JP2008539894A - Controlled intermittent stress augmentation pacing - Google Patents

Abstract

  Devices and methods are disclosed for delivering electrical stimulation to the heart in a manner that provides a protective effect against later ischemia. The protective effect is that from the normal mode of operation, the spatial pattern of depolarization changes, thereby completely switching one or more specific regions of the ventricular myocardium to a stress enhancement mode that is subject to increased mechanical stress. Generated by configuring a cardiac pacing device.

Description

Related applications

(Claiming priority)
For US Patent Application No. 60/678338, filed May 6, 2005, and US Patent Application No. 11 / 151,015, filed June 13, 2005, the application of which is incorporated herein by reference. The benefit of priority is claimed here.

(Cross-reference of related applications)
This application also relates to US patent application Ser. No. 11/030575 filed Jan. 6, 2005, entitled “INTERMITTENT STRESS AUGMENTATION PACING FOR CARDIOPROTECTED EFFECT”, the disclosure of which is incorporated herein by reference.

  The present invention relates to an apparatus and method for treating a heart disease and a device for applying electrical stimulation to the heart, such as a cardiac pacemaker.

  Coronary artery disease (CAD) occurs when the coronary arteries that supply blood to the heart muscle become stiff and narrow due to atherosclerosis. Arteries become stiff and narrow due to the build-up of plaque on the inner wall or lining of the artery. Blood flow to the heart decreases as the plaque narrows the coronary artery. This reduces the supply of oxygen to the myocardium. CAD is the most common type of heart disease and is the leading cause of death for both men and women in the United States.

  Atherosclerotic plaques are inflammatory reaction sites in the arterial wall, consisting of inflammatory cells surrounded by a lipid-containing core and connective tissue capsule. Myocardial infarction (MI) or heart attack is a rupture of an atheroma plaque in the coronary artery, causing blood to clot in the artery by exposing the plaque's highly thrombogenic lipid core to the blood (thrombosis). Sometimes happens. Complete or near-complete occlusion to coronary blood flow can damage a significant area of heart tissue and lead to sudden death, generally due to abnormal heart rhythms that inhibit effective pumping.

In addition to causing MI, CAD may also produce milder cardiac ischemia due to narrowing of the coronary lumen by atheroma plaques. When blood flow and oxygen supply to the heart are reduced, patients often experience chest pain or discomfort called angina. Angina pectoris serves as a useful warning for inadequate myocardial perfusion that can lead to more serious situations such as heart attacks or cardiac arrhythmias. Patients experiencing the development of angina are generally treated by medication or surgical revascularization. However, it has also been found that patients who experience angina prior to a heart attack often have a lower mortality rate than patients with a heart attack who do not experience such an episode. This phenomenon may be due to ischemic preconditioning of the heart due to angina, thereby making the myocardial tissue less likely to infarct if the blood supply is dramatically reduced by later coronary thrombus, It is theorized.
US Patent Application No. 60/678338 US patent application Ser. No. 11 / 151,015 US Patent Application No. 11/030575 US Patent Application No. 10/436876 US patent application Ser. No. 10 / 669,170

  Devices and methods are disclosed for delivering electrical stimulation to the heart in a manner that provides a protective effect against later ischemia. The protective effect is that the heart is intermittently switched from the normal mode of operation to a stress-enhanced mode in which the spatial pattern of depolarization changes, thereby causing one or more specific regions of the ventricular myocardium to experience increased mechanical stress. Generated by configuring a pacing device. Techniques for performing stress-enhanced pacing at optimal times are also described based on actual delay times, indications of posture changes, changes in autonomic balance, and the like.

  The present disclosure relates to a method and apparatus for using pacing therapy to precondition the heart so that it is less vulnerable to a sudden decrease in blood flow. It has been found that intermittent pacing of the heart provides a cardioprotective effect that makes the myocardium more resistant (ie, less prone to infarctions) during subsequent manifestations of myocardial ischemia. As described below, pacing therapy is applied in such a way that certain areas of the ventricular myocardium are subjected to increased mechanical stress. Increased myocardial stress is thought to precondition the heart to better withstand the effects of subsequent ischemia through signal transduction cascades that release certain cellular components and / or induce expression of specific genes. The mechanism responsible for the cardioprotective effect of increased stress may or may not be similar to the mechanism by which previous ischemia preconditions the heart. However, in animal studies, experiments have observed that pacing treatments that produce increased stress on specific areas of the myocardium produce a cardioprotective effect without making the area ischemic.

