Patent Application
20110093026
This document relates generally to implantable medical devices and particularly to an implantable cardiorenal stimulation system providing for electrical stimulation modulating cardiac and renal functions.
The heart is the center of a person's circulatory system. It includes an electromechanical system performing two major pumping functions. The left side of the heart draws oxygenated blood from the lungs and pumps it to the organs of the body to supply their metabolic needs for oxygen. The right side of the heart draws deoxygenated blood from the body organs and pumps it to the lungs where the blood gets oxygenated. These pumping functions result from contractions of the myocardium (cardiac muscles). In a normal heart, the sinoatrial (SA) node, the heart's natural pacemaker, generates electrical impulses, called action potentials, that propagate through an electrical conduction system to various regions of the heart and excite the myocardial tissues of these regions. Coordinated delays in the propagations of the action potentials in a normal electrical conduction system cause the various portions of the heart to contract in synchrony and result in efficient pumping function.
A blocked or otherwise damaged electrical conduction system causes irregular contractions of the myocardium, a condition generally known as arrhythmia. Arrhythmia reduces the heart's pumping efficiency and hence diminishes the blood flow to the body. A deteriorated myocardium has decreased contractility, also resulting in diminished blood flow. A heart failure patient usually suffers from both a damaged electrical conduction system and a deteriorated myocardium. The diminished blood flow results in insufficient blood supply to various body organs, preventing them from functioning properly and causing various symptoms. For example, in a patient suffering from acute worsening of heart failure, an insufficient blood supply to the kidneys results in avid salt and water retention and edema in the lungs and peripheral parts of the body, a condition referred to as decompensation. Acute decompensated heart failure is a significant cause for hospitalization. Reportedly, about 25-45% of patients with compensated heart failure exhibit combined cardiac and renal dysfunction, known as cardiorenal syndrome, which is a strong risk factor for morbidity and mortality. Because acute decompensated heart failure progresses rapidly after onset, quick treatment is required upon early indications. Thus, there is a need for an efficient method and system for prompt treatment of decompensation in a heart failure patient.
An implantable cardiorenal stimulator controls delivery of cardiorenal stimulation using a detected level of water retention in a patient's body. The cardiorenal stimulation includes delivering renal electrical stimulation pulses to promote diuresis and/or natriuresis and delivering cardiac electrical stimulation pulses to enhance the diuretic and/or natriuretic effects of the renal electrical stimulation pulses.
In one embodiment, an implantable cardiorenal stimulator includes a sensing circuit, a decompensation detector, a cardiac stimulation circuit, a renal stimulation circuit, and a stimulation control circuit. The sensing circuit senses one or more physiological signals. The decompensation detector detects a level of water retention in the patient's body using the one or more physiological signals and produces a decompensation signal indicating the detected level of water retention. The cardiac stimulation circuit delivers cardiac stimulation pulses modulating cardiovascular functions. The renal stimulation circuit delivers renal stimulation pulses modulating renal functions. The stimulation control circuit controls the delivery of the cardiac stimulation pulses and the renal stimulation pulses according to a cardiorenal stimulation mode using the decompensation signal.
In one embodiment, a method for operating an implantable cardiorenal stimulator is provided. One or more physiological signals are sensed using the implantable cardiorenal stimulator. A decompensation signal indicating a level of water retention in the patient is produced using the one or more physiological signals. Delivery of cardiac stimulation pulses modulating cardiovascular functions and renal stimulation pulses modulating renal functions is controlled according to a cardiorenal stimulation mode using the decompensation signal. The cardiac stimulation pulses and the renal stimulation pulses are delivered from the implantable cardiorenal stimulator.
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 of the invention 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. The scope of the present invention is defined by the appended claims and their legal equivalents.
The drawings illustrate generally, by way of example, various embodiments discussed in the present document. The drawings are for illustrative purposes only and may not be to scale.
In the following detailed description, reference is made to the accompanying drawings which form a part hereof; and in which is shown by way of illustration specific embodiments in which the invention may be practiced. These embodiments are described in sufficient detail to enable those skilled in the art to practice the invention, and it is to be understood that the embodiments may be combined, or that other embodiments may be utilized and that structural, logical and electrical changes may be made without departing from the spirit and scope of the present invention. The following detailed description provides examples, and the scope of the present invention is defined by the appended claims and their legal equivalents.
