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WO2006041421A1 - Stimulation de champ pres d'une discontinuite du myocarde visant a capturer le coeur a des seuils de stimulation reduits - Google Patents

Stimulation de champ pres d'une discontinuite du myocarde visant a capturer le coeur a des seuils de stimulation reduits Download PDF

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Publication number
WO2006041421A1
WO2006041421A1 PCT/US2002/040017 US0240017W WO2006041421A1 WO 2006041421 A1 WO2006041421 A1 WO 2006041421A1 US 0240017 W US0240017 W US 0240017W WO 2006041421 A1 WO2006041421 A1 WO 2006041421A1
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Prior art keywords
cardiac tissue
cardiac
discontinuity
pacing
forming
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English (en)
Inventor
Vinod Sharma
Xiaohong Zhou
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Medtronic Inc
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Medtronic Inc
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Priority to AU2002368545A priority Critical patent/AU2002368545A1/en
Priority to PCT/US2002/040017 priority patent/WO2006041421A1/fr
Anticipated expiration legal-status Critical
Publication of WO2006041421A1 publication Critical patent/WO2006041421A1/fr
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    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/02—Details
    • A61N1/04—Electrodes
    • A61N1/05—Electrodes for implantation or insertion into the body, e.g. heart electrode
    • A61N1/056—Transvascular endocardial electrode systems
    • A61N1/0565—Electrode heads
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/02—Details
    • A61N1/04—Electrodes
    • A61N1/05—Electrodes for implantation or insertion into the body, e.g. heart electrode
    • A61N1/056—Transvascular endocardial electrode systems
    • A61N1/057—Anchoring means; Means for fixing the head inside the heart
    • A61N1/0573—Anchoring means; Means for fixing the head inside the heart chacterised by means penetrating the heart tissue, e.g. helix needle or hook
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/02—Details
    • A61N1/04—Electrodes
    • A61N1/05—Electrodes for implantation or insertion into the body, e.g. heart electrode
    • A61N1/0587—Epicardial electrode systems; Endocardial electrodes piercing the pericardium

Definitions

  • the present invention relates to methods and electrode configurations for pacing the heart, particularly by pacing the heart at reduced pacing energy through inducement of virtual anodes and cathodes along lesions formed in the heart tissue.
  • IMDs implantable medical devices
  • ICDs implantable medical devices
  • pacing systems are incorporated into a wide variety of implantable pacemakers and also into implantable cardioverter defibrillators (ICDs).
  • Such pacing systems comprise an implantable pulse generator (IPG) and one or more lead interconnecting the IPG circuitry with pace/sense electrodes implanted against or into the myocardium of the heart.
  • IPG implantable pulse generator
  • Each heart cell contains positive and negative charges due to the selective permeation of certain ions, such as potassium and sodium through the cell membrane.
  • ions such as potassium and sodium
  • the negative charge is dissipated when the cell is disturbed by an electrical signal that causes the permeability of the cell membrane to change and allows the ingress of positive charge ions.
  • the resulting dissipation of the negative charges constitutes the "depolarization" of the cell.
  • the cell contracts causing (in conjunction with the contraction of adjoining cells) the heart muscle to contract.
  • the stimulation of the heart muscle affects both the depolarization and the contraction of the once- polarized myocardial cells that make up the muscle.
  • the "repolarization" or recovery of the cell commences so that the cell is ready to respond to the next applied stimulus.
  • the cell membrane begins to pump out the positive-charged ions that have entered following the application of the stimulus, that is, during the depolarization of the cell.
  • the inside of the cell membrane starts to become negative again, the cell relaxes, and the potential difference builds up again.
  • the individual myocardial cells are arranged to form muscle fibers and sheets that, in gross, constitute the heart itself.
  • the depolarization of the atrium is characterized by a P-wave viewed on an electrocardiogram (ECG), and depolarization and repolarization signals of the ventricle, are referred to as the QRS complex and the T wave, respectively.
  • ECG electrocardiogram
  • QRS complex depolarization and repolarization signals of the ventricle
  • Depolarization signals are generated in the SA node of specialized cardiac cells located in the atria at a rate that is appropriate for the body's physiologic demand for cardiac output.
  • the system then conducts these impulses rapidly to all the muscle fibers of the ventricles, ensuring coordinated, synchronized pumping.
  • a pacing system may be needed to generate and deliver trains of pacing pulses through pace/sense electrodes to maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart.
  • the pacing circuitry of pacemaker and ICD IPGs is powered by a battery, and each delivered pacing pulse consumes a discrete bolus of the battery energy.
  • the IPG longevity is primarily governed by the battery lifetime.
  • the IPG longevity can range from approximately 3 to 10 years depending on the type of IPG (e.g., pacemaker or ICD).
  • the IPG must be replaced when the battery is depleted, an expensive procedure that also poses significant discomfort and risk to the patient.
  • each pacing pulse is a major factor that impacts the battery life and device longevity, although its impact is greater for some devices than the others.
  • pacing current drawn by each pacing pulse is a major factor that impacts the battery life and device longevity, although its impact is greater for some devices than the others.
  • bi-ventricular pacing systems incorporated into pacemakers and ICDs present a high current drain since two pacing pulses must be delivered to synchronously pace both ventricles at a pacing rate that typically depends upon the patient's physiologic need for cardiac output as determined by an activity sensor, for example.
  • the reduction in delivered pacing current would certainly increase the
  • IPG longevity and could allow the battery and corresponding IPG size to be reduced, and therefore positively impact lives of thousands of patients receiving battery powered IMDs.
