Source: http://www.google.com/patents/US20020087089
Timestamp: 2017-12-16 19:32:33
Document Index: 308910507

Matched Legal Cases: ['art.\n85', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20', 'art 20']

Patent US20020087089 - Method of pacing a heart using implantable device - Google Patents
A method of determining an optimal location for implanting a pacemaker electrode includes the steps of pacing a heart from a first location and generating a first map of the heart associated with pacing at the first location. The heart is paced from a second location and a second map is generated of...http://www.google.com/patents/US20020087089?utm_source=gb-gplus-sharePatent US20020087089 - Method of pacing a heart using implantable device
Publication number US20020087089 A1
Also published as US6915149
Publication number 043663, 10043663, US 2002/0087089 A1, US 2002/087089 A1, US 20020087089 A1, US 20020087089A1, US 2002087089 A1, US 2002087089A1, US-A1-20020087089, US-A1-2002087089, US2002/0087089A1, US2002/087089A1, US20020087089 A1, US20020087089A1, US2002087089 A1, US2002087089A1
Original Assignee Shlomo Ben-Haim
US 20020087089 A1
15. A method according to any of claims 1-14, wherein the local physiological value comprises a thickness of the heart at the location.
16. A method according to claim 15, wherein the thickness of the heart is determined using an ultrasonic transducer mounted on the invasive probe.
analyzing the map to determine underperfused portions of the heart.
85. A method according to any of claims 81-84, wherein the cardiac parameter comprises intra-cardiac pressure.
[0005]FIG. 1C shows a second phase, called rapid filling phase and indicates the start of a diastole. During this phase, right ventricle 24 relaxes and fills with blood flowing from right atrium 22 through a tricuspid valve 40, which is open during this phase. pulmonic valve 34 is closed, so that no blood leaves right ventricle 24 during this phase. Left ventricle 28 also relaxes and is filled with blood flowing from left atrium 26 through a mitral valve 42, which is open. Aortic valve 36 is also closed to prevent blood from leaving left ventricle 26 during this phase. The filling of the two ventricles during this phase is affected by an existing venous pressure. Right atrium 22 and left atrium 26 also begin filling during this phase. However, due to relaxation of the ventricles, their pressure is lower than the pressure in the atria, so tricuspid valve 40 and mitral valve 42 stay open and blood flows from the atria into the ventricles.
[0006]FIG. 1D shows a third phase called diastatis, which indicates the middle of the diastole. During this phase, the ventricles fill very slowly. The slowdown in filling rate is due to the equalization of pressure between the venous pressure and the intra-cardiac pressure. In addition, the pressure gradient between the atria and the ventricles is also reduced.
[0007]FIG. 1E shows a fourth phase called atrial systole which indicates the end of the 15 diastole and the start of the systole of the atria During this phase, the atria contract and inject blood into the ventricles. Although there are no valves guarding the veins entering the atria, there are some mechanisms to prevent backflow during atrial systole. In left atrium 26, sleeves of atrial muscle extend for one or two centimeters along the pulmonary veins and tend to exert a sphincter-like effect on the veins. In right atrium 22, a crescentic valve forms a rudimentary valve called the eustachian valve which covers the inferior vena cava In addition, there may be muscular bands which surround the vena cava veins at their entrance to right atria 22.
[0008]FIG. 1F is a graph showing the volume of left ventricle 24 as a function of the cardiac cycle. FIG. 1F clearly shows the additional volume of blood injected into the ventricles by the atria during atrial systole as well as the variance of the heart volume during a normal cardiac cycle. FIG. 1G is a graph which shows the time derivative of FIG. 1F, i.e., the left ventricle fill rate as a function of cardiac cycle. In FIG. 1G two peak fill rates are shown, one in the beginning of diastole and the other during atrial systole.
[0015]FIG. 3 shows the main conduction pathways in heart 20. An SA node 50, located in right atrium 22, generates an activation signal for initiating contraction of muscle fibers 44. The activation signal is transmitted along a conduction pathway 54 to left atria 26 where the activation signal is locally disseminated via bachman bundles and Crista terminals. The activation signal for contracting the left and right ventricles is conducted from SA node 50 to an AV node 52, where the activation signal is delayed. The ventricles are normally electrically insulated from the atria by non-conducting fibrous tissue, so the activation signal must travel through special conduction pathways. A left ventricle activation signal travels along a left pathway 58 to activate left ventricle 28 and a right ventricle activation signal travels along a right pathway 56 to activate right ventricle 24. Generally, the conduction pathways convey the activation signal to apex 46 where they are locally disseminated via purkinje fibers 60 and propagation over the rest of the heart is achieved by conduction in muscle fibers 44. In general, the activation of the heart is from the inner surface towards the outer surface. It should be noted that electrical conduction in muscle fibers 44 is generally faster along the direction of the muscle fibers. Thus, the conduction velocity of the activation signals in heart 20 is generally anisotropic.
