Abstract:
An apparatus and method for relieving stress on a heart muscle tissue in a wall of a heart having a chamber. A plurality of biocompatible and implantable elongate strips are configured to be connected to the heart wall and disposed about the chamber such that the elongate strips are arranged in spaced relation to one another. The elongate strips are bendable and are sufficiently resistant to elongation such that natural stretching of the heart wall does not cause elongation of the plurality of strips.

Description:
REFERENCE TO CO-PENDING APPLICATION 
     The present application is a continuation application of U.S. patent application Ser. No. 09/064,370, filed Apr. 22, 1998 entitled “SYSTEM FOR STRESS RELIEVING THE HEART MUSCLE AND FOR CONTROLLING HEART FUNCTION” and assigned to the same assignee as the present application now U.S. Pat. No. 6,110,100. 
    
    
     BACKGROUND OF THE INVENTION 
     The present invention deals with treatment of heart disease. More particularly, the present invention deals with a system and method for treating heart disease by regulating blood flow in the vasculature. 
     Congestive heart failure is a common heart disease. The prevalence of incidents of congestive heart failure has recently increased, and there is considerable morbidity and mortality associated with its diagnosis. In fact, congestive heart failure is an extremely lethal disease with an estimated five year mortality for a vast majority of both men and women who encounter the disease. 
     Congestive heart failure results from loss of, or impairment of, normal heart function. This loss or impairment reduces cardiac output. This, in turn, results in a reduction in both blood flow and blood pressure in the kidneys. This reduction in flow and pressure causes a renin-angiotensin response that exacerbates congestive heart failure. 
     Briefly, as blood flow and pressure is reduced in the kidneys, cells in the kidneys referred to as juxtaglomerular apparatus secret an enzyme referred to as renin into the blood. The enzyme renin cleaves a ten-amino acid polypeptide called angiotensin I from a plasma protein in the blood called angiotensinogen. A converting enzyme in the blood removes two amino acids from the angiotensin I polypeptide leaving an eight amino acid polypeptide called angiotensin II. Angiotensin II has numerous effects on the smooth muscle layers of arterioles, including causing vasoconstriction. Further, an indirect effect of an increase in angiotensin II increases blood volume. Blood volume is increased because angiotensin II stimulates secretion of aldosterone from the adrenal cortex which, in turn, causes an increase in salt and water retention in the kidneys. Angiotensin II also stimulates thirst centers in the hypothalamus causing more water to be ingested. The increase in blood volume and the corresponding vasoconstriction cause an increase in blood pressure and hence a volume overload on the heart which causes further deterioration of the heart condition. 
     Another response is also related to congestive heart failure. Baroreceptors, referred to as stretch receptors, reside in the aortic arch and carotid sinuses. The baroreceptors are essentially pressure sensors sensing blood pressure in that area. The baroreceptors provide physiological feedback in two ways. First, in response to a reduction in blood pressure, the baroreceptors provide a neurohormonal feedback response which acts to increase the heart rate in an attempt to increase cardiac output. The increased heart rate causes the heart to work harder which, in turn, causes the heart muscle to stretch further. Also, a reduction in pressure caused by a reduction in cardiac output causes the baroreceptors to provide a feedback response which acts to constrict the distal vasculature thus increasing pressure in that area. 
     It can thus be seen that impairment of heart function can lead to a cyclical feedback response which increases, rather than reduces, the impairment. Such a cyclical feedback response is sometimes referred to as a cascade. 
     For instance, if the heart muscle is stressed, the heart works harder and begins to stretch. This reduces the efficiency of the heart in the following way. Muscles are thought of as being composed of many fibers which contract and lengthen to accomplish muscular action. Each fiber includes many densely packed subunits referred to as myofibrils which are on the order of 1 μm in diameter and extend in parallel from one end of the muscle fiber to the other. Each myofibril has spaced regions of thick filaments (about 110 Å thick) and thin filaments (about 50-60 Å thick) The thick filaments are formed of a protein, myosin, and the thin filaments are formed of a protein, actin. The actin and myosin filaments overlap in regions periodically spaced along the myofibrils. The units in the repeated overlapping pattern are referred to as sarcomeres. 
