Source: http://www.google.com/patents/US7346394?dq=5,987,610
Timestamp: 2017-10-18 02:38:36
Document Index: 540266510

Matched Legal Cases: ['art.\n7', 'art.\n8', 'art.\n15', 'art.\n16', 'art 401', 'art 401', 'art 401', 'art 401', 'art 401', 'art 401', 'art 401', 'art 401', 'art 401', 'art 590', 'art 1']

Patent US7346394 - Cardiac stimulation at high ventricular wall stress areas - Google Patents
An apparatus and method for reversing ventricular remodeling with electro-stimulatory therapy. A ventricle is paced by delivering one or more stimulatory pulses in a manner such that a stressed region of the myocardium is pre-excited relative to other regions in order to subject the stressed region to...http://www.google.com/patents/US7346394?utm_source=gb-gplus-sharePatent US7346394 - Cardiac stimulation at high ventricular wall stress areas
Publication number US7346394 B2
Application number US 10/952,346
Filing date Sep 28, 2004
Also published as EP1807151A1, US7725185, US20050065568, US20080140144, WO2006037108A1
Publication number 10952346, 952346, US 7346394 B2, US 7346394B2, US-B2-7346394, US7346394 B2, US7346394B2
Inventors Lili Liu, Rodney Salo
Patent Citations (64), Non-Patent Citations (3), Referenced by (37), Classifications (9), Legal Events (3)
Cardiac stimulation at high ventricular wall stress areas
US 7346394 B2
1. A lead implantation method, comprising:
accessing a heart of a patient, the heart having a heart wall;
detecting, proximate the heart wall, a target region of the heart wall having a level of abnormal wall motion relative to neighboring regions of the heart wall;
implanting an electrode of the lead at the target region; and
pre-exciting the target region relative to the neighboring regions of the heart wall using the lead electrode in order to alter stress at the target region for treating cardiac remodeling, wherein pre-exciting the target region is initiated in response to an atrial sense or an atrial pace.
2. The method of claim 1, wherein the wall motion is detected using an acceleration measurement.
3. The method of claim 1, wherein the wall motion is detected using a strain measurement.
4. The method of claim 1, wherein the wall motion is detected using an ultrasonic velocity measurement.
5. The method of claim 1, further comprising adjusting the pre-excitation in accordance with activity level measurements reflective of metabolic demand.
6. The method of claim 1, wherein accessing the patient's heart comprises accessing an epicardial surface of the patient's heart.
7. The method of claim 1, wherein accessing the patient's heart comprises accessing an endocardial surface of the patient's heart.
8. The method of claim 1, wherein accessing the patient's heart comprises accessing the heart through coronary vessels.
9. A lead implantation method, comprising:
detecting, proximate the heart wall, a target region of the heart wall having asynchronic depolarization characteristics relative to neighboring regions of the heart wall;
pre-exciting the target region relative to the neighboring regions of the heart wall using the lead electrode in order to alter stress of the target region for treating cardiac remodeling, wherein pre-exciting the target region is initiated in response to an atrial sense or pace event.
10. The method of claim 9, wherein detecting the target region of the heart comprises sensing activation characteristics of heart wall tissue at a plurality of heart wall sites.
11. The method of claim 9, wherein detecting the target region of the heart comprises detecting one or more electrophysiologic characteristics of heart wall tissue.
12. The method of claim 9, wherein detecting the target region of the heart comprises detecting complex impedance characteristics of heart wall tissue.
13. The method of claim 9, further comprising adjusting the pre-excitation in accordance with activity level measurements reflective of metabolic demand.
14. The method of claim 9, wherein accessing the patient's heart comprises accessing an epicardial surface of the patient's heart.
15. The method of claim 9, wherein accessing the patient's heart comprises accessing an endocardial surface of the patient's heart.
16. A cardiac system, comprising:
a controller provided in the housing and configured to control cardiac monitoring and cardiac stimulation;
detection circuitry provided in the housing and coupled to the controller;
energy delivery circuitry provided in the housing and coupled to the controller; and
a lead coupled to the detection circuitry and the energy delivery circuitry, the lead comprising:
at least one cardiac electrode coupled to the lead body; and
at least one sensor supported by the lead body and configured to detect abnormal cardiac wall motion, the sensor providing information useful for positioning the cardiac electrode proximate a target heart wall location associated with increased stress relative to neighboring heart wall locations;
wherein the controller is configured to coordinate delivery of a pre-excitation stimulus to the target heart wall location prior to at least one of an intrinsic conduction or delivery of a pace pulse.