  • pace/sense electrode technologies have included pace/sense electrode materials including substrates, coatings and surface treatments, pace/sense electrode shapes, pace/sense electrode surface areas, and pace/sense electrode configurations as well as minimizing local tissue injury when the pace/sense electrode fixed in place by a tissue penetrating active fixation mechanisms, delivery of steroids to the stimulation site by incorporation of steroid eluting elements in the lead body adjacent to the fixation mechanism or coatings on the fixation mechanism.
  • ICDs Today's implantable pacemakers and pacing systems incorporated into ICDs are far more versatile and offer a wider variety of therapies for medical conditions that were not imagined in the infancy of cardiac pacing.
  • electrical stimulation generated by a pacemaker or ICD IPG is in the form of pacing pulses typically having a fixed duration in the order of about 0.5 ms, a voltage of less than 5 volts, and a resulting delivered current dependent upon the collective impedance or load that the pulse is delivered through a cardiac lead conductor and the pace/sense electrode-tissue interface at an active pace/sense electrode.
  • the exponential decaying voltage, cathodal (negative going) pacing pulse shape achieved by a relatively simple, monophasic capacitive discharge output circuit has become accepted as the standard pacing pulse for many years.
  • a negative voltage pulse is typically delivered at the active pace/sense electrode, whereby the active pace/sense electrode is characterized as a cathode pace/sense electrode and the return or indifferent pace/sense electrode in the discharge path is characterized as an anode pace/sense electrode.
  • a cathodic electrical field of sufficient strength and current density has to be impressed upon the excitable tissue in the vicinity of the active site to initiate conduction of a depolarization wave through the entire cardiac tissue mass of a heart chamber that causes the heart chamber to contract and expel blood from the heart chamber, i.e., to capture the heart.
  • the minimum pacing pulse energy necessary to produce that effect is referred to as the "stimulation threshold” or “pacing threshold.”
  • pacing threshold The greater the efficiency of the cathode in impressing the electric field on the tissue, the smaller is the amplitude and/or duration of the pulse required to exceed the stimulation threshold.
  • the present invention provides improved pacing thresholds through adoption of technologies that heretofore have not been employed in the provision of pacing via pace/sense electrodes to a heart chamber.
  • Improved pacing thresholds for capturing the heart are achieved by forming a discontinuity in the cardiac tissue of the heart chamber, disposing a pacing electrode at a distance exceeding a space constant of the cardiac tissue from the discontinuity in the cardiac tissue, and applying a stimulus of a first polarity at an energy insufficient to cause the directly stimulated tissue adjacent to the pacing electrode to propagate a depolarization wave through the cardiac tissue mass of the heart chamber but sufficient to induce a transmembrane potential change at the tissue adjacent to the discontinuity that results in a propagated wave front.
  • pacing energy is advantageously reduced employing the methods and apparatus of the present invention.
  • the present invention is preferably implemented in unipolar and bipolar pacing leads having an electrode head at the lead body distal end wherein the electrode head supports at least one active, cathodal pacing electrode to bear against or be disposed into the myocardium at the space constant distance from the discontinuity.
  • the electrode head supports the active, cathodal pacing electrode and the indifferent, anodal pacing electrode with the discontinuity formed between the pacing electrodes at the space constant distance from each pacing electrode.
  • the lesion or cleft is preferably created by a non-conductive cutting blade or fixation screw supported by the electrode head to be directed into the myocardium upon fixation of the electrode head against the endocardium or epicardium.
  • FIGs. IA and IB are graphical depictions of anodal and cathodal, intracellular stimulation
  • FIGs. 1C and ID are graphical depictions of anodal and cathodal, extracellular stimulation
  • FIGs. 2 A and 2B are schematic illustrations of excitation of an isotropic cardiac tissue
  • FIGs. 3A and 3B are schematic illustrations of excitation of realistic anisotropic cardiac tissue with unequal anisotropy ratio in the extracellular and intracellular domain;
  • FIGs. 4A and 4B are graphical depictions of steady state polarization of a cardiac fiber;
  • FIGs. 5 A - 5D are graphical depictions of the formation of virtual sources bracketing an intracellular discontinuity
  • FIGs. 6 A and 6B are schematic illustrations of excitation of anisotropic cardiac tissue inducing virtual sources bracketing an intracellular discontinuity
  • FIG. 7 is a schematic illustration of an experimental setup for determining pacing thresholds in cardiac tissue prior to and following forming a lesion in the cardiac tissue;
  • FIGs. 8A - 8C are schematic illustrations depicting stimulation sites of heart chambers of hearts stimulated using the test setup of FIG. 7;
  • FIGs 9A - 9C are tracings of the cardiac ECG as well as the applied pacing pulses and depolarization responses obtained from a heart stimulated using the test setup of FIG. 7;
  • FIGs. 1OA and 1OB are graphical depictions of pacing threshold data obtained using the test setup of FIG. 7 for unipolar stimulation applied prior to and following formation of linear lesions in guinea pig hearts;
  • FIGs. 1 IA and 1 IB are graphical depictions of pacing threshold data obtained using the test setup of FIG. 7 for bipolar stimulation applied prior to and following formation of linear lesions in guinea pig hearts;
  • FIGs. 12A and 12B are graphical depictions of time dependent pacing threshold data obtained using the test setup of FIG. 7 for unipolar and bipolar stimulation prior to and following formation of linear lesions in guinea pig hearts;
  • FIGs. 13A and 13B are graphical depictions of the percent reduction in unipolar and bipolar pacing thresholds following formation of lesions in guinea pig hearts subjected to threshold testing using the test setup of FIG. 7;
  • FIGs. 14A and 14B are graphical depictions comparing unipolar and bipolar pacing thresholds prior to and following formation of lesions in guinea pig hearts subjected to threshold testing using the test setup of FIG. 7;
  • FIG. 15 is a plan view of a first embodiment of a pacing lead incorporating a retractable and extendable cutting blade made from an insulating material for forming a discontinuity in cardiac tissue between anodic and cathodic pacing electrodes disposed on an electrode head distal end;
  • FIG. 16 is an expanded end view of the electrode head distal end of the lead of FIG. 15;
  • FIG. 17 is an expanded side view of the electrode head distal end of the lead of FIG. 15;
  • FIG. 18 is an expanded side view in partial cross-section of the electrode head of the lead of FIG. 15 depicting the cutting blade extended to form a discontinuity in cardiac tissue between the anodic and cathodic pacing electrodes;
  • FIG. 19 is an expanded side view in partial cross-section of the electrode head of the lead of FIG. 15 depicting the cutting blade retracted into a chamber of the electrode head during transvenous advancement to an implantation site;
  • FIG. 20 is a side view of an electrode head of an epicardial pacing lead that supports a cutting blade to form a discontinuity in cardiac tissue between the anodic and cathodic pacing electrodes;
  • FIG. 21 is a bottom view of the electrode head of FIG. 20;
  • FIG. 22 is a side view of an electrode head of an epicardial pacing lead that supports a solid screw to form a discontinuity in cardiac tissue between the anodic and cathodic pacing electrodes;
  • FIG. 23 is a bottom view of the electrode head of FIG. 21.