  In the following, an exemplary device is described that performs pacing therapy in a manner that preconditions the heart to better withstand later ischemia, referred to herein as intermittent stress-enhancing pacing. Also described is an explanation of how pacing can generate increased mechanical stress on the myocardial region and an exemplary pacing algorithm.

1. The mechanical effect of pacing therapy The degree of tension or stress on the heart muscle fibers as the heart muscle fibers contract is called the afterload. As the blood is pumped into the aorta or pulmonary artery, the pressure in the ventricle quickly rises from the dilation value to the contraction value, so that the part of the ventricle that contracts first will have a lower afterload than the part of the ventricle that contracts later. Shrink against. The extent to which heart muscle fibers are stretched before contraction is called preload. The maximum tension and speed at which muscle fibers shorten is increased with increasing preload, and the increased contractile response of the heart associated with increasing preload is known as the Frank Stirling principle. As the myocardial region contracts later relative to other regions, earlier contraction of the opposing region extends the later contracting region and increases its preload. Thus, myocardial regions that contract after other regions during systole undergo both increased preload and increased afterload, which causes the region to experience increased wall stress.

  When the ventricle is stimulated to contract by a pacing pulse applied via an electrode placed at a particular pacing site, excitement spreads from the pacing site by transmission through the myocardium. This is different from the normal physiological situation where the spread of excitement from the AV node to the ventricle utilizes a specialized transmission system in the heart composed of Purkin fibers that allows rapid and synchronized excitation of the entire ventricular myocardium. On the other hand, the excitement that is the result of a pacing pulse applied to a single site produces a relatively asynchronous contraction because the rate at which the excitement is transmitted through the myocardium is slower. Regions of the myocardium that are located more distal to the pacing site are excited later than the regions adjacent to the pacing site and are subject to increased mechanical stress for the reasons described above.

  Thus, ventricular contractions that are the result of pacing pulses are generally not synchronized to the same extent as intrinsic contractions and may therefore be less hemodynamically efficient. For example, in conventional bradycardia pacing, the pacing site is located in the right ventricle, so that excitement must spread from the right ventricular pacing site through the rest to the myocardium. In that case, the contraction of the left ventricle is performed in a manner that is less regulated than the normal physiological situation in which cardiac output is reduced. This problem can be overcome by pacing the left ventricle in addition to or instead of the right ventricle to produce a more coordinated ventricular contraction, referred to as cardiac resynchronization pacing . Resynchronized pacing also adds to patients suffering from inherent ventricular transmission defects to improve the efficiency of ventricular contractions and increase cardiac output, in addition to overcoming the desynchronization effects of conventional pacing therapies. Sometimes. Ventricular resynchronization therapy is performed as pacing delivered to the left ventricle only, biventricular pacing, or multiple sites in either or both ventricles.

  In contrast to resynchronization therapy, pacing therapy performed to produce a cardioprotective effect is a relatively asynchronous contraction such that the myocardial region located more distal to the pacing site is subjected to increased mechanical stress. Is a pacing that is intended to generate Such pacing, called stress-enhanced pacing, produces a myocardial depolarization pattern that is different from the dominant or chronic depolarization pattern that is the result of intrinsic or pacing activation. However, if stress-enhancing pacing is delivered relatively constant, ventricular regions that contract later may undergo hypertrophy and other remodeling processes in response to increased stress, such remodeling being May offset the cardioprotective effect. Thus, the effectiveness of stress-enhancing pacing is increased when such pacing is performed as a single treatment or multiple treatments spread over a period of time so that no remodeling is performed. Stress enhanced pacing can be performed by various means. In one embodiment, an external pacing device sends pacing pulses to the heart via pacing electrodes incorporated into a catheter that can be placed near the heart. Such catheters can also be used for other types of heart treatment or diagnosis, such as angiography or angioplasty. Stress enhanced pacing can also be performed by an implantable pacing device. As described below, a cardiac pacing device can be programmed to perform pacing that stresses a specific myocardial region intermittently. The device can also be configured to intermittently pace multiple pacing sites to provide a cardioprotective effect to multiple cardiac regions.