17. The system of claim 16, wherein the sensor is situated at a distal region of the lead.
18. The system of claim 16, wherein the sensor comprises an accelerometer.
19. The system of claim 16, wherein the sensor comprises a strain-gage.
20. The system of claim 16, wherein the sensor comprises an ultrasonic velocimeter.
21. The system of claim 16, wherein the sensor is supported within a lumen of the lead.
22. The system of claim 16, wherein the controller is configured to coordinates delivery of the pre-excitation stimulus to the target heart wall location in response to an atrial sense or pace event.
23. The system of claim 16, further comprising an activity sensor situated in or on the housing and coupled to the controller, wherein the controller is programmed to adjust a pacing therapy in response to signals indicative of metabolic demand received from the activity sensor.
means for detecting, proximate the heart wall, a target region of the heart wall having asynchronic depolarization characteristics relative to neighboring regions of the heart wall; and
means for pre-exciting the target region relative to the neighboring regions in order to alter stress at the target region.
This application is a continuation-in-part of U.S. patent application Ser. No. 10/649,468, filed on Aug. 27, 2003, now issued as U.S. Pat. No. 7,103,410, which is a continuation of U.S. patent application Ser. No. 09/844,256, filed on Apr. 27, 2001, now issued as U.S. Pat. No. 6,628,988 and which are hereby incorporated herein by reference.
The present invention relates generally to medical devices and, more particularly, to implantable cardiac stimulation therapy devices and methods of cardiac stimulation therapy.
Congestive heart failure (CHF) is a clinical syndrome in which an abnormality of cardiac function causes cardiac output to fall below a level adequate to meet the metabolic demand of peripheral tissues. CHF can be due to a variety of etiologies with that due to ischemic heart disease being the most common. Inadequate pumping of blood into the arterial system by the heart is sometimes referred to as “forward failure,” with “backward failure” referring to the resulting elevated pressures in the lungs and systemic veins which lead to congestion.
Backward failure is the natural consequence of forward failure as blood in the pulmonary and venous systems fails to be pumped out. Forward failure can be caused by impaired contractility of the ventricles or by an increased afterload (i.e., the forces resisting ejection of blood) due to, for example, systemic hypertension or valvular dysfunction.
One physiological compensatory mechanism that acts to increase cardiac output is due to backward failure which increases the diastolic filling pressure of the ventricles and thereby increases the preload (i.e., the degree to which the ventricles are stretched by the volume of blood in the ventricles at the end of diastole). An increase in preload causes an increase in stroke volume during systole, a phenomena known as the Frank-Starling principle. Thus, heart failure can be at least partially compensated by this mechanism, but at the expense of possible pulmonary and/or systemic congestion.
When the ventricles are stretched due to the increased preload over a period of time, the ventricles become dilated. The enlargement of the ventricular volume causes increased ventricular wall stress at a given systolic pressure. Along with the increased pressure-volume work done by the ventricle, this acts as a stimulus for hypertrophy of the ventricular myocardium, which leads to alterations in cellular structure, a process referred to as ventricular remodeling.
Hypertrophy can increase systolic pressures but also decreases the compliance of the ventricles and hence increases diastolic filling pressure to result in even more congestion. It also has been shown that the sustained stresses causing hypertrophy may induce apoptosis (i.e., programmed cell death) of cardiac muscle cells and eventual wall thinning which causes further deterioration in cardiac function. Thus, although ventricular dilation and hypertrophy may at first be compensatory and increase cardiac output, the process ultimately results in both systolic and diastolic dysfunction. It has been shown that the extent of ventricular remodeling is positively correlated with increased mortality in CHF patients.
The present invention relates to devices and method for reversing ventricular remodeling with electro-stimulatory therapy. In accordance with embodiments of the present invention, a ventricle is paced by delivering one or more stimulatory pulses in a manner such that a previously stressed and remodeled region of the myocardium is pre-excited relative to other regions in order to reverse the tissue remodeling.
A method of cardiac remodeling reversal in accordance with the present invention involves accessing a patient's heart, and detecting, proximate the heart wall, a target region having a level of abnormal wall motion relative to neighboring regions. An electrode may be implanted near the target region. The target region is pre-excited relative to the neighboring regions of the heart wall using the electrode in order to alter stress at the target region for treating cardiac remodeling.
