Source: https://patents.google.com/patent/US9808260B2/en
Timestamp: 2019-09-20 23:13:01
Document Index: 160540948

Matched Legal Cases: ['Application No. 61', 'art 11', 'art 11', 'art 11', 'art 11', 'art 11', 'Application No. 15788567']

US9808260B2 - Noninvasive protection from emboli - Google Patents
Noninvasive protection from emboli Download PDF
US9808260B2
US9808260B2 US14/703,669 US201514703669A US9808260B2 US 9808260 B2 US9808260 B2 US 9808260B2 US 201514703669 A US201514703669 A US 201514703669A US 9808260 B2 US9808260 B2 US 9808260B2
US14/703,669
US20150313607A1 (en
Zhadkevich Medical Inc
2014-05-04 Priority to US201461988217P priority Critical
2015-05-04 Application filed by Zhadkevich Medical Inc filed Critical Zhadkevich Medical Inc
2015-05-04 Priority to US14/703,669 priority patent/US9808260B2/en
2015-05-08 Assigned to Zhadkevich Medical, Inc. reassignment Zhadkevich Medical, Inc. ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: Zhadkevich, Michael
2015-11-05 Publication of US20150313607A1 publication Critical patent/US20150313607A1/en
2017-11-07 Publication of US9808260B2 publication Critical patent/US9808260B2/en
This application claims priority to U.S. Provisional Patent Application No. 61/988,217, filed May 4, 2014, titled NON-INVASIVE METHOD OF PROTECTION FROM EMBOLI, the entire contents of which are incorporated herein by reference.
The subject technology relates to prevention of embolic and ischemic injury (such as ischemia and stroke) as a consequence of emboligenic event and interventions.
Arterial embolism, leading to embolic ischemia or stroke, is one of the most dreadful complications of cardiac, aortic and vascular procedures, diagnosed in 1-22% of patients undergoing cardiovascular surgery. Even more frequently, in up to 70% of cases, patients undergoing heart, valve, coronary artery bypass or aortic surgery experience subclinical embolic events. These embolic events lead to cognitive impairment and disability, extremity ischemia and multiple organ failure, having a significant impact on patients' recovery.
The main sources of emboli in this setting reside in the heart, heart valves, thoracic aorta, and great vessels when these structures are intervened thereon (i.e. when an emboligenic procedure is performed). Even simple cardiac catheterization with an endovascular catheter can induce microtrauma of the atherosclerotic thoracic aorta leading to formation of embolic particles with subsequent embolic brain, liver, kidney and extremity injury ranging from latent ischemic foci to a massive or even fatal event. Multiple devices are known that attempt to prevent embolization of the carotid arteries during endovascular and cardiac interventions by using different types of filters, deflection devices or endoluminal balloons. These anti-embolic devices, however, have not received wide acceptance in surgery of the heart, heart valves and thoracic aorta due to their complexity and invasive character with the risk of additional trauma to the inner vessel wall resulting in a high risk to benefit ratio. Known devices require insertion of additional hardware into the arterial system or aorta, a procedure that is known by itself to be associated with all classical risks of endovascular intervention, including aortic dissection, bleeding, thrombosis, and arterial embolization. One known intra-aortic filter device that is inserted into the ascending portion of the thoracic aorta via an aortic cannula to capture potential embolic material released from the heart and aortic wall during heart surgery was found to be quite difficult to implement and was reported to be associated with major trauma to aortic wall and acute aortic dissection.
The subject technology is illustrated, for example, according to various aspects described below. Various examples of aspects of the subject technology are described as numbered clauses (1, 2, 3, etc.) for convenience. These are provided as examples and do not limit the subject technology. It is noted that any of the dependent clauses may be combined in any combination, and placed into a respective independent clause, e.g., clause 1, 6, 14, or 21. The other clauses can be presented in a similar manner.
Clause 1. A system for diverting emboli within a patient, comprising:
a detection device configured to detect a presence of emboli in a first blood vessel of a patient;
a compression member configured to be aligned with a second blood vessel of the patient when a collar supporting the compression member is positioned at least partially around a portion of the patient;
a controller configured to actuate the compression member, when the presence of emboli is detected, from an unactuated state to an actuated state in which at least a portion of the compression member (i) is closer to the second blood vessel than while in the unactuated state and (ii) compresses and limits blood flow through the second blood vessel.
Clause 2. The system of clause 1, wherein the second blood vessel is downstream of the first blood vessel.
Clause 3. The system of clause 1, wherein the detection device blood vessel is configured to detect a threshold amount of emboli in the first blood vessel, wherein the controller is configured to actuate the compression member when the detected emboli exceeds the threshold amount.
Clause 4. The system of clause 1, wherein the detection device comprises a Doppler ultrasound device, a Doppler probe device, an oscillotonometry device, an electroencephalography device, a transcranial Doppler device, a pulse indicator device, a cardiac Echo device, a pulse oximeter, or a cerebral oximeter.
Clause 5. The system of clause 1, further comprising a supplemental detection device configured to detect a presence of emboli in a third blood vessel of a patient, upstream of the second blood vessel.
Clause 6. A method for diverting emboli within a patient, comprising:
Clause 7. The method of clause 6, wherein the second vascular location is downstream of the first vascular location.
determining whether the detected emboli exceeds a threshold amount;
wherein the compression member is actuated when the detected emboli exceeds the threshold amount.
Clause 9. The method of clause 6, further comprising:
determining whether the detected emboli does not exceed a threshold amount;
transitioning the compression member to the unactuated state when the detected emboli does not exceed the threshold amount.
Clause 10. The method of clause 6, further comprising transitioning the compression member to the unactuated state after the compression member has been actuated for a predetermined time limit.
Clause 11. The method of clause 6, wherein the detecting is by a Doppler ultrasound device, a Doppler probe device, an oscillotonometry device, an electroencephalography device, a transcranial Doppler device, or a cerebral oximetry device.
Clause 12. The method of clause 6, wherein the first vascular location is a heart valve, an aorta, a calf vein, a femoral vein, a popliteal vein, an iliofemoral vein, an iliac vein, an inferior vena cava, or a peripheral vein of the patient.
Clause 13. The method of clause 6, wherein the second vascular location is a carotid artery or a vertebral artery of the patient.