  • the drawing figures are not necessarily to scale.
  • a typical mammalian cardiac cell is cylindrical in shape, approximately 120 ⁇ m in length and 20 ⁇ m in diameter.
  • a single cardiac cell can be excited either by intracellular stimulation illustrated in FIGs. IA and IB or by extracellular stimulation illustrated in FIGs. 1C and ID.
  • the horizontal axis is space or distance, and the vertical axis is either extracellular potential ( ⁇ j) or intracellular potential ( ⁇ e ) or transmembrane potential (V m ). Note that an electrode of a given polarity can depolarize or hyperpolarize the cell depending on its extracellular or intracellular location.
  • a micro-electrode e.g. a micropipette
  • the intracellular micro-electrode can then be used to inject or withdraw current from the cell.
  • the intracellular micro-electrode can be referred to as an "anodal electrode” when positive (anodal) current is injected into the cardiac cell and as a “cathodal electrode” when negative (cathodal) current is injected into the cardiac cell.
  • anodal current is injected into the cell through the intracellular micro-electrode that raises the intracellular potential ⁇ , relative to the extracellular potential ⁇ e .
  • the increase in intracellular potential is uniform along the cell length because the cell is small in size and has high intracellular conductivity.
  • the transmembrane potential (V m - ⁇ i ⁇ e ) is raised, and the cell is depolarized.
  • the conductance of sodium channels small proteins spanning the cell membranes undergoes a very rapid increase when the transmembrane potential V m attains a threshold value ( — 60 mV from resting value of — 90 mV).
  • Sodium ions then flood the intracellular space and further raise the transmembrane potential V m resulting in a cascade of time-dependent and voltage-dependent changes in the conductance of other cell membrane channels (e.g., Ca 2+ and K + channels) causing the cell to fire an action potential.
  • the cell is hyperpolarized and not depolarized if cathodal current is injected into the cell through the intracellular micro-electrode as shown in FIG. IB.
  • the intracellular potential ⁇ ,- is lowered relative to the extracellular potential ⁇ e .
  • the decrease in intracellular potential is uniform along the cell length because the cell is small in size and has high intracellular conductivity.
  • a single cardiac cell can be stimulated with an extracellular electrode disposed outside the cell membrane.
  • the application of positive (anodal) stimulation through the extracellular electrode results in a positive extracellular potential ⁇ e that falls monotonically with distance from the electrode.
  • the intracellular potential ⁇ ,- is raised to a uniform value that is a weighted average of extracellular potential ⁇ e around the cell.
  • the transmembrane potential V 1n has the profile shown in FIG. 1C. Note that the center of the cell now is hyperpolarized. Thus, the excitation would occur only if the depolarization at the ends of the cell exceeds the threshold value, and would require a large extracellular current.
  • the transmembrane potential V 1n profile is reversed as shown in FIG. ID.
  • the cell center is depolarized resulting in easier cell excitation.
  • a cardiac cell can be excited by anodal or cathodal stimulation applied through respective anodal or a cathodal stimulating electrodes, depending on stimulating electrode location (extracellular versus intracellular).
  • pace/sense electrodes i.e., electrodes employed to deliver pacing pulses and to sense intrinsic heart signals
  • pacemaker or ICD IPGs are not designed to and cannot penetrate a viable cell membrane to apply intracellular stimulation to a single cardiac cell. Any penetration of cardiac cells that may occur during implantation or fixation of a pace/sense electrode into the myocardium irreparably damages the cell(s) and results in scar tissue contacting the electrode or fixation mechanism. Therefore, when pacemaker or ICD IPGs generate and deliver narrow pulse width (-0.5 ms), negative going or cathodal pulses to a pacing site of the heart in order to pace a heart chamber, the pacing current is injected in the extracellular space.
  • the cathodal pacing pulse is generated by discharge of a capacitor, typically charged to a voltage of 5 volts or less between discharges, through a discharge circuit or load.
  • the discharge load comprises the lead conductor(s), the cathodal, active pace/sense electrode at the pacing site, an anodal return or indifferent pace/sense electrode, the cardiac and other body tissues and fluids between the active and indifferent pace/sense electrodes, and the electrode-tissue interfaces at the electrode surfaces.