It is also known to pace using multiple electrodes, where the activation signal is initiated from a selected one or more of the electrodes, depending on sensed electrical values, such as sequence, activation time and depolarization state. Typically, the pacing regime is adapted to a specific arrhythmia. Sometimes, logic is included in the pacemaker which enables it to identify and respond to several types of arrhythmia
U.S. Pat. No. 5,403,356 to Hill et al. describes a method of preventing atrial arrhythmias by adapting the pacing in the right atrium in response to a sensed atrial depolarization, which may indicate an arrhythmia
Lameh Fananapazir, Neal D. Epstein, Rodolfo V. Curiel, Julio A. Panza, Dorothy Tripodi and Dorothea McAreavey, in “Long-Term Results Of Dual-Chamber (DDD) Pacing In Obstructive Hypertrophic Cardiomyopathy ”, Circulation, Vol. 90, No. 60, pp. 2731-2742, Dec. 1994, the disclosure of which is incorporated herein by reference, describes the effects of pacing a HCM-diseased heart using DDD pacing at the apex of the right ventricle. One effect is that the muscle mass near the pacing location is reduced, i.e., the ventricular septum is atrophied. The atrophy is hypothesized to be caused by the changes in workload at the paced location which are due to the late activation time of ventricular segments far from the pacing location.
(b) determining the position of the distal end of the catheter, and
Although the above maps are described as being time based or cardiac-phase based, in a preferred embodiment of the invention, measurements are binned based on geometrical characteristics of the heart or on ECG or electrogram characteristics. Preferably, the ECG characteristics comprise pulse rate and /or ECG morphology. Maps associated with different bins can be compared to determine pathologies and under utilization of the heart, for example, an abnormal activation profile due to a conduction abnormality, such as a block, for assessing the effects of tachycardia or for assessing changes in the activation profile as a function of heart rate.
(d) repeating (a)-c) for a plurality of locations of the heart; and
There is also provided in accordance with a preferred embodiment of the invention, a method of determining a preferred pacing regime, including generating a map of the heart; and determining, using the map, a preferred pacing regime for a heart which is optimal with respect to a physiological variable. Preferably, the method includes pacing the heart using the preferred pacing regime. Alternatively or additionally, the map includes an electrical map. Preferably, determining a preferred pacing regime includes generating a map of the activation profile of the heart. Alternatively or additionally, the map includes a mechanical map. Preferably, determining a preferred pacing regime includes generating a map of the reaction profile of the heart. Alternatively or additionally, the method includes analyzing an activation map or a reaction map of the heart to determine portions of the heart which are under-utilized due to an existing activation profile of the heart. Alternatively or additionally, pacing is initiated by implanting at least one pacemaker electrode in the heart s preferably, the at least one pacemaker electrode includes a plurality of individual electrodes, each attached to a different portion of the heart.
[0171]FIG. 1A is a schematic cross-section diagram of a heart;
[0172]FIG. 1B-1E are schematic cross-section diagrams showing the heart in each of four phases of a cardiac cycle;
[0173]FIG. 1F is a graph showing the blood volume in a left ventricle of the heart during a cardiac cycle;
[0174]FIG. 1G is a graph showing the filling rate of the left ventricle during a cardiac cycle;
[0175]FIG. 2 is a partial schematic view of a heart showing the arrangement of cardiac muscle fibers around a left ventricle; FIG. 3 is a schematic cross-section diagram of a heart showing the electrical conduction system of the heart;
[0176]FIG. 4 is a graph showing changes in the voltage potential of a single cardiac muscle cell in reaction to an activation signal;
[0178]FIG. 6 is a schematic cross-sectional side view of a heart showing a preferred apparatus for generating a map of the heart;
[0179]FIG. 7 is a flowchart of a preferred method of constructing the map utilizing the apparatus of FIG. 6;
[0180]FIG. 8 is a generalized graph showing the dependence of a resistance on the distance of the catheter from heart muscle tissue;
[0182]FIG. 10 shows a multi-headed catheter for sensing local geometric changes according to a preferred embodiment of the invention;
[0183]FIG. 11 is a flowchart showing a preferred binning method;
[0184]FIG. 12A-D show pathological cases where a change in pacing of a heart is desirable; and
[0185]FIG. 13 is a schematic side view of an implanted pacemaker according to a preferred embodiment of the invention.
Reconstructing the surface of heart 20 may comprise reconstructing inner or outer surfaces of heart 20, depending on the location of catheter tip 74. Methods of reconstructing a surface from a plurality of data points are well known in the art
Preferably, catheter 72 is a steerable tip catheter, so that repositioning of tip 74 is facilitated. Steerable catheters are further described in PCT application US95/01103 and in U.S. Pat. No. 5,404,297, 5,368,592, 5,431,168, 5,383,923, 5,368,564, 4,921,482, 5,195,968, the disclosures of which are incorporated herein by reference.
[0204]FIG. 8 is a generalized graph showing the dependence of a resistance, between tip 74 and an external lead attached to the patient, on the distance of tip 74 from location 75, at 50 KHz.
