WO2021034546A1 - Procédé de thérapie de resynchronisation cardiaque - Google Patents

Procédé de thérapie de resynchronisation cardiaque Download PDF

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Publication number
WO2021034546A1
WO2021034546A1 PCT/US2020/045764 US2020045764W WO2021034546A1 WO 2021034546 A1 WO2021034546 A1 WO 2021034546A1 US 2020045764 W US2020045764 W US 2020045764W WO 2021034546 A1 WO2021034546 A1 WO 2021034546A1
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WIPO (PCT)
Prior art keywords
heart
cardiac
pacing device
lbbb
pacing
Prior art date
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PCT/US2020/045764
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English (en)
Inventor
Barry Yomtov
Robert Pacheco
Original Assignee
Catheter Precision, Inc.
Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.)
Filing date
Publication date
Priority claimed from US16/670,672 external-priority patent/US11458320B2/en
Application filed by Catheter Precision, Inc. filed Critical Catheter Precision, Inc.
Publication of WO2021034546A1 publication Critical patent/WO2021034546A1/fr

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Classifications

    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/362—Heart stimulators
    • A61N1/3627—Heart stimulators for treating a mechanical deficiency of the heart, e.g. congestive heart failure or cardiomyopathy
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61B—DIAGNOSIS; SURGERY; IDENTIFICATION
    • A61B5/00—Measuring for diagnostic purposes; Identification of persons
    • A61B5/24—Detecting, measuring or recording bioelectric or biomagnetic signals of the body or parts thereof
    • A61B5/316—Modalities, i.e. specific diagnostic methods
    • A61B5/318—Heart-related electrical modalities, e.g. electrocardiography [ECG]
    • A61B5/367—Electrophysiological study [EPS], e.g. electrical activation mapping or electro-anatomical mapping
    • 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
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61N—ELECTROTHERAPY; MAGNETOTHERAPY; RADIATION THERAPY; ULTRASOUND THERAPY
    • A61N1/00—Electrotherapy; Circuits therefor
    • A61N1/18—Applying electric currents by contact electrodes
    • A61N1/32—Applying electric currents by contact electrodes alternating or intermittent currents
    • A61N1/36—Applying electric currents by contact electrodes alternating or intermittent currents for stimulation
    • A61N1/372—Arrangements in connection with the implantation of stimulators
    • A61N1/375—Constructional arrangements, e.g. casings
    • A61N1/3756—Casings with electrodes thereon, e.g. leadless stimulators
    • G—PHYSICS
    • G16—INFORMATION AND COMMUNICATION TECHNOLOGY [ICT] SPECIALLY ADAPTED FOR SPECIFIC APPLICATION FIELDS
    • G16H—HEALTHCARE INFORMATICS, i.e. INFORMATION AND COMMUNICATION TECHNOLOGY [ICT] SPECIALLY ADAPTED FOR THE HANDLING OR PROCESSING OF MEDICAL OR HEALTHCARE DATA
    • G16H50/00—ICT specially adapted for medical diagnosis, medical simulation or medical data mining; ICT specially adapted for detecting, monitoring or modelling epidemics or pandemics
    • G16H50/50—ICT specially adapted for medical diagnosis, medical simulation or medical data mining; ICT specially adapted for detecting, monitoring or modelling epidemics or pandemics for simulation or modelling of medical disorders

Definitions

  • Conduction disorders can have a variety of causes, including age, heart (muscle) damage, medications and genetics.
  • a common cause for conduction disorders results from defects in the left and/or right ventricle fast activation fibers, the His-Purkinje system, or scar tissue. As a result, the left and right ventricles may not be synchronized. This is referred to as Left Bundle Branch Block (LBBB) or Right Bundle Branch Block (RBBB).
  • LBBB Left Bundle Branch Block
  • RBBB Right Bundle Branch Block
  • CRT cardiac resynchronization therapy
  • RV right ventricle
  • LV left ventricle
  • the basic goal of CRT is to improve the mechanical functioning of the LV by restoring LV synchrony in patients with dilated cardiomyopathy and a widened QRS period, which is predominantly a result of LBBB.
  • pacemaker leads to obtain maximum cardiac synchronization involves a certain amount of guesswork on the part of an operating physician.
  • current methods do not allow for the determination of the optimal location for pacemaker leads, on a patient by patient basis. Further, current methods do not allow for the real time determination of whether leads have been properly positioned.
  • Various embodiments provide methods for performing cardiac resynchronization therapy and a system implementing the methods.
  • Various embodiments may include generating, using a processing unit, a three-dimensional (3D) activation map showing the propagation of electrical signals through a heart of a patient; determining the location of a left bundle branch block (LBBB), based on the cardiac activation map; implanting a first pacing device and a second pacing device into the patient; stimulating the His Bundle of the heart, using the first pacing device; and stimulating the left ventricle (LV) of the heart, at a position downstream of the LBBB with respect to a direction of electrical conduction through the LV, using the second pacing device, after the stimulating of the His bundle.
  • 3D three-dimensional
  • Various embodiments may include a method of cardiac resynchronization therapy (CRT), comprising: generating, using a processing unit, a cardiac activation map comprising a three-dimensional (3D) heart model of the heart and coronary vessels of a patient and showing the propagation of electrical signals through the 3D heart model; determining the location of a left bundle branch block (LBBB) based on the cardiac activation map; implanting a first pacing device and a second pacing device into the patient; stimulating the right ventricle (RV) using the first pacing device; and stimulating the left ventricle (LV) of the heart at a position downstream of the LBBB with respect to a direction of electrical conduction through the LV using the second pacing device after stimulating the His bundle.