  • the active pace/sense electrode is located typically at the distal end of a cardiac lead, and the indifferent pace/sense electrode is either located on the same lead or located more remotely, typically on the conductive housing of the IPG.
  • the active pace/sense electrode either is fixed to bear against the endocardial or epicardial heart surface (referred to as passive fixation) or penetrates through the endocardial or epicardial heart surface into the myocardium (referred to as active fixation).
  • the pacing pulse For a single cardiac cell that is stimulated with an extracellular electrode shown in FIG. ID, the pacing pulse must raise the transmembrane potential, Vm, of a critical length of the cell above a threshold value to cause a regenerative action potential.
  • Vm transmembrane potential
  • the cathodal stimulation energy applied to the extracellular domain through the typical active pace/sense electrode must depolarize a critical volume of the tissue as illustrated in FIGs. 2A and 2B so that the depolarized volume of cells acts as a foci of depolarization of the entire heart chamber.
  • a pacing pulse having a pulse energy exceeding the threshold value and causing the heart chamber to depolarize is said to "capture" the heart.
  • a depolarization wave produced by a pacing pulse of threshold energy is able to invade the entire heart is that the cardiac tissue is an electrical syncytium in which every cardiac cell is connected to the next cardiac cell via intercellular gap junctions (i.e., small pore-like proteins structures that connect two adjacent cells) as shown in the inset to FIG. 2A.
  • intercellular gap junctions i.e., small pore-like proteins structures that connect two adjacent cells
  • the applied excitation fails to result in a conducted depolarization through the cardiac muscle as shown in FIG. 2B.
  • the current sink from the adjacent tissue is so large that the tissue excitation is suppressed.
  • the source-to-sink mismatch decreases with an increase in the amount of tissue directly depolarized by the applied cathodal stimulus.
  • the applied pacing pulse energy must provide enough current to excite a critical mass of cardiac tissue to result a conducted depolarization to occur that captures the heart.
  • the amount of cathodal stimulation energy required to excite the critical mass of cardiac cells illustrated in FIG. 2A that in turn captures the heart is referred to as the stimulation threshold or pacing threshold.
  • the pacing pulse energy (pulse width or pulse voltage) is periodically adjusted by an auto-threshold algorithm or by programming so that the applied pacing pulse energy exceeds the pacing threshold by a sufficient safety margin to conserve battery energy. From the above discussion any strategy that can decrease source-sink interaction would decrease the critical mass required for excitation, and consequently will decrease current consumption and prolong battery life.
  • the heart as a whole is much more complex than the cells or cell masses depicted in FIGs. IA - ID and 2A - 2B.
  • the cardiac cells that contract and relax in the normal heart cycle and that can be stimulated with a pacing pulse to contract are organized in sheets and fibers that define the muscular atrial and ventricular heart chamber walls, the atrial and ventricular septum, and that merge with tissues that do not contract and relax at the base of the heart and that form valves and arterial and venous valves, etc.
  • the sheets and fibers forming the muscular ventricles change orientation as they wrap longitudinally and transversely around and across the atrial and ventricular walls.
  • the cardiac tissue is anisotropic in both the intracellular and extracellular domains rather than being an isotropic medium with uniform conductivity in all directions.
  • the anisotropy ratio (longitudinal to transverse) is unequal in the two domains (4:1 for extracellular domain versus 10:1 for the intracellular domain). Therefore, the anisotropic cardiac tissue responds to an externally applied stimulus in a very interesting fashion.
  • FIGs. 3A and 3B Schematically illustrated responses of myocardial fibers to anodal and cathodal extracellular stimuli are illustrated in FIGs. 3A and 3B, where L represents the longitudinal direction and T represents the transverse direction of the myocardial fibers.
  • polarized regions or fields of the myocardial fibers that are marked with a "+” are depolarized by an applied stimulus
  • polarized regions or fields of the myocardial fibers that are marked with a "-” are hyperpolarized by an applied stimulus.
  • a dog-bone shaped region of depolarization marked "-" and extending in the transverse direction T forms directly beneath a stimulation electrode applying cathodal stimulation to the myocardial fibers as shown in FIG. 3 A.
  • Two regions of hyperpolarization marked "+” also form at a distance in the longitudinal direction L away from and flanking the dog- bone shaped region of depolarization marked "-” in response to the applied cathodal stimulation as also shown in FIG. 3 A.
  • depolarization and hyperpolarization regions are reversed in polarity in response to an anodal stimulus applied through the same electrode, such that the central hyperpolarized region marked "+” is flanked by two regions of depolarization marked "-" as shown in FIG. 3B.
  • Such virtual sources can arise not only from the tissue anisotropy but also from several other factors that disrupt the flow of the intracellular or extracellular currents, e.g., fiber bending, gradient in the extracellular electrical field, and changes in intracellular and extracellular conductance. See Sobie et al., "A Generalized Activating Function for
  • the intracellular current encounters an abrupt barrier caused by an intracellular cleft (no intracellular space) or an intracellular lesion (an induced injury to cardiac cells resulting in scar tissue), and therefore the intercellular current must exit the intracellular space and reenter on the other side of the cleft or lesion.
  • discontinuity at the cleft or lesion impedes the flow of intracellular current and results in changes in the transmembrane potential V n , far from the electrode (x> ⁇ ) as shown in FIG. 5B.
  • FIG. 5D The anodic current and the accompanying hyperpolarization on the other side of the cleft or lesion can be thought to be arising from a virtual anodal electrode or source indicated at ⁇ +> in FIG. 4D.
  • the virtual cathodal electrode or source on one side of a discontinuity is referred to herein as a “virtual cathode", and the virtual anodal electrode or source on the other side of the discontinuity is referred to herein as a "virtual anode”.