It should be noted that 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.
This document discusses, among other things, a system including an implantable cardiorenal stimulator and an implantable lead system for cardiorenal electrical stimulation. The system detects physiological changes indicative of worsening heart failure in a patient and provides prompt intervention to treat the patient, with the potential of avoiding hospitalization. In various embodiments, the worsening heart failure includes occurrence of acute decompensated heart failure, with symptoms of decompensation. The cardiorenal electrical stimulation reduces or eliminates use of diuretic drugs and hence their undesirable side effects such as hypotension, electrolyte disturbances, arrhythmia, and neurohormonal activation. In various embodiments, the cardiorenal electrical stimulation includes renal electrical stimulation (referred to as renal stimulation hereinafter) and cardiac electrical stimulation (referred to cardiac stimulation hereinafter). The renal stimulation includes delivery of electrical stimulation pulses to the kidneys and/or nerves modulating renal functions to promote diuresis and/or natriuresis. The cardiac stimulation includes delivery of electrical stimulation pulses to the heart and/or nerves modulating cardiovascular functions for enhancing the diuretic and/or natriuretic effects of the rental stimulation.
Implantable system 105 includes, among other things, implantable cardiorenal stimulator 110 and an implantable lead system including a cardiac stimulation lead 108 and a renal stimulation lead 109. In various embodiments, implantable cardiorenal stimulator 110 provides for the cardiorenal stimulation as well as other therapies such as cardioversion/defibrillation, neurostimulation, drug therapy and biological therapy. Cardiac stimulation lead 108 represents one or more implantable cardiac stimulation leads. Renal stimulation lead 109 represents one or more implantable renal stimulation leads. While
In the illustrated embodiment, implantable cardiorenal stimulator 110 is implanted in a body 102. Implantable cardiorenal stimulator 110 includes a hermetically sealed implantable housing 130 and a header 132 including a lead connector attached to housing 130. Housing 130 encapsulates electronic circuitry that performs sensing and therapeutic functions including cardiorenal stimulation. Header 132 provides for mechanical and electrical connections between leads 108 and 109 and implantable cardiorenal stimulator 110. In various embodiments, implantable cardiorenal stimulator 110 detects decompensation associated with heart failure using one or more sensed physiological signals and delivers cardiac stimulation pulses modulating cardiovascular functions and renal stimulation pulses modulating renal functions according to a cardiorenal stimulation mode in response to a detection of the decompensation.
Lead 108 provides electrical connections between implantable cardiorenal stimulator 110 and a heart 101 and/or nerves modulating cardiovascular functions. Lead 108 includes a proximal end portion 121 configured to be connected to header 132, a distal end portion 123 including one or more electrodes for delivering cardiac stimulation pulses and/or sensing one or more physiological signals, and an elongate lead body 122 coupling between proximal end portion 121 and distal end portion 123. In various embodiments, lead 108 represents one or more implantable transvenous leads for sensing physiological signals and delivering pacing pulses, cardioversion/defibrillation shocks, neurostimulation, pharmaceutical agents, biological agents, and/or other types of energy or substance for treating cardiac disorders. In various embodiments, the one or more electrodes of lead 108 are placed in a heart 101 or other portions of body 102 for sensing physiological signals and delivering pacing pulses, cardioversion/defibrillation shocks, neurostimulation, pharmaceutical agents, biological agents, and/or other types of energy or substance for treating cardiac disorders. In one embodiment, lead system 108 includes one or more pacing-sensing leads each including at least one electrode placed in or on heart 101 for sensing one or more electrograms and/or delivering pacing pulses. In a specific embodiment, lead system 108 allows pacing pulses to be delivered to multiple atrial and ventricular sites. In various embodiments, distal end portion 123, which includes the one or more pacing electrodes, is placed in the right atrium (RA) of heart 101 for baroreceptor pacing, atrial stretch receptor pacing, and/or RA pacing (for RA contraction), in the right ventricle (RV) of heart 101 for RV pacing (for RV contraction), and/or in the coronary sinus or vein over the left ventricle (LV) of heart 101 for LV pacing (for LV contraction).