     Contraction of a muscle fiber results from shortening of the myofibrils which form the muscle fiber. The myofibrils are shortened, but the individual filaments in the myofibrils do not decrease in length. Instead, the actin and myosin filaments slide longitudinally relative to one another to shorten the overall length of the myofibrils. Sliding occurs as a result of cross-bridges extending from the myosin toward the actin attaching to the actin at bonding sites. The cross bridges are oriented to draw overlapping actin filaments on either longitudinal side of the myosin filament toward the longitudinal center of the myosin filament. When the muscle fiber is stretched such that the actin and myosin only overlap a short distance, only a small number of cross-bridges are available for bonding to the adjacent actin, and contraction is highly inefficient. When the muscle is stretched to a point where the actin and myosin filaments no longer overlap, contraction is rendered impossible. 
     This inefficient or impaired heart function causes blood pressure in the areas of both the kidneys and the baroreceptors to decrease. The feedback response generated by the kidneys causes further overload and stress on the heart. The feedback response generated by the baroreceptors causes increased heart rate. Both of these feedback responses cause the heart to work harder, causing further stretching of the heart muscle and thus leading to greater inefficiencies. In response, the feedback responses become even more acute—and the cascade continues. 
     This cascade effect, which is a natural progression of congestive heart failure, leads to increased muscle mass and stretching of the heart muscle fibers which, in turn, leads to muscular hypertrophy,of the left ventricle. The hypertrophy is a compensatory mechanism which, if maintained at a given level such that muscle fibers maintain inherent contractile properties (i.e., actin-myosin overlap), can be beneficial for maintaining proper heart function. However, prolonged and continuous stretching causes muscular fatigue and reduced muscle performance as explained by the known Frank-Starling mechanism. 
     SUMMARY OF THE INVENTION 
     An apparatus and method restrict elongation of heart muscle tissue in a wall of a heart having a chamber. A plurality of biocompatible and implantable elongate strips are configured to be connected to the heart wall and disposed about the chamber such that the elongate strips are arranged in spaced relation to one another. The elongate strips are bendable and are sufficiently resistant to elongation such that natural stretching of the heart wall does not cause elongation of the plurality of strips. 
    
    
     BRIEF DESCRIPTION OF THE DRAWINGS 
     FIG. 1A is a side sectional view of a heart. 
     FIG. 1B is a greatly enlarged sectional view of a portion of the heart shown in FIG.  1 A. 
     FIG. 2 illustrates a retention strip in accordance with one aspect of the present invention. 
     FIG. 3 illustrates the retention strip shown in FIG. 2 embedded in the heart wall. 
     FIG. 4 illustrates a plurality of the strips as shown in FIG. 2 embedded in the wall of the left ventricle. 
     FIG. 5 illustrates a second embodiment of a retention mechanism in accordance with one aspect of the present invention. 
     FIG. 6A shows the retention mechanism illustrated in FIG. 5 deployed on the outer surface of the left ventricle. 
     FIG. 6B is a sectional view of a portion of the heart wall shown in FIG.  6 A. 
     FIG. 7 illustrates another embodiment of a monitoring system in accordance with one aspect of the present invention. 
     FIG. 8 illustrates a portion of the monitoring system shown in FIG. 7 in schematic and partial block diagram form. 
     FIG. 9 illustrates another embodiment of a monitoring and control system in schematic and partial block diagram form. 
    
    
     DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS 
     FIG. 1A illustrates a portion of a heart  10 . FIG. 1A illustrates a plurality of chambers in heart  10  including right ventricle  12  and left ventricle  14 . FIG. 1A also illustrates heart wall  16  which extends around chambers  12  and  14 , and separates chambers  12  and  14 . As discussed in the background portion above, congestive heart failure can lead to hypertrophy of the muscle fibers in heart  10 , particularly those surrounding left ventricle  14 . 