Clause 14. A device for diverting emboli from cerebral circulation of a patient, comprising:
a first carotid compression member configured to be aligned with a first carotid artery of the patient radially between the first carotid compression member and a cervical spine of the patient when the device is positioned at least partially around a neck of a patient, the first carotid compression member having an unactuated state and an actuated state in which at least a portion of the first carotid compression member (i) is closer to the first carotid artery than while in the unactuated state and (ii) compresses and limits blood flow through the first carotid artery;
a first vertebral compression member configured to be aligned with a first vertebral artery of the patient radially between the first vertebral compression member and the cervical spine when the device is positioned at least partially around the neck, the first vertebral compression member having an unactuated state and an actuated state in which at least a portion of the first vertebral compression member (i) is closer to the first vertebral artery than while in the unactuated state and (ii) compresses and limits blood flow through the first vertebral artery.
Clause 15. The device of clause 14, wherein an internal volume of the first carotid compression member and an internal volume of the first vertebral compression member are in fluid communication with each other.
Clause 16. The device of clause 14, wherein first carotid compression member has a maximum height, parallel to a central axis of the device, that is greater than a maximum height of the first vertebral compression member.
Clause 17. The device of clause 14, further comprising:
a second carotid compression member configured to be aligned with a second carotid artery of the patient radially between the second carotid compression member and the cervical spine when the device is positioned at least partially around the neck, the second carotid compression member having an unactuated state and an actuated state in which at least a portion of the second carotid compression member (i) is closer to the second carotid artery than while in the unactuated state and (ii) compresses and limits blood flow through the second carotid artery;
a second vertebral compression member configured to be aligned with a second vertebral artery of the patient radially between the second vertebral compression member and the cervical spine when the device is positioned at least partially around the neck, the second vertebral compression member having an unactuated state and an actuated state in which at least a portion of the second vertebral compression member (i) is closer to the second vertebral artery than while in the unactuated state and (ii) compresses and limits blood flow through the second vertebral artery.
Clause 18. The device of clause 17, wherein an internal volume of the second carotid compression member and an internal volume of the second vertebral compression member are in fluid communication with each other.
Clause 19. The device of clause 17, wherein an internal volume of the first carotid compression member, an internal volume of the first vertebral compression member, an internal volume of the second carotid compression member, and an internal volume of the second vertebral compression member are in fluid communication with each other.
Clause 20. The device of clause 17, wherein second carotid compression member has a maximum height, parallel to a central axis of the device, that is greater than a maximum height of the second vertebral compression member.
Clause 21. A method of diverting emboli from cerebral circulation of a patient, comprising:
while a device is positioned around a neck of a patient, expanding a first carotid compression member of the device toward a first carotid artery of the patient to compress and limit blood flow through the first carotid artery;
while the device is positioned around the neck, expanding a first vertebral compression member of the device toward a first vertebral artery of the patient to compress and limit blood flow through the first vertebral artery.
Clause 22. The method of clause 21, wherein expanding the first carotid compression member comprises radially advancing a portion of the first carotid compression member toward a cervical spine of the patient.
Clause 23. The method of clause 21, wherein expanding the first vertebral compression member comprises radially advancing a portion of the first vertebral compression member toward a cervical spine of the patient.
Clause 24. The method of clause 21, further comprising:
while the device is positioned around the neck, expanding a second carotid compression member of the device toward a second carotid artery of the patient to compress and limit blood flow through the second carotid artery;
while the device is positioned around the neck, expanding a second vertebral compression member of the device toward a second vertebral artery of the patient to compress and limit blood flow through the second vertebral artery.
Clause 25. The method of clause 24, wherein expanding the second carotid compression member comprises radially advancing a portion of the second carotid compression member toward a cervical spine of the patient.
Clause 26. The method of clause 24, wherein expanding the second vertebral compression member comprises radially advancing a portion of the second vertebral compression member toward a cervical spine of the patient.
FIG. 1 is a view of the blood vessel with the blood carrying emboli. The blood vessel branches into the vessels carrying blood to different areas and organs.
FIG. 2 is a view of the blood vessel, containing emboli, where an external compression of its branch, carrying blood to an organ (such as brain) will divert potential emboli to another vessel.
FIG. 3 is a schematic representation of the method of protection from vascular emboli with an option of an automated external compression of an artery carrying blood to an organ.
FIG. 4 represents a mechanism of detection of embolic particles upstream from the organ to be protected with an automated feedback signaling system that is able to trigger the process of arterial compression to limit the entry of emboligenic particles into this organ.
FIGS. 5 and 6 show compression of an artery, triggered by detection of the embolic particles in the afferent vessel, with subsequent diversion of emboli into the less important blood vessel.
FIG. 7 shows release of arterial compression once embolic particles are diverted away from the organ to be protected on the basis of the negative feedback mechanism, triggered by disappearance of embolic particles in the afferent vascular pathway.
FIG. 8 is a front view of a patient with embolic particles in the heart and ascending thoracic aorta with a potential for propagation into both carotid arteries and other vessels with the source of emboli being diseased aorta, aortic valve and the heart.
FIG. 9 is a front view of a patient with the release of embolic particles arising in the heart, aortic valve and aorta, into the systemic circulation, including both carotid and vertebral arteries, and descending thoracic aorta.
FIG. 10 shows accentuation of the process of arterial embolization during cardiac contraction (systole).
FIG. 11 is a front view of a patient with external compression of both carotid and vertebral arteries that leads to temporary interruption of the cerebral arterial inflow, protecting the brain from potential emboli.
FIG. 12 is a front view of a patient with external compression of both carotid and vertebral arteries during cardiac contraction.
FIG. 13 is a front view of a patient with external compression of carotid and/or vertebral arteries by virtue of an external compression device and mechanism, actuated by certain physiological parameters.
FIG. 14 is a schematic view of the device for carotid and vertebral compression, depicted on FIG. 13.
FIG. 15 is a cross-sectional view of a neck of a patient and a device attached thereto in an unactuated state.
FIG. 16 is a cross-sectional view of a neck of a patient and a device attached thereto in an actuated state.
FIG. 17 is a front view of a patient with a compression device in accordance with another exemplary embodiment, leading to selective compression of vertebral arteries.
FIG. 18 is a front view of a patient with a compression device for vertebral arteries in accordance with yet another exemplary embodiment.
FIG. 19 is a schematic view of the device for vertebral compression, similar to the one depicted on FIG. 18, but carrying features of an additional exemplary embodiment.