Lead 109 provides electrical connections between implantable cardiorenal stimulator 110 and kidneys 103A-B and/or nerves modulating renal functions. Lead 109 includes a proximal end portion 124 configured to be connected to header 132, a distal end portion 126 including one or more electrodes for delivering renal stimulation pulses and/or sensing one or more physiological signals, and an elongate lead body 125 coupling between proximal end portion 124 and distal end portion 126. In various embodiments, lead 109 represents one or more implantable transvenous leads for sensing physiological signals and delivering renal stimulation pulses, pharmaceutical agents, biological agents, and/or other types of energy or substance for treating renal disorders. In various embodiments, distal end portion 126, which includes the one or more electrodes, is placed on kidneys 103A-B, renal veins 104A-B, an inferior vena cava (IVC) 106, or other portions of body 102 to sense physiological signals and deliver renal stimulation pulses, pharmaceutical agents, biological agents, and/or other types of energy or substance for treating renal disorders. In various embodiments, distal end portion 126 is placed in a location in body 102 that allows for delivering renal stimulation pulse to block nerve traffic in renal nerves or interconnected nerves/ganglia within the plexus.
In various embodiments, system 100 allows for bipolar cardiac stimulation using a pair of electrodes on distal end portion 123 of lead 108 and/or unipolar cardiac stimulation using an electrode on distal end portion 123 and another electrode on implantable cardiorenal stimulator 110. In various embodiments, system 100 allows for bipolar renal stimulation using a pair of electrodes on distal end portion 126 of lead 109 and/or unipolar renal stimulation using an electrode on distal end portion 126 and another electrode on implantable cardiorenal stimulator 110. In one embodiment, a portion of implantable housing 130 functions as the electrode on implantable cardiorenal stimulator 110.
External system 115 allows a user such as a physician or other caregiver or the patient to control the operation of implantable cardiorenal stimulator 110 and obtain information acquired by implantable cardiorenal stimulator 110. In one embodiment, external system 115 includes a programmer communicating with implantable cardiorenal stimulator 110 bi-directionally via telemetry link 112. In another embodiment, external system 115 is a patient management system including an external device communicating with a remote device through a telecommunication network. The external device is within the vicinity of implantable cardiorenal stimulator 110 and communicates with implantable cardiorenal stimulator 110 bi-directionally via telemetry link 112. The remote device allows the user to monitor and treat a patient from a distant location.
Telemetry link 112 provides for data transmission from implantable cardiorenal stimulator 110 to external system 115. This includes, for example, transmitting real-time physiological data acquired by implantable cardiorenal stimulator 110, extracting physiological data acquired by and stored in implantable cardiorenal stimulator 110, extracting therapy history data stored in implantable cardiorenal stimulator 110, and extracting data indicating an operational status of implantable cardiorenal stimulator 110 (e.g., battery status and lead impedance). Telemetry link 112 also provides for data transmission from external system 115 to implantable cardiorenal stimulator 110. This includes, for example, programming implantable cardiorenal stimulator 110 to acquire physiological data, programming implantable cardiorenal stimulator 110 to perform at least one self-diagnostic test (such as for a device operational status), and programming implantable cardiorenal stimulator 110 to deliver one or more therapies.
Sensing circuit 240 senses one or more physiological signals via one or more electrodes on lead 108, lead 109, and/or sensor 250. The one or more physiological signals include one or more signals indicative of water and/or salt retention in body 102. Examples of such signals includes signals indicative of body tissue volume, blood volume, and effects of abnormal tissue or blood volumes, as further discussed below. Decompensation detector 242 detects a level of water retention in body 102 using the one or more physiological signals and produces a decompensation signal indicative of the detected level of water retention. In one embodiment, decompensation detector 242 detects occurrence of decompensation associated with heart failure using the one or more physiological signals and one or more specified thresholds. In one embodiment, the one or more thresholds are each specified according to a need to deliver therapy indicated by one of the one or more physiological signals. In one embodiment, the decompensation signal includes a decompensation alert signal indicative of an occurrence of decompensation. In various embodiments, the decompensation alert signal indicates onset and cessation of the detected decompensation and/or a status or degree of the detected decompensation. For example, the decompensation alert signal includes a parameter value that quantitatively indicates the status or degree of the detected decompensation.
