WO1997027797A2

WO1997027797A2 - Electrical muscle controller

Info

Publication number: WO1997027797A2
Application number: PCT/US1997/001921
Authority: WO
Inventors: Shlomo Ben-Haim; Maier Fenster
Original assignee: Individual
Current assignee: Individual
Priority date: 1996-02-05
Filing date: 1997-02-05
Publication date: 1997-08-07
Anticipated expiration: 1998-08-05
Also published as: AU1954597A

Abstract

Procédé pour commander un segment de muscle cardiaque, qui consiste à capter un moment d'activation dudit segment et à appliquer un champ électrique non excitant au segment un certain temps t1 après le moment d'activation, pendant une durée t2. Cette commande est utilisée, de préférence, pour augmenter la durée du plateau du segment et augmenter ainsi sa contractilité. Le champ électrique peut, de plus ou autrement, être utilisé pour commander la période de réfraction ou la vitesse de conduction.Method for controlling a segment of cardiac muscle, which consists in sensing a moment of activation of said segment and in applying a non-exciting electric field to the segment a certain time t1 after the moment of activation, for a duration t2. This command is preferably used to increase the duration of the segment plateau and thus increase its contractility. The electric field can, moreover or otherwise, be used to control the period of refraction or the speed of conduction.

Description

ET.rr-TRTt-AT. MHSCT.T. ΓONTROLLER

FIELD OF THE INVENTION

The present invention relates to cardiac muscular control, in particular control using non-excitatory electrical signals.

BACKGROUND OF THE INVENTION The heart is a muscular pump whose activation is by electrical stimulation of the cardiac muscle. In a normal heart, an activation signal is generated in the right atrium of the heart, conducted to the left atrium of the heart and after a delay, conducted to the left ventricle and the right ventricle. Since the electrical resistance of the heart is relatively high, the activation signal is not merely conducted from muscle cell to muscle cell. Rather, each muscle cell amplifies the activation signal which reaches it before passing it on to the next cell after a short delay.

In a particular muscle cell, the normal voltage potential across its cellular membrane is approximately -90 millivolts (the inside is negatively charged with respect to the outside) . When an activation signal reaches one end of the fiber, a depolarization wave rapidly advances along the cellular membrane until the entire membrane is depolarized, usually to approximately +20 millivolts. Complete depolarization of the cell membrane occurs in a very short time, such as less than one millisecond. After the rapid depolarization, the cell slowly repolarlzes by about 20 millivolts over a period of approximately 200-300 milliseconds, called the plateau. It is during the plateau that the muscle contraction occurs. At the end of the plateau, the cell rapidly rβpolarizes to its previous voltage.

The electrical activi-ty mirrors chemical activity in the cell. In a resting cell, the concentration of sodium ions inside the cell is about one tenth the concentration outside the cell. Potassium ions are about thirty-five times more concentrated inside the cell than outside. Calcium ions are over ten thousand times more concentrated outside the cell than inside the cell. These abnormal concentration differentials are maintained by ionic pumps in the membrane of the cell which continuously pump sodium and calcium ions out and potassium ions in. One result of the concentration differences between the cell and the environment external to the cell is a large negative potential in the cell, about 90 millivolts as indicated above. When a portion of the cell membrane is depolarized, such as by an action potential, two things happen. First, the depolariza-tlon wave is spread along the membrane. Second, a plurality of voltage-gated sodium gates are opened. An enormous influx of sodium through these gates changes the potential of the membrane from negative to positive. Once the voltage becomes less negative, these gates close, and do not open until the cell is again depolarized. It should be noted that many sodium gates require a minimal negative voltage in order to be primed for reopening. The sodium gates usually open faster than they close. During the plateau stage, voltage-gated potassium gates and voltage-gated calcium gates open. Potassium then flows out of the cell, to repolarize it, and calcium flows into the cell to activate the muscle proteins. In general, the flow of potassium and calcium is many times slower than the flow of the sodium, which is the source of the long plateau. In fact, the potassium gates may also open as a result of the action potential, however, due to their βlow reaction time and low flow rates, their effect is negligible during the depolarization of the cell. The calcium gates also conduct sodium back into the cell, which helps extend the plateau duration. For some reason, the potassium gates have a significantly higher flow after the influx of calcium is over, resulting in a further increase in the plateau duration.

After the cell is repolarized, it enters a state of hyper polarization, during which the cell cannot be depolarized. This state is probably caused by the potassium gates remaining open. In addition, since the sodium gates must be primed by a negative voltage, the cell cannot be depolarized during the entire time it is depolarized.