  • CTR cardiac resynchronization therapy
  • Various embodiments provide methods for performing cardiac resynchronization therapy and a system implementing the methods.
  • Various embodiments may include generating, using a processing unit, a cardiac activation map comprising a three-dimensional (3D) heart model of the heart and coronary vessels of a patient and showing the propagation of electrical signals through the 3D heart model; determining the location of a right bundle branch block (RBBB) based on the cardiac activation map; implanting a first pacing device and a second pacing device into the patient; stimulating the right ventricle (RV) of the heart at a position downstream of the RBBB with respect to a direction of electrical conduction through the RV using the first pacing device; and stimulating the left ventricle (LV) of the heart using the second pacing device.
  • a cardiac activation map comprising a three-dimensional (3D) heart model of the heart and coronary vessels of a patient and showing the propagation of electrical signals through the 3D heart model
  • RBBB right bundle branch block
  • FIG. 1 A is a sectional view of a human heart including the cardiac electrical conduction system
  • FIGS. IB and 1C are sectional views of human hearts showing pacemaker lead locations for CRT.
  • FIG. 2 is an example of a three-dimensional model of a heart.
  • FIG. 3A is a plan view of a 3D model of electrical activation of a heart.
  • FIG. 3B is a plan view of a 3D model of electrical activation of a heart.
  • FIG. 3C is a plan view of an activation map according to various embodiments of the present disclosure.
  • FIG. 3D is a plan view of an activation map according to various embodiments of the present disclosure.
  • FIG. 4 is a schematic representation of a cardiac imaging system according to various embodiments of the present disclosure.
  • FIGS. 5 A and 5B are plan views of 3D models of the electrical activation of a heart according to various embodiments of the present disclosure.
  • FIGS. 5C and 5D are plan views of cardiac activation maps according to various embodiments of the present disclosure.
  • FIG. 6 is a schematic representation of a cardiac imaging system according to various embodiments of the present disclosure.
  • FIG. 7 is a flow chart illustrating a method according to various embodiments of the present disclosure.
  • FIG. 8A shows the ECG pattern of one beat of a heart
  • FIG. 8B is an example of a 3D cardiac activation map of LBB activation patterns of the heart during the beat
  • FIG. 8C is a sectional view of 3D cardiac activation map of FIG. 8B showing a conduction delay indicating the location of a LBBB.
  • FIGS. 9 A and 9B are schematic cardiac views showing pacemaker lead locations that may be utilized for CRT in a patient having LBBB, according to various embodiments of the present disclosure.
  • FIGS. 10A and 10B are schematic cardiac views showing pacemaker lead locations that may be utilized for CRT in a patient having LBBB according to various embodiments of the present disclosure.
  • LIG. 11 is a process flow diagram illustrating a method of CRT according to various embodiments of the present disclosure.
  • FIG. 12A and 12B are cardiac activation maps, according to various embodiments of the present disclosure.
  • An ECG is defined herein as any method that (preferably non-invasively) correlates actual electrical activity of the heart muscle to measured or derived (electrical activity) of the heart. In case of a classical electrocardiogram the differences in potential between electrodes on the body surface are correlated to the electrical activity of the heart. Derived ECG's can also be obtained in other ways (e.g. by measurement made by a so-called ICD (Implantable Cardioverter Defibrillator)).
  • ICD Implantable Cardioverter Defibrillator
  • Cardiac dyssynchrony has deleterious effects on cardiac function by depressing left ventricular (LV) mechanical performance, while increasing myocardial oxygen consumption. In addition, it probably causes LV remodeling. Therefore, cardiac dyssynchrony accelerates the progression of chronic congestive heart failure (CHF) and reduces patient survival.
  • CHF chronic congestive heart failure
  • cardiac activation begins within both the left ventricular and right ventricular endocardium.
  • electrical impulses i.e., depolarization waves
  • FIG. 1 A is a sectional view of a human heart including the electrical conduction system.
  • the human heart includes a sinoatrial node 1, an atrioventricular (AV) node 2, a His bundle 3, a left bundle branch (LBB) 4, a left posterior fascicle 5, a left- anterior fascicle 6, a left ventricle (LV) 7, a ventricular septum 8, a right ventricle (RV) 9, and a right bundle branch (RBB) 10.
  • AV atrioventricular
  • LBB left bundle branch
  • LV left- anterior fascicle
  • RV right ventricle
  • RBV right ventricle
  • the cardiac electrical conduction system includes heart muscle cells specialized for electrical conduction, and is situated within the myocardium. There is a skeleton of fibrous tissue that surrounds the conduction system which can be seen on an ECG. Dysfunction of the conduction system can cause irregular, fast, or slow cardiac rhythms.
  • the His bundle 3 is an important part of the electrical conduction system, as it transmits impulses from the AV node 2, located at the inferior end of the interatrial septum, to the left and right ventricles 7, 9.
  • the His bundle branches into the LBB 4 and the RBB 10, which run along the interventricular septum.
  • the LBB 4 further divides into the left posterior fascicle 5 and the left-anterior fascicle 6.