In one embodiment, decompensation detector 242 detects conditions indicative of decompensation that occur during acute decompensated heart failure. In another embodiment, decompensation detector 242 detects conditions that may lead to acute decompensated heart failure or conditions indicative of recovery from acute decompensated heart failure. Heart failure results in diminished blood flow from the heart as measured by cardiac output or stroke volume. Cardiac output is the amount of blood pumped by the heart during a unit period of time. Stroke volume is the amount of blood pumped during each contraction or stroke. Decompensated heart failure occurs when the heart becomes significantly weakened such that the body's compensatory mechanisms cannot restore a normal cardiac output/stroke volume. One principal consequence of the decompensated heart failure is that the heart fails to provide the kidneys with sufficient blood to support normal renal functions. As a result, a patient suffering decompensated heart failure progressively develops increased neurohormonal activation, retention of salt and water, and ultimately pulmonary and peripheral edema, a process referred to as decompensation.
In one embodiment, sensor 250 includes an implantable impedance sensor to measure pulmonary impedance, or impedance of a portion of the thoracic cavity. In another embodiment, sensor 250 includes an implantable impedance sensor to measure blood impedance indicative of hemodilution resulting from water retention. Decompensation detector 242 produces the decompensation alert signal when the impedance is out of its normal range. For example, pulmonary edema, i.e., fluid retention in the lungs resulting from the decreased cardiac output, increases the pulmonary or thoracic impedance. In one specific embodiment, decompensation detector 242 produces the decompensation alert signal when the pulmonary or thoracic impedance exceeds a specified threshold impedance. In one embodiment, the impedance sensor is a respiratory sensor that senses the patient's minute ventilation. An example of an impedance sensor sensing minute ventilation is discussed in U.S. Pat. No. 6,459,929, “IMPLANTABLE CARDIAC RHYTHM MANAGEMENT DEVICE FOR ASSESSING STATUS OF CHF PATIENTS,” assigned to Cardiac Pacemakers, Inc., which is incorporated herein by reference in its entirety.
In one embodiment, sensor 250 includes a pressure sensor. Acute decompensated heart causes pressures in various portions of the cardiovascular system to deviate from their normal ranges. Decompensation detector 242 produces the decompensation alert signal when a pressure is outside of its normal range. Examples of the pressure sensor include a central venous pressure (CVP) sensor, left atrial (LA) pressure sensor, a left ventricular (LV) pressure sensor, an artery pressure sensor, a pulmonary artery pressure sensor, and an intra-abdominal pressure sensor. In various embodiments, one or more of such pressure sensors are incorporated into one or more of lead 108, lead 109, and housing 130. Pulmonary edema results in elevated LA and pulmonary arterial pressures. A deteriorated LV results in decreased LV and arterial pressures. In various embodiments, decompensation detector 242 produces the decompensation alert signal when the LA pressure exceeds a specified threshold LA pressure level, when the pulmonary arterial pressure exceeds a predetermined threshold pulmonary arterial pressure level, when the LV pressure falls below a predetermined threshold LV pressure level, and/or when the arterial pressure falls below a predetermined threshold LV pressure level. In other embodiments, decompensation detector 242 derives a parameter from one of these pressures, such as a rate of change of a pressure, and produces the decompensation alert signal when the parameter deviates from its normal range. In one embodiment, the LV pressure sensor senses the LV pressure indirectly, by sensing a signal having known or predictable relationships with the LV pressure during all or a portion of the cardiac cycle. Examples of such a signal include an LA pressure and a coronary vein pressure. One specific example of measuring the LV pressure using a coronary vein pressure sensor is discussed in U.S. patent application Ser. No. 10/038,936, “METHOD AND APPARATUS FOR MEASURING LEFT VENTRICULAR PRESSURE,” filed on Jan. 4, 2002, assigned to Cardiac Pacemakers, Inc., which is hereby incorporated by reference in its entirety.
