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IMPLANTABLE CARDIAC STIMULATION DEVICE FOR AND METHOD OF MONITORING PROGRESSION OR REGRESSION OF HEART DISEASE BY MONITORING EVOKED RESPONSE 5 FEATURES
FIELD OF THE INVENTION
The present invention is generally directed to an implantable device for monitoring the progression or regression of heart disease. The present invention is more particularly directed to a system and method for use in an implantable cardiac stimulation device, which quantifies and stores evoked response features. Relative changes in the quantified evoked response features, over time, are indicative of the progression or regression of the heart disease.
BACKGROUND OF THE INVENTION
More people die of heart disease than any other single cause. One common form of heart disease is congestive heart failure.
Congestive heart failure (CHF) is a debilitating, end-stage disease in which abnormal function of the heart leads to 25 inadequate bloodflow to fulfill the needs of the body's tissues. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not appropriately fill with blood between heartbeats and the valves regulating blood flow 30 may become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness, and inability to carry out daily tasks may result.
Not all CHF patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive.
As CHF progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it 40 triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles to grow in volume in an attempt to pump enough blood with each heartbeat. This places a still 45 higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in ventricular filling. 50
Current standard treatment for heart failure is typically centered around medical treatment using ACE inhibitors, diuretics, and digitalis. It has also been demonstrated that aerobic exercise may improve exercise tolerance, improve quality of life, and decrease symptoms. Only an option in 1 55 out of 200 cases, heart transplantation is also available. Other cardiac surgery is also indicated for only a small percentage of patients with particular etiologies. Although advances in pharmacological therapy have significantly improved the survival rate and quality of life of patients, go patients who are refractory to drug therapy have a poor prognosis and limited exercise tolerance. Cardiac pacing has been proposed as a new primary treatment for patients with drug-refractory CHF.
In patients with heart failure and atrial fibrillation (AF), 65 the heart has often remodeled due to the disease, such that there is interstitial fibrosis and myocyte lengthening. There
is also decreased myocyte density with increased collagenation in the connective structure of the myocardium. There is further abnormal calcium handling at both the sarcoplasmic reticulum and membrane levels. Manifestations of these effects are increased fractionation of heart electrical activity, decreased conduction velocity, and increased heterogeneity of repolarization.
Bi-chamber pacing (biventricular or biatrial) has been proposed as an emerging therapy for the treatment of heart failure and atrial fibrillation. The patients who appear to gain the greatest benefit from this pacing therapy are those with the greatest dyssynchrony, since the benefit of bi-chamber pacing appears dependent upon chamber synchronization and/or appropriate sequencing.
It is desirable to have a system, which would track the progression or regression of the patient's disease, particularly as it relates to the success of any therapy in halting or reversing the remodeling. By tracking the progression or regression of heart disease, such as CHF, more closely, treatments could be managed more effectively. Commonly, patients with heart disease have an implanted cardiac stimulation device. Hence, it would be advantageous if the implanted cardiac stimulation device were able to aid in the tracking of the progression or regression of the heart disease. The present invention provides a system and method for use in such a device capable of tracking heart disease progression or regression.
SUMMARY OF THE INVENTION
The present invention provides a system and method, for use in an implantable cardiac stimulation device, for monitoring progression or regression in heart disease such as congestive heart failure. In accordance with the present invention, isolated features in evoked responses of a heart are quantified and stored in a memory over time to monitor or track the progression or regression in a patient's heart disease, such as CHF. The evoked response, especially when stimulated and sensed in a unipolar configuration, is well suited to measurement of myocardial status since it measures the course of the action potentials of the group of cells in the region of stimulation immediately beneath and surrounding the stimulation electrode. Use of the evoked response is likened to a controlled experiment since, during stimulation, propagation of the wavefront spreads out from the stimulation point, a fixed, consistent region relative to the stimulation electrode.
Hence, in accordance with the present invention, a pulse generator delivers pacing pulses to the heart to cause evoked responses of the heart. The evoked responses are sensed by a sensing circuit to generate evoked response signals which are analyzed by isolating a given feature of the evoked responses and quantifying the isolated features to provide quantified values. The quantified values are stored in a memory over time and then conveyed by a telemetry circuit to an external receiver for analysis of the progression or regression of the heart disease.