  • These bundles and fascicles give rise to thin filaments known as Purkinje fibers.
  • the Purkinje fibers distribute the impulse to the LV 7 and RV 9.
  • the ventricular conduction system comprises the bundle branches 4, 10 and Purkinje networks. It takes about 0.03-0.04 seconds for the impulse to travel from the His bundle 3 to the LV 7 and RV 9.
  • Heart blocks are separated into different categories based on the location of the cellular damage. Damage to any of the conducting cells in or below the His bundle are collectively referred to as "infra- Hisian blocks.”
  • blocks that occur in the right or left bundle branches 4, 10 are called “bundle branch blocks,” and blocks that occur in either the left anterior or the left posterior fascicles 5, 6 are called “fascicular blocks,” or “hemiblocks.”
  • the conditions in which both the RBB 10 and either the left anterior fascicle 6 or the left posterior fascicle 5 are blocked are collectively referred to as bifascicular blocks, and the condition in which the right bundle branch 10, the left anterior fascicle 6, and the left posterior fascicle 5 are blocked is called trifascicular block.
  • pacing device may refer to one or more micro-pacemakers or pacemaker connected to leaded electrodes.
  • a pacemaker is an electronic device, approximately the size of a pocket watch, which senses intrinsic heart rhythms and provides electrical stimulation to electrodes attached to tissues in particular locations when indicated.
  • a micro-pacemaker (or leadless pacemaker) is a pacemaker of reduced size that stimulates the heart without electrical wires.
  • Permanent pacing is most commonly accomplished through transvenous placement of leads to the endocardium (i.e., right atrium or ventricle) or epicardium (i.e., the LV surface via the coronary sinus), which are subsequently connected to a pacing generator placed subcutaneously in the infra-clavicular region.
  • miniaturized pacemakers i.e., leadless micro-pacemakers
  • the present disclosure encompasses endocardial and epicardial pacing, which may be accomplished using pacing electrodes connected to a pacing generator and/or implantable leadless micro pacemakers.
  • Cardiac resynchronization therapy is a specialized type of pacemaker therapy that provides biventricular pacing. CRT is carried out with or without the use of an implantable cardioverter-defibrillator (ICD), a device employed for treatment and prophylaxis in patients at risk for ventricular tachycardia (VT) or ventricular fibrillation (VF).
  • ICD implantable cardioverter-defibrillator
  • CRT is performed by pacing methods, such as apical pacing for example, in which electrodes are placed on one or more points on one or both ventricles to stimulate the cardiac muscle and increase cardiac synchronicity.
  • the stimulation points i.e., lead placements
  • the stimulation points may be based on a difference between LV and RV activation times, earliest and/or latest activation of the LV and/or RV, a detected depolarization wave blockage, or the like.
  • the process of determining placement locations for pacing leads may include the use of a patient- specific cardiac activation map showing a three-dimensional (3D) model of the electrical activation of the patient’ s heart.
  • the LV and RV pacing electrodes should be placed in optimal locations and the delay between the RV and LV pacing pulses should be set with the goal to shorten the QRS duration for achieving ventricular synchrony.
  • FIGS. IB and 1C show the conventional locations for CRT pacing electrodes.
  • a pacing electrode is placed in the RA and at the apex of the RV to stimulate the right side of the heart.
  • an electrode may be threaded through the coronary sinus (FIG. IB), or may be disposed on the epicardial surface of the LV (FIG. 1C) in order to stimulate the LV.
  • the RA lead provides right atrial pacing.
  • DHBP Direct His bundle pacing
  • HBP Direct His bundle pacing
  • His-Purkinje tissue of the heart which may produce a more synchronous ventricular depolarization and improved cardiac function as compared to right ventricular apical pacing.
  • DHBP has been shown to result in a reduction of left ventricular dimensions and heart failure hospitalization, and improved cardiac function.
  • DHBP may be utilized for CRT in place of right ventricular apical pacing.
  • the improved cardiac function provided thereby,
  • DHBP may also be used as a treatment for congestive heart failure.
  • the His bundle is formed of conduction fibers that extend through the cardiac septum. If the His bundle is not stimulated directly, only the surrounding tissue will be stimulated. In other words, such stimulation will not increase cardiac synchronicity. As such, a stimulation lead should be precisely positioned to directly stimulate the His bundle for DHBP to be effective.
  • methods of CRT include generating a cardiac activation map showing the electrical activation pattern on a three-dimensional (3D) model of a heart in order to identify the origin or cardiac activation and/or conduction delays caused by BBBs, such as a LBBB in particular.
  • pacing locations on the His bundle and/or the LV can be identified that are predicted provide maximum levels of resynchronization.
  • the locations may be highlighted on the cardiac activation map to facilitate electrode placement.
  • FIG. 2 shows a three-dimensional (3D) model 21 of a heart seen in two different directions.
  • the 3D model 21 includes a mesh 26 representing an outer surface of the heart, here the myocardial surface.
  • the 3D model also may include the septal wall.
  • the mesh 26 has a plurality of nodes 28.
  • the mesh 26 is a triangular mesh in which the surface of the heart is approximated by adjoining triangles.
  • FIG. 3A is a 3D activation map 24 showing the initial electrical activation of a heart from a single stimulation location 30.