In one embodiment, sensor 250 includes a cardiac output or stroke volume sensor. Examples of stroke volume sensing are discussed in U.S. Pat. No. 4,686,987, “BIOMEDICAL METHOD AND APPARATUS FOR CONTROLLING THE ADMINISTRATION OF THERAPY TO A PATIENT IN RESPONSE TO CHANGES IN PHYSIOLOGIC DEMAND,” and U.S. Pat. No. 5,284,136, “DUAL INDIFFERENT ELECTRODE PACEMAKER,” both assigned to Cardiac Pacemakers, Inc., which are incorporated herein by reference in their entirety. Decompensation detector 242 produces the decompensation alert signal when the stroke volume falls below a specified threshold level.
In one embodiment, sensor 250 includes a neural activity sensor to detect activities of the sympathetic nerve and/or the parasympathetic nerve. A significant decrease in cardiac output immediately stimulates sympathetic activities, as the autonomic nervous system attempts to compensate for deteriorated cardiac function. Sympathetic activities sustain even when the compensation fails to restore the normal cardiac output. In one specific embodiment, the neural activity sensor includes a neurohormone sensor to sense a hormone level of the sympathetic nerve and/or the parasympathetic nerve. Decompensation detector 242 produces the decompensation alert signal when the hormone level exceeds a specified threshold level. In another specific embodiment, the neural activity sensor includes an action potential recorder to sense the electrical activities in the sympathetic nerve and/or the parasympathetic nerve. Decompensation detector 242 produces the decompensation alert signal when the frequency of the electrical activities in the sympathetic nerve exceeds a predetermined threshold level. Examples of direct and indirect neural activity sensing are discussed in U.S. Pat. No. 5,042,497, “ARRHYTHMIA PREDICTION AND PREVENTION FOR IMPLANTED DEVICES,” assigned to Cardiac Pacemakers, Inc., which is hereby incorporated by reference in its entirety. In one embodiment, decompensation detector 242 includes a heart rate variability detector. Patients suffering acute decompensated heart failure exhibit abnormally low heart rate variability. An example of detecting the heart rate variability is discussed in U.S. Pat. No. 5,603,331, “DATA LOGGING SYSTEM FOR IMPLANTABLE CARDIAC DEVICE,” assigned to Cardiac Pacemakers, Inc., which is incorporated herein by reference in their entirety. Decompensation detector 242 produces the decompensation alert signal when the heart rate variability falls below a specified threshold level.
In one embodiment, sensor 250 includes a renal function sensor. Acute decompensated heart failure results in peripheral edema primarily because of fluid retention by the kidneys that follows the reduction in cardiac output. The fluid retention is associated with reduced renal output, decreased glomerular filtration, and formation of angiotensin. Thus, in one specific embodiment, the renal function sensor includes a renal output sensor to sense a signal indicative of the renal output. In one embodiment, decompensation detector 242 produces the decompensation alert signal when the CVP exceeds a threshold CVP pressure (such as 15-20 mm Hg) or when intra-abdominal pressure exceeds a threshold intra-abdominal pressure. In another embodiment, decompensation detector 242 produces the decompensation alert signal when the sensed renal output falls below a predetermined threshold. In another specific embodiment, the renal function sensor includes a filtration rate sensor to sense a signal indicative of the glomerular filtration rate. Decompensation detector 242 produces the decompensation alert signal when the sensed glomerular filtration rate falls below a specified threshold. In yet another specific embodiment, the renal function sensor includes a chemical sensor to sense a signal indicative of increased rennin or angiotensin levels. Decompensation detector 242 produces the decompensation alert signal when the sensed rennin or angiotensin level exceeds a specified threshold level.
In one embodiment, sensor 250 includes an acoustic sensor being a heart sound sensor and/or a respiratory sound sensor. Acute decompensated heart failure causes abnormal cardiac and pulmonary activity patterns and hence, deviation of heart sounds and respiratory sounds from their normal ranges of pattern and/or amplitude. Decompensation detector 242 produces the decompensation alert signal when the heart sound or respiratory sound is out of its normal range. For example, detection of the third heard sound (S3) is known to indicate heart failure. In one specific embodiment, decompensation detector 242 produces the decompensation alert signal when the S3 amplitude exceeds a predetermined threshold level.
Embodiments of sensor 250 and decompensation detector 242 are discussed in this document by way of example, but not by way of limitation. Other methods and sensors for directly or indirectly detecting decompensation, as known to those skilled in the art, are useable as sensor 250 and decompensation detector 242.