FIG. 20 is a cross-sectional view of a neck of a patient and a device of FIGS. 18 and 19 for selective compression of vertebral arteries attached thereto in an actuated state with an option of restrictive pad at the external surface of the compression member.
FIG. 21A is a front view of a patient with a compression device in accordance with another exemplary embodiment.
FIG. 21 B is a cross-sectional view of a neck of a patient and a device of FIG. 21A attached thereto in an actuated state when both carotid and vertebral arteries are compressed.
FIG. 22 is a front view of a patient with another embodiment of the compression device, designed for selective compression of carotid arteries.
FIG. 23A is a cross-sectional view of a neck of a patient and a device of FIG. 22 attached thereto in an actuated state with selective compression of carotid, but not vertebral arteries.
FIG. 23B is a cross-sectional view of the device of FIG. 23A in a unactuated state.
FIG. 23C is a cross-sectional view of the device of FIG. 23A in an actuated state.
FIG. 23D is a schematic view of the device of FIGS. 23A, 23B and 23C
FIG. 24A is a front view of patient with yet another embodiment of the anti-embolic compression device.
FIG. 24B is a cross-sectional view of the device of FIG. 24A in a partially unactuated state.
FIG. 24C is a cross-sectional view of the device of FIG. 24A in a fully actuated state.
FIG. 24D is a schematic view of the device of FIG. 24A.
FIG. 25 is a block diagram illustrating a system of the subject technology.
FIG. 26 is an exemplary diagram illustrating modules implementing methods of the subject technology.
The subject technology relates to prevention of emboli and ischemic injury (such as ischemia and stroke) as a consequence of emboligenic event and interventions, e.g., on the heart, heart valves, coronary arteries and aorta. More particularly, the subject technology relates to an external compression method and device that induce temporary noninvasive external compression of the blood vessels supplying the organs at risk for embolic damage. The device can be actuated at the moment of emboligenic intervention and may be triggered and deactivated on demand and automatically on the basis of patient's physiological parameters and detection of emboligenic particles.
Reference will now be made in detail to embodiments of the subject technology, one or more examples of which are illustrated in the drawings. Each example is provided by way of explanation of the subject technology, and not meant as a limitation of the subject technology. For example, features illustrated or described as part of one embodiment can be used with another embodiment to yield still a third embodiment. It is intended that the present subject technology include these and other modifications and variations.
The subject technology provides for a method of preventing arterial embolization by diverting emboli from the circulation to be protected, such as cerebral circulation, arm circulation, leg circulation or else.
With reference to FIG. 1, a schematic view of a branching vessel such an aortic arch is shown in which emboli 8 are transferred from the more proximal arterial trunk 1, such an ascending aorta, into more distal branches 2 and 3, such as carotid 16, vertebral 12, subclavian 13 arteries causing ischemic injury to the organ they supply (such as stroke in the case of embolization of cerebral arteries).
FIG. 1 shows a hypothetical blood vessel 1 branching into the blood vessels 2 and 3. The antegrade flow 5 in the vessel 1 carries blood, containing emboligenic particles 8 to different areas in the human body, including the organ more vulnerable to ischemic injury (such as brain)—via the blood vessel 3, and less vulnerable (such as soft tissues)—via blood vessel 2. As shown on FIG. 1 the emboli 8 entering vessel 1 will follow the path of branching into the vessels 2 and 3 and will enter both vessels 2 and 3 proportionally to the magnitude of flow through these vessels. The more flow would occur via the blood vessel 2, the more emboli will enter the organ to be protected (such as brain) leading to serious ischemic injury (such as stroke).
FIGS. 2-7 show the disclosed method of diverging emboli 8 from important structures such as brain by exerting external pressure 10 on the blood vessel 3 (such as carotid or vertebral artery) to create an area of the pressure gradient 9 leading to limitation of the blood flow 5 carrying emboli 8 to the compressed blood vessel 3. Such compression will lead to flow reversal 7 diverting emboli 8 into other less important vessel 2. Acceleration of flow via the blood vessel 2 while the blood vessel 3 is compressed will lead to a Venturi effect providing additional force 7 deflecting the emboli 8 from the vessel 3 into the vessel 2. In order to avoid prolonged limitation of flow to the most important area of the human body (such as brain) the time of the protective compression of the blood vessel 2 should be brief. This goal is achieved by a disclosed method of vascular compression “on demand”, i.e. at the brief periods of time when the emboligenic particles are released. As shown on FIGS. 3-7 the detectors of emboli “A” and/or “E” can be placed over the source of emboli (such as heart, heart valve, aorta, etc.) or the blood vessels 1 and 3, carrying said emboli to the target organ (such as brain). The appearance of emboli in said areas when detected as echogenic signal or as another physiological parameter(s), reflecting cardiac ejection and systole (such as EKG, arterial Doppler, pulse oximetry, arterial waveform etc.) will be recorded by monitor “B” and will actuate the compression mechanism “C” that would temporarily compress the blood vessel 3 leading to limitation, interruption and/or reversal of the flow to the organ to be protected. Detection can occur during and be sensitive to flight of emboli or other debris in transit within a blood vessel. The length of compression and its intensity will be recorded by monitoring system “D” with a capacity of overruling the act of compression if its length or intensity exceed the safe limit Thus, a positive and negative feedback mechanisms will be assured with a potential for an automated auto-regulatory function of such a device.
Once the emboli 8 disappear from the inflow vessel 1 and/or deflected from the blood vessel 3 into the blood vessel 2, the detectors “A” and/or “E” will signal such events to the device “B”, that in turn will provide negative feedback to the device “C” thus interrupting the act of compression 10 and restoring circulation via the blood vessel 3 to the organ to be protected (such as brain). Considering the fact that the majority of embolic events leading to the organ damage and stroke in cardiovascular procedures are very short, this method and system appear to be feasible and reliable, thus providing anti-embolic protection at the moments of surgery when the risk of embolism is maximal, while restoring circulation to such organs when the risk of embolism is minimal. The process of vascular compression alternating with vascular release can be repeated on multiple occasions throughout the course of cardiovascular procedure or a cardiac cycle.