  • FIG. 3A shows a ventricular surface of the myocardium with a septal wall 22.
  • the activation map 24 may include a mesh 26 representing a ventricular surface of the heart, here an outer surface of the ventricular myocardium with septal wall 22 as represented in FIG. 2.
  • the mesh 26 has a plurality of nodes 28.
  • the heart is electrically stimulated at a stimulation location 30.
  • the electrical signals will travel through the heart tissue.
  • Each location on the heart has a particular delay relative to the initial stimulation.
  • Each node 28 has associated therewith a value representative of a time delay between stimulation of the heart at the stimulation location 30 and activation of the heart at that respective node 28.
  • Locations that share the same delay time are connected by isochrones 32 in FIG. 3A.
  • isochrones are defined as lines drawn on a 3D heart surface model connecting points on this model at which the activation occurs or arrives at the same time.
  • the delay time for nodes across the heart surface in this example is also displayed by differing rendering colors.
  • the vertical bar indicates the time delay in milliseconds associated with the respective colors.
  • the stimulation location 30 can be the location of intrinsic activation of the heart. In other embodiments, the stimulation location 30 may be disposed on the His bundle.
  • FIG. 4 is a schematic representation of a system 100 for providing a representation of synchronicity of electrical activation of heart tissue.
  • the system 100 includes a processing unit 102 and a memory 104.
  • the 3D activation map 24 can be obtained by combining electrocardiographic and medical imaging data. This data may be stored in the memory 104.
  • the processing unit 102 may be connected to an electrocardiographic system 106, a medical imaging system 108, and a 3D camera 109, for retrieving the data and storing corresponding data in the memory 104.
  • An electrocardiographic imaging (ECGI) method able to determine the cardiac activation from a 12 lead ECG may be applied by the processing unit 102 for determining the 3D activation map 24 of electrical activation of the heart.
  • the ECG signals may be combined with a patient-specific 3D anatomical model of the heart, lungs, and/or torso, in order to compute the positions of the cardiac isochrones.
  • the patient-specific 3D anatomical model may be obtained from a magnetic resonance image (MR I) or computed tomography (CT) images.
  • MR I magnetic resonance image
  • CT computed tomography
  • a 3D anatomical model showing closest conformity to the patient may be selected, and optionally modified, from a database including a plurality of 3D anatomical models.
  • the selected, and optionally modified, 3D anatomical model may serve as the patient- specific 3D anatomical model.
  • the 3D activation map 24 may also include further information.
  • the 3D activation map 24 may include cardiac blood vessels 34, veins on the myocardium.
  • the activation map 24 may include detailed representations of internal cardiac features, such as the His bundle, fibrous tissue that surrounds the His bundle, the AV junction, and/or the cardiac septum. This information may be added to the activation map 24 with nodes indicated as being associated with such cardiac features.
  • the processing unit 102 may include a first recognition unit 110 arranged for automatically retrieving information representative of the location of such cardiac features from the patient's 3D anatomical model of the heart. The processing unit 102 may then automatically insert this information into the activation map 24.
  • the activation map 24 may also include information on scar tissue. Scar tissue locations may be obtained from delayed enhancement MRI images and added to the activation map 24. Scar tissue can be simulated in the activation map 24 by reducing the propagation velocity of electrical signals there through. Scar tissue can also be accounted for by selling the transition from one node to another to very slow or non-transitional for the areas in the heart wall where scar tissue is present.
  • the processing unit 102 may include a second recognition unit 112 arranged for automatically retrieving information representative of the location of such scar tissue from the patient-specific three-dimensional anatomical model of the heart. The processing unit 102 may then automatically insert this information into the activation map 24.
  • the obtained activation map 24 may be used for obtaining further information on electrical activation of the heart. For example, the time delay of activation from one node to another may be determined. This may be used to generate, on the basis of the activation map 24, other views resulting from initial stimulation at other nodes of the mesh 6.
  • the processing unit 102 may include an insertion unit 114.
  • the insertion unit 114 may take the activation map 24 and define a certain node as a stimulation location.
  • the activation map 24 may assume stimulation at a predetermined node.
  • the insertion unit 114 may remove stimulation at that predetermined node for calculation purposes.
  • FIG. 3B shows an example resulting from initial stimulation at another stimulation location 30’.
  • a view resulting from initial stimulation at other nodes of the mesh 26 may be generated for each node of the mesh 26.
  • a particular electrical activation sequence of the entire heart, resulting from stimulation at a particular node, may be summarized in a single parameter, namely, heart activation synchronicity.
  • the heart activation synchronicity provides an indication of how synchronously the entire heart is activated. For common situations, a more synchronous activation of the heart is considered beneficial.
  • the measure for heart activation synchronicity in this example is standard deviation (std) of the depolarization (dep) times of the heart.
  • the heart activation synchronicity provides an indication of synchronicity of activation of the entire heart as a result of stimulation at the respective node.
  • the processing unit 102 may include a synchronicity determination unit 116 configured to determine the heart activation synchronicity.
  • the heart activation synchronicity may be determined separately for stimulation at each node.
  • a measure of heart activation synchronicity for each node of the mesh may be provided.
  • the processing unit 102 may include a cardiac activation map generation unit 118 configured to generate a cardiac activation map based on the calculation of the heart activation synchronicity for each node, by the synchronicity determination unit 116.