The isolated features may be: the positive slope of the evoked response (which is related to conduction velocity); evoked response continuity (which is related to fractionation); evoked response maximum positive or negative amplitudes (which are related to myocardium wall thickness and dilation); or T-wave slope and amplitude (which are related to heterogeneity of repolarization).
The monitoring of the disease progression or regression may be performed for either one of the ventricles, or both, or either one of the atria, or both. The quantified values may
further be employed by the implantable cardiac stimulation device for automatic adjustment of pacing parameters.
BRIEF DESCRIPTION OF THE DRAWINGS
Further features and advantages of the present invention 5 may be more readily understood by reference to the following description taken in conjunction with the accompanying drawings, in which:
FIG. 1 is a simplified diagram illustrating an implantable stimulation device embodying the present invention in electrical communication with at least three leads implanted into a patient's heart for delivering multichamber stimulation and shock therapy;
FIG. 2 is a functional block diagram of the device of FIG. 15 1 illustrating the basic elements for monitoring evoked responses in accordance with the present invention and providing cardioversion, defibrillation and pacing stimulation in four chambers of the heart;
FIG. 3 is a typical unipolar ventricular evoked response 20 identifying possible features, which may be extracted and quantified in accordance with the present invention;
FIG. 4 illustrates an example of the changes in several features of the ventricular evoked response while in two different states of congestive heart failure, separated in time 25 by 1 month and after treatment for CHF; and
FIG. 5 is a flow chart describing an overview of the operation of a preferred embodiment of the present invention.
DESCRIPTION OF THE PREFERRED
The following description is of the best mode presently contemplated for practicing the invention. This description 3J is not to be taken in a limiting sense but is made merely for the purpose of describing the general principles of the invention. The scope of the invention should be ascertained with reference to the issued claims. In the description of the invention that follows, like numerals or reference designa- 4Q tors will be used to refer to like parts or elements throughout.
As shown in FIG. 1, there is a stimulation device 10 in electrical communication with a patient's heart 12 by way of three leads, 20, 24 and 30 suitable for delivering multichamber stimulation and shock therapy. To sense atrial 45 cardiac signals and to provide right atrial chamber stimulation therapy, the stimulation device 10 is coupled to an implantable right atrial lead 20 having at least an atrial tip electrode 22, which typically is implanted in the patient's right atrial appendage. 50
To sense left atrial and ventricular cardiac signals and to provide left-chamber pacing therapy, the stimulation device 10 is coupled to a "coronary sinus" lead 24 designed for placement in the "coronary sinus region" via the coronary sinus os so as to place a distal electrode adjacent to the left 55 ventricle and additional electrode(s) adjacent to the left atrium. As used herein, the phrase "coronary sinus region" refers to the vasculature of the left ventricle, including any portion of the coronary sinus, great cardiac vein, left marginal vein, left posterior ventricular vein, middle cardiac go vein, and/or small cardiac vein or any other cardiac vein accessible by the coronary sinus.
Accordingly, the coronary sinus lead 24 is designed to receive atrial and ventricular cardiac signals and to deliver: left ventricular pacing therapy using at least a left ventricular 65 tip electrode 26, left atrial pacing therapy using at least a left atrial ring electrode 27, and shocking therapy using at least
a left atrial coil electrode 28. For a complete description of a coronary sinus lead, see U.S. patent application Ser. No. 09/457,277, filed Dec. 18, 1999, entitled A SELFANCHORING, STEERABLE CONARY SINUS LEAD (Pianca et. al); and U.S. Pat. No. 5,466,254, "Coronary Sinus Lead with Atrial Sensing Capability" (Helland), which patents are hereby incorporated herein by reference.
The stimulation device 10 is also shown in electrical communication with the patient's heart 12 by way of an implantable right ventricular lead 30 having, in this embodiment, a right ventricular tip electrode 32, a right ventricular ring electrode 34, a right ventricular (RV) coil electrode 36, and an SVC coil electrode 38. Typically, the right ventricular lead 30 is transvenously inserted into the heart 12 so as to place the right ventricular tip electrode 32 in the right ventricular apex so that the RV coil electrode will be positioned in the right ventricle and the SVC coil electrode 38 will be positioned in the superior vena cava. Accordingly, the right ventricular lead 30 is capable of receiving cardiac signals, and delivering stimulation in the form of pacing and shock therapy to the right ventricle.