2. Exemplary Cardiac Devices Cardiac rhythm management devices such as pacemakers are typically implanted subcutaneously on the patient's chest and inserted into the heart from the vein to connect the device to the electrodes used for sensing Have a lead. With a programmable electronic controller, pacing pulses are output in response to elapsed time intervals and sensed electrical activity (ie, intrinsic heart beats not as a result of the pacing pulse). A pacemaker senses intrinsic cardiac electrical activity by internal electrodes located near the sensed chamber. The depolarization wave associated with the intrinsic contraction of the atrium or ventricle detected by the pacemaker is called atrial sensing or ventricular sensing, respectively. To cause such a contraction in the absence of an intrinsic beat, a pacing pulse (atrial pace or ventricular pace) having an energy greater than a pacing threshold is delivered to the chamber.

  FIG. 1 shows a system diagram of a microprocessor-based cardiac rhythm management device or pacemaker suitable for implementing the present invention. The pacemaker controller is a microprocessor 10 that communicates with the memory 12 via a bidirectional data bus. The memory 12 typically includes a ROM (Read Only Memory) for storing programs and a RAM (Random Access Memory) for storing data. The controller can be implemented by other types of logic circuits (eg, discrete components or programmable logic arrays) using a state machine type design, but a microprocessor-based system is preferred. As used herein, the term “circuit” should be construed to refer to programming of a discrete logic circuit or microprocessor.

  The instrument is equipped with multiple electrodes, each capable of being incorporated into a pacing channel and / or a sensing channel. The figure designates “a” to “d” with bipolar leads having ring electrodes 33a-d and tip electrodes 34a-d, sense amplifiers 31a-d, pulse generators 32a-d, and channel interfaces 30a-d. Four exemplary sensing and pacing channels are shown. Thus, each channel includes a pacing channel consisting of a pulse generator connected to the electrode and a sensing channel consisting of a sense amplifier connected to the electrode. By properly placing the electrodes, the channel is configured to sense and / or pace a specific atrial or ventricular site. Channel interfaces 30a-d communicate bi-directionally with the microprocessor 10, each interface outputting an analog-to-digital converter that digitizes the sense signal input from the sense amplifier, pacing pulses, and pacing pulses. It is possible to include registers that can be written by the microprocessor to change the amplitude and adjust the gain and threshold of the sense amplifier. A pacemaker sensing circuit is atrial sensing or ventricular sensing when an electrogram signal generated by a particular channel (ie, a voltage sensed by an electrode representing cardiac electrical activity) exceeds a specified detection threshold. Detect room sensing. The pacing algorithm used in a particular pacing mode uses such sensing to trigger or prevent pacing, and the intrinsic atrial rate and / or ventricular rate is between atrial sensing and ventricular sensing, respectively. Can be detected by measuring the time interval.

  The electrode of each bipolar lead is connected via a conductor in the lead to a MOS switching network 70 controlled by the microprocessor. The switching network is used to switch the electrode to the input of a sense amplifier to detect intrinsic cardiac activity and to switch the electrode to the output of a pulse generator to send pacing pulses. Depending on the switching network, the instrument is in bipolar mode using both the lead ring electrode and tip electrode, or in monopolar mode using only one of the lead electrodes and the instrument housing or can 60 acts as a ground electrode. It can also be sensed or paced. As will be described below, one way in which the device can change the spatial distribution of pacing is to switch from unipolar pacing to bipolar pacing (or vice versa), or between bipolar leads during bipolar pacing. The electrode is exchanged between the cathode and the anode. The shock pulse generator 50 is also interfaced to the controller to deliver a defibrillation shock to the atrium or ventricle via a pair of shock electrodes 51 when detecting a shocking tachyarrhythmia.