     FIG. 1B illustrates a greatly enlarged sectional view of a portion of wall  16  of heart  10  shown in FIG.  1 A. FIG. 1B is taken from the portion labeled  1 B in FIG.  1 A. FIG. 1B illustrates that wall  16  is formed of an endocardium layer  18  which comprises the inner tissue of heart wall  16 . Heart wall  16  also includes an epicardium layer  20  which comprises the outer tissue in heart wall  16 . Mid-wall portion  22  comprises a portion of wall  16  between the endocardium  18  and epicardium  20 . The pericardium is a double-walled sac which encloses the heart. The inner layer of the pericardial sac comprises the epicardium  20 . 
     Photomicrographs available from the American Heart Association libraries show that the alignment of cardiac muscle fibers are generally perpendicular to the ventricular cavity wall in the endocardium  18  and epicardium  20 . Also, the muscle fibers are typically nearly parallel to the ventricular cavity wall in the mid-wall portion  22 . During hypertrophy of the muscular wall  16  around the left ventricle  14 , the muscle fibers stretch and elongate in a direction generally parallel to their longitudinal orientation. Thus, the muscle fibers in the endocardium  18  and epicardium  20  elongate in a direction generally perpendicular to the ventricular cavity wall. Also, the muscle fibers in the mid-wall region  22  elongate in a direction generally parallel to the ventricular cavity wall. Additional muscle fibers also develop. All of these effects contribute to an increase in muscle mass and stretching of the heart muscle fibers. 
     FIG. 2 illustrates a retention strip  24  in accordance with one aspect of the present invention. Retention strip  24 , in one preferred embodiment, includes a generally longitudinal strut  26  with a first set of protrusions  28 ,  30  and  32  extending from strut  26  in a first direction and a second plurality of protrusions  34  and  36  extending from longitudinal strut  26  in a second direction, generally opposite the first direction. While protrusions  28 ,  30  and  32  are shown to have a generally T-shaped conformation, and while protrusions  34  and  36  have a generally linear conformation, it should be noted that all of struts  28 - 36  could either have a T conformation or a linear conformation. 
     Retention strip  24  is also shown having a plurality of apertures  38  which are used for suturing retention strip  24  in place. Of course, the number and placement of the suture apertures  38  shown in FIG. 2 is illustrative only. More or less apertures  38 , and apertures having different placement on retention strip  24  are contemplated as well. 
     Also, while only three protrusions  28 ,  30 , and  32  are shown and two protrusions  34  and  36  are shown, any suitable number of protrusions can be used on either side of retention strip  24 . Strut  26  and protrusions  28 - 36  are preferably formed of a material which allows repeated bending cycles, without permanent deformation or breakage. However, strut  26  and protrusions  28 - 36  are also preferably formed of a material which exhibits high resistance to elongation in the longitudinal direction. Suitable materials include collagen, or biocompatable and implantable polymer strips, as well as biocompatable and implantable metals, cartilage, or composite materials, Nitinol and bovine and porcine byproducts, as examples. 
     FIG. 3 illustrates a portion of wall  16  with retention strip  24  implanted therein. In a preferred embodiment, longitudinal strut  26  is implanted. in the mid-wall region  22  of wall  16 . Protrusions  28 ,  30  and  32  (and any other number of protrusions) extend into the endocardium layer  18 , while protrusions  34  and  36  (and any other suitable number of protrusions) extend into the epicardium layer  20 . Retention strip  24  is then sutured in place by an appropriate suturing technique using apertures  38  in retention strip  24 . Retention strip  24  preferably extends throughout substantially the entire longitudinal length of the ventricular cavity wall, such as from the base to the apex of the ventricular cavity wall. 
     FIG. 4 illustrates a plurality of retention strips  24  embedded in wall  16  about left ventricle  14 . Retention strips  24  are preferably arranged at regular intervals about left ventricle  14  to encircle left ventricle  14  in wall  16 . Such placement forms a restrictive cage around left ventricle  14  of heart  10 . Strips  24  thus provide very little, or no impedance to the natural contractile motion of the heart. However, fixturing of retention strips  24  to the tissue of the heart with sutures prevents enlargement or substantially eliminates enlargement and extensive stretch of the muscle fibers. 