  • FIG. 6A and 6B The two-dimensional spatial fields of virtual anodes and virtual cathodes occurring on either side of an intracellular discontinuity, e.g., a cleft or lesion, formed in a cardiac tissue fiber in response to an anodal stimulus, for example, applied to the cardiac tissue fiber at a distance x ⁇ l .5-2.5 ⁇ from the cleft or lesion are illustrated in FIGs. 6A and 6B. It will be understood that the virtual anodes and virtual cathodes would appear on the opposite sides of the intracellular discontinuity in response to a cathodal stimulus applied to the cardiac tissue fiber at the distance x ⁇ l .5-2.5 ⁇ from the cleft or lesion. In FIG.
  • the elongated cleft or lesion is formed in the same direction as the longitudinal direction L of the cardiac tissue fibers.
  • the elongated cleft or lesion is formed transverse to the longitudinal direction L of the cardiac tissue fibers, i.e., in the transverse direction T.
  • These virtual anodes and virtual cathodes flanking the cleft or lesion are conceptually similar to the hyperpolarization regions marked by "-" flanking the dog-bone shaped depolarization regions marked by "+” below the real cathodal electrode that are also depicted in FIGS. 6 A and 6B.
  • the regions of hyperpolarization flanking the central depolarized region of anisotropic cardiac tissue stimulated with cathodal stimulation depicted in FIG. 3B serve as electrotonic current sinks.
  • the electrotonic current sinks limit the ability of the depolarized region directly stimulated by the real electrode to excite the entire cardiac tissue.
  • the current practice is to apply sufficient pulse energy to increase the depolarized region sufficiently to overcome the effects of the electrotonic current sinks.
  • the electrotonic interaction between the virtual anode and the virtual cathode bracketing the lesion will be small, provided the cleft or lesion depicted in FIG. 6 A is long enough (i.e., longer than space constant ⁇ ).
  • the electrotonic current sink is minimal at the location of the virtual cathode, and the strength of the cathodic virtual source, and consequently the accompanied depolarization could potentially be stronger than the real source.
  • the pacing threshold would be reduced, resulting in a reduced pacing pulse energy of a pacing pulses applied at the real electrode sufficient to capture the heart.
  • the lesion may decrease the electrotonic load on the centrally depolarized region and help reduce the pacing threshold if the lesion is made perpendicular to the fibers (i.e. along the transverse direction T) approximately at the location of the hyperpolarization region, as shown in FIG. 6B.
  • ECG type signals were derived from the monitoring electrodes and used to monitor health of the heart and to determine unipolar and bipolar control pacing thresholds and post-lesion pacing thresholds as explained below.
  • the unipolar and bipolar pacing electrodes used to stimulate the heart to determine pacing thresholds had surface areas of 1.2 mm 2 and were made of porous platinum black, a material similar to one used on pace/sense electrodes of commercially available pacing leads.
  • the pacing electrodes were mounted on a manual micro-manipulator and pressed against the myocardium until a reliable and stable capture response to pacing stimuli was observed.
  • the three sites on the heart where unipolar and bipolar pacing thresholds were measured comprise an anterior left ventricular site shown in FIG. 8A, a posterior left ventricular site shown in FIG. 8B, and an interventricular septum site shown in FIG. 8C.
  • the right ventricle was cut open along the interventricular connection to access the septum.
  • both the active cathodal and the return anodal pacing electrodes were affixed at each of the three sites at an inter-electrode spacing ⁇ 5 mm apart.
  • the lead from the stimulator was removed from the return anodal pacing electrode and connected to another return anodal electrode in the bath.
  • the unipolar and bipolar control pacing thresholds were measured for each site after the initial stabilization period. A lesion was then formed in the myocardial tissue approximately midway between the two pacing electrodes affixed at each site as shown.
  • the lesion was formed using a scalpel to make a cut ⁇ 3-5 mm long and orthogonal to an imaginary line between the two pacing electrodes affixed at each site.
  • the distance I was about ⁇ 1.5-2.5 ⁇ (the space constant) for the cardiac tissue.
  • the unipolar and bipolar, control and test, pacing thresholds were detennined by applying a train of constant current pulses (each 0.5 ms in duration with inter-pulse duration of 300 ms) using a Bloom stimulator to each site.
  • the pulse current amplitude was gradually increased in increments of 0.02 mA from a sub-threshold value until capture of the myocardium occurred as revealed by the ECG recordings for every pulse in the pulse train.
  • the current amplitude at which a delivered pulse achieved capture was labeled as the pacing threshold for that site.
  • the mean pacing threshold using unipolar electrodes decreased by -50% from a control value of 0.3 l ⁇ O.13 mA to 0.16 ⁇ 0.08 mA
  • a train of sub-threshold amplitude pacing pulses was applied to the heart to explore the pacing threshold.
  • the recorded ECG reflected sinus rhythm of the heart as shown in FIG. 9A as long as the train of sub-threshold pacing pulses did not capture the myocardium.
  • the pulse amplitude was then gradually raised in increments of 0.02 mA.
  • Myocardial capture occurred for some pulses in the pulse train but not for all as shown in FIG. 9B when the mean pulse amplitude was slightly below the threshold value.
  • myocardial capture occurred for every pulse as shown in FIG. 9C when the pulse amplitude was raised by another 0.02 mA, and this pulse amplitude was recorded as the pacing threshold for that site.
  • FIG. 1OA The reduction in pacing threshold after lesion formation is shown in FIG. 1OA for unipolar stimulation.
  • the data includes measurement from 26 sites in 8 guinea pigs. The threshold was found to decrease after lesion formation for all sites except one.