[0206]FIG. 9B shows another way of determining the reaction of muscle tissue to an activation signal. A first location 92 is located a distance D1 from a second location 94 and a distance D2 from a third location 96. In a normal heart D1 and D2 can be expected to contract at substantially the same time by a substantially equal amount However, if the tissue between location 92 and location 94 is non-reactive, D1 might even grow when D2 contracts (Laplace's law). In addition a time lag between the contraction of D1 and of D2 is probably due to blocks in the conduction of the activation signal. A map of the reaction of the heart to an activation signal may be as important as an activation map, since it is the reaction which directly affects the cardiac output, not the activation.
[0207]FIGS. 9C and 9D show the determination of local changes in the radius of heart 20, which can be together with the pressure to determine the local tension using Laplace's law. In FIG. 9C a plurality of locations 98, 100 and 102 exhibit a local radius R1 and in FIG. 9D, the local radius decreases to R2, which indicates that the muscle fiber at locations 98, 100 and 102 is viable. It should be noted, that since the pressure in heart 20 is spatially equalized, a ratio between the tension at different parts of heart 20 can be determined even if an absolute value cannot be determined.
Alternatively or additionally, a cold-tip catheter is used to map the effect of ablating a portion of the heart. It is known in the art that hypothermic cardiac muscle does not initiate or react to electrical signals. Cold-tip catheters, such as disclosed in PCT publication WO 95/19738 of July 27, 1995, the disclosure of which is incorporated herein by reference, can be used to inhibit the electrical activity of a local wall segment while simultaneously mapping the local geometrical effects of the inhibition.
[0236]FIG. 12A shows a heart 20′ having a hyper trophied ventricular septum 109. The activation of the left ventricle of heart 20′ typically starts from a location 108 at the apex of heart 20′, with the result that the activation times of a location 110 in an external wall 111 is substantially the same as the activation time of a location 112 in septum 109. If the initial activation location is moved from location 108 to location 112, e.g. by external pacing, septum 109 will be more efficiently utilized, while wall 111 will be activated later in the systole, resulting in a shorter plateau duration of wall 111. As a result, wall 111 will hypertrophy and septum 109 will atrophy, which is a desired result. It should be appreciated, that not all pathological changes in muscle-mass distribution are reversible, especially if slippage of muscle fibers and/or formation of scar tissue are involved.
[0242]FIG. 12D shows heart 20″ having a substantially inactive muscle segment 126 which is closer to natural pacing location 108 of the left ventricle and a healthy muscle segment 130 which is further away from pacing location 108. Muscle segment 130 is not called upon to perform as much work as it can because of its late activation time, on the other hand, segment 126 cannot perform as much work as it should since it is infarcted. pacing the left ventricle from location 128 transfers the demand from segment 126 to segment 130, which is able to answer the demand. As a result, the output and efficiency of heart 20″ increase. If heart 20″ hypertrophied to compensate for its reduced output, the hypertrophy may be reversed. Other compensatory mechanisms, such as increased heart rate may also be reversed, resulting in less stress on heart 20″.
Alternatively, a pacemaker can be implanted. Typically, the AV node is ablated and the ventricle is paced as described hereinabove. Alternatively, the AV node is not ablated, the SA node activation signal is sensed and the ventricles are activated artificially before the signal from the AV node arrives at the ventricles. In some embodiments of the invention, such as those explained. with reference to FIG. 12B, pacing can proceed in parallel both through the natural pathways and through the artificial ones, with similar beneficial results.
[0262]FIG. 13 shows an implanted pacemaker according to a preferred embodiment of the invention. A control unit 140 electrifies a plurality of electrodes 142 implanted in various locations in heart 20″, in accordance with at least one of the pacing regimes described above. Various local physiological values of the heart can be determined using electrodes 142, for example, local activation time and plateau length. Alternatively or additionally, at least one implanted sensor 146 is used to determine local physiological values, such as perfusion and thickness. Alternatively or additionally, a cardiac physiological variable is measured using a sensor 144. Examples of physiological variables include, the intra-cardiac pressure which may be measured using a solid state pressure transducer and the stroke volume, which may be measured using a flow velocity sensor in the aorta. Other variables include: heart rate, diastolic interval, long and short axis shortening, ejection fraction and valvular cross-section. In addition, vascular variables may be measured in any particular vessel, for example, blood-vessel cross-section, vascular flow velocity, vascular flow volume and blood pressure. Any one of these variables can be used to asses the functionality of the heart under a new pacing regime.
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International Classification A61B5/029, A61B18/20, A61B5/06, A61N1/368, A61B5/042, A61N1/362, A61B5/0215, A61N1/32, A61B5/00, A61N1/365, A61B17/00
Cooperative Classification A61N1/32, A61N1/36564, A61N1/3627, A61B2018/00392, A61B5/02014, A61N1/368, A61B5/0422, A61B5/06, A61B5/6859, A61B18/20, A61B5/145, A61B5/0215, A61B2017/00247, A61B5/029, A61M2025/0166, A61B5/6843
European Classification A61B5/145, A61B5/68B5, A61B5/68D1H6, A61B5/02D2, A61N1/362C, A61N1/32, A61B5/029, A61B5/042D, A61B18/20, A61B5/0215, A61B5/06, A61N1/365B9