|Numéro de publication||US20090149900 A1|
|Type de publication||Demande|
|Numéro de demande||US 12/371,153|
|Date de publication||11 juin 2009|
|Date de dépôt||13 févr. 2009|
|Date de priorité||11 avr. 2005|
|Autre référence de publication||EP1871460A1, EP2277583A2, EP2277583A3, EP2301623A2, EP2301623A3, US7499748, US8929990, US20060229677, US20110082537, US20150119790, WO2006110338A1|
|Numéro de publication||12371153, 371153, US 2009/0149900 A1, US 2009/149900 A1, US 20090149900 A1, US 20090149900A1, US 2009149900 A1, US 2009149900A1, US-A1-20090149900, US-A1-2009149900, US2009/0149900A1, US2009/149900A1, US20090149900 A1, US20090149900A1, US2009149900 A1, US2009149900A1|
|Inventeurs||Julia Moffitt, Imad Libbus|
|Cessionnaire d'origine||Julia Moffitt, Imad Libbus|
|Exporter la citation||BiBTeX, EndNote, RefMan|
|Citations de brevets (3), Référencé par (19), Classifications (18)|
|Liens externes: USPTO, Cession USPTO, Espacenet|
This application is a continuation of U.S. application Ser. No. 11/103,245, filed Apr. 11, 2005, which is hereby incorporated by reference in its entirety.
This patent document pertains generally to neural stimulation devices and methods, and more particularly, but not by way of limitation, to transvascular neural stimulation devices and methods.
The automatic nervous system (ANS) regulates “involuntary” organs. The ANS includes the sympathetic nervous system and the parasympathetic nervous system. The sympathetic nervous system is affiliated with stress and the “fight or flight response” to emergencies. The parasympathetic nervous system is affiliated with relaxation and the “rest and digest response.” The ANS maintains normal internal function and works with the somatic nervous system. Autonomic balance reflects the relationship between parasympathetic and sympathetic activity. A change in autonomic balance is reflected in changes in heart rate, heart rhythm, contractility, remodeling, inflammation and blood pressure. Changes in autonomic balance can also be seen in other physiological changes, such as changes in abdominal pain, appetite, stamina, emotions, personality, muscle tone, sleep, and allergies, for example.
Reduced autonomic balance (increase in sympathetic and decrease in parasympathetic cardiac tone) during heart failure has been shown to be associated with left ventricular dysfunction and increased mortality. Research also indicates that increasing parasympathetic tone and reducing sympathetic tone may protect the myocardium from further remodeling and predisposition to fatal arrhythmias following myocardial infarction. Direct stimulation of the vagal parasympathetic fibers has been shown to reduce heart rate via the sympathetic nervous system. In addition, some research indicates that chronic stimulation of the vagus nerve may be of protective myocardial benefit following cardiac ischemic insult.
Some target areas can be difficult to stimulate or isolate. For example, it may be difficult to stimulate a nerve that is located deep in the body or behind an organ. Improved neural stimulation devices are needed.
Various aspects of the present subject matter relate to an implantable apparatus. In an example, an apparatus is configured to transvascularly stimulate a nerve trunk through a blood vessel. The apparatus includes an expandable electrode that is chronically implantable in a blood vessel proximate a nerve trunk. The expandable electrode is configured to abut an area of the vessel wall along a length of the vessel. An electrical lead is coupled to the expandable electrode. An implantable pulse generator is coupled to the lead and configured to deliver an electrical stimulation signal to the electrode through the lead.
Various aspects of the present subject matter relate to a method. In an example method, an electrical signal is delivered from an implanted medical device to an electrode chronically implanted in a blood vessel proximate a nerve trunk to transvascularly deliver neural stimulation from the electrode to the nerve trunk.
This Summary is an overview of some of the teachings of the present application and not intended to be an exclusive or exhaustive treatment of the present subject matter. Further details about the present subject matter are found in the detailed description and appended claims. Other aspects will be apparent to persons skilled in the art upon reading and understanding the following detailed description and viewing the drawings that form a part thereof, each of which are not to be taken in a limiting sense. The scope of the present invention is defined by the appended claims and their equivalents.