  • FIG. 1OB shows the same data after normalizing the control threshold to 100%. In some experiments the reduction in pacing threshold was up to 70%.
  • the findings for bipolar stimulation were similar to those for unipolar stimulation.
  • the normalized data shown in FIG. 1 IB shows that reduction in pacing threshold for some sites was up to 80%, slightly larger than that observed for unipolar stimulation.
  • the unipolar and bipolar pacing thresholds measured 5 minutes and 10 minutes after the lesion formation are shown in FIG. 12A and 12B, respectively. After the 5 minutes wait, 13 sites ( ⁇ 62%) showed a decrease in the pacing threshold, and 7 sites (-33%) showed an increase in the pacing threshold. For unipolar stimulation, the increase in the pacing threshold was restricted to a small range of 0.08 mA for all sites except one exceptional site where the pacing threshold changed by ⁇ 0.25 mA. Possible reasons for such a large change in the pacing threshold are discussed below. The pacing threshold increased at only one site after 10 minutes wait, and this increase was less than 0.02 mA. Similar data as set forth in FIG.
  • Table 1 depicts percentage of sites with variation in pacing threshold from the control value by various fixed amounts. Note, that the variation in pacing threshold ranged from -0.1 mA to 0.08 mA after 5 minutes wait, and the variation ranged from -0.08 mA to 0.02 mA after 10 minutes wait.
  • the reduction in pacing threshold showed a trend of being slightly larger for sites with higher baseline pacing threshold as shown in FIGs. 13A and 13B.
  • the pacing thresholds for the unipolar and bipolar stimulation before (control) and after the lesion formation were compared.
  • the control pacing threshold for the two electrodes were approximately equal (0.31 ⁇ 0.13 mA for unipolar versus 0.30 ⁇ 0.17 mA for bipolar; .PO.33) as shown in FIG. 14A.
  • the pacing threshold for the two electrodes reduced but again remained approximately equal as shown in FIG. 14B (0.16 ⁇ 0.18 mA for unipolar versus 0.17 ⁇ 0.08 mA for bipolar; PO.ll).
  • the pacing thresholds were found to be quite stable for the majority of the measurement sites for up to 5 to 10 minutes (FIGs. 12A and 12B and Table 1).
  • the reduction in pacing threshold was slightly larger for higher values of baseline pacing threshold for both unipolar and bipolar electrodes (FIGs. 13A and 13B).
  • the threshold reduction for unipolar and bipolar electrodes were found to be quite similar (FIGs. 14 A and 14B).
  • the control pacing threshold for unipolar and bipolar electrodes varied from 0.1 mA to 0.7 mA.
  • pacing threshold for normal myocardium should be in the range of 0.3 - 0.6 mA as derived from voltage and impedance values reported by Hidden-Lucet et al., "Low Chronic Pacing Thresholds of Steroid-Eluting Active-Fixation Ventricular Pacemaker Leads: A Useful Alternative to Passive-Fixation Leads", Pacing Clin Electrophysiol. 2000; 23:1798-800.
  • Abnormally low pacing threshold for some hearts might have occurred because the hearts experienced transient global ischemia during the extraction procedure.
  • the percent decrease in the pacing threshold in hearts with low pacing threshold was found to be smaller compared to the hearts with higher control values as shown in FIGs. 13A-13B.
  • reduction in baseline threshold might be correlated with severity of ischemia experienced by a heart during the extraction procedure.
  • any electrotonic interaction between the two electrodes is expected to be minimal, i.e., current flow pattern from one electrode is unlikely to be influenced by the other electrode.
  • the inter-electrode distance should be of the order of space constant ⁇ for a significant electrotonic interaction to occur.
  • the two electrodes were to be a space constant ⁇ apart, then the distance between the lesion to any one electrode will be only half a space constant 0.5 ⁇ . This would be insufficient distance for intracellular current density to reach a steady state maximal value.
  • the two electrodes should at least be two space constants away (2 ⁇ ). However, this guarantees that electrotonic interaction between the two electrodes will be small or negligible, and therefore the unipolar and bipolar electrodes should yield identical results as observed in this study.
  • the present invention can be embodied in epicardial and endocardial pacing leads of the types known in the prior art.
  • a first embodiment of a pacing lead that both forms a discontinuity and provides pacing stimulation is depicted in FIGs. 15 - 19.
  • the endocardial pacing lead 10 comprising a lead body 26 extending between a proximal connector assembly 20 and a distal electrode head 50.
  • a stylet 30 is also depicted in FIG. 15 having an elongated stylet wire 32 extending from a stylet knob 34 and inserted down the lumen of the lead body 26.
  • Lead body 26 is formed of a length of outer insulating sheath 12 having proximal and distal ends and a sheath lumen, the sheath 12 operating as an electrical insulator formed of a biocompatible silicone rubber or polyurethane compound substantially inert to body fluids.
  • a multi-filar, coiled wire conductor 18 having proximal and distal ends and a coil lumen formed therein is loosely received within the sheath lumen of sheath 12.
  • the proximal connector assembly 20 comprises a connector ring 22 and a connector pin 24 that are electrically connected to separately insulated anodic and cathodic wires of the multi-filar coiled wire conductor 18.
  • Sealing ring sets 28 and 28' are compressed and serve to seal the lead body lumen and the gap between the connector pin 24 and connector ring 22 from ingress of body fluids upon insertion of connector assembly 20 into a mating bore of an implantable pulse generator connector block in a manner well known in the art.
  • Sheath 12 and coiled wire conductor 18 extend between the connector assembly 20 and the electrode head 50 shown in cross- section in FIGs. 18 and 19.