The emboli 8 (FIG. 1) may be fragments of atherosclerotic plaque 19 (FIGS. 8, 9) of the ascending thoracic aorta that become dislodged during surgical or catheter manipulations on the aorta. Also shown in FIGS. 8 and 9 is calcification of the aortic valve 15 and intra-cardiac embolic particles 20 of the heart 11 that can also be the origin of emboli 17 eventually present in any artery such as the carotid artery 16 or vertebral artery 12. The intra-cardiac emboli 20 may include air, gas, thrombi and atherosclerotic materials. Although all of the various emboli in the heart 11, aorta and aortic valve 15 need not be present in all instances, they are all shown in FIGS. 8 and 9 for sake of example. Trauma to the heart 11, aortic valve 15 and aortic structures during placement and removal of items such as an aortic clamps, guidewires, catheters, balloons and electrophysiological instruments, along with manipulations such coronary artery bypass grafting, aortic and mitral valve replacement, catheter ablation, endovascular grafting of the aorta, percutaneous implantation of the aortic or mitral valves, endovascular manipulations on the aorta, aortic branches and the heart 11 may give rise to the presence of emboli 17 in the carotid arteries 16, vertebral arteries 12, and subclavian arteries 13. Critical moments of the aforementioned procedures (for example during the aortic cross clamp manipulation, aortic valvuloplasty or valve implantation, coronary interventions, and endovascular procedures on the aorta) may cause emboli 17 to form and cause stroke and are referred to as emboligenic events.
The method and system described can be also applied for prevention of venous and pulmonary artery emboli. In this case the detection of the moving venous thrombus/embolus traveling from the peripheral vein toward the heart and pulmonary artery may initiate the measures for prevention of embolism by virtue of compression of the veins on its path, and signaling and initiating of other measures of prophylaxis of pulmonary embolism if necessary (such as deployment of the embolic trap or starting thrombolytic therapy).
A device similar to the embodiments depicted in FIGS. 13-24 may be placed around the part of the body containing the target vessel that is noninvasive and can include a vascular compression member(s) 27 and/or 27-V applied to the area of the artery at the certain angle (ranging from 0 to 90) to the axis of the artery. The device may comprise a transverse vascular compression member 32. The members 27, 27-V and 32 can be converted from an unactuated state to an actuated state in which the members 27, 27-V and 32 create an area of compression 23 and 23-V at the target arteries such as carotid (16), vertebral (12), subclavian (13) or femoral or any other hypothetical vessel 2 to limit blood flow therethrough into the circulation to be protected such as cerebral or any other circulation. Emboli 8, 17, 18, 20 that are formed in the patient secondary to emboligenic intervention are diverted into a descending aorta 14 and other less important vascular structures.
As shown in FIG. 9 the emboligenic particles 18 and 20, formed in the heart 11, aortic valve 15 and aorta may enter the carotid arteries 16 and vertebral arteries 12, thus becoming cerebral emboli 17 leading to obstruction of cerebral circulation and stroke. As shown on FIG. 10, the degree of embolization may significantly increase at the time of cardiac contraction (systole) when intra-cardiac (20) and aortic (18) particles are forcefully ejected into the systemic circulation, leading to a massive entry of emboli 17 into the carotid 16 and vertebral 13 arteries. With respect to our method of anti-embolic protection disclosed above it seems to be feasible to protect cerebral circulation by applying temporary pressure on the carotid and, if needed, vertebral arteries for the brief period of time when the risk of embolization is maximal (FIG. 11). Using detectors of potential emboligenic particles and emboli in the heart (by ECHO), aorta and its branches (as assessed by Doppler ultrasound) with timely signaling and immediate initiation of the protective compression of the target blood vessels such as carotid arteries 16 and/or vertebral arteries 12 will lead to temporary limitation of the blood inflow such as carotid and/or vertebral flow, thus protecting the organ, such as brain, from embolic load. Upon creation of the areas of vascular compression 23 (carotid) and 23-V (vertebral), a relative pressure gradient and a “no-flow” or “low-flow” condition is produced in the proximal segments of the compressed arteries such as carotid 16 and vertebral 12 arteries that prevents emboli 18 from entering the circulation to be protected such as cerebral circulation. The proximal carotid 16 and vertebral 12 arteries are areas of said arteries upstream from the areas of compression 23 and 23-V that have interrupted or diminished blood flow due to the compression. Potential cerebral vascular emboli such as emboli 18 are diverted into the more distal vessels such as descending aorta 14 and are illustrated as emboli 21. The thin arrow at the level of aortic arch on FIG. 11 shows preferential direction of the blood flow that carries potential emboli such as cerebral emboli 17 into the descending aorta 14 when the areas of compression 23 and 23-V are created. To protect the brain from an augmented embolic load at the time of cardiac systole (FIGS. 12 and 13) we disclose a method of carotid 16 and/or vertebral 12 compression synchronized with systolic phase of cardiac activity. The compression system 49 (box C on FIG. 7) is actuated and deactuated by the device 58 (Box B) depending on the phase of cardiac activity. Thus, the timing of the vascular compression 23 and 23-V in order to limit the inflow of emboli 17 can be triggered by electrophysiological, hemodynamic and/or pulse-oximetric indices of cardiac contraction, received and processed by the detector 58. On the other hand, the deactuation of the compression in order to restore arterial perfusion to the brain may be triggered by the same indices, but in the phase of cardiac relaxation.
FIGS. 13-16 disclose an exemplary embodiment that can selectively limit flow to either carotid 16 or vertebral arteries 12, or if necessary, limit flow to all or any combination of these vessels. Said device can be used to create the areas of compression 23 and 23-V as previously described to deflect emboli 18 and 20 from the target arteries such as carotid arteries 16 and vertebral arteries 13. The goal of this compression is to prevent the entry of emboli in the circulation to be protected such as cerebral circulation. The device can be positioned on the neck of the patient so that a pair of straps 33 and 43 extend around the neck 38 of the patient and are secured to one another via hooks 44 and loops 45 that form a hook and loop type arrangement. However, it is to be understood that other mechanisms of securing the straps 33 and 43 to one another are possible and that the disclosed arrangement is only one exemplary embodiment. Securement of the hooks 44 and loops 45 causes the device 26 to be retained onto the body part such as the neck 38 of the patient. This retention may be loose so that the device 26 has some room to give on the body part such as the neck 38, or the retention may be of a tightness that firmly secures the device into the body part such as the neck 38 and prevents same from moving or twisting. The compression device may be a neck collar 26, combination of compression elements, bars, levers, pads, inserts and screws to provide compression of the target vessel in accordance with various exemplary embodiments. In other arrangements the compression device 26 may be a strap that lays on the front of the body part to be protected such as the neck 38 of the patient, or may be made of multiple components that are not directly attached to one another but are positioned proximate to the neck 38 of the patient. The device 26 may include two semi-oval halves that may be positioned around body part of the patient such as the neck 38 or extremity of the patient in accordance with one exemplary embodiment. The device 26 need not be circular in shape. Even if the device 26 is not circular in shape it may still have a central axis 56 (FIG. 23A) as the central axis 56 can be located at the center of the vessel and the body part to be protected such as a carotid artery and the neck 38 of the patient and thus may still be a central axis 56 of the device 26.