Cardiac stimulation circuit 244 delivers cardiac stimulation pulses modulating cardiovascular functions. In one embodiment, cardiac stimulation circuit 244 delivers cardiac pacing pulses to the heart via lead 108 having one or more electrodes placed in or on the heart. In another embodiment, cardiac stimulation circuit 244 delivers neural pacing pulses to deliver neural pacing pulses to a nervous system modulating cardiac functions via lead 108 having one or more electrodes placed on or adjacent baroreceptors and/or other components of the autonomic neural system.
Renal stimulation circuit 244 delivers renal stimulation pulses modulating renal functions. In one embodiment, renal stimulation circuit 244 delivers renal stimulation pulses to the kidneys via lead 109 having one or more electrodes placed on or adjacent to the kidneys. In another embodiment, renal stimulation circuit 244 delivers renal stimulation pulses to renal nerves via lead 109 having one or more electrodes placed on or adjacent one or more of nerves, ganglia, and plexuses that innervate the kidney, including the aorticorenal ganglion, renal ganglia, celiac plexus, intermesenteric plexus, paravertebral sympathetic chain, prevertebral ganglia, splanchnic nerve, renal nerves, and vagus nerve.
Stimulation control circuit 248 controls the delivery of the cardiac stimulation pulses and the renal stimulation pulses according to a cardiorenal stimulation mode using renal stimulation parameters and cardiac stimulation parameters. In various embodiments, stimulation control circuit 248 temporally coordinates delivery of the cardiac stimulation pulses and the renal stimulation pulses according to the cardiorenal stimulation mode. In various embodiments, stimulation control circuit 248 controls the delivery of the cardiac stimulation pulses and the delivery of the renal stimulation pulses using the decompensation signal produced by decompensation detector 242. In one embodiment, stimulation control circuit 248 provides closed-loop control of the delivery of the cardiac stimulation pulses and the delivery of the renal stimulation pulses using the decompensation signal as a feedback input. In one embodiment, stimulation control circuit 248 controls the delivery of the cardiac stimulation pulses and the delivery of the renal stimulation pulses using the decompensation signal and one or more additional control signals. In various embodiments, stimulation control circuit 248 uses the one or more additional control signals to control timing and/or intensity of the cardiac stimulation pulses and the renal stimulation pulses. Examples of such control signals include signals indicative of drug therapy received by the patient and time of the day.
In one embodiment, stimulation control circuit 248 initiates the delivery of the cardiac stimulation pulses and the renal stimulation pulses according to the cardiorenal stimulation mode in response to the onset of the decompensation as indicated by the decompensation signal. In one embodiment, stimulation control circuit 248 stops the delivery of the cardiac stimulation pulses and the renal stimulation pulses according to the cardiorenal stimulation mode in response to the cessation of the decompensation as indicated by the decompensation signal.
In one embodiment, stimulation control circuit 248 controls the delivery of the renal stimulation pulses using renal stimulation parameters selected for increasing diuresis and natriuresis by modifying renal adrenergic drive and/or renal cholinergic drive. In one embodiment, the renal stimulation parameters are selected for partially or completely blocking renal adrenergic drive. In another embodiment, the renal stimulation parameters are selected for enhancing renal cholinergic drive, in place of or in addition to partially or completely blocking renal adrenergic drive. The delivery of the renal stimulation pulses is controlled to increase renal perfusion, reduce renin secretion and renin-angiotensin-aldosterone system (RAAS) activation, or alter renal filtration or renal reabsorption (such as by reducing sodium reabsorption in the proximal tubule), thereby promoting diuresis and natriuresis. In one embodiment, stimulation control circuit 248 controls the delivery of the renal stimulation pulses to override the renal nerve traffic using a neurostimulation frequency substantially higher than the frequency of the intrinsic action potential impulses in the renal nerves. In another embodiment, stimulation control circuit 248 controls the delivery of the renal stimulation pulses to hyperpolarize the renal nerves.
