Abstract:
A system and method for electrically stimulating the heart muscle to improve heart function requires identifying a site in the venous system adjacent a sympathetic nerve. An electrode is then positioned at the site to electrically stimulate the nerve. In turn, this stimulation releases norepinephrine from the nerve to improve heart muscle contraction.

Description:
[0001]    This application is a continuation-in-part of application Ser. No. 12/190,097, filed Aug. 12, 2008, which is currently pending. The contents of application Ser. No. 12/190,097 are incorporated herein by reference. 
     
    
     FIELD OF THE INVENTION 
       [0002]    The present invention pertains generally to systems and methods for treating heart disease. More particularly, the present invention pertains to systems and methods for electrically stimulating the heart muscle to improve heart function. The present invention is particularly, but not exclusively, useful as a system or method wherein an electrode is positioned in the coronary sinus, or a vein connected with the coronary sinus, to be adjacent a sympathetic nerve for stimulation of the nerve and muscle to improve heart muscle contractions. 
       BACKGROUND OF THE INVENTION 
       [0003]    Normal heart function is characterized by a rhythmic contraction of the heart muscle, wherein each contraction is followed by a refractory period and cardiac diastole during which the heart muscle relaxes to be refilled with circulating blood. A diseased heart, however, may experience filling disorders or ineffective contractions under certain conditions that diminish heart and circulatory function leading to heart failure. In response to a diminished heart function, a relatively common practice has been to place electrodes via the cardiac veins on the epicardial surface of the heart&#39;s left ventricle, and to then electrically stimulate the area of placement for the purpose of synchronizing heart contractions. Such a technique, however, is not predictably effective and has resulted in no benefit in significant numbers of patients where substantial benefit would have been predicted. Moreover, the possibility of cell damage in the area of electrode placement from observed loss in contractile function has raised additional concerns. 
         [0004]    Though several mechanisms are known to contribute to contractions of the heart muscle, they each do so in different ways. As indicated above, one such mechanism involves a direct electrical stimulation of the heart muscle and control of the sequence of muscle activation. Another mechanism for improving muscle function, however, involves the stimulation of sympathetic nerves. More specifically, it is known that norepinephrine (a derivative of adrenaline released from the nervous system nerve endings at the heart) is a potent stimulant of contraction on the heart muscle. It is also known that sympathetic nerves can be electrically stimulated to secrete norepinephrine in response to relatively low intensity stimulation patterns. Importantly, stimulation of the sympathetic nervous system can be efficacious for energizing the heart muscle by causing the release of norepinephrine at low stimulation intensities that do not have any direct effects to electrically stimulate the heart muscle itself. 
         [0005]    In light of the above, it is an object of the present invention to provide a system and method that will improve heart function by indirectly stimulating the sympathetic nervous system. Another object of the present invention is to provide a system and method that avoids direct stimulation of the heart muscle while improving heart function with indirect electrical stimulation. Yet another object of the present invention is to improve heart function using low intensity, electrical stimulation patterns during the heart&#39;s refractory period that will not adversely affect the heart muscle, or otherwise diminish its local muscle function. Another object of the present invention is to provide a system and method for improving heart function by electrical stimulation that alters the sequence of muscle activation but is also focused on activation of the cardiac sympathetic nervous system, is simple to implement, is easy to use and is comparatively cost effective. 
       SUMMARY OF THE INVENTION 
       [0006]    In accordance with the present invention, a system and method for electrically stimulating a sympathetic nerve to improve heart function employs an electrode that is positioned in the vasculature of a patient for epicardial heart stimulation. More particularly, the electrode is positioned in the coronary sinus, or in a vein connected to the coronary sinus. And, it is positioned adjacent to a sympathetic nerve (i.e. nerve bundle). Selective stimulation of the sympathetic nerve by the electrode then causes a secretion (release) of norepinephrine that improves the heart muscle contraction (i.e. left ventricle) in the area of the electrode, blood vessel (vein) and nerve. 
         [0007]    Structurally, the system of the present invention, includes a voltage source (e.g. a pacemaker), a stimulator, and a sensor that are respectively connected to a deployment catheter. Specifically, the voltage source and stimulator are electrically connected to an electrode that is located at/near the distal end of the deployment catheter. Similarly, the sensor is electrically connected to a probe that is also located at/near the distal end of the deployment catheter. Further, the system can include a computer having pre- programmed instructions for concertedly controlling the operation of the voltage source and the stimulator. As envisioned for the present invention, the voltage source can be either a pacemaker or a pacing catheter of a type well known in the pertinent art. In use, the voltage source (pacemaker) is programmed to establish heart muscle contractions at a predetermined rate. Specifically, this is done to control the desired frequency of heart cycles per minute, and to thereby support a more synchronous activation of cardiac pump function. 