The following detailed description of the present subject matter refers to the accompanying drawings which show, by way of illustration, specific aspects and embodiments in which the present subject matter may be practiced. These embodiments are described in sufficient detail to enable those skilled in the art to practice the present subject matter. Other embodiments may be utilized and structural, logical, and electrical changes may be made without departing from the scope of the present subject matter. References to “an”, “one”, or “various” embodiments in this disclosure are not necessarily to the same embodiment, and such references contemplate more than one embodiment. Additionally, the identified embodiments are not necessarily exclusive of each other, as some embodiments may be able to be combined with other embodiments. The following detailed description is, therefore, not to be taken in a limiting sense, and the scope is defined only by the appended claims, along with the full scope of legal equivalents to which such claims are entitled.
Referring now to
Referring again to
In an example, the entire surface area of the expandable electrode that touches the blood vessel wall is conductive. In an alternative example, at least a part of the surface area of the electrode is non-conductive. For example, an electrode can be formed and positioned to deliver stimulation to through a conductive part of the electrode to a portion 330 (
In an example, the expandable electrode is covered with a drug, such as a drug that prevents occlusion, or a drug that reduces inflammation of the blood vessel near the electrode.
The expandable electrode 305 is coupled to a power source that delivers an electrical stimulation. In
The electrode may be implanted in various locations in the body, including a variety of locations near a trunk or branch of a sympathetic or parasympathetic nerve system.
Referring again to the example shown in
In another example, a cardiac fat pad is transvascularly stimulated by an implanted electrode.
Referring now to
In other examples, nerve trunks innervating other organs, such as the lungs or kidneys are transvascularly stimulated. In an example, an expandable electrode such as a stent is implanted in a blood vessel proximate a nerve or nerve trunk that innervates the lungs or kidneys.
Referring again to the example shown in
Neural stimulation therapies can be used to treat one or more of a variety of conditions, including but not limited to arrhythmias, heart failure, hypertension, syncope, or orthostatic intolerance. In an example, an efferent peripheral nerve is transvascularly stimulated by an implanted expandable electrode. In another example, an afferent peripheral nerve is stimulated.
In an example, electrical stimulation is transvascularly delivered to a parasympathetic nerve to reduce chronotropic, ionotropic, and dromotropic responses in the heart. In a therapy example, electrical stimulation is transvascularly delivered to a parasympathetic nerve trunk during heart failure. In another therapy example, electrical stimulation is transvascularly delivered to a parasympathetic nerve trunk following a myocardial infarction to protect against arrhythmias or prevent cardiac remodeling.
Transvascular stimulation of a vagus nerve trunk is used in a number of therapies. In an example, vagal nerve stimulation simultaneously increases parasympathetic tone and decreases sympathetic myocardial tone. In an example, a vagus nerve trunk is transvascularly stimulated following cardiac ischemic insult. Increased sympathetic nervous activity following ischemia often results in increased exposure of the myocardium to epinephrine and norepinephrine. These catecholamines activate intracellular pathways within the myocytes, which lead to myocardial death and fibrosis. This effect is inhibited by stimulation of the parasympathetic nerves, such as vagus nerves. In an example, vagal stimulation from the SVC lowers heart rate, overall blood pressure, and left ventricular pressure. Stimulation of the vagal cardiac nerves following myocardial infarction, or in heart failure patients, can be beneficial in preventing further remodeling and arrhythmogenesis.
In other examples, transvascular neural stimulation is used to treat other conditions such as hypertrophic cardiomyopathy (HCM) or neurogenic hypertension, where an increase parasympathetic cardiac tone and reduction in sympathetic cardiac tone is desired. In another example, a bradycardia condition is treated by transvascularly stimulating a sympathetic nerve trunk. In another example, the ionotropic state of the heart is increased by transvascularly stimulating a sympathetic nerve trunk.
Referring now to
In an example, transvascularly stimulating a parasympathetic nerve inhibits cardiac remodeling or delivers an antiarrhythmia therapy following a myocardial infarction. In another example, transvascularly stimulating a sympathetic nerve delivers an antibradycardia therapy.
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|Classification aux États-Unis||607/3, 607/116, 607/9|
|Classification coopérative||A61N1/362, A61N1/37288, A61N1/3611, A61N1/37217, A61M31/00, A61N1/056, A61N1/36053, A61N1/0558, A61N1/3627, A61N1/36114, A61N1/36117|
|Classification européenne||A61N1/36Z, A61N1/05N, A61N1/36|