  • the processing unit 102 may be connected with an output unit 120 arranged for outputting the cardiac activation map and/or alternative data to a user.
  • the output unit 120 may be a display unit, a printer, a messaging unit, or the like.
  • FIG. 3C shows an example of a cardiac activation map 35.
  • heart activation synchronicity is indicated for each node in the activation map 35.
  • the indication may be show by providing false colors and/or iso- sync lines 36.
  • the iso-sync lines 36 connect nodes having the same heart activation synchronicity.
  • the activation map 35 provides a singular 3D overview showing which locations on the heart result in good heart activation synchronicity, and which locations on the heart result in poor heart activation synchronicity, if the heart were stimulated at such locations.
  • the original stimulation location 30 does not provide particularly good synchronization, with a heart activation synchronicity value of approximately 45 ms standard deviation of the depolarization times of the heart.
  • the least favorable stimulation location here the location with the highest heart activation synchronicity value, is indicated at S-.
  • the most favorable stimulation location, where the lowest heart activation synchronicity value occurs is indicated at S+. It is noted that the most favorable stimulation location S+ may best be seen when looking at the cardiac activation map 35 from another direction, as shown in FIG. 3D.
  • Another example of a measure for heart activation synchronicity is a range in depolarization times (maximum depolarization time - minimum depolarization time). The range in depolarization times may be corrected for cycle length.
  • Another example of a measure for heart activation synchronicity is a standard deviation of the LV depolarization times only.
  • Another example of a measure for heart activation synchronicity is a delay between stimulus and septum activation.
  • Another example of a measure for heart activation synchronicity is an AV delay.
  • Another example of a measure for heart activation synchronicity is a VV delay.
  • the measure for heart activation synchronicity may be chosen in dependence of the task at hand and/or in dependence of a specific condition or abnormality experienced in the patient.
  • FIG. 5 A a second example is shown in which a second stimulation location 38 is defined. Then electrical activation of the heart is calculated using the activation map 24 and simultaneous stimulation at the first stimulation location 30 and the second stimulation location 38. In this example, the insertion unit 114 does not remove stimulation at the first location 30 for calculation purposes.
  • FIG. 5A shows the calculated resulting electrical activation of the heart. The total activation time shortens due to the addition of the second stimulation location 38.
  • the first stimulation location 30 represents the location of intrinsic activation of the heart, or a first chosen location to stimulate or a stimulation generated by an already present pacemaker lead within the heart.
  • FIG. 5B shows an example resulting from initial stimulation at a second stimulation location 38’ simultaneous with stimulation at first stimulation location 30.
  • a view resulting from initial stimulation at second nodes of the mesh 26 simultaneous with stimulation at a first node associated with the first stimulation location 30 may be generated for each node of the mesh 26.
  • a particular electrical activation sequence of the entire heart is combined and shown as the heart activation synchronicity.
  • the electrical activation sequence involves stimulation at the second stimulation location 38 simultaneous with stimulation at the first stimulation location 30.
  • the heart activation synchronicity again provides an indication of how synchronous the entire heart is activated.
  • the heart activation synchronicity may be determined separately for stimulation at each node simultaneously with stimulation at the first 30 and second 38 stimulation locations.
  • This provides a measure of heart activation synchronicity for each node acting as third stimulation location of the mesh 26.
  • FIG. 5C shows an example of a heart activation map 35 showing which locations on the heart result in good heart activation synchronicity and which location on the heart result in poor heart activation synchronicity. If the heart were stimulated at such locations simultaneous with stimulation at the first stimulation location 30 and the second stimulation location 38.
  • the least favorable third stimulation location S- had the highest heart activation synchronicity value of approximately 41 ms, when the first stimulation location 30 and the second stimulation location 38 were stimulated simultaneously.
  • the most favorable third stimulation location S+ had the lowest heart activation synchronicity value, when with the first stimulation location 30 and the second stimulation location 38 were stimulated simultaneously. It is noted that the most favorable stimulation location S+ may best be seen when looking at the activation map 35 from another direction, as shown in FIG. 5D.
  • FIG. 6 shows another schematic representation of a system 100 for providing a cardiac activation map.
  • FIG. 7 illustrates a method of determining heart synchronicity using the system 100 according to an embodiment.
  • the system includes a processing unit 102 which receives data from hardware modules.
  • the processing unit 102 may receive ECG data from an electrocardiographic system 106.
  • the processing unit may receive patient-specific anatomical data from a medical imaging system 108.
  • the anatomical data may include detailed representations of internal cardiac features, such as the His bundle, fibrous tissue that surrounds the His bundle, the AV junction, and/or the cardiac septum.
  • the processing unit 102 may receive information on the positions of ECG leads relative to the anatomy of the patient from a 3D camera 109, such as a 3D image and the torso model mapped to the 3D image. ECG lead positions may also be entered into the system manually.
  • the processing unit 102 may determine the cardiac activation map.
  • the processing unit 102 may include the following units, and may perform the operations illustrated in FIG. 7 and described below to generate a cardiac activation map.
  • the processing unit 102 may use a patient- specific 3D anatomical model of the thorax of the patient and the size, orientation, and location of the heart within the thorax. Such a model may be selected in step 201 for further use by the processing unit. Such model may already be available in step 202. If the model is not yet available, a retrieval unit 103 may check whether a suitable anatomical model for this patient is present in a database 117 in step 204. If so, the retrieval unit 103 may retrieve the suitable anatomical model from the database 117.