         [0008]    As envisioned for the present invention, the stimulator can be incorporated as an additional feature of the voltage source, or it can be used as an independent component. In either case, operations of the voltage source and the stimulator are coordinated by the computer. Thus, in addition to the heart muscle contractions that are stimulated by the voltage source at the predetermined rate to establish heart function cycles, the stimulator component will create a train of electrical pulses that are generated during the refractory period in the heart cycle. More specifically, this train of electrical pulses will preferably have a pulse frequency that is less than 600 pulses per second, and will extend over a time duration in the heart cycle that is less than approximately 300 ms. Also, the intensity of the pulses in this pulse train will be less than the level that would be effective for directly stimulating a heart muscle contraction. Structurally, the voltage source (pacemaker) and the stimulator can be electrically connected with the electrode by a same wire. 
         [0009]    For an operation of the present invention, an appropriate sympathetic nerve (nerve bundle) on the epicardial surface of the left ventricle is identified. Importantly, the nerve needs to be located either adjacent the coronary sinus or a vein that is connected to the coronary sinus. Location of this nerve can be accomplished by well known mapping techniques, such as by using a loop catheter. Once the site of an appropriate sympathetic nerve has been identified, the electrode is advanced through the venous system to be positioned at the site adjacent to the nerve in the vein. The electrode can then be activated. 
         [0010]    Activation of the electrode can be accomplished either actively, in accordance with pre-programmed instructions from the computer, or reactively in response to the contractions of the heart muscle. In either case, an activation of the electrode is done twice during each heart cycle, for two different reasons. For one, the electrode is activated to cause contractions of the heart muscle at the predetermined rate established for heart cycles by the voltage source. For another, within the refractory period of each heart cycle, a train of pulses is generated to stimulate the sympathetic nerve for a release of norepinephrine. Importantly, the sympathetic nerve should be stimulated while the heart muscle is not able to electrically respond to electrical stimuli. Nevertheless, the released norepinephrine is available for stimulation of the heart muscle when the heart is ready for its next contraction. Thus, stimulation of the sympathetic nerve only indirectly assists a heart muscle contraction. Further, the voltage level necessary for stimulating the sympathetic nerve is lower than the threshold necessary for a direct stimulation of the heart muscle. 
         [0011]    An important feature of the present invention is that whenever a heart function cycle is interrupted (e.g. a premature contraction during diastole) the system will reset itself. Specifically, when competing electrical activity interrupts a heart cycle, the sensor will detect the competing activity, and will accordingly inhibit the voltage source output until a time interval is sensed wherein there is no competing electrical activity. At that time (i.e. when there is no longer any competing electrical activity), the voltage source (pacemaker) is returned to its normal operation. Thus, the system returns to the function of concertedly stimulating heart muscle contractions and the secretions of norepinephrine from a sympathetic nerve that will assist the heart muscle contractions. 
         [0012]    A computer program for the present invention is required to coordinate and control the electrical stimulation functions of the voltage source and the stimulator. Specifically, in an operation of the present invention, the voltage source (pacemaker) may be used to activate an electrode that will directly stimulate contractions of the heart muscle at the predetermined rate for heart function cycles. Importantly, the intensity of these electrical stimulations is computer-controlled and must be sufficient to cause a heart muscle contraction. As envisioned for the present invention, however, the required intensity is mitigated due to the assist that is provided by the secretion of norepinephrine from a sympathetic nerve. For the present invention, these secretions of norepinephrine are stimulated by an activation of the electrode. Specifically, for this purpose, a train of electrical pulses are generated whose duration and intensity are both computer-controlled. Thus, both heart muscle contractions and sympathetic nerve secretions are concertedly controlled by the computer. 
         [0013]    As envisioned for the present invention, and as implied above, the system of the present invention may operate in any of several modes. For one, the computer can be pre-programmed with low-intensity stimulation patterns. For another, the sensor can be used to identify when electrical activation of the heart muscle occurs, and can then activate the voltage source for stimulation of the nerve during the heart&#39;s refractory period. Still another mode would be to couple the system into a larger assembly for the execution of other stimulation plans. 