It is known that by applying a positive potential across the membrane, a cell may be made more sensitive to activation signal. Some cells in the heart, such as the cells in the SA node (the natural pacemaker of the heart) have a negative potential of only -55 millivolts. As a result, their voltage-gated sodium gates are permanently inactivated and action potentials in these cells is slow to develop. In general, it appears that when the potential of a cell stay below about -60 millivolts for a few milliseconds, the voltage-gated sodium gates are blocked. Applying a negative potential across its membrane make a cell less sensitive to activation and also hyper-polarizes the cell membrane, which seems to reduce conduction velocity.

In an experimental methodology called voltage clamping, an electrical potential is maintained across at least a portion of a cell membrane to study the effects of voltage on ionic pumps and on the reactivity of the cell.

In the above discussion, activation signals are propagated in the heart by sequentially activating connected muscle fibers. Regular electrical currents can be conducted in the heart, using the electrolytic properties of the body fluids, however, due the relatively large resistance of the heart muscle, this conduction cannot be used to transmit the activation signal.

In modern cardiology many parameters of the heart's activation can be controlled. Pharmaceuticals can be used to control the excitability, contractility and duration of the refractory periods in the heart. These pharmaceuticals may be used to treat arrhythmias, prevent fibrillations and strengthen the heart. A special kind of control can be achieved using a pacemaker. A pacemaker is an electronic device which is typically implanted to replace the heart's electrical excitation system or to bypass a blocked portion of the conduction system. Typically in pacemaker implantation, portions of the heart's conduction system must be removed in order for the pacemaker to operate correctly. Another type of electronic device is a defibrillator.

As an end result of many diseases, the heart may become more susceptible to fibrillation, in which the activation of the heart is substantially random. A defibrillator, senses this randomness and resets the heart by applying a very high voltage to the heart.

Pharmaceuticals are generally limited in effectiveness in that they affect both healthy and diseased portions of the heart, usually, with a relatively low precision. Electronic pacemakers, are further limited in that they are invasive, generally require destruction of heart tissue and are not usually optimal in their effects. Defibrillators have substantially only one limitation. The act of defibrillatlon is very painful to the patient and traumatic to the heart. SUMMARY

It is an object of some aspects of the present invention to provide a method of locally controlling the electrical and mechanical activity of cardiac muscle cells. Preferably, the control is continuous in degree. Further preferably, the control may be freely varied between cardiac cycles. One example of electrical control is shortening the refractory period of a muscle fiber by applying a negative voltage to the outside of the cell. The cell may be totally blocked from reacting by maintaining a sufficiently positive voltage to the outside of the cell, so that an activation signal fails to sufficiently depolarize the cellular membrane. One example of mechanical control includes, extending or shortening the plateau duration be applying voltage potentials across the cell, thus, increasing or decreasing the strength of contraction and the duration of the contraction.

It is a further object of some aspects of the present invention to provide a complete control system for the heart which includes controlling the pacing rate, refractory period, conduction velocity and mechanical force of the heart. Except for heart rate, each of these parameters may be locally controlled. It should be noted that heart rate may also be locally controlled, however, in most cases this is detrimental to the heart's pumping efficiency.

In one preferred embodiment of the present invention, electrical and/or mechanical activity of a segment of cardiac muscle is controlled by applying a non-exciting voltage across the segment. A non-exciting voltage is a voltage which does not cause depolarization of the muscle cell. Depolarization may be averted either by the voltage being of the wrong polarity, being applied when the cell is not sensitive to it or by the amplitude of the voltage being too small to depolarize the cell. Optionally, this control is exerted in combination with a pacemaker which applies an exciting voltage to the heart.

In another preferred embodiment of the present invention, arrhythmias and fibrillation are treated using fences. Fences are portions of cardiac muscle which are temporarily inactivated using electrical fields. In one example, atrial fibrillation is treated by channeling the activation signal from an SA node to an AV node by fencing it in. In another example, fibrillations are damped by fencing in the multitude of incorrect activation signals, so that only one path of activation is conducting. In still another example, ventricular tachycardia is treated by dividing the heart into insulated segments, using electrical fields and deactivating the fences in sequence with a normal activation sequence of the heart, so that at most only one segment of the heart will be prematurely activated.