With reference in particular to FIGS. 23B, 23C and 23D, a pair of insertion pockets 41 and 42 are present on the device 26 and may be sealed at their tops and bottoms with respect to the vertical direction 55. As used herein, the vertical direction 55 may be the direction of the device 26 that is parallel to the direction of extension of the central axis 56. Strap 33 may extend from the first insertion pocket 41, and strap may extend from the second insertion pocket 42. The first insertion pocket 41 forms a cavity into which a first vascular compression member 27 is located. Member 27 is shown in a relaxed or unactuated state in FIG. 23 and may be made of a flexible material that can be stretched or otherwise deformed. The material making up member 27 can be nonporous such that member 27 is capable of being filled with gas or liquid that enables the member 27 to expand and at the same time hold the gas or liquid therein. The pocket 41 may be made of a material that is different than the material making up member 27.
The second insertion pocket 42 forms a cavity into which the second vascular compression member 46 is retained. Member 46 may be configured in a manner similar to member 27 and a repeat of this information is not necessary. Member 46 may be completely sealed or connected to an opening that leads into connecting tube 54. Member 46 is in an unactuated state in FIG. 23B. Similarly, for compression of vertebral arteries 13 two insertion pockets 41-V and 42-V may be created. Said pockets may contain compression members 27-V and 46-V and other components to facilitate arterial compression as described in previous paragraphs. If necessary, only vertebral compression members can be actuated (FIG. 17). The specific anatomic location of the vertebral compression members is disclosed and should correspond to the level of the C5-C7 vertebra in order to assure adequate compression of the vertebral arteries 13 against the body of C-7 (FIGS. 16 and 20). In other embodiments, however, only the carotid (FIGS. 22 and 23A) or, conversely, only vertebral (FIGS. 18-20) compression members could be present. Other arrangements and combinations of compression members are possible in order to achieve selective compression of any combination of the carotid and vertebral arteries. Some of these embodiments are shown on FIGS. 17-23.
A pressure or compression source 49 is included and is placed into communication with the first vascular compression member 27 by the way of tubing 29 that extends through a port of member 27. A manometer 30 may be included in the device 26 at some point between the member 27 and the pressure/compression source 49 in order to monitor and measure pressure in the system. A detector of emboli and/or EKG, pulse oxymeter, arterial waveform monitor 58 can be bundled with the pressure source 49 to assure an option of initiation of the vascular compression once the potential emboli are ejected or anticipated. FIGS. 23C and 23D illustrate the device 26 once the pressure/compression source 49 is activated in order to cause the device 26 to be pressurized. The pressure source 49 may be a pump that injects air, gas or liquid, such as water, through the pressure tubing 29. Injection of air or otherwise increasing the pressure causes the first vascular compression member 27 to expand. Due to fluid communication through the connecting tube 54, the second vascular compression member 46 will likewise expand and the two members 27 and 46 may expand at the same rate to the same size. Expansion may be in the radial direction 57 such that the expandable members 27 and 46 expand towards the central axis 56 and away from the central axis 56. In some exemplary embodiments, the members 27 and 46 may expand in the radial direction 57 towards the central axis 56 but not in the radial direction 57 away from the central axis 56. This arrangement may be accomplished by making portions of the compression members 27 and 46, for example the portions facing away from the central axis 56 in the radial direction 57, such that they cannot expand while the portion facing towards the central axis 56 are in fact expandable. Said arrangements can be also applied to the vertebral compression elements 41-V, 42-V, 46-V and 27-V and their repetition of them is not necessary.
Another exemplary embodiment of the device 26 is illustrated in FIGS. 24A-24D. The device 26 in this exemplary embodiment also functions to compress the carotid arteries 16 to create the areas of compression 23. The device 26 includes a first insertion pocket 41 and a second insertion pocket 42 but lacks first and second vascular compression members 27 and 46. Instead a first compression member 52 is located within the first insertion pocket 41, and a second compression member 53 is located within the second insertion pocket 42. The compression members 52 and 53 are not expandable but may be made of a material, such as foam, that can be compressed and then can subsequently expand back into its original shape. The compression members 52 and 53 may alternatively be made of a material that does not exhibit any give upon the application of forces thereto that would be encountered in a procedure of the type described herein. The compression members 52 and 53 may be elongated in the vertical direction 55 and may have a convex shape that faces the central axis 56. The shape of the compression members 52 and 53 at their surfaces that face away from the central axis 56 in the radial direction 57 may be different than those that face towards the central axis 56.
The device 26 may include a transverse carotid compression section 31 that is located outward from the compression members 52 and 53 in the radial direction 57 from the central axis 56. A transverse carotid expandable member 32 may be held by the section 31 and can have an arc length about the central axis 56 that extends beyond both of the compression members 52 and 53. The transverse carotid expandable member 32 has a height in the vertical direction 55 that is the same as, larger or smaller than the height of the compression members 52 and 53 in the vertical direction 55. The member 32 is made of a material that will hold air, gas or liquid such that it can be expanded upon the application of fluid thereto. The member 32 has a single port that is in fluid communication with the pressure tubing 29. Application of pressure to the member 32 will cause the member 32 to expand as shown for example in FIGS. 24C and 24D. In other embodiments, the compression members 52 and 53 can be removed and not present so that only the expandable member 32 is present to compress the carotid arteries 16.