     Since longitudinal strut  26  is substantially resistant to elongation in its longitudinal direction, it helps to prevent elongation of the muscle fibers in mid-wall region  22 . Also, since protrusions  28 ,  30  and  32  are highly resistant to elongation in their longitudinal directions, they greatly inhibit elongation or stretch of the muscle fibers in endocardium layer  18 . Similarly, since protrusions  34  and  36  are highly resistant to elongation in their longitudinal direction, they greatly inhibit elongation or stretch of the muscle fibers in epicardium layer  20 . 
     Placement of retention strips  24  in the positions illustrated in FIG. 4 thus restrict the progression of congestive heart failure of the muscle due to the pressure overload on left ventricle  14 . The muscle is supported in such a way that it is not allowed to progressively increase its mass, and also such that uncontrolled stretching is limited by physically restricting its growth and stretch. Thus, heart failure scan be controlled. Further, since the recruitable muscle mass can still perform a satisfactory job due to the limited constraint on its contraction, no additional or compensatory muscle mass is generated, which also restricts growth of new muscle tissue in wall  16 . This aspect of the present invention thus reduces fatigue of the heart muscle and allows for natural regeneration of healthy cardiac tissue. Also, it is believed that supporting the cardiac muscle tissue relives tension on the chordae tendinae which, in turn, helps prevent mitral valve regurgitation which prevents higher mean atrial pressures and thus pulmonary edema. 
     FIG. 5 illustrates another embodiment of a retention device  40  in accordance with another aspect of the present invention. With progressive congestive heart failure, heart  10  may already have started to hypertrophy and thus may be vulnerable to trauma. Thus, extensive incision in heart  10  may be undesirable. In that case, retention device  40  can be used by attaching it to the epicardial surface of heart  10  with only minimal intrusion into the heart muscle (such as with sutures, adhesives, staples, or other connection techniques). 
     Retention device  40  includes a first generally circular strap  42  and a second generally circular strap  44 . Straps  42  and  44  are connected to one another by a plurality of generally longitudinal straps  46 ,  48 ,  50 ,  52  and  54 . Straps  46 - 54  are preferably attached to circular strips  42  and  44  by a suitable adhesive, by welding, or by another suitable mechanism, or are formed integrally with circular straps  42 . Straps  42 - 54  are preferably formed of collagen, polymer or metal fibers which exhibit the capability of undergoing many bending cycles, without permanent deformation of damage. Straps  42 - 54  are also formed to exhibit high resistance to elongation in the generally longitudinal directions. In addition, straps  42 - 54  have a plurality of apertures  56  therein which are used to attach retention device  40  to the heart wall  16  with an appropriate suturing technique. Of course, as with the embodiment illustrated in FIGS. 2-4, any suitable number of straps  42 - 54  can be used. The arrangement of straps  42 - 54  can also be changed as desired. Further, the number and placement of suture apertures  56  can be changed to any suitable number and location on straps  42 - 54 . 
     FIG. 6A illustrates retention device  40  deployed on wall  16  of left ventricle  14 . FIG. 6A illustrates that, in one preferred embodiment, straps  42 - 54  are periodically, and alternately, sutured to the outer surface of epicardium  20 , and embedded within wall  16 . FIG. 6A also illustrates that more longitudinal straps can be used than are illustrated in FIG.  5 . This simply illustrates that any desired number of longitudinal straps can be used. In the preferred embodiment, in the areas where straps  42 - 54  are embedded in wall  16 , they are embedded only in the epicardium layer  20  such that extensive incisions into wall  16  need not be made. 
     FIG. 6B better illustrates embedding of straps  42 - 54  in the wall  16  of heart  10 . FIG. 6B is a greatly enlarged cross-section of wall  16  taken in the region labeled  6 B in FIG.  6 A. FIG. 6B illustrates that strap  46 , at alternate portions  58  is simply sutured to the exterior of epicardium layer  20 , while at other portions  60  is embedded within the epicardium layer  20 . Of course, straps  42 - 54  could be embedded more deeply in the wall  16 . However, embedding in epicardial layer  20  is preferred. 
     As with the embodiment illustrated in FIGS. 2-4, retention device  40  restricts the progression of failure of heart muscle  16  due to pressure overload on the left ventricle  14  of heart  10 . Heart  10  is not allowed to progressively increase its mass and since the uncontrolled stretching of the heart muscle is physically restricted, heart failure can be controlled. Further, since the recruitable muscle mass is still capable of operating satisfactorily, no additional, compensatory muscle mass needs to be generated. Retention device  40  thus restricts growth of new muscle. Further, retention device  40  allows for minimal internal damage to heart  10 . 