In still another preferred embodiment of the invention, the muscle mass of the heart is redistributed using electrical fields. In general, changing the workload on a segment of cardiac muscle activates adaptation mechanisms which tend to change the muscle mass of the segment. Changing the workload may be achieved directly by increasing or decreasing the plateau duration of the segment, using electrical fields. Alternatively or additionally, the workload may be changed indirectly by changing the activation time of the activation sequence in the segment of the heart.

In yet another preferred embodiment of the invention, the operation of the heart is optimized by changing the activation sequence of the heart and/or by changing plateau length at segments of the heart.

There is therefore provided in accordance with a preferred embodiment of the invention a method of controlling a segment of cardiac muscle including sensing an activation time of the segment and applying a non-exciting electric field to the segment at a time delay tl after the activation time, for a duration of t2. Preferably, this controlling is used to increase the plateau duration of the segment and thereby increase the contractility thereof.

There is also provided in accordance with another preferred embodiment of the invention a method of controlling a segment of cardiac muscle, including, providing at least one electrode near the muscle segment and electrifying the at least one electrode to apply non-exciting electric fields to the muscle segment. BRIEF DESCRIPTION OF THE DRAWINGS The present invention will be more clearly understood from the detailed description of the preferred embodiments and from the attached drawings in which:

Fig. 1 is a schematic model of a cardiac muscle cell in an electrical field;

Fig. 2 is a schematic diagram of a heart controlled in accordance with embodiments of the present invention;

Fig. 3 is a schematic diagram of a portion of right atrial tissue with a plurality of conduction pathways, which illustrates using fences in accordance with a preferred embodiment of the present invention;

Fig. 4 is a schematic diagram of an electrical controller connected to a portion of cardiac muscle, in accordance with a preferred embodiment of the invention;

Fig. 5 is a schematic diagram of an experimental setup used for testing the feasibility of some embodiments of the present invention; and

Figs. 6A-6C are graphs showing different experimental results.

DETAIX-ED DESCRIPTION OF THE PREFERRED EMBODIMENTS One preferred embodiment of the present invention relates to increasing the plateau duration in a segment of heart muscle by applying a voltage across the segment.

Fig. 1 shows a model illustrating one possible explanation for the relation between applied voltage and plateau duration. A cell 20, having a membrane 26 surrounded by extra-cellular fluid 28 is located in an electrical field generated by an electrode 22 and an electrode 24. Cell 20 is shown to have a -40 millivolts potential across membrane 26, electrode 22 has a potential of 40 millivolts and electrode 24 is grounded (to the rest of the body). During the plateau, calcium ions enter the cell and potassium ions leave the cell. In this model, the external electric field caused by the voltage on electrodes increases the potential of extra-cellular fluid 28. This inhibits the movement of potassium ions from inside cell 20 and/or forces calcium ions into cell 20.

In an additional or alternative model, the electric field generated by electrodes 22 and 24 causes an ionic flow between them. This flow is carried mainly by calcium and potassium ions, since these are the ions to which membrane 26 is permeable. Thus, calcium ions are drawn into cell 20 by the current while potassium ions are removed. Alternatively or additionally sodium ions are removed instead of potassium ions. In any case, the additional calcium ions increase the contractility of cell 20 and probably extend the plateau duration.

Another additional or alternative model is that the electric field and/or the ionic current affect the opening and closing of voltage-gated gates (sodium, potassium and sodium-calcium). Further, the field may affect the operation of ionic pumps.

Most probably, different model may be used to explain the activity of cell 20 during different parts of the activation cycle. However, several major effects, including, extension of plateau duration, hyperpolarization of cells, changing of conduction velocity and inactivation of cells using electric fields, can be effected without knowing which model, if any, is correct.

As can be appreciated, the direction of the electric field may be important. First, conduction in cardiac cells is very anisotropic. Second, there exist voltage potentials in the heart which are caused the depolarization and repolarization of the heart which may interfere with an applied electric field. Alternatively, it may be that the purpose of a particular electric field is to induce an ionic current which is opposite to an ionic current induced by the voltage potential caused by the rhythmic depolarization of the heart. For example, the plateau duration in cardiac muscle cells further from the activation location is typically shorter than the duration of those cells near the activation location. This shortening may result from ionic currents caused by the depolarization and repolariaztion of the heart. This current can be negated by applying an electric field of an equal magnitude and opposite direction to the field generated by the rhythmic depolarization.