In one embodiment, stimulation control circuit 248 controls the delivery of the cardiac stimulation pulses using cardiac stimulation parameters selected for enhancing one or more effects of the delivery of the renal stimulation pulses. Examples of such one or more effects include diuretic and natriuretic effects. The cardiac stimulation pulses include cardiac pacing pulses and/or neural pacing pulses. In one embodiment, stimulation control circuit 248 controls the delivery of the cardiac pacing pulses according to an anti-bradycardia pacing mode using a pacing rate that is substantially higher than the patient's intrinsic heart rate. In another embodiment, stimulation control circuit 248 controls the delivery of the cardiac pacing pulses according to a cardiac resynchronization therapy (CRT) pacing mode to improve hemodynamic performance using cardiac pacing. In one embodiment, stimulation control circuit 248 controls delivery of the neural pacing pulses for atrial stretch pacing. In one embodiment, stimulation control circuit 248 controls delivery of the neural pacing pulse for baroreceptor pacing.
In various embodiments, implantable housing 130 encapsulates at least sensing circuit 240, decompensation detector 242, cardiac stimulation circuit 244, renal stimulation circuit 246, and stimulation control circuit 248. Header 132 is electrically connected to sensing circuit 240, cardiac stimulation circuit 244, and renal stimulation circuit 246.
In various embodiments, implantable cardiorenal stimulator 210 is implemented using a combination of hardware and software. In various embodiments, each element of implantable cardiorenal stimulator 210 may be implemented using an application-specific circuit constructed to perform one or more specific functions or a general-purpose circuit programmed to perform such function(s). Such a general-purpose circuit includes, but is not limited to, a microprocessor or a portion thereof, or other programmable logic circuit or a portion thereof. In one embodiment, decompensation detector 242 and stimulation control circuit 248 are implemented as a microprocessor-based circuit programmed to perform various functions discussed in this document.
In the illustrated embodiment, pulse delivery stein 560 is placed in aorta 316, which allows electrodes to be placed in a location closer to the target renal nerves than IVC 106. Pulse delivery stent 560 includes electrodes 558A-B, a receiver 556, and a pulse delivery circuit 557. Receiver 556 receives the power and the renal stimulation pulses. In one embodiment, transmitter 554 and receiver 556 each include a coil (or antenna) to form the magnetic (inductive) couple via which the power and the renal stimulation pulses are transmitted. In one embodiment, transmitter 554 and receiver 556 each include an acoustic transducer to form the acoustic couple via which the power and the renal stimulation pulses are transmitted. Pulse delivery circuit 557 operates with the received power and delivers electrical stimulation pulses corresponding to the received renal stimulation pulses.
In various embodiments, distal end portion 526 of renal stimulation lead 509 and pulse delivery stent 560 are configured and placed with considerations on desirable stimulation target(s) and/or stability of the placement. In one embodiment, one or more leads with electrodes are connected to pulse delivery stent 560 to allow pulse delivery stent 560 to be placed in aorta 316 while the electrodes are placed in renal arteries 314A-B. In another embodiment, distal end portion 526 is placed in renal vein 104A or 104B, and pulse delivery stent 560 is placed in the adjacent renal artery 314A or 314B. In another embodiment, multiple leads or a lead with multiple distal end portions, as well as multiple pulse delivery stents, are used, such that a distal end portion is placed in each of renal veins 104A-B, and pulse delivery stents are placed in each of renal arteries 314A-B.
At 910, one or more physiological signals are sensed using an implantable medical device such as implantable cardiorenal stimulator 110. The one or more physiological signals indicate a level of water retention in a patient's body. Occurrence of decompensation during acute decompensated heart failure is detected using the one or more physiological signals. At 920, decompensation associated with heart failure is detected using the one or more physiological signals. At 930, a decompensation signal is produced in response to a detected decompensation. In one embodiment, the decompensation signal is indicative of an onset and cessation of the detected decompensation. In another embodiment, the decompensation signal is quantitatively indicative of a status or degree of the detected decompensation. In yet another embodiment, the decompensation signal is quantitatively indicative of a status or degree of a condition that may lead to acute decompensated heart failure or recovery from acute decompensated heart failure.