     FIG. 7 illustrates another embodiment of retention device  40  in accordance with one aspect of the present invention. Retention device  40 , shown in FIG. 7, is similar to that shown in FIG. 5, and similar items are similarly numbered. However, the longitudinal straps  46 - 54  (only four of which are shown in FIG. 7) are each provided with a plurality of sensors  62  which are configured to sense stretching, and/or other physiologic parameters, such as electrical activity, acceleration or physicochemical activity, of the cardiac muscle wall  16 . In the illustration of FIG. 7, sensors  62  are only provided on longitudinal strap  48 , it will be appreciated that, in a preferred embodiment, sensors  62  are similarly disposed on each of the straps  42 - 54 . 
     Sensors  62  are preferably wire bond strain gauges, piezopolymer strips, or other strain measuring sensors. As is generally known, some such strain gauges are provided with a resistive bridge having a signal, such as a voltage, applied thereacross. As strain on the bridge changes, the values of signals received from the bridge change in a differential manner. In piezopolymer elements, application of a mechanical stress to the device generates electric polarization which can also be sensed. Thus, each sensor  62  provides one or more conductors  64  which carry signals indicative of the stretching of muscle wall  16 . Such conductors are preferably provided through a suitable cable  66  to monitor circuit  68  which, in turn, is coupled to a user input/output (I/O) device  70 . 
     In one preferred embodiment, the strain information captured by the signals conducted by conductors  64  to monitor circuit  68  is processed to obtain a total stretch response in the myocardium of heart  10 . Such processing preferably occurs in monitor circuit  68  and is described below. The total stretch response is preferably monitored for variations and thus provides information about the stretching and condition of heart  10 . This information is preferably used for the treatment and management of the heart failure condition, either by itself through observation, or used to generate a feedback signal which can be used to pace heart  10  for maximal contraction (which is described in greater detail with respect to FIG.  9 ). 
     User I/O device  70  is preferably any suitable I/O device, such as a cathode ray tube, an LCD display, a strip or other printer, or any other suitable I/O device. I/O device  70  may also allow user input functions by including a keypad, a keyboard, or other user actuable elements. 
     FIG. 8 illustrates a more detailed block diagram of one embodiment of monitor circuit  68 . Monitor circuit  68  preferably includes a plurality of differential amplifiers  72 ,  74  and  76 , a circuit (such as a summing amplifier, multiplexer, etc.)  78  and a microprocessor or microcontroller based circuit  80 . Of course, monitor circuit  68  may also include other signal filtering and amplification, and other general signal conditioning circuitry, which is generally known for conditioning signals from strain sensors and is not described here in detail. 
     In the embodiment illustrated in FIG. 8, differential amplifiers  72 - 76  are provided for amplifying the signals received from strain sensors  62 . In one preferred embodiment, each strain sensor  62  has a corresponding differential amplifier. Alternatively, of course, multiplexing circuity can be used to switch the signals from sensors  62  into a single, or into one or more of the differential amplifiers. In any case, the output signals from differential amplifiers  72 - 76  are provided to circuit  78 . In the embodiment in which circuit  78  is a summing amplifier, the signals are summed in a desired manner to obtain the total stretch response of the myocardium of heart  10 . The signal from amplifier  78  is provided to microprocessor  80  where it is preferably corrected for any non-linearities and temperature affects, in a known manner. Microprocessor  80  then generates a suitable output signal to user I/O device  70 . 
     In another embodiment in which circuit  78  is a multiplexer, each of the signals from amplifiers  72 - 76  are switched into microprocessor  80  under the control of microprocessor  80 . Alternatively, circuit  78  can also be eliminated. In that embodiment, the outputs from amplifiers  72 - 76  are provided as discrete inputs to microprocessor  80 . It should also be noted that other inputs can be provided to microprocessor  80  as well, such as EKG information, blood pressure information, or other sources of information. In any case, microprocessor  80  generates a signal to user I/O device  70  based on the signals from amplifiers  72 - 76 . 