  • the retrieval unit 103 may adapt the anatomical model from the database to the 3D image of the patient so as to transform the selected anatomical model into a (quasi) patient-specific 3D anatomical model. If no suitable patient- specific anatomical model is available in the database 117, the retrieval unit 103 may generate the patient- specific anatomical model on the basis of the received patient- specific anatomical 3D image data in step 208.
  • the patient-specific 3D model also may include the size, orientation and/or location of other structures in the patient, such as the lungs and/or other organs.
  • the patient-specific 3D model may be a volume conductor model.
  • a lead locator module 105 may determine corresponding positions of the ECG leads in the patient-specific 3D model, to provide an enhanced patient-specific model in step 210.
  • step 212 when the patient-specific anatomical model and/or the enhanced patient-specific model available, a determination is made as to whether ECG data representative of intrinsic or stimulated activation is available.
  • step 214 if intrinsic activation data or pacing stimulation from one or more already present pacemaker leads is available, an activation unit 107 may generate a 3D electrical conduction model (e.g., activation map) showing the current activation of the heart of the patient, on the basis of the patient- specific model and the ECG data.
  • a 3D electrical conduction model e.g., activation map
  • a virtual stimulation unit 111 may add an initial virtual stimulation to an electrical model of the heart based on previously determined and/or assumed transition velocities between nodes in step 216.
  • An assumed transition velocity may be 0.8 ms, for example.
  • the electrical model may include arteries, veins, and or scar tissue as explained above.
  • a 3D electric model of virtual activation of the heart of the patient may be generated.
  • a synchronicity determination unit 116 may generate a cardiac activation map 35 in step 222, as described above.
  • the processing unit 102 may determine whether the artificial stimulation location or virtual stimulation location resulted in optimal activation and synchronicity in step 230. If so, the processing unit 102 may calculate optimal stimulation locations for a patient’s heart in step 234.
  • step 230 If it is determined in step 230 that optimum synchronicity has not been reached, the method proceeds to step 232 in which it is determined whether an extra virtual stimulation location should be added, or if a virtual stimulation location should be moved or changed with respect to the timing parameters. This determination may be made by a clinician, by the processing unit, or by the clinician based on information or recommendations presented on a display by the processing unit. If it is determined that a virtual stimulation location should be moved or changed, the artificial or virtual stimulation location may be adjusted accordingly in step 225. In step 226, activation may be determined again. Synchronicity may then be recalculated in step 222. The process may be repeated until a desired activation is determined to be achieved in step 230.
  • the system may also virtually adapt the current artificial stimulation locations (i.e., pacemaker lead locations) with respect to its current stimulation parameters to reach optimum synchronicity.
  • current artificial stimulation locations i.e., pacemaker lead locations
  • the system may also be used for assessing multiple stimulations.
  • the multiple stimulations may be a combination of intrinsic activation and stimulated activation (pacing).
  • the multiple stimulations may be multiple stimulated pacing, for example.
  • the user, the processing unit 102, or the clinician based on information or recommendations presented on a display by the processing unit may determine in step 232 whether an additional stimulation location (e.g., an additional pacemaker lead) would be desirable.
  • an additional stimulation location may be inserted by the insertion unit 114. Then activation for the situation with the original stimulation location and the added virtual stimulation location may be determined again in step 226, and synchronicity may be recalculated in step 222.
  • the processing unit 102 may determine in step 230 whether the additional virtual stimulation location resulted in optimum synchronicity. If the optimum synchronicity has not been reached, the method proceeds to step 232, in which it is determined whether an extra virtual stimulation location should be added, or if a virtual stimulation location should be moved or removed, with respect to the timing parameters. In such a case, the process may be repeated one or more times.
  • a cardiac synchronicity model may be generated.
  • the synchronicity model may be a 3D heart surface model including iso- sync lines.
  • the iso sync lines represent the activation synchronicity of the heart. This synchronicity may be based on specific activation conditions, such as right ventricle activation at a lead position of a pacemaker.
  • the synchronicity model may be generated as follows.
  • the activation isochrones for the intrinsic LBBB pattern may be determined in the following steps.
  • a patient-specific anatomical 3D model of the heart, lungs, and thorax may be generated, e.g. on the basis of an MRI or CT image of the patient, or derived from a model taken from a database adapted to the patient’s dimensions, e.g. with use of the 3D camera.
  • the anatomical 3D model may e.g. include a 3D surface model of the heart, a 3D surface model of the lungs and a 3D surface model of the thorax.
  • a 3D surface model may be a close approximation of the actual surface, by means of a mesh of a plurality of polygons, such as triangles, connected at their corners. The interconnected corners form nodes of the mesh.
  • the anatomical 3D model may include detailed depictions of the His bundle and adjacent structures, such as the AV junction and cardiac septum.
  • the His bundle may be identified by detecting the fibrous tissue that surrounds the His bundle using ECG, MRI, and/or CT imaging data.
  • An ECG e.g. a 12-lead ECG
  • the exact locations of the electrodes of the ECG device on the thorax may be recorded.
  • the positions of the electrodes in the 3D anatomical model are used for estimating the distribution, fluctuation, and/or movement of electrical activity through heart tissue.