Heart wall motion may be detected using, for example, an acceleration measurement, a strain measurement, and/or an ultrasonic velocity measurement such as a local Doppler tissue velocity measurement. The electrode may be used to pre-excite the target region in response to an atrial sense, an atrial pace, a ventricular sense or pace event, or other timing event or methodology. The remodeling reversal pre-excitation may be adjusted in accordance with activity level measurements reflective of metabolic demand. Detecting the target region of the heart may involve sensing activation characteristics of heart wall tissue, such as one or more electrophysiologic characteristics, complex impedance characteristics, or other characteristics of the heart wall tissue indicative of remodeling.
The pulse output sequence best suited for reversal of remodeling may not be the optimum pulse output sequence for maximizing hemodynamic performance. In another embodiment, therefore, the pulse output sequence is adjusted automatically in accordance with activity level measurements reflective of metabolic demand. The pulse output sequence is then alternated between one designed to produce more hemodynamically-effective contractions when metabolic needs of the body are great to one designed for remodeling reversal when metabolic needs are less.
A cardiac system suitable for cardiac remodeling reversal in accordance with the present invention includes an implantable housing having a controller configured to control cardiac monitoring and stimulation. Detection circuitry and energy delivery circuitry are provided in the housing and coupled to the controller. A lead is coupled to the detection circuitry and the energy delivery circuitry. The lead includes a lead body with at least one cardiac electrode and at least one sensor supported by the lead body and configured to detect abnormal cardiac wall motion. The sensor provides information useful for positioning the cardiac electrode proximate a target heart wall location associated with increased stress relative to neighboring heart wall locations. The sensor may be situated at a distal region of the lead, or the cardiac electrode may be situated at a distal end of the lead, and the sensor situated proximal of the cardiac electrode.
Embodiments of a device in accordance with the present invention may include leads having a fixation arrangement configured to fix the lead at the target heart wall location. Further embodiments include an activity sensor situated in or on the housing and coupled to the controller, wherein the controller is programmed to adjust a pacing therapy in response to signals indicative of metabolic demand received from the activity sensor.
FIG. 1 is a block diagram of an example of a cardiac rhythm management device in accordance with present invention;
FIGS. 2 and 3 are diagrams showing examples of sensing/pacing electrode placement according to embodiments of the present invention;
FIG. 4A is an illustration of an implantable cardiac device including a lead assembly shown implanted in a sectional view of a heart, the device configured for ventricular wall remodeling reversal in accordance with embodiments of the present invention;
FIG. 4B is an illustration of an implantable cardiac device including a mesh configured for local stress measurements, the device configured for ventricular wall remodeling reversal in accordance with embodiments of the present invention;
FIG. 5 illustrates an epicardial lead having a helical fixation arrangement in the myocardium for ventricular wall remodeling reversal in accordance with an embodiment of the present invention; and
FIG. 6 is a flow chart directed to methods of cardiac tissue remodeling reversal in accordance with the present invention.
A device employing cardiac stimulation methods and devices in accordance with the present invention may incorporate one or more of the features, structures, methods, or combinations thereof described herein below. For example, a cardiac monitor or stimulator and cardiac implantation devices may be implemented to include one or more of the advantageous features and/or processes described below. It is intended that such devices or methods need not include all of the features and functions described herein, but may be implemented to include selected features and functions that, in combination, provide for unique structures and/or functionality.
Conventional cardiac pacing with implanted pacemakers involves excitatory electrical stimulation to the heart by use of an electrode in electrical contact with the myocardium. As the term is used herein, “excitatory stimulation” refers to stimulation sufficient to cause contraction of muscle fibers, which is also commonly referred to as pacing. Furthermore, the term “pacemaker” should be taken to mean any cardiac rhythm management device with a pacing functionality, regardless of any other functions it may perform such as cardioversion/defibrillation or drug delivery. A pacemaker is usually implanted subcutaneously on the patient's chest, and is typically connected to an electrode for each paced heart chamber by leads threaded through the vessels of the upper venous system into the heart, and/or placed epicardially. In response to sensed electrical cardiac events and elapsed time intervals, the pacemaker delivers to the myocardium a depolarizing voltage pulse of sufficient magnitude and duration to cause an action potential. A wave of depolarizing excitation then propagates through the myocardium, resulting in a heartbeat.