  The controller controls the pace feed through the pacing channel, interprets the sensing signal received from the sensing channel, timers to determine the refill contraction interval, sensing refractory period, and other specified time intervals. The overall operation of the device is controlled according to programmed instructions stored in the memory. The exercise level sensor 330 (eg, accelerometer, minute ventilation sensor, or other sensor that measures parameters related to metabolic demand) allows the controller to measure the pacing rate according to changes in the patient's physical activity. It becomes possible to adapt. A posture sensor is also interfaced to the controller to determine the patient's posture when heart rate and activity levels are measured. In one embodiment, the accelerometer 330 is a multi-axis accelerometer that allows the controller to calculate the patient's posture from accelerations measured along multiple axes.

  A telemetry interface 40 is also provided that allows the controller to communicate with an external device 300 such as an external programmer via a wireless telemetry link. An external programmer is a computerized device with an associated display and input means that can query the pacemaker, receive stored data, and directly adjust pacemaker operating parameters. The external device 300 shown in the figure can also be a remote monitoring unit. The external device 300 can also be interfaced and remotely programmed to a patient management network 91 that allows the implantable device to send data and alert messages over the network to the clinician. The network connection between the external device 300 and the patient management network 91 can be implemented, for example, by an internet connection, on a telephone line, or via a cellular radio link.

  The controller can operate the instrument in several programmed pacing modes that determine how pulses are output in response to sensing events and the expiration of time intervals. Most pacemakers for treating bradycardia are programmed to operate synchronously in a so-called demand mode in which sensed cardiac events that occur within a defined interval trigger or block pacing pulses. The blocked demand pacing mode uses a supplemental contraction interval so that a pacing pulse is delivered to the ventricle during the cardiac cycle only after expiration of a defined supplemental contraction interval in which no chamber-specific beats are detected. Control pacing according to perceived specific activity. The ventricular pacing replacement interval can be restarted by a ventricular or atrial event, which allows the pacing to track the intrinsic atrial beat. Multiple excitatory stimulation pulses can be delivered to multiple sites during the cardiac cycle to pace the heart according to the bradycardia mode and provide additional excitement to the selected site.

3. Implementation of Intermittent Stress Enhanced Pacing The device shown in FIG. 1 is configured to perform intermittent stress enhanced pacing in several different ways. In one embodiment that may be appropriate for patients who do not require bradycardia or resynchronization pacing, the device may not perform any pacing therapy except at periodic intervals (eg, 5 minutes daily). Programmed. In that case, pacing therapy is performed in any selected pacing mode, such as right ventricular only pacing, left ventricular only pacing, or biventricular pacing. In some patients with an embedded pacemaker, intermittent pacing may occur accidentally if the patient is relatively chronologically acceptable, has no AV block, and the pacemaker's program refill interval is long enough Is possible. However, to ensure enhanced stress pacing and cardioprotective effects, the pacemaker should be programmed so that pacing occurs at scheduled intervals regardless of the patient's intrinsic rate. Another embodiment that may be appropriate for patients requiring bradycardia and / or resynchronization pacing is pacing applied by intermittently switching from a normal mode of operation to one or more stress-enhancing pacing modes. -Intermittent stress-enhancing pacing is performed by intermittently changing the spatial distribution of pulses. Switching to the stress enhancement mode may cause the pacing pulse output configuration and / or pulse output of the device to excite different myocardial regions first, and thereby later excite different regions distal to one or more pacing sites. Changing the sequence, where the pulse output configuration specifies a particular subset of available electrodes used to deliver the pacing pulses, and the pulse output sequence is inter-pulse Specify the timing relationship. The pulse output configuration is determined by the controller selecting the specific pacing channel used to output the pacing pulse and selecting the specific electrode used by the channel having the switch matrix 70. It is done. If the normal mode of operation is the primary pacing mode for performing ventricular pacing therapy, the stress enhancement mode changes the spatial pattern of depolarization so that certain myocardial regions experience increased mechanical stress. It is possible to excite the ventricular myocardium at one or more sites different from the primary pacing mode. Intermittent spatial changes in pacing can be achieved by, for example, intermittent switching from left ventricular pacing mode to right ventricular pacing mode or vice versa, or biventricular pacing mode or other multiple ventricular pacing modes. Generated by switching intermittently from mode to single ventricular pacing mode or vice versa. Spatial variation of pacing can also be achieved by using a bipolar pacing lead with relatively spaced electrodes and intermittently switching from unipolar pacing to bipolar pacing or vice versa, or during bipolar pacing It can also be produced by intermittently switching which bipolar lead electrode is a cathode or an anode.