  • the exact locations of the recording leads or the ECG device may be entered in the anatomical 3D representation of the thorax.
  • scar tissue and/or coronary vessels may be incorporated in the anatomical 3D representation of the heart.
  • the presence and location of scar tissue may be derived from delayed enhancement MRI images.
  • the measurements per recording lead of the ECG device may be related to the heart and torso geometry. Using an inverse procedure, the intrinsic activation may be determined. The distribution, fluctuation, and/or movement of electrical activity through heart tissue may be based upon a myocardial distance function, a fastest route algorithm, shortest path algorithm, and/or fast marching algorithm.
  • a stimulus site may be added to the intrinsic activation for each node on the heart and the desired synchronicity of the heart may be computed from the outcome.
  • a “node” refers to an intersection point of the triangles of upon which the anatomical 3D heart model is based.
  • the above methods may also be used to determine optimal location(s) for placement of cardiac pacemaker electrode(s).
  • activation maps may be computed.
  • the intrinsic activation map, in combination with a determined stimulation point(s) may be applied to a new cardiac isochrone positing map.
  • FIG. 8A shows the ECG pattern of one beat of a heart
  • FIG. 8B is an example of a 3D cardiac activation map of LBB activation patterns of the heart during the beat
  • FIG. 8C is a sectional view of 3D synchronization map of FIG. 8B, showing a conduction delay 80 indicating the location of a LBBB.
  • red line LI indicates the start of the Q wave
  • blue line L2 indicates the end of the S wave
  • green line L3 indicates the end of the T wave.
  • a cardiac activation map corresponding to the ECG pattern displays the dynamic electrical depolarization of the heart over time as corresponding colors. Accordingly, an origin O of an ECG beat may be determined.
  • a potential area of conduction delay or branch blockage may appear on the cardiac activation map as an area that exhibits a more rapid color change as compared to adjacent areas of the heart.
  • a rapid color change in area 80 indicates a slowdown or blockage in cardiac signal conduction, which may be consistent with a BBB in the His Purkinje conduction system, and in particular, a LBBB.
  • the cardiac activation map may be utilized to identify the location of conduction problems, such as LBBB.
  • RBBB locations may also be identified, but in general, a RBBB is not considered as clinically significant as a LBBB with respect to CRT.
  • FIGS. 9 A and 9B are schematic cardiac views showing pacing lead locations that may be utilized for CRT in a patient having LBBB according to various embodiments of the present disclosure.
  • the method may include generating a cardiac activation map as shown in FIGS. 8B and 8C.
  • the method may include positioning CRT electrodes.
  • the cardiac activation map may be used to identify the location of the first activation and/or the location of the LBBB.
  • an RA lead 90, a RV lead 92, and/or an LV lead 94 may be positioned with respect to the heart.
  • the RA lead 90 may include a sensing electrode and/or a stimulation electrode disposed in the RA.
  • the RV lead 92 may be positioned at the apex of the RV.
  • the LV lead 94 may be positioned via the coronary sinus and the great cardiac vein or the middle cardiac vein, in a location downstream (e.g., distal) to the LBBB with respect to the direction of electrical conduction through the LV. This location should activate the Purkinje fibers for improved synchronization.
  • the LV lead 94 may be implanted epicardially on the left ventricle (LV).
  • the LV lead 94 may be in the form of a leadless pace maker 94A, in some embodiments.
  • the leadless pacemaker 94A can wirelessly communicate to receive the signal for the left ventricular pulse (with adjustable delay) from a primary pacemaker system.
  • FIGS. 9 A and 9B exemplify CRT pacing with the implanted RV lead 94 or leadless micro-pacemaker 94A located in the LV.
  • the RA lead 90 would sense/pace the RA.
  • the RV lead 92 may stimulate at the apex of the RV and the LV lead 94 may pace the LV downstream of the LBBB to activate the Purkinje fibers that would otherwise experience a conduction delay due to the LBBB.
  • FIGS. 10A and 10B are schematic cardiac views showing lead locations that may be utilized for CRT in a patient having LBBB according to various embodiments of the present disclosure. The method may be similar to the method illustrated in FIGS. 9A and 9B, so only the differences there between will be discussed in detail.
  • the RV lead 92 may be positioned in a location selected for stimulating at the His bundle.
  • the RA lead 90 may be disposed in the RA and may be configured to detect the presence or absence of the natural heartbeat.
  • the LV lead 94 may be inserted via the coronary sinus and the great cardiac vein or the middle cardiac vein in a location downstream (e.g., distal) to the LBBB with respect to the direction of electrical conduction through the LV. As shown in FIG. 10B, the LV lead 94 may be in the form of a leadless pacemaker 94A in some embodiments.
  • the RA lead 90 may sense/pace the RA.
  • the RV lead 92 may stimulate at the HIS bundle, and the LV lead may pace the LV downstream of the LBBB to activate the Purkinje fibers that would otherwise experience a conduction delay due to the LBBB.
  • the pacing time of the RV lead 92 and the LV lead 94 may be adjustable and may be set according to the distance therebetween and/or the locations thereof.
  • the pacing time of the LV lead 94 may be set to occur at approximately the same time as the depolarization wave reaches the LBBB.
  • the pacing time of the LV lead 94 may be set to occur after the pacing time of the RV lead 92 and/or the RA lead 90.