     
    
     
       BRIEF DESCRIPTION OF THE DRAWINGS 
         [0014]    The novel features of this invention, as well as the invention itself, both as to its structure and its operation, will be best understood from the accompanying drawings, taken in conjunction with the accompanying description, in which similar reference characters refer to similar parts, and in which: 
           [0015]      FIG. 1  is a schematic drawing of the components of a system for the present invention; 
           [0016]      FIG. 2  is a drawing of the diaphragmatic surface of the heart showing only veins and proximate nerve bundles; 
           [0017]      FIG. 3  is a time graph of the electrical and mechanical cycles of the heart; and 
           [0018]      FIG. 4  is a time graph of electric pulse intensities provided for stimulating the heart muscle and a sympathetic nerve during a heart function cycle. 
       
    
    
     DESCRIPTION OF THE PREFERRED EMBODIMENTS 
       [0019]    Referring initially to  FIG. 1 , a system for transvascular activation of sympathetic cardiac nerves that are useful for improving heart function in accordance with the present invention is shown and is generally designated  10 . As shown, the system  10  includes a deployment catheter  12  having an electrical probe  14  and an electrode  16  mounted at its distal end  18 . The proximal end  20  of the deployment catheter  12  is affixed to an electrical connector  22 . As also shown in  FIG. 1 , the system  10  includes a voltage source  24  that is electrically connected to the connector  22 . For purposes of the present invention, the voltage source  24  may be a pacemaker or a pacing catheter of a type well known in the pertinent art. Further, the voltage source  24  may include a stimulator  25  or, alternatively, the stimulator  25  may be an independent component. In either case, both the voltage source  24  and the stimulator  25  are electrically connected to the electrode  16 . 
         [0020]    Still referring to  FIG. 1 , it will be seen that the system  10  further includes a sensor  26  and a computer  28  that are each electrically connected to the voltage source  24 . Also, the voltage source  24  is connected, through the connector  22 , with the electrode  16  that is mounted at the distal end  18  of the deployment catheter  12 . Further, the sensor  26  is connected with the probe  14  through the connector  22 . With these connections, it is to be appreciated that the voltage source  24  is responsive to both the sensor  26  and to the computer  28 . 
         [0021]    A heart muscle is shown in  FIG. 2  and is generally designated  30 . Anatomically, a view of the diaphragmatic surface of the heart muscle  30 , ( FIG. 2 ), shows its coronary sinus  32  and several connecting veins. In particular, the posterior vein  34  of the left ventricle, and the middle cardiac vein  36  are shown. Also shown are sympathetic nerve(s)  38  in the nervous system, of which the nerve bundles  38   a,    38   b  and  38   c  are only exemplary. Importantly, the nerves  38  are located on the epicardial surface of the left ventricle  40 , and they are adjacent to either the coronary sinus  32  or one of the veins connected with the coronary sinus  32  (e.g. veins  34  or  36 ). 
         [0022]    For the operation of the system  10  of the present invention, the heart muscle  30  is initially mapped to identify an appropriate nerve(s)  38 . Specifically, as implied above, an appropriate nerve  38  is one that is adjacent the coronary sinus  32  or a vein that is connected with the coronary sinus  32  (e.g. vein  34  or  36 ). Also, it is important that the nerve  38  be at a location on the epicardial surface of the left ventricle  40  of heart muscle  30  where it will be efficacious for stimulating the heart muscle  30 . Once an appropriate nerve(s)  38  has been identified, the deployment catheter  12  is advanced through the vasculature of the patient (not shown) to position the electrode  16  in the vein (e.g.  32 ,  34  or  36 ) for stimulation of the adjacent nerve (e.g. respectively  38   a,    38   b  or  38   c ). 
         [0023]      FIG. 3  provides a generalized time graph for the cyclical activity of the heart muscle  30 . More specifically,  FIG. 3  provides a sequential time line for the interaction between the system  10  and the heart muscle  30  during a beat of the heart muscle  30 . This includes, an electrical activation of system  10 , the subsequent mechanical activation of the heart muscle  30  (i.e. contraction), and the subsequent relaxation or diastole that follows each contraction. The cycle, of course, is repetitive. 
         [0024]    As shown for a single beat (i.e. cycle) of the heart muscle  30 , activation of the heart muscle  30  begins at the time “t 0 ”. This activation continues from the time “t 0 ” to the time “t 1 ”, through what is known as the refractory period  42 . In more detail, the refractory period  42  lasts for a time duration of about 120 to 300 ms, and occurs when the heart muscle  30  is not able to respond to an electrical stimulation. The nerve  38 , however, is able to respond during a refractory period  42  by secreting norepinephrine. As envisioned for the system  10  of the present invention, the magnitude of the electric pulse that is provided by stimulator  25  for use in stimulating the nerve  38  during the refractory period  42  can be controlled. Specifically it can be programmed to be less than a level that would otherwise be efficacious for directly stimulating a contraction of the heart muscle  30 . 