Various forms of cardiac pacing can often benefit CHF patients. For example, sinus node dysfunction resulting in bradycardia can contribute to heart failure that can be corrected with conventional bradycardia pacing. Also, some CHF patients suffer from some degree of AV block such that their cardiac output is improved by synchronizing atrial and ventricular contractions with dual-chamber pacing using a programmed AV delay time (i.e., atrial triggered ventricular pacing or AV sequential pacing).
CHF patients may also suffer from conduction defects of the specialized conduction system of the heart (a.k.a. bundle branch blocks) so that a depolarization impulse from the AV node reaches one ventricle before the other. Stretching of the ventricular wall brought about by CHF can also cause slowed conduction of depolarization impulses through the ventricle. If conduction velocity is slowed in the left ventricle more than the right, for example, the contraction of the two ventricles during ventricular systole becomes uncoordinated which lessens pumping efficiency. In both of these situations, cardiac output can be increased by improving the synchronization of right and left ventricular contractions.
Cardiac pacemakers have therefore been developed which provide pacing to both ventricles. For example, any device of the present invention may incorporate features of one or more of the following references: U.S. Pat. No. 4,928,688, commonly owned U.S. Pat. No. 7,260,432 and U.S. Pat. Nos. 6,411,848; 6,285,907; 4,928,688; 6,459,929; 5,334,222; 6,026,320; 6,371,922; 6,597,951; 6,424,865; and 6,542,775, each of which is hereby incorporated herein by reference.
The specialized His-Purkinje conduction network of the heart rapidly conducts excitatory impulses from the sinoatrial node to the atrioventricular node, and then to the ventricular myocardium to result in a coordinated contraction of both ventricles. Artificial pacing with an electrode fixed into an area of the myocardium does not take advantage of the heart's normal specialized conduction system for conducting excitation throughout the ventricles. This is because the specialized conduction system can only be entered by impulses emanating from the atrioventricular node. Thus, the spread of excitation from a ventricular pacing site must proceed only via the much slower conducting ventricular muscle fibers, resulting in the part of the ventricular myocardium stimulated by the pacing electrode contracting well before parts of the ventricle located more distally to the electrode. Although the pumping efficiency of the heart is somewhat reduced from the optimum, most patients can still maintain more than adequate cardiac output with artificial pacing.
In multi-site pacing, the atria and/or ventricles are paced at more than one site in order to effect a spread of excitation that results in a more coordinated contraction. Biventricular pacing, as described above, is one example of multi-site pacing in which both ventricles are paced in order to synchronize their respective contractions. Multi-site pacing may also be applied to only one chamber. For example, a ventricle may be paced at multiple sites with excitatory stimulation pulses in order to produce multiple waves of depolarization that emanate from the pacing sites. This may produce a more coordinated contraction of the ventricle and thereby compensate for intraventricular conduction defects that may exist. Stimulating one or both ventricles with multi-site pacing in order to improve the coordination of the contractions and overcome interventricular or intraventricular conduction defects is termed resynchronization therapy.
A block diagram of a cardiac rhythm management device suitable for practicing the present invention is shown in FIG. 1. The controller of the device is made up of a microprocessor 10 communicating with a memory 12 via a bidirectional data bus, where the memory 12 typically includes a ROM (read-only memory) for program storage and a RAM (random-access memory) for data storage. The controller could also include dedicated circuitry either instead of, or in addition to, the programmed microprocessor for controlling the operation of the device. The device has atrial sensing/stimulation channels including electrode 34, lead 33, sensing amplifier 31, pulse generator 32, and an atrial channel interface 30 which communicates bi-directionally with a port of microprocessor 10. The device also has multiple ventricular sensing/stimulation channels for delivering multi-site univentricular or biventricular pacing. Two such ventricular channels are shown in the figure that include electrodes 24 a-b, leads 23 a-b, sensing amplifiers 21 a-b, pulse generators 22 a-b, and ventricular channel interfaces 20 a-b where “a” designates one ventricular channel and “b” designates the other. For each channel, the same lead and electrode may be used for both sensing and stimulation. The channel interfaces 20 a-b and 30 may include analog-to-digital converters for digitizing signal inputs from the sensing amplifiers and registers which can be written to by the microprocessor in order to output stimulation pulses, change the stimulation pulse amplitude, and adjust the gain and threshold values for the sensing amplifiers. A telemetry interface 40 is provided for communicating with an external programmer.