Fig. 2 shows a heart 30 which is controlled using an electrical controller 32. A segment 38 of the right atrium is a controlled segment. In one preferred embodiment of the invention, the casing of controller 32 is one electrode and an electrode 36 is a second electrode for applying an electric field to segment 38. In another preferred embodiment of the invention, a second electrode 34 is used instead of the casing of controller 32. in a further preferred embodiment of the invention, the body of controller 32 is a ground, so that both electrode 34 and electrode 36 can be positive or negative relative to the rest of the heart.

It should be appreciated that a current induced between the electrodes may cause electrolytic deposition on the electrodes over a period of time. In a preferred embodiment of the invention, the electric field is an AC electric field. In one preferred embodiment, the direction of the field is switched at a relatively low frequency, equal to or lower than the cardiac cycle. Preferably, the phase is inverted during a particular phase of the cardiac cycle, for example, during diastole. In another preferred embodiment of the invention, the electric field has a frequency which is significantly higher than the cardiac cycle. As is well known, the reaction times of some of the gates and pumps is significantly longer in closing than in opening, for example, the fast sodium gates require less than half a millisecond to open and close to a millisecond to close. Thus, if the frequency of the field is high enough, certain pumps can be activated and gates kept open even though the average voltage is zero.

The timing of the electric field relative to the local activity at segment 38 and relative to the entire cardiac cycle is important. In general, the activation of the field may be synchronized to the local activation time if a local effect is desired, such as increasing the plateau duration. The activation of the field is synchronized to the cardiac cycle in cases where a global effect is desired. For example, by hyperpolarizing cells in synchrony with the cardiac cycle it is possible to time their excitability window such that certain arrhythmias are prevented, as described in greater detail below. The activation of the field may also be synchronized in accordance with a model of how the heart should be activated, in order to change the activation profile of the heart. For example, to increase the output of the heart, conduction velocities and/or conduction pathways may be controlled so that the heart beats in a sequence deemed to be more optimal than a natural sequence.

If an electric field is applied before the activation signal reaches segment 38, the electric field can be used to reduce the sensitivity of segment 38 to the activation signal. One method to produce this effect is to apply a large electric field opposite to the direction of the activation signal. This field will reduce the amplitude of the activation signal, so that it cannot excite cardiac tissue. Another method is to apply a strong positive potential on segment 38, so that segment 38 is hyperpolarized and not sensitive to the activation signal. Removing the electric field does not immediately cancel the effect. Segment 36 stays insensitive for a short period of time and for a further period of time, the conduction velocity in segment 38 is reduced.

Fig. 3 illuminates one use of extending the refractory periods of cardiac tissue. Segment 40 is a portion of a right atrium. An activation signal normally propagates from an SA node 42 to an AV node 44. Several competing pathways, marked 46A-46D, may exist between SA node 42 and AV node 44, however, in healthy tissue, only one signal reaches AV node 44 within its excitability window. In diseased tissue, several signal may excite AV node 44 in a single heart beat. Further, in atrial fibrillation, the entire right atrium may have random signal running through it. In a preferred embodiment of the invention, electric fields are applied to a plurality of regions which act as "fences" 48A and 48B. The action of a fence is to be non¬ conducting to activation signals during a particular, predetermined critical time, depending on the activation time of the electric fields. Thus, the activation signal is fenced in between SA node 42 and AV node 44. It is known to perform a surgical procedure with a similar effect, however, in the surgical procedure, many portions of the right atrium need to be ablated to produce permanent insulating regions (fences). In the present embodiment of the invention, at least portions of fences 48A and 48B may be deactivated after the activation signal has passed, so that the atrium can contract.

Still another preferred embodiment of the invention relates to treating ventricular fibrillation (VF). In VF, a ventricle is activated by more than one activation signal, which do not activate the ventricle in an orderly fashion. Rather, each portion of the ventricle is randomly activated asynchronously with the other portions of the ventricle and asynchronously with the cardiac cycle. As a result, no pumping action is achieved. In a preferred embodiment of the invention, a plurality of electrical fences are applied in the affected ventricle to damp the fibrillations. In general, by changing the window during which portions of the ventricle are sensitive to activation, a fibrillation causing activation signal can be blocked, without affecting the natural contraction of the ventricle. In one embodiment of the invention, the fences are used to channel activation signals along correct pathways, for example, only longitudinal pathways. Thus, activation signals cannot move in transverse direction and will quickly fade away, harmlessly. Healthy activation signals from the AV node will not be adversely affected by the fences. Alternatively or additionally, fences are generated in synchrony with the activation signal from the AV node, so that fibrillation causing activation signals are blocked. Further alternatively, entire portions of the ventricle are desensitized to the activation signals by applying a positive potential to those portions deemed sensitive to fibrillation.