Placement of the device 26 onto the patient may result in the first compression member 52 overlaying the target artery such as carotid artery 16 femoral or brachial artery so that the artery to be compressed is between compression member 52 and the central axis 56 in the radial direction 57. The second compression member 52 will be arranged so that it overlays the second carotid artery 16 causing it to be between the second compression member 52 and the central axis 56 in the radial direction 57. The expandable members 27, 32 and 46 may be located at the neck 38, upper chest, shoulder, lower abdomen or an extremity of the patient such that they are secured to the neck 38 or extremity or otherwise proximate. The compression members 27, 32 and 46 need not be in direct contact with the body part of the patient such as the neck 38, chest, abdomen or extremity but only located near them. Application of pressure via the pressure source 49 causes the transverse compression member 32 that may be expandable to exert pressure in the radial direction 57. This inward radial pressure causes the compression members 52 and 53 to move inwards and be urged against the target vessels such as carotid arteries 16, femoral, brachial or other compressible arteries. The positioning and configuration of the members 52 and 53 function to impart compressive forces onto the arteries to be compressed such as carotid arteries 16, femoral, brachial or other arteries when the device 26 is pressurized thus resulting in the creation of the areas of compression 23. The other components of the device 26 may be made as those previously described and a repeat of this information is not necessary.
An alternative exemplary embodiment of the device 26 would be the one in which both a pair of longitudinal vascular compression members 27 and 46 are present along with a transverse vascular compression member 32. A pair of compression members 52 and 53 may be missing from this embodiment, or they may be present in certain arrangements. This exemplary embodiment may include additional pressure tube lines 47 and 48 that are separate from pressure tubing 29 that actuates the transverse vascular compression member such as carotid compression member 32. Pressure tube lines 47 and 48 provide pressure to the first and second longitudinal vascular compression members 27 and 46 so that these members 27 and 46 can be actuated at different rates, amounts, and/or times than compression member 32. This flexibility provides selective pressure adjustments between the transverse vascular compression member 32 and longitudinal vascular compression members such as carotid members 27 and 46. This feature will provide an option to decrease or completely eliminate the degree of circumferential compression of the body part such as the neck 38 or extremity when selective inflation of the longitudinal vascular compression members is adequate. Conversely, if inflation of longitudinal compression members such as carotid members 27 and 46 does not lead to sufficient reduction of the arterial flow, an additional inflation of the transverse vascular compression member such as carotid member 32 would allow one to achieve the desired effect by combining the effect of pressure created in all of the members described.
An alternative exemplary embodiment of the device 26 that is being disclosed is similar to that previously disclosed with respect to FIGS. 23 and 24 and a repeat of the features and functionality that are similar between the two need not be repeated. The pressurization of the members 27, 32 and 46 are different in that the second pressure tube 47 feeds into the first longitudinal vascular compression member 27, and in that the third pressure tube 48 supplies the second longitudinal vascular compression member 46 to allow the members 27 and 46 to be pressurized independently from one another. In this regard, one can apply more or less pressure to member 27 than member 46 so that compression of the arteries, such as carotid arteries 16 or femoral and brachial arteries can be more precisely controlled. The transverse vascular compression member 32 is supplied by pressure tubing 29 and is independent from the expansion of members 27 and 46 such that it can be pressurized to a greater or lesser extent than members 27 and 46. The manometer 30 may be capable of measuring pressures in all of the lines 29, 47 and 48 so that their individual pressures can be monitored. In use, one may adjust the pressures in members 27 and 46 first, then subsequently if needed one may apply pressure into member 32 to cause its actuation so that adequate compression of the carotid arteries 16 is realized.
The arrangement of the device 26 in this case includes a pair of longitudinal vascular compression members 27 and 46 along with a transverse vascular compression member 32. The circumferential distance about the central axis 56 may be the circumferential distance about the neck 38 or extremity of the patient when the device 26 is worn by a patient and thus these two terms can be interchangeable when discussing the arc length of the member 32. In other exemplary embodiments, the arc length of the member 32 may be from 50-65% (180 degrees-234 degrees) about the circumference of the body part of the patient, from 25%-50% (90 degrees-180degrees) about the circumference of the body part patient, or from 15%-25% (54degrees-90 degrees) about the circumference of the body part of the patient. In yet other exemplary embodiments, the member 32 may extend 360 degrees completely about the body part of the patient.
FIGS. 13-22 disclose modifications of the geometry of the vascular compression members 27 and 46 with respect to the geometry and anatomy of the patient in order to achieve compression of carotid and/or vertebral arteries in any combination.
FIGS. 15, 16, 20, 21B, and 23A demonstrate the method of use and the effect of inflation of the vascular compression device such as device 26 and it's different embodiments resulting in external compression of carotid arteries 16 and/or vertebral arteries 12 leading to transient interruption of carotid and/or vertebral flow. These figures demonstrate the anatomic relationship of the device 26 to carotid arteries 16, vertebral arteries 12 and surrounding structures 34, 35, 36, 37 and 40 of the neck 38. The carotid arteries 16 are bordered by neck muscles 36, esophagus 35, trachea 34 and fat tissues 40. These structures provide a protective cushion, minimizing the risk of the carotid and vertebral artery injury during external compression. In fact, an external compression of arteries 16 and 12 in this setting would lead to significantly lower risk of injury to carotid intima than intravascular carotid occlusion with the balloon or umbrella devices used for cerebral protection in patients undergoing carotid stenting. The longitudinal carotid (42, 46) and/or vertebral (42-V, 46-V) expandable members are positioned along the course of both carotid arteries 16 and/or vertebral arteries 12 on the neck 38. Similar considerations are applicable to protective compression of all other compressible arteries such as femoral and brachial arteries and the repeat description of identical processes is not necessary.
The exemplary embodiment of the device 26 may be any one of those previously disclosed that lacks a transverse carotid expandable member 32. However, it is to be understood that this is just one example and that other devices 26 that include member 32 can function in a similar manner to the device 26 disclosed in FIGS. 8A and 8B. As shown in FIGS. 15, 16, 20, 21B, and 23 longitudinal vascular compression members are placed along the course the target arteries such as carotid and/or vertebral artery, or brachial and femoral artery, or any other combination of compressible vessels. The lumen of the target arteries such as carotid or vertebral arteries is compressed between the vascular compression members anteriorly (outward in the radial direction 57) and the cervical spine 37 (or brachial and femoral bones in the case of the arteries of the extremities) posteriorly (inward in the radial direction 57). Actuation of the members 27 and 46 and/or 27-V, 46-V cause the members to move radially inward and compress fat tissue 40 that is immediately adjacent the device 26. I the case of the carotid artery compression the vascular compression members 27 and 46 are shown moving in the radial direction 57 inward of portions of the trachea 34 and neck muscles 36 so that portions of the vascular compression members 27 and 46 are closer to the central axis 56 in the radial direction 57 than portions of the trachea 34 and neck muscles 36. Full expansion of the vascular compression members 27 and 46 may result in inward radial movement so that they are not radially closer to the axis 56 than any portion of the esophagus 35. However, other embodiments are possible in which at least some portion of the vascular compression members 27 and 46 are closer to the central axis 56 than a portion of the esophagus 35. Actuation of the compression members 27-V and 46-V achieve similar compression of the vertebral arteries against the cervical spine, that would be most efficient at the level of C5-C7 vertebrae.