The controller is capable of operating the device in a number of programmed pacing modes that define how pulses are output in response to sensed events and expiration of time intervals. Most pacemakers for treating bradycardia are programmed to operate synchronously in a so-called demand mode where sensed cardiac events occurring within a defined interval either trigger or inhibit a pacing pulse. Inhibited demand pacing modes utilize escape intervals to control pacing in accordance with sensed intrinsic activity such that a pacing pulse is delivered to a heart chamber during a cardiac cycle only after expiration of a defined escape interval during which no intrinsic beat by the chamber is detected. Escape intervals for ventricular pacing can be restarted by ventricular or atrial events, the latter allowing the pacing to track intrinsic atrial beats. Rate-adaptive pacing modes can also be employed where the ventricular and/or atrial escape intervals are modulated based upon measurements corresponding to the patient's exertion level.
As shown in FIG. 1, an activity level sensor 52 (e.g., a minute ventilation sensor or accelerometer) provides a measure of exertion level to the controller for pacing the heart in a rate-adaptive mode. Multiple excitatory stimulation pulses can also be delivered to multiple sites during a cardiac cycle in order to both pace the heart in accordance with a bradycardia mode and provide resynchronization of contractions to compensate for conduction defects. In accordance with the invention, the controller may also be programmed to deliver stimulation pulses in a specified pulse output sequence in order to effect reduction of stress to a selected myocardial region.
Methods and devices in accordance with the present invention may be beneficially employed to unload a stressed myocardial region that is either hypertrophied or thinned. FIG. 2 depicts a left ventricle 200 with pacing sites 210 and 220 to which may be fixed epicardial stimulation/sensing electrodes. The myocardium at pacing site 210 is shown as being hypertrophied as compared to the myocardium at pacing site 220. A cardiac rhythm management device such as shown in FIG. 1 may deliver stimulation pulses to both sites in accordance with a pacing mode through its ventricular stimulation/sensing channels. In order to unload the hypertrophied site 210 during systole and thereby promote reversal of the hypertrophy, the ventricle is paced with a pulse output sequence that stimulates the hypertrophied site 210 before the other site 220. The lessened mechanical stress during systole then allows the site 210 to undergo reversal of the hypertrophy. FIG. 3 shows a left ventricle 200 in which the pacing site 240 is relatively normal while the site 230 is a myocardial region that has been thinned due to late state remodeling or other stresses such as ischemia. Again, pacing of the ventricle with pre-excitation stimulation of site 230 relative to the site 240 unloads the thinned region and subjects it to less mechanical stress during systole. The result is either reversal of the remodeling or reduction of further wall thinning.
In one embodiment, a pre-excitation stimulation pulse is applied to a stressed region either alone or in a timed relation to the delivery of a stimulation pulse applied elsewhere to the myocardium. For example, both the right and left ventricles can be paced at separate sites by stimulation pulses delivered with a specified interventricular delay between the pulses delivered to each ventricle. By adjusting the interventricular delay so that one of the ventricular pacing sites is pre-excited relative to the other, the spread of activation between the two pacing sites can be modified to change the wall stresses developed near these sites during systolic contraction. Other embodiments may employ multiple electrodes and stimulation channels to deliver pulses to multiple pacing sites located in either of the atria or the ventricles in accordance with a specified pulse output sequence. A multi-site pacemaker may also switch the output of pacing pulses between selected electrodes or groups of electrodes during different cardiac cycles. Pacing is then delivered to a heart chamber through a switchable configuration of pacing electrodes, wherein a pulse output configuration is defined as a specific subset of two or more electrodes fixed to the paced chamber and to which pacing pulses are applied as well as the timing relations between the pulses. Two or more different pulse output configurations may be defined as subsets of electrodes that can be selected for pacing. By switching the pulse output configuration to a different configuration, pacing to the heart chamber is thereby temporally distributed among the total number of fixed electrodes. The principle remains the same in these embodiments, however, of unloading a stressed myocardial site by pre-exciting it relative to other regions of the myocardium.
In other embodiments, a stressed region of the ventricular myocardium is pre-excited in a timed relation to a triggering event that indicates an intrinsic beat has either occurred or is imminent. For example, a pre-excitation stimulation pulse may be applied to a stressed region immediately following the earliest detection of intrinsic activation elsewhere in the ventricle. Such activation may be detected from an electrogram with a conventional ventricular sensing electrode. An earlier occurring trigger event may be detected by extracting the His-Purkinje bundle conduction potential from a special ventricular sensing electrode using signal-processing techniques.