Dividing the heart into insulated segments using fences is useful for treating many types of arrhythmia. By insulated, it is meant that conduction of the activation signal is blocked by deactivating portions of the heart conduction system. For example, many types of VT (ventricular tachycardia) and premature beats in the heart are caused by local portions of tissue which generate a pacemaking signal. Theses portions can be insulated from other portions of the heart so that only a small, local portion is affected by the irregular pacing. Alternatively, These diseased portions can be desensitized using an electric field, so that they do not generate incorrect activation signals.

Premature beats are usually caused by an oversensitive portion of the heart. By applying a local electric field to the portion, the sensitivity of the portion can be controlled and brought to similar levels as the rest of the heart, solving the major cause of premature beats.

It should be appreciated that it is not necessary to know the exact geometrical origin of an arrhythmia to treat it using the above described methods. Rather, entire portions of the heart can be desensitized in synchrony with the cardiac cycle εo that they do not react before the true activation signal reaches them. Further, the heart can be divided into isolated portions or fenced in without mapping the electrical system of the heart. For example, electrodes can be inserted in the coronary vessels to create fences in the heart. Theses fences can block most if not all of the irregular activation signals in the heart.

In an additional preferred embodiment of the present invention, portions of the heart are continuously controlled using an electric field, so that their resting potential is below 60 millivolts. Below this level, the voltage-gated sodium gates cannot be opened by an activation signal. Thus, the reaction of the portions of the heart to an activation signal is reduced and has a longer delay. Other resting potentials may affect the opening of other voltage-gated gates in the cell. A further benefit of applying electric fields to cardiac cells is that the field may be able to force more calcium ions into the cells during short cardiac cycles than are usually carried in through the calcium gates, resulting in a stronger contraction.

Another preferred embodiment of the present invention relates to treating ischemic portions of the heart. Ischemic portions, which may be automatically identified from their injury currents using locally implanted sensors, may be desensitized to the activation signal of the heart. Thus, the ischemic cells are not required to perform work and may be able to heal.

U.S. provisional application titled "Cardiac Electromechanics", filed on January 10, 1996, by Shlomo Ben-Haim and Maier Fenster, and its corresponding Israeli patent application titled "Cardiac Electromechanics", filed on January 6, 1996 by applicant Biosense Ltd., the disclosures of which are incorporated herein by reference describe methods of cardiac modeling and heart optimization. In cardiac modeling, the distribution of muscle mass in the heart is changed by changing the workload of portions of the heart or by changing the plateau duration at portions of the heart. These changes may be achieved by changing the activation profile of the heart. Using methods of the present invention, plateau duration can be readily controlled using methods as described hereinabove. Further, by controlling the conduction pathways in the heart, according to methods of the present invention, the entire activation profile of the heart can be affected. In cardiac optimization as described in the references, the activation profile of the heart is changed so that global parameters of cardiac output are increased. Alternatively, local physiological values, such as stress are redistributed, such as to relieve stress from the heart. In a

II preferred embodiment of the present invention, the activation profile may be usefully changed using methods as described hereinabov .

As can be appreciated, in order to best implement many embodiments of the present invention, it is useful to first generate an electrical, geometrical or mechanical map of the heart. U.S. Patent Application titled "Cardiac Electromechanics", filed on February 1, 1996, by Shlomo Ben-Haim, the disclosure of which is incorporated herein by reference describes maps and methods and means for generating such maps. U.S. Patent 5,391,199, U.S. Patent application 08/293,859 "means and method for remote object position and orientation detection system" and PCT US95/01103, the disclosures of which are incorporated herein by reference, describe position sensing means suitable for mounting on a catheter which are especially useful for generating such maps. Such position sensing means may also be useful for correctly placing electrodes in the heart.

One benefit of most embodiments of the present invention, is that they can be implemented without making any structural or permanent changes in the conduction system of the heart. Further, most embodiments may be practiced in conjunction with an existing pacemaker or in conjunction with drug therapy which affects the electrical conduction in the heart.

It must be appreciated however, that by changing the activation profile of the heart, some changes may be affected on the structure of the heart. For example, cardiac modeling, as described above , may result from the activation profile changes, over time.