  By using multiple pacing electrodes placed at different pacing sites, several stress enhancement modes may be switched intermittently to provide enhanced stress to multiple myocardial regions. Each such stress augmentation mode is determined by a certain pulse output configuration and pulse output sequence, and includes intermittent stress enhancement implementations and temporary switching to each mode according to a programmed schedule, in which case the instrument Stay in the stress enhancement mode for a specified time called the stress enhancement period (eg, 5 minutes). By properly positioning the pacing electrodes, a cardioprotective effect can be imparted to a large area of the ventricular myocardium. Such multiple pacing sites are provided by multiple leads or by leads having multiple electrodes incorporated therein. For example, multiple electrode leads are screwed into the coronary sinus to provide multiple left ventricular pacing sites. In one embodiment, stress enhanced pacing is performed during each cardiac cycle as multi-site pacing via multiple multiple electrodes. In other embodiments, stress enhanced pacing is performed as single site pacing, where pacing sites can be alternated between multiple electrodes during successive cardiac cycles or during different stress enhancement periods. . Switching to stress augmentation mode also includes adjusting one or more pacing parameters such as the supplemental contraction interval that determines the pacing rate to ensure that the stress augmentation pace is not blocked by intrinsic cardiac activity. It is also possible.

  As described above, the device controller can be programmed to intermittently switch from the normal operation mode to the stress enhancement mode. In the normal mode of operation, the device may perform no therapy or primary pacing with a different pacing configuration, different pulse output sequence, and / or different pacing parameter settings than the stress enhancement mode. It is possible to perform pacing therapy in mode. The device can be equipped with a single ventricular pacing channel or multiple ventricular pacing channels each having pacing electrodes disposed at different pacing sites. In one example, the stress enhancement mode uses at least one pacing channel that is not used in the primary pacing mode. When the device receives a command to switch to stress enhancement mode for a specified time, it initiates stress enhancement pacing, where such commands are generated internally according to a defined schedule or externally It can be received from a programmer or via a patient management network. After the command is received, the device then simply switches to stress enhancement mode for a specified time when the pacing parameter is a predetermined value. For example, in an atrial-triggered synchronization mode (eg, DDD or VDD) with a pre-established atrial-ventricular (AV) supplemental systole period and a ventricular-ventricular (VV) supplemental systole period, stress enhanced pacing is performed on the ventricles. A non-atrial triggered ventricular pacing mode (e.g., with a pre-determined VV supplemental systole period that can be set to a value that results in a high pacing frequency or , VVI), stress enhanced pacing can be performed. However, it is desirable to incorporate additional steps into the algorithm before switching. For example, the refill contraction interval for the stress enhancement mode can be determined dynamically prior to mode switching to ensure a high pacing frequency. In embodiments where the stress enhancement mode is a non-atrial trigger pacing mode, the instrument measures the patient's intrinsic heart rate prior to mode switching, and then the pacing rate of the stress enhancement mode is slightly higher than the intrinsic rate Thus, it is possible to set the VV replenishment contraction period. If the patient is undergoing rate-adapted ventricular pacing therapy in the primary pacing mode, the VV supplemental contraction period in stress enhancement mode can be similarly modulated by the exercise level measurement. In embodiments where stress enhanced pacing is performed by an atrial trigger pacing mode, the device can measure the patient's intrinsic AV interval prior to mode switching (eg, some prior to mode switching). As an average over a period), it is thereby possible to set the AV supplemental contraction period during which ventricular pacing is performed so that the ventricle is paced at a high frequency during the stress augmentation period. Also, in some patients, it may be desirable for the device to examine the patient's exercise level before switching to stress enhancement mode and cancel the mode switch if the exercise level is above a certain threshold. . This may be the case if the patient's ventricular function is somewhat impaired by stress enhanced pacing. The device can also measure the patient's intrinsic AV interval prior to mode switching (eg, as an average over several cycles preceding mode switching), thereby increasing the ventricle during the stress enhancement period. An AV supplement systole period can be set during which ventricular pacing is performed in the atrial trigger mode to pace at frequency.