     FIG. 9 illustrates another embodiment of a monitoring and control system  82  in accordance with one aspect of the present invention. Some items in system  82  are similar to those shown in FIGS. 7 and 8 and are similarly numbered. In system  82 , each sensor  62  is provided with a strain sensing element  84 , as discussed above, and an excitation electrode  86 . Excitation electrodes  86  are preferably conventional pacing electrodes capable of delivering pacing voltages to the myocardium of heart  10 . While the sensing elements  84  and pacing electrodes  86  are shown attached to one another in FIG. 9, it should be noted that they can be separated from one another, but are preferably closely proximate one another when deployed on one of straps  42 - 54 . 
     In one preferred embodiment, microprocessor  80  receives the stretch response information from sensor elements  84  which indicates not only long term stretching of the heart muscle fibers, but which also indicates contractile motion of the heart  10  in a pulsatile fashion. Based upon this information, microprocessor  80  generates a plurality of feedback signals which are provided to each of pacing electrodes  86 . The feedback signals are used to energize pacing electrodes  86  to deliver the necessary pacing voltages to the myocardium of heart  10  in order to pace heart  10 . 
     In one preferred embodiment, microprocessor  80  simply energizes all of electrodes  86  at one time to cause contraction of the heart muscle. In another preferred embodiment, however, the microprocessor  80  selectively and sequentially energizes each of the excitation electrodes  86  in order to sequentially pace different sets of electrodes  86  to achieve optimal contraction of the ventricles. In that embodiment, the output of each of differential amplifiers  72 ,  74  and  76  can be individually provided to microprocessor  80 , as well as through, for example, a summing amplifier  78 . Microprocessor  80 , in a preferred embodiment, also calculates and delivers appropriate pacing voltages to the various sets of excitation electrodes  86  being controlled. 
     As with the other embodiments discussed herein, system  82 , when used in conjunction with retention device  40  restricts the progression of failure of the muscle of heart  10  due to the pressure overload in the left ventricle  14 . The muscle in heart  10  is preferably supported such that it is not allowed to progressively increase its mass, and so as to restrict uncontrolled stretch of the heart muscle in order to control heart failure. Since the muscle is not allowed to reach a point of destructive stretching, the muscle fibers maintain their inherent contractile properties (actin-myosin overlap) and the progression to failure (or cascade) can be stopped. Also, since the recruitable muscle mass is still performing satisfactorily, no additional or compensatory muscle mass needs to be generated, thus further restricting growth of new muscle. 
     In another preferred embodiment, the present invention is used to deliver a drug or other therapeutic agent to the tissue with which it is used. For example, in one embodiment, the struts, protrusions, retention strips, etc. are coated or impregnated with or otherwise provided with the therapeutic agent which is preferably engineered to be released into the adjacent tissue over time. Such drugs or therapeutic agents illustratively include genetic therapeutic agents like growth factors, angiogenics, angiotensin converting enzymes, or contractibility promoters (such as that sold under the name Digitalis) or other suitable drugs. 
     In addition, it is believed that the heart muscle can benefit from suturing or other manipulations of the heart muscle in accordance with the present invention. This benefit results from myocardial revascularization which is a known angiogenic effect which regenerates cardiac tissue. 
     The present invention reduces fatigue of the heart and allows for natural regeneration of healthy cardiac tissue, or increases the efficiency of pharmacologically administered treatments. It is also believed that supporting the cardiac muscle in this way relieves tension on the chordae tendinae which in turn prevents mitral. valve regurgitation thus preventing higher mean atrial pressures and pulmonary edema. All of these factors contribute to the cascade of failures in organs and systems associated with congestive heart failure. Once the relaxed heart muscle has regained many of its own contractile properties, it can be weaned from the pacing routine. 
     It should also be noted that the present invention contemplates implementing the techniques and devices described herein not only on the left ventricle, but also on the right ventricle or the other chambers of the heart. Further, the present invention can be implemented on any desired combination of chambers. 
     Although the present invention has been described with reference to preferred embodiments, workers skilled in the art will recognize that changes may be made in form and detail without departing from the spirit and scope of the invention.