  • each cardiac chamber can be independently detected and paced based on the sequence of activation between the atrium and the ventricle.
  • a dual electrode site e.g. HIS bundle and LV distal to the LBBB
  • FIG. 11 is a process flow diagram illustrating a method of CRT according to various embodiments of the present disclosure. Referring to FIG. 11, in step 400, a 3D cardiac activation map of a patient’s heart is generated as discussed above.
  • the activation map may be used to identify a point of earliest activation and/or the location of a conduction blockage. For example, regions of the activation map that show a relatively rapid color change may be detected and used to locate a BBB, in particular LBBB.
  • pacing devices such as pacing leads and/or micro-pacemakers may be implanted within the heart.
  • a first pacing device e.g., an RV lead
  • a second pacing device e.g., an LV lead
  • a third pacing device e.g., an RA lead
  • RA RA lead
  • the onset of cardiac activation may be detected by detecting the initiation of the intrinsic activation signal, for example, using the RA lead. Once onset has been detected, the RV lead may be used to pace the His bundle. In step 408, after a delay sufficient to allow the depolarization wave to reach the LBBB, the LV lead may be used to pace the LV downstream of the LBBB.
  • a determination may be made as to whether a predetermined amount of cardiac function has been achieved.
  • the cardiac activation map may be updated based on the pacing of the heart and used to determine whether the heart has at least the predetermined amount of function. Determining whether the heart has the desired amount of function may include determining whether the heart has at least predetermined amount of synchronization, activation, or both synchronization and activation. In some embodiments, determining whether the heart has the predetermined amount of function includes determining whether the pacing device has provided a sufficient amount of stimulation to the His bundle, the LV, or both the His bundle and the LV. If the heart has at least the desired amount of function, the method ends.
  • step 412 may additionally or alternatively include increasing or decreasing a voltage applied by the respective pacing devices. The method then returns to step 406 to detect the onset of cardiac activation.
  • FIG. 12A shows a single-beat activation map 500 that may be generated during step 400, according to various embodiments of the present disclosure.
  • the activation map 500 may include a 3D heart model that is modified to reflect patient- specific features detected during an MRI or CT scan.
  • the model may include patient- specific cardiac features such as the RV 502, LV 504, myocardium 506, etc.
  • step 400 may further include modifying the activation map 500 to further display coronary vessel structures 512, as shown in FIG. 12B.
  • the activation map 500 may include coronary vessel structures applicable to endocardial lead implantation, such as the left anterior descending artery (LAD) 514.
  • LAD left anterior descending artery
  • the coronary vessel structures may be determined based on data from MRI and/or CT images of a patient.
  • step 402 may optionally include using the processing unit to identify a suspected BBB location by adding an LBBB marker 520 to the activation map 500.
  • the LBBB marker 520 may identify cardiac tissue in which the progression of a depolarization wave has been slowed or disrupted, due to a LBBB.
  • the LBBB marker 520 may include cardiac tissue downstream of a LBBB that exhibits a conduction delay relative to an expected rate of conduction and/or asynchronous contraction relative to adjacent tissue.
  • step 402 may optionally include adding a virtual stimulation point 522 to the activation map 500.
  • the stimulation point 522 may be used to identify a portion of the LAD 514 that is predicted to provide optimal stimulation for restoring synchronicity lost due to the LBBB identified by the LBBB marker 520.
  • the virtual stimulation point 522 may be located in the LAD 514, downstream of the LBBB marker 520 with respect to a direction of electrical conduction through the heart, and as close as possible to the LBBB marker 520.
  • step 402 may optionally include providing multiple stimulation points 522 disposed in the same coronary vessel, or in different coronary vessels, at positions downstream from the LBBB marker 520.
  • the stimulation points 522 may be positioned substantially the same distance from the LBBB marker 520 but in different coronary vessels.
  • the stimulation points 522 may be positioned in different coronary vessels at positions where the corresponding vessels are closest to the LBBB marker 520.
  • the activation map 500 may allow for a clinician to precisely position a stimulation electrode at an optimized location within a corresponding coronary vessel.
  • an activation map including a heart model having cardiac vascular structure along with the location of a LBBB
  • a clinician may be provided with a single image that identifies an optimal endocardial implantation placement location of the LV pacing lead, as well as shows the path of the coronary vessel through which the pacing lead can be threaded to reach the implantation placement location for CRT patients who also have LBBB.

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Abstract

Divers modes de réalisation comprennent des procédés de thérapie de resynchronisation cardiaque (CRT). Divers modes de réalisation peuvent comprendre : la génération, à l'aide d'une unité de traitement, d'une carte d'activation cardiaque comprenant un modèle cardiaque tridimensionnel (3D) du cœur qui montre des vaisseaux coronaires d'un patient et montre la propagation de signaux électriques à travers le modèle cardiaque 3D ; la détermination de l'emplacement d'un bloc de branche de faisceau gauche (LBBB) sur la base de la carte d'activation cardiaque ; l'implantation d'un premier dispositif de stimulation et d'un second dispositif de stimulation dans le patient ; la stimulation du faisceau de His du cœur à l'aide du premier dispositif de stimulation ; et la stimulation du ventricule gauche (LV) du cœur à une position en aval du LBBB par rapport à une direction de conduction électrique à travers le ventricule gauche à l'aide du second dispositif de stimulation après stimulation du faisceau de His.
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