4). Controlled Implementation of Stress Enhanced Pacing As explained above, stress enhanced pacing performs a cardioprotective effect by creating mechanical asynchrony in the heart. Asynchrony increases cell stretch in later contraction areas, which protects the heart from ischemic events temporarily (hours to days) (ie, minimizes damage) intracellular signaling cascade It is possible to start. Since some of the cardioprotective effects are very short, treatment is best performed when the patient is likely to have an ischemic event. It has been reported that there is circadian variation in the risk of having MI. In particular, patients are at highest risk, especially in the morning after waking up from sleep. The implantable pacing device determines the time of the day or when the patient wakes up from sleep and performs a treatment that is optimized for this circadian variation by correspondingly stress-enhancing pacing. Can be programmed. For example, the device can be programmed to perform treatment at a particular day time from the device time stamp. Alternatively, the device may be configured to detect when the patient is awake by using a posture sensor (such as a multi-axis accelerometer) to detect a change from standing to standing or sitting. it can. Arousal can also be detected by changes in heart rate variability (HRV) due to sympathetic uplift associated with arousal as assessed by LF / HF ratio, SDANN, or an autonomous balance monitor. After wakefulness is detected (or morning time is specified), the device can be programmed to initiate stress enhanced pacing (at VDD or DDD, specific AV delay and LV offset). is there. As described above, pacing can be performed for a specified length of time (eg, 5 minutes), then turned off for a certain length of time and started again, and the amount of time that treatment is performed is programmable Or it can be hard coded into the device. Pacing site, AV delay, LV offset can also be changed each time the treatment is turned on to provide greater variation in mechanical contraction and thus greater stress enhancement. . Also, depending on the degree of change in posture or HRV, different parameter settings for single or multiple pacing sites, AV delays, and LV offsets can be used.

  FIG. 2 shows an exemplary algorithm in which stress-enhancing pacing is performed at a scheduled period according to the patient's predicted wake time. In step Al, the device waits for the timer to expire to switch to the stress enhancement mode, where the timer is determined to expire when it matches the time the patient is expected to wake up from sleep. Yes. When the timer expires, the instrument sets an AV delay and VV supplemental contraction period for stress enhanced pacing in atrial trigger pacing mode in step A2, where the supplemental contraction period is the current measured heart rate of the patient. It can be set according to a number or intrinsic AV interval, set to a pre-programmed fixed value, or set to a value that changes each time stress-enhanced pacing is performed. In step A3, the device switches to the stress enhancement mode for a specified time period. When the designated time for stress enhanced pacing expires in step A4, the device stops stress enhanced pacing in step A5, returns to step A1, and waits for the expiration of another timer.

  However, performing stress-enhanced pacing with a strict time schedule assumes that the patient wakes up at the same time every day. FIG. 3 illustrates another exemplary algorithm in which stress-enhanced pacing is performed according to a signal received from a posture sensor that indicates when a patient has changed from a supine position to a standing or sitting position and is awake from sleep. Show. Of course, the patient may lie down and wake up at other times of the day. Thus, in order to add better specificity to this technique, a timer can optionally be used to determine the wake-up window, so that stress-enhanced pacing allows the patient to wake This is only done when changing from standing to standing during the up window. For example, the wake-up window can be determined as between 6:00 AM and 8:00 AM to take into account that the patient may not wake up at the same time every day. When the posture sensor signal indicates that the patient is waking up from standing to standing during the wake-up window, the patient is at an optimal time for stress-enhanced pacing as described above. It is very likely that you are awake from sleep. In step B1, the device waits for a signal from the posture sensor indicating that the patient is getting up from the prone position. In step B2, the device checks whether the time of the day is within the determined wake-up window. If so, the instrument sets the AV delay and VV refill contraction period for stress enhanced pacing as described above in step B3. Next, in step B4, the device switches to the stress enhancement mode for a specified time period. When the specified time period for stress-enhancing pacing expires in step B5, the device stops stress-enhancing pacing in step B6, returns to step B1, and waits for another posture change.