The soft tissues such as the fat tissues 40, neck muscles 36, esophagus 35 and trachea 34 around carotid arteries 16 provide a smooth cushion assuring adequate protection against carotid trauma. Same considerations will hold true in the case of compression of the arteries of upper and lower extremities and the repetition of them is not necessary. In the case of protection of both carotid arteries, the actuation of the members 27, 46 and/or 27-V, 46-V causes the areas of compression to restrict blood flow through the carotid arteries 16 and/or vertebral arteries 12 which leads to transient limitation or interruption of cerebral flow. The trachea 34 and esophagus 35 are not closed or restricted upon actuation of the expandable members 27 and 46 due to the placement and specific configuration of said expandable members. The fact that in most cases this maneuver is performed while the patient is intubated and sedated makes the risk of compression of trachea minimal. Performing the same procedure on the ambulatory basis, however, or while the patient is not intubated, may prove to be hazardous. However, in some arrangements some degree of restriction of the trachea 34 and/or esophagus 35 may occur and is considered acceptable in the setting of general anesthesia with endotracheal intubation and mechanical ventilation. It is advisable, however, to obtain Duplex scan in all patients planned for this procedure to rule out significant atherosclerotic disease of these vessels, especially if carotid arteries 16 are compressed. The mere presence of carotid artery disease in these patients should be considered a contraindication to carotid compression due to increased risk of carotid atherosclerotic plaque injury leading per se to distal cerebral embolization and stroke i.e. defeating the purpose of such a procedure.
Various types of mechanisms capable of compressing the carotid arteries 16, vertebral arteries 12 and other vessels can be included in the device 26 in addition to or alternatively to those previously discussed. For example, the device 26 can be supplied with different vascular compression mechanisms, including different forms and shapes of longitudinal or transverse bladders, cuffs, compression pads or inserts with the same effect of vascular compression to the point of transient limitation or interruption of blood flow. The fluid provided to pressurize the expandable components of the device 26 from the pressure source 49 may be a liquid substance in some embodiments. Fluid that is a liquid may be used in the device 26 to effect pressurization and more uniform constriction of the carotid arteries 16 than gas or air fluid because liquid is more non-compressible at the operating range of pressures. Liquid fluid in the members 27, 32 and 46 may more directly transmit pressure to the carotid area than gas or air fluid.
A monitoring system 58 may be included with the device 26 to assure a safe, adequate, easily manageable and controllable compression of carotid, vertebral and other vessels. The monitoring system 58 may comprise Doppler ultrasound, Doppler probe, oscillotonometry, electroencephalography, transcranial Doppler, cerebral oximetry and/or other techniques. The device 26 may be actuated to such a degree that the one, two or more areas of vascular compression formed completely stop the flow of blood into the distal artery such as carotid artery 22, or to an extent that partial flow of blood passes through the areas of compression 23 and into the distal artery such as carotid artery 22.
The device 26 provided is a noninvasive and precise apparatus with an option of assessing a degree and an effectiveness of an interruption of the arterial flow by the optional inclusion of a monitoring system 58. The device 26 assures a uniform and reproducible interruption or limitation of the arterial flow bilaterally minimizing the risk of trauma to the artery compressed such as carotid and vertebral artery and subsequent distal emboli, such as cerebral emboli 17. An alarm system 59 can be included in the device 26 that is triggered by excessive or lengthy compression of the target artery, such as carotid arteries 16, brachial or femoral arteries. The alarm system 59 may be a part of the monitoring system 58 or may be a different component that is not part of the monitoring system 58. The alarm system 59 may thus measure the time of compression, and the magnitude of compression. Constant monitoring of arterial, such as carotid 16, brachial or femoral and systemic arterial and device 26 pressures with pressure in the device 26 exceeding only slightly the pressure in the arterial system may be conducted to ensure safe operation and use of the disclosed device 26. The device 26 provides a noninvasive compression apparatus that does not require the insertion of intravascular devices.
The central axis 56 may be present even when the device 26 is not configured with straps 33, 43 to form a generally circular member when viewed from the top as for example in FIG. 6A. In some embodiments of the device 26, a circular member is not formed when viewed from the top by the straps 33, 43. For instance, the straps 33, 43 may be missing such that the section 31 is attached to sides of a bed or otherwise secured so that the device 26 is located at the neck 38 of the patient. In such instances, the central axis 56 is still present. The central axis 56 may be located at a location within the neck 38 of the patient, for examples shown with reference to FIGS. 8A and 8B. This location may be at the spinal column 37 of the patient, or may be at the center of the neck 38 of the patient. It is to be understood that various embodiments of the device 26 exist in which the device 26 does not wrap completely around the neck 38 of the patient but instead only wraps around a portion of the neck 38 of the patient less than 360 degrees fully about the neck of the patient.
The apparatus and methods discussed herein are not limited to the detection and compression of any particular vessels or combination of vessels, but can include any number of different types of vessels. For example, in some aspects, vessels can include arteries or veins. In some aspects, the vessels can be suprathoracic vessels (e.g., vessels in the neck or above), intrathoracic vessels (e.g., vessels in the thorax), subthoracic vessels (e.g., vessels in the abdominal area or below), lateral thoracic vessels (e.g., vessels to the sides of the thorax such as vessels in the shoulder area and beyond), or other types of vessels and/or branches thereof.