  • the electrode head 50 can include a plurality of soft, pliant tines 52 (shown in FIG. 15 but omitted from FIGs. 16 - 19 for convenience of illustration) that provide passive fixation of the electrode head
  • Anodic and cathodic pacing electrodes 56 and 58 and a cutting element or blade 60 extend distally from the electrode head distal surface 54.
  • the anodic and cathodic pacing electrodes 56 and 58 are electrically connected through the separately insulated anodic and cathodic wires of the multi-filar coiled wire conductor 18 to the connector ring 22 and connector pin 24, respectively.
  • the electrode head distal surface 54 is preferably non-conductive and supports the anodic and cathodic pacing electrodes 56 and 58 on either side of a centrally disposed cutting element or blade 60.
  • the anodic and cathodic pacing electrodes 56 and 58 are spaced apart by an inter-electrode distance 2-£; which may be on the order or 3.0 mm to 5.0 mm apart.
  • the anodic and cathodic pacing electrodes 56 and 58 can be formed of any of the known pacing materials and have an electrode surface area of about 1-2 mm 2 or 1.2 mm 2 for example.
  • the pacing electrodes 56 and 58 can be formed on the surface of the electrode head distal surface 54 or can project distally from the surface of the electrode head distal surface 54.
  • the pacing electrodes 56 and 58 are coupled through conductors 66 and 68, respectively, to wires of the coiled wire conductor 18.
  • the cutting element or blade 60 is adapted to be retracted into the distal electrode head 50 during implantation as shown in FIG. 19 and ejected distally of the electrode head distal surface 54 at the implantation site to cut through the endocardium and form the discontinuity as shown in FIG. 18.
  • the cutting element or blade 60 is preferably formed of a non-conductive ceramic or a similar material that can have a highly sharpened cutting edge 62.
  • the cutting edge 62 preferably extends about 2 mm further distally when ejected as shown in FIG. 18 than the anodic and cathodic pacing electrodes 56 and 58.
  • the electrode head 50 of lead 10 is advanced via a percutaneous access into a vein with the cutting element or blade 60 retracted into a slit 64 and cylindrical chamber 70 of the electrode head 50 as shown in FIG. 19.
  • a first stylet 30 having stylet wire 32 length that extends to the distal electrode head 40 can be used to stiffen and steer the lead body 26 during implantation.
  • a second stylet 30 having a stylet wire 32 length that extends through the length of the distal electrode head 40 can then be used to distally advance the cutting element or blade 60 from the distal electrode head 40 to form a lesion or cleft in endocardial tissue.
  • the proximal end of the cutting blade 60 is mounted to a mounting block 76 embedded within a sealing block 80 having a plurality of sealing rings 78 bearing tightly against the surface of the cylindrical chamber 70.
  • a proximal recess 74 of the movable mounting block 76 can be engaged by the distal surface of stylet wire 32.
  • the stylet wire 32 is advanced distally within the lead body lumen to engage the recess 74 to move the assembly of the sealing block 80, the mounting block 76, and the cutting blade 60 distally from the retracted position of FIG. 19 to the extended position of FIG. 18.
  • the movement of the cutting blade 60 is done with sufficient force to penetrate through the cardiac tissue layers.
  • the cutting edge 62 is shaped like the edge of a razor blade.
  • the electrode head is firmly advanced against the cardiac tissue in initial implantation, and the tines hold the advanced position.
  • the present invention may also be employed in an epicardial pacing lead where it may not be necessarily necessary to move cutting element or blade.
  • the electrode head 150 of an exemplary epicardial pacing lead 100 is depicted in part in FIGs. 20 and 21.
  • the lead body 126, coiled wire conductor 118, and proximal connector assembly can take the forms employed in the endocardial lead 10, except that a stylet lumen and stylet are not necessary.
  • the electrode head 150 is provided with a mesh 112 on the electrode head surface 154 adapted to encourage tissue ingrowth and that can be sutured through or adhered to the epicardium employing a medical adhesive following procedures known in the prior art.
  • the anodic and cathodic pacing electrodes 156 and 158 are spaced apart by an inter-electrode distance 2£; which may be on the order or 3.0 mm to 5.0 mm apart.
  • the anodic and cathodic pacing electrodes 156 and 158 can be formed of any of the known pacing materials and have an electrode surface area of about 1-2 mm 2 or 1.2 mm 2 for example.
  • the pacing electrodes 156 and 158 can be formed on the surface of the electrode head distal surface 154 or can project distally from the surface of the electrode head distal surface 154.
  • the pacing electrodes 156 and 158 are coupled through wires of the coiled wire conductor 118 to the connector pin and ring of the proximal connector assembly.
  • the movement of the cutting blade 160 is done with sufficient force to penetrate through the cardiac tissue layers.
  • the cutting blade 160 is shaped like an arrow that has a point 164 that first penetrates the tissue layer before the arrow edge
  • FIGs. 22 and 23 An electrode head 250 of a further exemplary epicardial pacing lead 200 that supports a solid, non-conductive, screw 260 to form a discontinuity in cardiac tissue between the anodic and cathodic pacing electrodes 256 and 258 is depicted in FIGs. 22 and 23.
  • the anodic and cathodic pacing electrodes 256 and 258 are spaced apart by an inter-electrode distance 2t; which may be on the order or 3.0 mm to 5.0 mm apart.
  • the anodic and cathodic pacing electrodes 256 and 258 can be formed of any of the known pacing materials and have an electrode surface area of about 1-2 mm 2 or 1.2 mm 2 for example.
  • the pacing electrodes 256 and 258 can be formed on the surface of the electrode head distal surface 254 or can project distally from the surface of the electrode head distal surface 254.