At 940, delivery of cardiac stimulation pulses modulating cardiovascular functions and renal stimulation pulses modulating renal functions is controlled according to a cardiorenal stimulation mode using the decompensation signal. In one embodiment, the delivery of the cardiac stimulation pulses and the delivery of the renal stimulation pulses are temporally coordinated such that the cardiac stimulation pulses are delivered to enhance one or more effects of the delivery of the renal stimulation pulses. In one embodiment, the delivery of the cardiac stimulation pulses and the renal stimulation pulses according to the cardiorenal stimulation mode is initiated in response to the onset of the detected decompensation and stopped in response to the cessation of the detected decompensation. In one embodiment, the delivery of the cardiac stimulation pulses and the renal stimulation pulses is controlled according to the cardiorenal stimulation mode using the decompensation signal as a feedback input in a closed-loop control system. In one embodiment, timing and intensity of the delivery of the cardiac stimulation pulses and the renal stimulation pulses is controlled using the decompensation signals and one or more additional signals.
At 950, the cardiac stimulation pulses and the renal stimulation pulses are delivered from the implantable medical device such as implantable cardiorenal stimulator 110. In various embodiments, the cardiac stimulation pulses include cardiac pacing pulses delivered to a heart and/or neural pacing pulses delivered to a nervous system modulating cardiovascular functions. The renal stimulation pulses include renal stimulation pulses delivered to one or more kidneys and/or one or more renal nerves to increase diuresis or natriuresis by blocking renal adrenergic drive and/or enhancing renal cholinergic drive. In one embodiment, the renal stimulation pulses are delivered via one or more electrodes placed in the IVC and/or renal vein(s) adjacent to renal nerve(s). In another embodiment, the renal stimulation pulses are delivered via one or more electrodes placed in an artery adjacent to renal nerve(s) and a wireless link coupling the one or more electrodes to the implantable medical device.
At 960, one or more effects of the delivery of the cardiac stimulation pulses and the renal stimulation pulses are verified by monitoring one or more signals each indicative of diuresis or natriuresis. In one embodiment, a Foley type catheter with one or more sensors is used. Examples of the one or more sensors include a flow sensor for direct diuresis measurement and a conductivity sensor for indirect measurement of sodium secretion. In another embodiment, ultrasonic or other imaging techniques are employed for measuring bladder volume before and after renal stimulation.
In one embodiment, method 900 is performed using system 100 as a chronic therapy for a heart failure patient. Sensing circuit 240 and decompensation detector 242 are chronically enabled. Cardiorenal stimulation is controlled using the compensation signal produced by decompensation detector 242 in response to each detection of decompensation. In one embodiment, cardiac stimulation parameters are adjusted as needed for enhancing diuresis and natriuresis. This includes, for example, applying CRT pacing to enhance diuresis and natriuresis by improving hemodynamic performance. The hemodynamic performance is monitored and approximately optimized by adjusting pacing parameters such as atrioventricular (AV) delay and interventricular (VV) delay. In various embodiments, the cardiac stimulation includes one or more of (1) stimulation of cardiopulmonary reflexes that improve diuresis via reduction of sympathetic activation (making renal nerve blocking more effective) or reduction of antidiuretic hormone (ADH), (2) hyperpolarization of sympathetic cardiac afferents that reduces sympathetic activation, (3) stimulation of cardiopulmonary receptors in the RA, LA, and coronary sinus that activates the cardiopulmonary stretch reflex, either during RA and LA refractory periods or using continuous stimulation of nerve endings using cardiac subthreshold stimulation currents, and (4) anti-bradycardia or CRT pacing that increases cardiac output. In one embodiment, when the patient's heart failure status is stable, the cardiorenal stimulation is applied on a periodic basis and/or based on the one or more physiological signals, to reduce dose of diuretic drug, preserve glomerular filtration rate (GFR) and prevent progression of chronic kidney disease (CKD) stage by reducing sympathetic drive to the kidneys, and/or control blood pressure.
It is to be understood that the above detailed description is intended to be illustrative, and not restrictive. Other embodiments will be apparent to those of skill in the art upon reading and understanding the above description. The scope of the invention should, therefore, be determined with reference to the appended claims, along with the full scope of equivalents to which such claims are entitled.
This application claims the benefit of provisional U.S. patent application Ser. No. 61/252,809, filed on Oct. 19, 2009, which is hereby incorporated by reference in its entirety.
| Number | Date | Country | |
|---|---|---|---|
| 61252809 | Oct 2009 | US |