In some aspects, the detection and compression systems disclosed herein can be applied to superthoracic vessels. The suprathoracic vessels can comprise at least one of intracranial vessels, cerebral arteries, and/or any branches thereof. For example, the suprathoracic vessels can comprise at least one of a common carotid artery, an internal carotid artery, an external carotid artery, a middle meningeal artery, superficial temporal arteries, an occipital artery, a lacrimal (ophthalmic) artery, an accessory meningeal artery, an anterior ethmoidal artery, a posterior ethmoidal artery, a maxillary artery, a posterior auricular artery, an ascending pharyngeal artery, a vertebral artery, a left middle meningeal artery, a posterior cerebral artery, a superior cerebellar artery, a basilar artery, a left internal acoustic (labyrinthine) artery, an anterior inferior cerebellar artery, a left ascending pharyngeal artery, a posterior inferior cerebellar artery, a deep cervical artery, a highest intercostal artery, a costocervical trunk, a subclavian artery, a middle cerebral artery, an anterior cerebral artery, an anterior communicating artery, an ophthalmic artery, a posterior communicating artery, a facial artery, a lingual artery, a superior laryngeal artery, a superior thyroid artery, an ascending cervical artery, an inferior thyroid artery, a thyrocervical trunk, an internal thoracic artery, and/or any branches thereof. The suprathoracic vessels can also comprise at least one of a medial orbitofrontal artery, a recurrent artery (of Heubner), medial and lateral lenticulostriate arteries, a lateral orbitofrontal artery, an ascending frontal (candelabra) artery, an anterior choroidal artery, pontine arteries, an internal acoustic (labyrinthine) artery, an anterior spinal artery, a posterior spinal artery, a posterior medial choroidal artery, a posterior lateral choroidal artery, and/or branches thereof. The suprathoracic vessels can also comprise at least one of perforating arteries, a hypothalamic artery, lenticulostriate arteries, a superior hypophyseal artery, an inferior hypophyseal artery, an anterior thalamostriate artery, a posterior thalamostriate artery, and/or branches thereof. The suprathoracic vessels can also comprise at least one of a precentral (pre-Rolandic) and central (Rolandic) arteries, anterior and posterior parietal arteries, an angular artery, temporal arteries (anterior, middle and posterior), a paracentral artery, a pericallosal artery, a callosomarginal artery, a frontopolar artery, a precuneal artery, a parietooccipital artery, a calcarine artery, an inferior vermian artery, and/or branches thereof.
In some aspects, the subthoracic vessels can comprise at least one of renal arteries, inferior phrenic arteries, a celiac trunk with common hepatic, left gastric and splenic arteries, superior suprarenal arteries, a middle suprarenal artery, an inferior suprarenal artery, a right renal artery, a subcostal artery, 1st to 4th right lumbar arteries, common iliac arteries, an iliolumbar artery, an internal iliac artery, lateral sacral arteries, an external iliac artery, a testicular (ovarian) artery, an ascending branch of deep circumclex iliac artery, a superficial circumflex iliac artery, an inferior epigastric artery, a superficial epigastric artery, a femoral artery, a ductus deferens and testicular artery, a superficial external pudendal artery, a deep external pudendal artery, and/or branches thereof. The subthoracic vessels can also comprise at least one of a superior mesenteric artery, a left renal artery, an abdominal aorta, an inferior mesenteric artery, colic arteries, sigmoid arteries, a superior rectal artery, 5th lumbar arteries, a middle sacral artery, a superior gluteal artery, umbilical and superior vesical arteries, an obturator artery, an inferior vesical and artery to ductus deferens, a middle rectal artery, an internal pudendal artery, an inferior gluteal artery, a cremasteric, pubic (obturator anastomotic) branches of inferior epigastric artery, a left colic artery, rectal arteries, and/or branches thereof.
2. The method of claim 1, wherein the second vascular location is downstream of the first vascular location.
determining whether the detected emboli exceed a threshold amount;
wherein the compression member is actuated when the detected emboli exceed the threshold amount.
determining whether the detected emboli do not exceed a threshold amount;
transitioning the compression member to the unactuated state when the detected emboli do not exceed the threshold amount.
5. The method of claim 1, further comprising transitioning the compression member to the unactuated state after the compression member has been actuated for a predetermined time limit.
6. The method of claim 1, wherein the detecting is by a Doppler ultrasound device, a Doppler probe device, an oscillotonometry device, an electroencephalography device, a transcranial Doppler device, or a cerebral oximetry device.
7. The method of claim 1, wherein the first vascular location is a heart valve, an aorta, a calf vein, a femoral vein, a popliteal vein, an iliofemoral vein, an iliac vein, an inferior vena cava, or a peripheral vein of the patient.
8. The method of claim 1, wherein the second vascular location is a carotid artery or a vertebral artery of the patient.
9. A method of diverting emboli from cerebral circulation of a patient, comprising:
10. The method of claim 9, wherein expanding the first carotid compression member comprises radially advancing a portion of the first carotid compression member toward a cervical spine of the patient.
11. The method of claim 9, wherein expanding the first vertebral compression member comprises radially advancing a portion of the first vertebral compression member toward a cervical spine of the patient.
13. The method of claim 12, wherein expanding the second carotid compression member comprises radially advancing a portion of the second carotid compression member toward a cervical spine of the patient.
14. The method of claim 12, wherein expanding the second vertebral compression member comprises radially advancing a portion of the second vertebral compression member toward a cervical spine of the patient.
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US14/703,669 US9808260B2 (en) 2014-05-04 2015-05-04 Noninvasive protection from emboli
US15/691,026 US20170360452A1 (en) 2014-05-04 2017-08-30 Noninvasive protection from emboli
US15/691,026 Division US20170360452A1 (en) 2014-05-04 2017-08-30 Noninvasive protection from emboli
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US14/703,669 Active 2036-01-19 US9808260B2 (en) 2014-05-04 2015-05-04 Noninvasive protection from emboli
US15/691,026 Pending US20170360452A1 (en) 2014-05-04 2017-08-30 Noninvasive protection from emboli
US (2) US9808260B2 (en)
EP (1) EP3139840A4 (en)
WO (1) WO2015171519A2 (en)
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2015-05-04 US US14/703,669 patent/US9808260B2/en active Active
2015-05-04 EP EP15788567.4A patent/EP3139840A4/en active Pending
2015-05-04 WO PCT/US2015/029104 patent/WO2015171519A2/en active Application Filing
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Owner name: ZHADKEVICH MEDICAL, INC., SOUTH CAROLINA
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