Fig. 4 is a schematic diagram of an electrical controller 50 in accordance with a preferred embodiment of the invention. A muscle segment 56, which is controlled by controller 50 is preferably electrified by at least one electrode 52 and preferably a second electrode 54. A sensor 58 may be used to determine the local activation time of segment 56, Alternatively, sensor 58 is located near the SA node for determining the start of the cardiac rhythm. Alternatively, sensor 58 is used to sense the mechanical activity of segment 56, of other portions of the heart or for sensing the cardiac output. In one embodiment, sensor 58 senses the electrical state of the heart, controller 50 determines a state of fibrillation and electrifies electrodes 52 and 54 accordingly.

Different embodiments of the present invention will typically require different control electrodes. For example, some embodiments require a large area electrode, for applying an electric field to a large portion of the heart. In this case, a net shaped electrode may be suitable. Alternatively, a large flat electrode may be placed against the outside of the heart. Other embodiments require long electrodes, for generating fences. In this case, wires are preferably implanted in the heart in parallel to the wall of the heart, optionally, in the coronary vessels outside the heart.

Fig. 5 shows an experimental setup designed and used by the inventor to test some embodiments of the present invention. A papillary muscle 60, from a guinea pig, was connected between a support 62 and a pressure transducer 64. Muscle 60 was stimulated by a pair of electrodes 66 which were connected to a pulsed constant current source 70. A pulse generator 74 generated constant current pacing pulses for electrodes 66. A pair of electrodes 68 were used to apply an electric field to muscle 60. A slave pulse generator 76, which bases its timing on pulse generator 74, electrified electrodes 68 via a pulsed constant current source 72. The force applied by the muscle was measured by transducer 64, amplified by an amplifier 78 and drawn on a plotter 80. Pulse generator 74 selectably generated activation pulses 500, 750, 1000 and 1500 milliseconds (tl) apart for variable activation of muscle 60. Pulse generator 76 generated a square wave pulse which started t2 seconds after the activation pulse, was t3 seconds long and had a selected current (in milliamperes) higher than zero.

Fig. 6A-6C are graphs showing some results of the experiments. In general, the results shown are graphs of the force of the muscle contractions after muscle 60 reaches a steady state of pulsed contractions. Fig. 6A is a graph of the results under the following conditions: tl» 750 milliseconds; t2» 150 milliseconds; t3= 100 milliseconds; and currents 100 milliamperes. As can be seen, the force exerted by the muscle was increased by a factor of 2.5 when the controlling pulse (electrodes 68) was used as opposed to when electrodes 6Θ were not activated.

Fig. 6B is a graph of the force of muscle contractions under the following conditions: tl«= 1000 milliseconds; t2= 20 milliseconds; t3» 300 milliseconds; and current= 75 milliamperes. As can be seen, the amplitude of the contractions is extremely attenuated. When the polarity of the controlling signal was inverted after a few contractions, the contractions of muscle 60 were almost completely attenuated.

Fig. 6C is a graph of the force of muscle contractions under the following conditions: tl=> 1000 milliseconds; t2= 20 milliseconds; t3= 300 milliseconds; and current- 10 milliamperes. In this case, the effects of increasing the contractile force of muscle 60 remained for about two minutes after the electrification of electrodes 68 was stopped. Thus, the contraction of muscle 60 is dependent not only on the instantaneous stimulation and control but also on prior stimulation and control.

Although the present invention has be described mainly with reference to the heart, it should be appreciated that preferred embodiments of the present invention may be applied to other types of excitable tissue. In one example, skeleton muscle and smooth muscle can be controlled as described hereinabove. It should however be appreciated, that most muscles have different ion gates and different resting potentials than cardiac muscle. So that the general principles must be adapted to the individual physiology. Further, the present invention may be applied to neural tissue. For example, epileptic fits and tetanization may be controlled by damping the excitability of neural tissue, as described above. Alternatively, electrical control may be used in conjunction with electrical stimulation of denervated or atrophied muscles to increase the precision of stimulation. It will be appreciated by a person skilled in the art that the present invention is not limited by what has thus far been particularly described. Rather, the present invention is limited only by the claims which follow.

Claims

1. A method of controlling a segment of cardiac muscle, comprising:

(a) sensing an activation time of said segment; and

(b) applying a non-exciting electric field to the segment at a time delay t1 after the activation time, for a duration of time t2.

2. A method of controlling a segment of cardiac muscle, comprising:

(a) providing at least one electrode near the muscle segment; and

(b) electrifying the at least one electrode to apply non- exciting electric fields to the muscle segment.