  Another surrogate indicator for patient arousal is changes in autonomic balance that can be determined by analyzing heart rate variability. Increased sympathetic nervous system activity occurs upon arousal and is therefore either alone or described above to indicate that the patient is awake from sleep so that stress enhanced pacing can be performed at an optimal time. Can be used in combination with other techniques. Also, regardless of whether it is associated with arousal, an increase in sympathetic activity can indicate metabolic stress and can therefore constitute the basis for optimal implementation of stress-enhancing pacing. One means by which increased sympathetic activity can be detected is through spectral analysis of heart rate variability. Heart rate variability refers to variability in time intervals between consecutive heart beats in sinus rhythm, mainly due to interactions between sympathetic and parasympathetic branches of the autonomic nervous system. Spectral analysis of heart rate variability involves decomposing a signal representing successive beats-beat intervals into separate components representing the amplitude of the signal at different oscillation frequencies. The amount of signal power in the low frequency (LF) band ranging from 0.04 Hz to 0.15 Hz is affected by both sympathetic and parasympathetic activity levels, while 0.15 Hz to 0.40 Hz. It has been found that the amount of signal power in the high frequency (HF) band of the range is mainly a function of parasympathetic activity. Thus, the signal power ratio expressed as LF / HF ratio is a good indicator of the state of autonomic balance, and a high LF / HF ratio indicates increased sympathetic activity. An LF / HF ratio that exceeds a specified threshold is interpreted as an indicator that cardiac function is not appropriate. The cardiac rhythm management device is programmed to determine the LF / HF ratio by analyzing data received from an atrial or ventricular sensing channel. The interval between successive atrial or ventricular senses, called beat-beat interval or BB interval, can be measured and collected for a period of time or a specified number of beats. The resulting series of RR interval values is then stored as a discrete signal and analyzed to determine energy in the high and low frequency bands as described above. A technique for assessing the LF / HF ratio based on interval data is the same, named “STATISTICAL METHOD FOR ASSESSING AUTONOMIC BALANCE” filed on May 12, 2003, the disclosure of which is incorporated herein by reference. U.S. Patent Application No. 10 / 436,766 assigned to the assignee and U.S. Patent Application No. 10 / 669,170 entitled "DEMAND-BASED CARDIAC FUNCTION THERAPY" filed on September 23, 2003.

  FIG. 4 illustrates an exemplary algorithm in which stress-enhancing pacing is performed according to an autonomic balance assessment. In step C1, the device waits until the LF / HF ratio determined by analyzing the data received from the atrial or ventricular sensing channel is greater than a specified threshold. If so, in step C2, the instrument sets the AV delay and VV refill contraction period for stress enhanced pacing as described above. Next, in step C3, the device switches to the stress enhancement mode for a specified time period. When the specified time for stress enhanced pacing to expire at step C4, the device stops stress enhanced pacing at step C5, returns to step C1, and waits for another indication of increased sympathetic activity.

  Although the invention has been described with reference to the above specific embodiments, many alternatives, changes, and modifications will be apparent to those skilled in the art. Other such alternatives, changes, and modifications are intended to be within the scope of the appended claims.

1 is a block diagram of an exemplary cardiac rhythm management device for implementing the present invention. FIG. FIG. 6 illustrates an exemplary algorithm for controlling and implementing intermittent stress-enhancing pacing. FIG. 6 illustrates an exemplary algorithm for controlling and implementing intermittent stress-enhancing pacing. FIG. 6 illustrates an exemplary algorithm for controlling and implementing intermittent stress-enhancing pacing.

