulation regime and diminishes slowly when the stimulation is discontinued. It is preferred to have the therapy invoked when a threshold is exceeded and then continue for a fixed period of time for example 1 hour then the therapy stops. Activity monitors or real time clocks may be used as well.
  • FIG 8. A representative but not limiting embodiment of a pacing device 50 to carry out the invention is shown in Figure 8.
  • the drawing shows a conventional heart stimulator capable of delivering heart stimulation to leads implanted at various locations in the heart.
  • a connection block 52 allows selection of lead configurations as set forth in Figures 1 through 7. Typically only a subset of the leads shown in the figure are required for carrying out the therapy. Both sensing and pacing can occur at each lead location in the heart. All rates and timing intervals are available in the heart stimulator.
  • a blood pressure sensor is located on a lead. Typical locations are in the RV or remotely in other regions of the vasculature.
  • left ventricular cavity pressure can be measured with a device placed in the right ventricle that penetrates the ventricular septum and emerges into the left ventricular cavity.
  • This device may also have a pressure transducer that lies within the septal wall, and measures intra-septal force as a surrogate for contractility.
  • a blood pressure transducer 54 is located on either a separate blood pressure lead or as a separate sensor 56 on a ventricular lead 10. It is important to note that other blood pressure transduction devices may be incorporated into the device. Although BP measurement is preferred other BP proxy measurements may be substituted within the scope of the invention.
  • a blood pressure transducer is provided to measure blood pressure to determine the existence of hypertension.
  • the blood pressure monitoring transducer may be located on a lead for example the RV ventricular lead or a separate BP lead may be provided.
  • a BP algorithm will be developed which provides a BP threshold.
  • the threshold may vary with time of day or patient activity. Once detected the stimulator will delivery a therapy for a treatment time. It is expected that the treatment time will be selected by the physician and it may be terminated automatically or it may time out. This episodic therapy may be used alone or in conjunction with a drug regime.
  • Proposed Mechanism of Action It is believed that the present invention induces a controlled and temporary "inefficiency" in the mechanical function of the heart. This inefficiency is produced and controlled by altering either or all, the normal pacing rate, the normal electrical path of ionic gradient flow through the heart, or dyssynchronization between the right and left ventricles.
  • initiation of the heart beat occurs in the sinoatrial node that resides towards the epicardial surface of the right atrium close to the junction of the superior vena cava.
  • Nodal cells have a constantly changing resting membrane potential measured in respect to the voltage difference between the outside and inside of the cell.
  • there are sodium and calcium channels that increase pacing rate by decreasing their resistance to ion flow from the outside to inside of the cell based on their diffusion gradients.
  • Contractile cells differ from pacemaker cells in that they maintain a stable resting membrane potential by allowing a controlled amount of potassium ions to leave the cell, determined by the membrane potential. They also differ in that when they are confronted with either a positively charged depolarization wavefront or an artificially induced electrical stimulus, a sodium channel, instead of a calcium channel, is activated and the cell becomes depolarized.
  • the depolarization in a contractile muscle cell then allows calcium ions to be release intracellularly from the sarcoplasmic reticulum and a cell contraction occurs.
  • the depolarization wavefront of positive charges reaches the atrioventricular node, those cells become depolarized and the unidirectional wavefront continues down the "bundle of his" to the apex of the ventricles.
  • Purkinje fibers rapidly conduct this depolarization wavefront away from the apex and into the muscle cells of the ventricles leading towards the base of the heart.
  • the natural pathway of electrical conduction from the apex towards the base also results in a slight spiraling pathway. This allows the ventricular muscle to effectively and efficiently "wring" out blood from the chambers.
  • the present invention allows for an artificial activation of the ventricular multidirectional depolarization wavefront. If the electrical stimulation leads are placed in the apex of the ventricles, a close approximation of the natural pathway of electrical-mechanical coupling occurs. If the pacing rate however is overdriven higher than the normal pacing rate, there will be less time for filling of blood into the chambers driven by the venous side filling pressure. In accordance with Starling's Law, less blood filling the chamber results in less stretch on the actin and myosin contractile filaments, and therefore less contractile force developed to eject blood from the chambers. Less ejection volume and ventricular pressure consequently results in less systemic blood pressure developed.
  • This invention also allows for de-synchronizing the right and left ventricular chambers.
  • the stimulation leads may be placed in one or both of the ventricular apices and stimulated in a fashion that allows one chamber to contract prior to the other. Because the right ventricle anatomically wraps around the left ventricle and produces a chamber containing part of the left ventricle wall, a dyssynchronous contraction between the right and left chambers results in an inefficiency in mechanical function and resultant ejection of blood, initially from the right ventricle that results in less filling in the left ventricle and less ejection and lowered systemic blood pressure.
  • Another aspect to this invention is the deliberate activation of single or multiple pacing sites in the ventricle (s) at locations other than the apex.