As illustrated in FIG. 2, a simplified block diagram is shown of the multi-chamber implantable stimulation device 10, which is capable of treating both fast and slow arrhythmias with stimulation therapy, including cardioversion, defibrillation, and pacing stimulation. While a particular multi-chamber device is shown, this is for illustration purposes only, and one of skill in the art could readily duplicate, eliminate or disable the appropriate circuitry in any desired combination to provide a device capable of treating the appropriate chamber(s) with cardioversion, defibrillation and pacing stimulation.
The housing 40 for the stimulation device 10, shown schematically in FIG. 2, is often referred to as the "can", "case" or "case electrode" and may be programmably selected to act as the return electrode for all "unipolar" modes. The housing 40 may further be used as a return electrode alone or in combination with one of the coil electrodes, 28, 36 and 38, for shocking purposes. The housing 40 further includes a connector (not shown) having a plurality of terminals, 42, 44, 46, 48, 52, 54, 56, and 58 (shown schematically and, for convenience, the names of the electrodes to which they are connected are shown next to the terminals). As such, to achieve right atrial sensing and pacing, the connector includes at least a right atrial tip terminal 42 adapted for connection to the atrial tip electrode 22.
To achieve left chamber sensing, pacing and shocking, the connector includes at least a left ventricular tip terminal 44, a left atrial ring terminal 46, and a left atrial shocking terminal 48, which are adapted for connection to the left ventricular tip electrode 26, the left atrial tip electrode 27, and the left atrial coil electrode 28, respectively.
To support right chamber sensing, pacing and shocking, the connector further includes a right ventricular tip terminal 52, a right ventricular ring terminal 54, a right ventricular shocking terminal 56, and an SVC shocking terminal 58, which are adapted for connection to the right ventricular tip electrode 32, right ventricular ring electrode, 34, the RV coil electrode 36, and the SVC coil electrode 38, respectively.
At the core of the stimulation device 10 is a programmable microcontroller 60 which controls the various modes of stimulation therapy. As is well known in the art, the microcontroller 60 typically includes a microprocessor, or equivalent control circuitry, designed specifically for controlling the delivery of stimulation therapy and may further
include RAM or ROM memory, logic and timing circuitry, state machine circuitry, and I/O circuitry. Typically, the microcontroller 60 includes the ability to process or monitor input signals (data) as controlled by a program code stored in a designated block of memory. The details of the design 5 and operation of the microcontroller 60 are not critical to the present invention. Rather, any suitable microcontroller 60 may be used that carries out the functions described herein. The use of microprocessor-based control circuits for performing timing and data analysis functions are well known 10 in the art.
As shown in FIG. 2, an atrial pulse generator 70 and a ventricular pulse generator 72 generate pacing stimulation pulses for delivery by the right atrial lead 20, the right ventricular lead 30, and/or the coronary sinus lead 24 via a :5 switch bank 74. It is understood that in order to provide stimulation therapy in each of the four chambers of the heart, the atrial and ventricular pulse generators, 70 and 72, may include dedicated, independent pulse generators, multiplexed pulse generators, or shared pulse generators. The 20 pulse generators, 70 and 72, are controlled by the microcontroller 60 via appropriate control signals, 76 and 78, respectively, to trigger or inhibit the stimulation pulses.
The microcontroller 60 further includes timing circuitry which is used to control the timing of such stimulation 25 pulses (e.g., pacing rate, atrio-ventricular (AV) delay, atrial interconduction (A—A) delay, or ventricular interconduction (V—V) delay, etc.) as well as to keep track of the timing of refractory periods, blanking periods, noise detection windows, evoked response windows, alert intervals, marker 30 channel timing, etc., which is well known in the art.
The switch bank 74 includes a plurality of switches for connecting the desired electrodes to the appropriate I/O circuits, thereby providing complete electrode programma- 3J bility. Accordingly, the switch bank 74, in response to a control signal 80 from the microcontroller 60, determines the polarity of the stimulation pulses (e.g., unipolar, bipolar, combipolar, etc.) by selectively closing the appropriate combination of switches (not shown) as is known in the art. 4Q
Atrial sensing circuits 82 and ventricular sensing circuits 84 may also be selectively coupled to the right atrial lead 20, coronary sinus lead 24, and the right ventricular lead 30, through the switch bank 74 for detecting the presence of cardiac activity in each of the four chambers of the heart. 45 Accordingly, the atrial and ventricular sensing circuits, 82 and 84, may include dedicated sense amplifiers, multiplexed amplifiers, or shared amplifiers. The switch bank 74 determines the "sensing polarity" of the cardiac signal by selectively closing the appropriate switches, as is also known in 50 the art. In this way, the clinician may program the sensing polarity independent of the stimulation polarity.