         [0025]    At the time “t 1 ” shown in  FIG. 3 , the refractory period  42  ends and a relative refractory period  44  begins wherein the heart muscle  30  electrically recovers from the refractory period  42 . The relative refractory period  44  then ends at the time “t 2 ” when the heart muscle  30  contracts. Importantly, this contraction is assisted by the norepinephrine that was secreted by nerve  38  in response to an activation of the voltage source  24  during the refractory period  42 . As shown, this contraction is followed by a relaxation or diastole that lasts from a time “t 3 ” until another cycle begins at the time “t 0 ′”. For purposes of the present invention, the computer  28  can be pre-programmed to accomplish the described cycle. Alternatively, the sensor  26  can receive a signal from the probe  14  that indicates a spontaneous electrical activation signal, and the voltage source  24  can then be responsive to the sensor  26  by activating the electrode  16  during the respective refractory period. 
         [0026]    It is to be appreciated that the above disclosed operation of the stimulator  25  may be accomplished in concert with a direct stimulation of the heart muscle  30  by the voltage source  24 . An example of this concerted operation is shown in  FIG. 4 , where a heart function cycle is shown to begin at a time “t 0 ” and extend to a time “t 0 ′”. Note: primed identifiers in  FIG. 4  pertain to a subsequent heart function cycle. For purposes of disclosure, it will be noted that a heart function cycle can also be considered as starting at the time “t 2 ” (when a heart contraction begins) and extending to a time “t 2 ′”. In either case, if the heart muscle  30  is to be directly stimulated by the voltage source  24 , this stimulation will be accomplished at a predetermined rate (e.g. 60/minute) to establish a desired duration for each heart function cycle. 
         [0027]    With reference to  FIG. 4 , consider a heart function cycle that begins at time “t 0 ”. Further, consider that a stimulation of a nerve bundle  38 ( a - c ), and a stimulation of the heart muscle  30 , will both occur during a same heart function cycle. As shown, a train of electrical pulses  46  is generated by the stimulator  25  during the refractory period  42  that extends from “t 0 ” to “t 1 ” (see  FIG. 3 ). Within this refractory period  42 , the pulse train  46  will continue through a time interval  48 , and each pulse in the pulse train  46  will have an intensity  50  that is below the intensity  52  that is required for a direct stimulation of the heart muscle  30 . As envisioned for the system  10  of the present invention, the time interval  48  will typically be less than 300 ms, and the frequency for electrical pulses in the pulse train  46  will be approximately 600/sec. Actual values for these variables are programmable, and will be controlled by the computer  28  during an operation of the system  10 . 
         [0028]    As noted above, several characteristics of the electrical pulses from the stimulator  25  are important for the present invention. For one, the magnitude and duration of each pulse can be pre-programmed and, thus, varied as required for the particular patient&#39;s needs. For another, the magnitude of each pulse should be and, indeed, is preferably below the voltage threshold that would otherwise be required to directly stimulate the heart muscle  30 . With these considerations in mind, low-intensity stimulation patterns can be crafted to meet specific patient needs. 
         [0029]    Still referring to  FIG. 4 , it will be seen that a stimulation of the heart muscle  30  can be programmed to occur, in concert with the stimulation of a nerve bundle (sympathetic nerve)  38 ( a - c ), during a same heart function cycle. Of particular importance here is that the actual intensity  54  of a direct stimulation  56  at time “t 2 ” will be assisted by the consequences of pulse train  46 . More specifically, the actual intensity  54  can be adjusted and set for subsequent control by the computer  28 . This can be done with the understanding that secretions from nerve bundle  38 ( a - c ), which result from pulse train  46 , will assist stimulation  56  in stimulating the heart muscle  30 . As envisioned for the system  10  of the present invention, operational parameters for both the pulse train  46  and the stimulation  56  can be programmed and controlled with the computer  28 . 
         [0030]    While the particular System and Method for Transvascular Activation of Cardiac Nerves With Automatic Restart as herein shown and disclosed in detail is fully capable of obtaining the objects and providing the advantages herein before stated, it is to be understood that it is merely illustrative of the presently preferred embodiments of the invention and that no limitations are intended to the details of construction or design herein shown other than as described in the appended claims.