Claims (19)

A pacing channel for delivering pacing pulses to selected ventricular myocardial sites;
A controller for controlling the delivery of pacing pulses according to a programmed pacing mode;
Stress from which the controller is subjected to increased mechanical stress from a normal operating mode when one or more specific regions of the ventricular myocardium are compared to the stress experienced by those regions during the normal operating mode Programmed to switch to augment mode,
The controller is programmed to switch to stress augmentation mode for a specified amount of time when the timer expires, and the timer expires to coincide with when the patient is predicted to be awake from sleep. Cardiac rhythm management equipment.   The device of claim 1, wherein the normal mode of operation is a primary pacing mode for performing ventricular pacing therapy, and the stress enhancement mode produces a different depolarization pattern from the primary pacing mode.   The apparatus of claim 2, wherein the stress enhancement mode excites the ventricular myocardium at one or more sites different from the primary pacing mode.   The device of claim 2, wherein the switching from a primary pacing mode to a stress enhancement mode includes switching from bipolar pacing to monopolar pacing or vice versa.   3. The apparatus of claim 2, wherein the switching from a primary pacing mode to a stress enhancement mode includes switching which electrode of a bipolar pacing lead is a cathode and which electrode is an anode. A plurality of pacing channels for delivering pacing pulses to a plurality of ventricular pacing sites;
The apparatus of claim 2, wherein the stress enhancement mode uses at least one pacing channel that is not used in the primary pacing mode. A pacing channel for delivering pacing pulses to selected ventricular myocardial sites;
A controller that controls the delivery of pacing pulses according to a programmed pacing mode;
An attitude sensor interfaced with the controller;
Stress from which the controller is subjected to increased mechanical stress from a normal operating mode when one or more specific regions of the ventricular myocardium are compared to the stress experienced by those regions during the normal operating mode Programmed to switch to augment mode,
The heart is programmed to switch to the stress enhancement mode for a specified time when the controller receives a signal from the posture sensor indicating that the patient's posture has changed from a supine position to a standing or sitting position. Rhythm management equipment.   8. The device of claim 7, wherein the normal mode of operation is a primary pacing mode for performing ventricular pacing therapy, and the stress enhancement mode produces a different depolarization pattern from the primary pacing mode.   9. The device of claim 8, wherein the stress enhancement mode excites the ventricular myocardium at one or more sites different from the primary pacing mode.   9. The device of claim 8, wherein the switching from a primary pacing mode to a stress augmentation mode includes switching from bipolar pacing to monopolar pacing or vice versa.   9. The apparatus of claim 8, wherein the switching from a primary pacing mode to a stress enhancement mode includes switching which electrode of a bipolar pacing lead is a cathode and which electrode is an anode. A plurality of pacing channels for delivering pacing pulses to a plurality of ventricular pacing sites;
9. The device of claim 8, wherein the stress enhancement mode uses at least one pacing channel that is not used in the primary pacing mode.   When the controller receives a signal from the posture sensor indicating that the patient's posture has changed from prone to standing or sitting, and the time of the day is determined by a time stamp 8. The device of claim 7, further programmed to switch to the stress augmentation mode for a specified period of time when within the window. A pacing channel for delivering pacing pulses to a selected ventricular myocardial site;
A sensing channel for detecting intrinsic cardiac activity;
A controller for controlling the delivery of pacing pulses according to a programmed pacing mode;
The controller is programmed to determine an LF / HF ratio by analyzing data received from the sensing channel;
Stress from which the controller is subjected to increased mechanical stress from a normal operating mode when one or more specific regions of the ventricular myocardium are compared to the stress experienced by those regions during the normal operating mode Programmed to switch to augment mode,
A cardiac rhythm management device, wherein the controller is programmed to switch to the stress enhancement mode for a specified time when the LF / HF ratio is higher than a specified threshold.   15. The device of claim 14, wherein the normal mode of operation is a primary pacing mode for performing ventricular pacing therapy, and the stress enhancement mode results in a depolarization pattern different from the primary pacing mode.   The apparatus of claim 15, wherein the stress enhancement mode excites the ventricular myocardium at one or more sites different from the primary pacing mode.   16. The device of claim 15, wherein the switching from a primary pacing mode to a stress augmentation mode includes switching from bipolar pacing to monopolar pacing or vice versa.   The apparatus of claim 15, wherein the switching from a primary pacing mode to a stress enhancement mode comprises switching which electrode of a bipolar pacing lead is a cathode and which electrode is an anode. A plurality of pacing channels for delivering pacing pulses to a plurality of ventricular pacing sites;
The apparatus of claim 15, wherein the stress enhancement mode uses at least one pacing channel that is not used in the primary pacing mode.

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