Referring to FIG. 4A, there is shown a body implantable device that represents one of several types of devices with implantable leads that may be used to reverse remodeling of the ventricular wall in accordance with embodiments of the present invention. For example, a patient internal medical device (PIMD) 400, illustrated in FIG. 4A as a pacemaker/defibrillator, may be representative of all or part of a pacemaker, defibrillator, cardioverter, cardiac monitor, or re-synchronization device (e.g., multichamber or multisite device).
The implantable device illustrated in FIG. 4A is an embodiment of the PIMD 400 including an implantable pacemaker/defibrillator electrically and physically coupled to an intracardiac lead system 402. The intracardiac lead system 402 is implanted in a human body with portions of the intracardiac lead system 402 inserted into a heart 401. Electrodes of the intracardiac lead system 402 may be used to detect and analyze cardiac signals produced by the heart 401 and to provide stimulation and/or therapy energy to the heart 401 under predetermined conditions, to treat cardiac arrhythmias of the heart 401.
The PIMD 400 depicted in FIG. 4A is a multi-chamber device, capable of sensing signals from one or more of the right and left atria 420, 422 and the right and left ventricles 418, 424 of the heart 401 and providing pacing pulses to one or more of the right and left atria 420, 422 and the right and left ventricles 418, 424. Low energy pacing pulses may be delivered to the heart 401 to regulate the heartbeat for remodeling reversal, for example. In a configuration that includes cardioversion/defibrillation capabilities, high-energy pulses may also be delivered to the heart 401 if an arrhythmia is detected that requires cardioversion or defibrillation.
The atrial lead system 405 includes A-tip and A-ring cardiac pace/sense electrodes 456, 454. In the configuration of FIG. 4A, the intracardiac lead system 402 is positioned within the heart 401, with a portion of the atrial lead system 405 extending into the right atrium 420. The A-tip and A-ring electrodes 456, 454 are positioned at an appropriate location within the right atrium 420 for pacing the right atrium 420 and sensing cardiac activity in the right atrium 420.
The lead system 402 illustrated in FIG. 4A also includes a left atrial/left ventricular lead system 406. The left atrial/left ventricular lead system 406 may include, one or more electrodes 434, 436, 417, 413 positioned within a coronary vein 465 of the heart 401. Additionally, or alternatively, one or more electrodes may be positioned in a middle cardiac vein, a left posterior vein, a left marginal vein, a great cardiac vein or an anterior vein.
Additional configurations of sensing, pacing and defibrillation electrodes may be included in the intracardiac lead system 402 to allow for various sensing, pacing, remodeling reversal, and defibrillation capabilities of multiple heart chambers. In other configurations, the intracardiac lead system 402 may have only a single lead with electrodes positioned in the right ventricle to implement single chamber cardiac pacing. In yet other embodiments, the intracardiac lead system 402 may not include the left atrial/left ventricular lead 406 and may support pacing and sensing of the right atrium and right ventricle only. Any intracardiac lead and electrode arrangements and configurations may be implanted within the scope of the present system in accordance with embodiments of the invention.
The PIMD 400 may include one or more sensors configured to detect local wall motion, velocity, and/or stress. For example, one or more accelerometers 491, 493 may be used to monitor local heart wall movement. This information can be used in closed loop fashion to control therapy by changing the pacing site (if multiple electrodes are available) or timing. A strain gauge 492 may alternately or additionally be used to detect flexing that occurs due to the local contraction of the ventricular wall. The strain gauge 492 and/or the accelerometers 491,493 may be provided in or on the intracardiac lead system 402 at a variety of locations. For example, the strain gauge 492 and/or the accelerometer 491 may be provided proximate the LV electrode 413, proximate the LV electrode 436, proximate the RV electrode 412, or at other locations suitable for determining local wall stress relative to a pace electrode. The strain gauge 492 and/or the accelerometers 491,493 may be of varying type, including, but not limited to, micro-electro-mechanical systems (MEMS) sensors.
PIMD 400 may be configured to treat problems in accordance with the present invention, such as by providing electrical pacing stimulation to one or both ventricles in an attempt to reverse remodeling of the ventricular wall to improve the coordination of ventricular contractions. The PIMD 400 may be configured structurally and functionally in a manner described in commonly owned U.S. Pat. Nos. 6,597,951; 6,574,506; 6,512,952; 6,501,988; 6,411,848; and 6,363,278, each of which is hereby incorporated herein by reference.