  • the pacing electrodes 256 and 258 are coupled through wires of the coiled wire conductor 218 to the connector pin and ring of the proximal connector assembly.
  • the electrode head 250 is provided with a mesh 212 adapted to encourage tissue ingrowth and that can be sutured through or adhered to the epicardium employing a medical adhesive following procedures known in the prior art.
  • fixation may be possible by the threads 262 of solid helix or screw 260 that are intended to be screwed into the myocardium employing a fixation tool, e.g., the tool disclosed in commonly assigned U.S. Patent No. 6,010,526.
  • the electrode head 250 is grasped by the tool and pressed against the epicardium as the tool and electrode head 250 are rotated so that sharpened tip 264 penetrates the epicardium, and the threads 262 screw into the myocardium and draw the epicardium against the pacing electrodes 256 and 258.
  • FIGs. 22 and 23 Although an epicardial lead is depicted in FIGs. 22 and 23, it will be understood that the solid helix or screw 260 can be substituted for the cutting blade 60 of the endocardial lead of FIGs. 15 - 19.
  • the virtual anode and virtual cathode are created in the cardiac tissue on the sides of the blade 60 or 160 or the screw 260 that are closest to the cathodic and anodic pacing electrodes as depicted in the figures. It will be understood that the above-described embodiments are particularly useful for bipolar pacing as shown or for unipolar pacing, wherein the indifferent anodal pacing electrode 56, 156, 256 is not present or is not employed by the IPG.

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  • Biomedical Technology (AREA)
  • Nuclear Medicine, Radiotherapy & Molecular Imaging (AREA)
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Abstract

Des seuils de stimulation cardiaque améliorés, destinés à capturer le coeur, sont obtenus par la formation d'une discontinuité dans le tissu cardiaque de la chambre, par le placement d'une électrode de stimulation à une distance supérieure à la constante spatiale du tissu cardiaque par rapport à la discontinuité dans le tissu cardiaque, et par l'application d'un stimulus d'une première polarité avec une énergie insuffisante pour faire en sorte que le tissu stimulé directement, adjacent à l'électrode de stimulation, propage une onde de dépolarisation à travers la masse du tissu cardiaque de la chambre mais suffisante pour induire un changement de potentiel transmembranaire dans le tissu adjacent à la discontinuité, ce qui résulte en un front d'onde propagé. De cette manière, on réduit avantageusement l'énergie de stimulation cardiaque.
PCT/US2002/040017 2002-12-04 2002-12-04 Stimulation de champ pres d'une discontinuite du myocarde visant a capturer le coeur a des seuils de stimulation reduits Ceased WO2006041421A1 (fr)

Priority Applications (2)

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AU2002368545A AU2002368545A1 (en) 2002-12-04 2002-12-04 Field stimulation about a discontinuity of the myocardium to capture the heart at reduced pacing thresholds
PCT/US2002/040017 WO2006041421A1 (fr) 2002-12-04 2002-12-04 Stimulation de champ pres d'une discontinuite du myocarde visant a capturer le coeur a des seuils de stimulation reduits

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PCT/US2002/040017 WO2006041421A1 (fr) 2002-12-04 2002-12-04 Stimulation de champ pres d'une discontinuite du myocarde visant a capturer le coeur a des seuils de stimulation reduits

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Cited By (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2024115937A1 (fr) * 2022-12-02 2024-06-06 Sorin Crm Sas Hélice de coupe pour fixation de conducteur

Citations (7)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
GB2025236A (en) * 1978-07-10 1980-01-23 Cordis Corp Suture-forming tool
US4280510A (en) * 1979-02-08 1981-07-28 Medtronic, Inc. Sutureless myocardial lead introducer
US4351345A (en) * 1978-10-10 1982-09-28 Carney Andrew L Methods of securing electrodes to the heart
EP0393265A1 (fr) * 1987-07-13 1990-10-24 Intermedics Inc. Mécanisme de fixation active pour électrode de stimulation cardiaque
US5575797A (en) * 1993-09-24 1996-11-19 Siemens Elema Ab Device for explanting a medical electrode device
US6010526A (en) 1998-09-18 2000-01-04 Medtronic, Inc. Epicardial lead implant tool and method of use
EP1062971A1 (fr) * 1999-06-25 2000-12-27 BIOTRONIK Mess- und Therapiegeräte GmbH & Co Ingenieurbüro Berlin Cathéter muni d'un port distal pour un fil

Patent Citations (7)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
GB2025236A (en) * 1978-07-10 1980-01-23 Cordis Corp Suture-forming tool
US4351345A (en) * 1978-10-10 1982-09-28 Carney Andrew L Methods of securing electrodes to the heart
US4280510A (en) * 1979-02-08 1981-07-28 Medtronic, Inc. Sutureless myocardial lead introducer
EP0393265A1 (fr) * 1987-07-13 1990-10-24 Intermedics Inc. Mécanisme de fixation active pour électrode de stimulation cardiaque
US5575797A (en) * 1993-09-24 1996-11-19 Siemens Elema Ab Device for explanting a medical electrode device
US6010526A (en) 1998-09-18 2000-01-04 Medtronic, Inc. Epicardial lead implant tool and method of use
EP1062971A1 (fr) * 1999-06-25 2000-12-27 BIOTRONIK Mess- und Therapiegeräte GmbH & Co Ingenieurbüro Berlin Cathéter muni d'un port distal pour un fil

Cited By (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2024115937A1 (fr) * 2022-12-02 2024-06-06 Sorin Crm Sas Hélice de coupe pour fixation de conducteur

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