Abstract

La présente invention concerne un procédé qui consiste à appliquer une stimulation électrique périodique au muscle cardiaque afin de modifier le profil d'éjection du coeur, ce qui permet de réduire la pression artérielle observée du patient. La méthode thérapeutique décrite dans cette invention peut être mise en oeuvre au moyen d'un capteur de pression artérielle implantable associé à un dispositif de type stimulateur cardiaque.
PCT/US2005/028415 2005-08-11 2005-08-11 Stimulateur cardiaque et procede de stimulation pour traiter l'hypertension WO2007021258A1 (fr)

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US8086315B2 (en) 2004-02-12 2011-12-27 Asap Medical, Inc. Cardiac stimulation apparatus and method for the control of hypertension
US9008769B2 (en) 2012-12-21 2015-04-14 Backbeat Medical, Inc. Methods and systems for lowering blood pressure through reduction of ventricle filling
US9370662B2 (en) 2013-12-19 2016-06-21 Backbeat Medical, Inc. Methods and systems for controlling blood pressure by controlling atrial pressure
US9370661B2 (en) 2008-09-08 2016-06-21 Backbeat Medical, Inc. Methods and apparatus to stimulate heart atria
US9427586B2 (en) 2006-09-25 2016-08-30 Backbeat Medical, Inc. Methods and apparatus to stimulate heart atria
US9687636B2 (en) 2005-03-02 2017-06-27 Backbeat Medical, Inc. Methods and apparatus to increase secretion of endogenous naturetic hormones
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US10485658B2 (en) 2016-04-22 2019-11-26 Backbeat Medical, Inc. Methods and systems for controlling blood pressure
US11969598B2 (en) 2022-08-09 2024-04-30 Backbeat Medical, Llc Methods and systems for controlling blood pressure

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US11406829B2 (en) 2004-02-12 2022-08-09 Backbeat Medical, Llc Cardiac stimulation apparatus and method for the control of hypertension
US8428729B2 (en) 2004-02-12 2013-04-23 Backbeat Medical, Inc. Cardiac stimulation apparatus and method for the control of hypertension
US10232183B2 (en) 2004-02-12 2019-03-19 Backbeat Medical, Inc. Cardiac stimulation apparatus and method for the control of hypertension
US9320903B2 (en) 2004-02-12 2016-04-26 Backbeat Medical, Inc. Cardiac stimulation apparatus and method for the control of hypertension
US8086315B2 (en) 2004-02-12 2011-12-27 Asap Medical, Inc. Cardiac stimulation apparatus and method for the control of hypertension
US11577059B2 (en) 2005-03-02 2023-02-14 Backbeat Medical, Llc Methods and apparatus to increase secretion of endogenous naturetic hormones
US9687636B2 (en) 2005-03-02 2017-06-27 Backbeat Medical, Inc. Methods and apparatus to increase secretion of endogenous naturetic hormones
US10369333B2 (en) 2005-03-02 2019-08-06 Backbeat Medical, Inc. Methods and apparatus to increase secretion of endogenous naturetic hormones
US9427586B2 (en) 2006-09-25 2016-08-30 Backbeat Medical, Inc. Methods and apparatus to stimulate heart atria
US11529520B2 (en) 2006-09-25 2022-12-20 Backbeat Medical, Llc Methods and apparatus to stimulate heart atria
US10596380B2 (en) 2006-09-25 2020-03-24 Backbeat Medical, Inc. Methods and apparatus to stimulate heart atria
US9370661B2 (en) 2008-09-08 2016-06-21 Backbeat Medical, Inc. Methods and apparatus to stimulate heart atria
US10252060B2 (en) 2008-09-08 2019-04-09 Backbeat Medical, Inc. Methods and apparatus to stimulate the heart
US9731136B2 (en) 2008-09-08 2017-08-15 Backbeat Medical, Inc. Methods and apparatus to stimulate the heart
US11083894B2 (en) 2008-09-08 2021-08-10 Backbeat Medical, Llc Methods and apparatus to stimulate the heart
US11759639B2 (en) 2008-09-08 2023-09-19 Backbeat Medical, Llc Methods and apparatus to stimulate the heart
US9656086B2 (en) 2012-12-21 2017-05-23 Backbeat Medical, Inc. Methods and systems for lowering blood pressure through reduction of ventricle filling
US9937351B2 (en) 2012-12-21 2018-04-10 Backbeat Medical, Inc. Methods and systems for lowering blood pressure through reduction of ventricle filling
AU2014367229B2 (en) * 2012-12-21 2019-04-04 Backbeat Medical, Llc Methods and systems for controlling blood pressure by controlling atrial pressure
US9008769B2 (en) 2012-12-21 2015-04-14 Backbeat Medical, Inc. Methods and systems for lowering blood pressure through reduction of ventricle filling
US10071250B2 (en) 2012-12-21 2018-09-11 Backbeat Medical, Inc. Methods and systems for lowering blood pressure through reduction of ventricle filling
US10441794B2 (en) 2012-12-21 2019-10-15 Backbeat Medical, Inc. Methods and systems for lowering blood pressure through reduction of ventricle filling
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