Referring now to FIG. 4B, the PIMD 400 is illustrated as including a mesh 481 configured for local measurements of the cardiac wall. The mesh 481 is coupled to the PIMD 400 using a cable 482. The mesh 481 may be configured as an (x,y) coordinate grid, where each vertical mesh element and each horizontal mesh element intersect at a node of the (x,y) coordinate system. For example, a node 483 is identified on the mesh 481 at the intersection of the third horizontal and third vertical mesh elements, if mesh elements are numbered starting at the upper left corner of the mesh 481 as illustrated in FIG. 4B. The node 483 would then correspond to the (x,y) coordinate (3,3). Each node may thus be associated with a strain measurement capability useful for local cardiac wall stress calculations.
FIG. 5 illustrates embodiments of the present invention using epicardial leads for cardiac remodeling reversal. FIG. 5 illustrates a patient's heart 590 in a cut-away view through the rib-cage 550. A lead 510 having a helical electrode 520 is implanted in a myocardium 580 in accordance with an embodiment of the present invention. During delivery of the lead 510, the electrode 520 is implanted within the myocardium 580 by rotating the lead 510. In another embodiment, the electrode 520 may be inserted into the myocardium 580 and actively extended out from the lead and into myocardial tissue.
In a fixed electrode arrangement, as the lead 510 is rotated, the sharp end 500 of the helical electrode 520 penetrates through an epicardium 560, through an epicardial space 565, and penetrates into the myocardium 580. As the lead 510 is further rotated, the sharp end 500 burrows through the tissue, penetrating further into myocardial tissue and acutely fixing the electrode within the myocardium 580. This process effectively screws the helical electrode 520 into the myocardial tissue.
The lead 510 may be affixed at a location pre-determined to have an abnormal wall stress, and/or the lead 510 may include one or more sensors, such as an acceleration sensor, a strain sensor, an ultrasonic velocity sensor, or other local stress sensor, to determine abnormal wall stress locations. For example, the helical electrode 520 may incorporate stress measurement capabilities by acting as a strain-gage, useful for determining local wall stress abnormalities after implantation. Optionally or additionally, the lead 510 may incorporate sensors capable of determining local wall stress, such as by using localized ultrasonic Doppler velocimetry. Leads incorporating ultrasonic Doppler systems are further described in commonly owned U.S. patent application Ser. No. 10/930,088 entitled “Sensor Guided Epicardial Lead,” filed on Aug. 31, 2004, which is hereby incorporated herein by reference.
Local wall stress abnormalities may be pre-determined prior to lead placement. For example, electrodes may be built into the mesh of a cardiac support device, such as the CORCAP, a trademarked device available from Acorn Cardiovascular Inc. in St. Paul, Minn., USA. Electrodes may be positioned about the heart on the epicardial surface and may be used for sensing delays in electrical activation. If, alternately or additionally, strain gauges are positioned at various points in the mesh of a CORCAP type device, delays in mechanical activation of the heart may be monitored. This would be one way to monitor mechanical dysnchrony and/or to determine wall stress abnormalities.
Referring now to FIG. 6, a method 600 of cardiac remodeling reversal in accordance with the present invention involves detecting 620, proximate the heart wall, a target region having a level of abnormal wall motion relative to neighboring regions. An electrode is implanted 630 near or at the target region. The target region is pre-excited 640 relative to the neighboring regions of the heart wall using the electrode in order to alter stress at the target region for treating cardiac tissue remodeling.
Heart wall motion 620 may be detected using, for example, an acceleration measurement, a strain measurement, and an ultrasonic velocity measurement such as a local Doppler tissue velocity measurement. The electrode may be used to pre-excite 640 the target region in response to an atrial sense, an atrial pace, a ventricular sense or pace event, or other timing methodology. The remodeling reversal pre-excitation 640 may be adjusted in accordance with activity level measurements reflective of metabolic demand. Detecting 620 the target region of the heart may involve sensing activation characteristics of heart wall tissue, such as one or more electrophysiologic characteristics, complex impedance characteristics, or other characteristics of the heart wall tissue indicative of remodeling.
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U.S. Classification 607/18, 607/19
International Classification A61N1/368, A61N1/362
Cooperative Classification A61N1/368, A61N1/3684, A61N1/3627
European Classification A61N1/362C, A61N1/368
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