Each sensing circuit, 82 and 84, preferably employs one or more low power, precision amplifiers with programmable gain and/or automatic gain control, bandpass filtering, and a 55 threshold detection circuit, as known in the art, to selectively sense the cardiac signal of interest. The automatic gain control enables the device 10 to deal effectively with the difficult problem of sensing the low amplitude signal characteristics of atrial or ventricular fibrillation. The outputs of 60 the atrial and ventricular sensing circuits, 82 and 84, are connected to the microcontroller 60 which, in turn, are able to trigger or inhibit the atrial and ventricular pulse generators, 70 and 72, respectively, in a demand fashion in response to the absence or presence of cardiac activity, 65 respectively, in the appropriate chambers of the heart. The sensing circuits, 82 and 84, in turn, receive control signals
over signal lines, 86 and 88, from the microcontroller 60 for purposes of controlling the gain, threshold, polarization charge removal circuitry (not shown), and the timing of any blocking circuitry (not shown) coupled to the inputs of the sensing circuits, 82 and 84, as is known in the art.
For arrhythmia detection, the device 10 utilizes the atrial and ventricular sensing circuits, 82 and 84, to sense cardiac signals to determine whether a rhythm is physiologic or pathologic. As used herein "sensing" is reserved for the noting of an electrical signal, and "detection" is the processing of these sensed signals and noting the presence of an arrhythmia. The timing intervals between sensed events (e.g., P-waves, R-waves, and depolarization signals associated with fibrillation which are sometimes referred to as "F-waves" or "Fib-waves") are then classified by the microcontroller 60 by comparing them to a predefined rate zone limit (i.e., bradycardia, normal, low rate VT, high rate VT, and fibrillation rate zones) and various other characteristics (e.g., sudden onset, stability, physiologic sensors, and morphology, etc.) in order to determine the type of remedial therapy that is needed (e.g., bradycardia pacing, antitachycardia pacing, cardioversion shocks or defibrillation shocks, collectively referred to as "tiered therapy").
Cardiac signals are also applied to the inputs of an analog-to-digital (A/D) data acquisition system 90. The data acquisition system 90 is configured to acquire intracardiac electrogram signals, convert the raw analog data into a digital signal, and store the digital signals for later processing and/or telemetric transmission to an external device 102. The data acquisition system 90 is coupled to the right atrial lead 20, the coronary sinus lead 24, and the right ventricular lead 30 through the switch bank 74 to sample cardiac signals across any pair of desired electrodes.
In accordance with this preferred embodiment, the data acquisition system 90 is coupled to the microcontroller and senses evoked responses from the heart 12 in response to applied stimulation pulses. The evoked response signals generated by the data acquisition system 90 are stored in a memory 94 by the microcontroller for processing by the microcontroller. More specifically, the microcontroller isolates a given feature from each evoked response signal generated by the data acquisition system 90 and quantifies the feature. The quantified feature value is then stored in memory 94. This process is repeated at regular intervals, as often as with every beat, or less often, as once or twice each day. Over time, the stored quantified values, and relative changes therein, are indicative of the progression or regression of the patient's heart disease, such as CHF. Specific evoked response features, which may be quantified for monitoring the progression or regression in the patient's heart disease, in accordance with this embodiment, will be described in detail subsequently.
The microcontroller 60 is coupled to the memory 94 by a suitable data/address bus 96. In addition to the quantified evoked response feature values, the memory 94 may store programmable operating parameters used or modified by the microcontroller 60, as required, in order to control the operation of the stimulation device 10 to suit the needs of a particular patient. Such operating parameters define, for example, pacing pulse amplitude, pulse duration, electrode polarity, rate, sensitivity, automatic features, arrhythmia detection criteria, and the amplitude, waveshape and vector of each shocking pulse to be delivered to the patient's heart 12 within each respective tier of therapy. A feature of the present invention is the ability of the microcontroller to modify or adjust the programmable parameters in response to the quantified evoked response feature values to titrate therapy delivered to the patient by the device.