36 results about "Ventricular cavity" patented technology

A tiny electrically powered hydrodynamic blood pump is disclosed which occupies one third of the aortic or pulmonary valve position, and pumps directly from the left ventricle to the aorta or from the right ventricle to the pulmonary artery. The device is configured to exactly match or approximate the space of one leaflet and sinus of valsalva, with part of the device supported in the outflow tract of the ventricular cavity adjacent to the valve. In the configuration used, two leaflets of the natural tri-leaflet valve remain functional and the pump resides where the third leaflet had been. When implanted, the outer surface of the device includes two faces against which the two valve leaflets seal when closed. To obtain the best valve function, the shape of these faces may be custom fabricated to match the individual patient's valve geometry based on high resolution three dimensional CT or MRI images. Another embodiment of the invention discloses a combined two leaflet tissue valve with the miniature blood pump supported in the position usually occupied by the third leaflet. Either stented or un-stented tissue valves may be used. This structure preserves two thirds of the valve annulus area for ejection of blood by the natural ventricle, with excellent washing of the aortic root and interface of the blood pump to the heart. In the aortic position, the blood pump is positioned in the non-coronary cusp. A major advantage of the transvalvular VAD is the elimination of both the inflow and outflow cannulae usually required with heart assist devices.

A method of treating a neurological disorder in a patient is provided. The method comprises intravascularly delivering a stimulation lead within the head of the patient, and placing the stimulation lead adjacent brain tissue (e.g., cortical brain tissue or deep brain tissue), the stimulation of which will treat the neurological disorder. The stimulation lead can be placed into indirect contact with the brain tissue (e.g., through a blood vessel) or indirect contact with the brain tissue (e.g., when placed within the ventricular cavity or by being introduced through an exit point within a vessel wall). Optionally, the method comprises implanting a source of stimulation within the patient's body, and then electrically coupling the proximal end of the stimulation lead, which conveniently extends from the access point within the circulatory system, to the implanted stimulation source. Using the stimulation lead, the brain tissue can then be stimulated in order to treat the neurological disorder.

A device used to treat heart disease by decreasing the size of a diseased heart, or to prevent further enlargement of a diseased heart. The device works by limiting the volume of blood entering the heart during each cardiac cycle. The device partitions blood within the heart, and protects the heart from excessive volume and pressure of blood. The device is placed within the interior of the heart, particularly within a ventricular cavity. The device is a hollow sac, with two openings, which simulates the shape and size of the interior lining of a ventricle of a normal heart. It allows the ventricle to fill through one opening juxtaposed to the annulus of the inflow valve to a predetermined, normal volume, and limits filling of the heart beyond that volume. It then allows blood to be easily ejected through the second opening through the outflow valve. By limiting the amount of blood entering the ventricle, the ventricle is not subjected to the harmful effect of excessive volume and pressure of blood during diastole, the period of the cardiac cycle when the heart is at rest. This allows the heart to decrease in size, or to reverse remodel, and to recover lost function. In some applications, a second device may be simultaneously placed inside the heart to take up excessive space between the heart and the primary device.

The disclosure provides methods and apparatus of left ventricular pacing including automated adjustment of a atrio-ventricular (AV) pacing delay interval and intrinsic AV nodal conduction testing. It includes—upon expiration or reset of a programmable AV Evaluation Interval (AVEI)—performing the following: temporarily increasing a paced AV interval and a sensed AV interval and testing for adequate AV conduction and measuring an intrinsic atrio-ventricular (PR) interval for a right ventricular (RV) chamber. Thus, in the event that the AV conduction test reveals a physiologically acceptable intrinsic PR interval then storing the physiologically acceptable PR interval in a memory structure (e.g., a median P-R from one or more cardiac cycles). In the event that the AV conduction test reveals an AV conduction block condition or if unacceptably long PR intervals are revealed then a pacing mode-switch to a bi-ventricular (Bi-V) pacing mode occurs and the magnitude of the AVEI is increased.

Methods and compositions are provided for magnetic resonance imaging of biological tissue, particularly methods and compositions for 23Na and 39K magnetic resonance imaging of cardiac tissue. In particular, methods of 23Na magnetic resonance imaging (MRI) cardiac imaging is presented for attenuating 23Na signals corresponding to ventricular cavity blood and viable well-perfused tissue and for visualizing myocardial infarction. Cardiac tissue is imaged using 23Na MRI after the introduction of an intravascular paramagnetic contrast agent. Optimally, the intravascular paramagnetic contrast agent is MION-46. The MION-46 suppresses the blood signal intensity in sodium images of ventricular cavities and signal for viable cardiac tissue. The quantity of MION-46 and the echo time (TE) for 23Na MRI of cardiac tissue may be selected to minimize signal intensity differences between ventricular cavity blood and well-perfused viable myocardium; maximize signal intensity differences between non-viable myocardium and ventricular cavity blood in myocardial infarction; and maximize signal intensity differences between non-viable myocardium and well-perfused viable myocardium in myocardial infarction.

A system and method for providing a dark-blood technique for contrast-enhanced cardiac magnetic resonance, improving visualization of subendocardial infarcts or perfusion abnormalities that may otherwise be difficult to distinguish from the bright blood pool. In one technique the dark-blood preparation is performed using a driven-equilibrium fourier transform (DEFT) preparation with motion sensitizing gradients which attenuate the signal in the ventricular cavities related to incoherent phase losses resulting from non-steady flow within the heart. This dark-blood preparation preserves the underlying contrast characteristics of the pulse sequence causing a myocardial infarction to be bright while rendering the blood pool dark. When applied to perfusion imaging, this dark-blood preparation will help eliminate artifacts resulting from the juxtaposition of a bright ventricular cavity and relatively dark myocardium.

A cardiovascular device (11), adapted to be fitted into a cardiac ventricular cavity (2) having a volume with blood flowing therethrough, which is bounded by walls (8) and has a larger longitudinal dimension (D1) and a smaller transverse dimension (D2), characterized in that it comprises diaphragm means (16) that can be disposed in said ventricular cavity (2) substantially transverse to said larger longitudinal dimension (D1), in such an arrangement as to reduce said volume, said diaphragm means (16) having a peripheral edge (15) which can be sealingly engaged with said walls (8) and being adapted to be alternately driven between an active blood pushing displacement and an inactive return displacement.

The invention relates to an application of miRNA in treating cardiac hypertrophy. Particularly, the miRNA is hsa-miR-15a-5p/hsa-miR-16-5p, and the nucleotide sequences of the miRNA are shown as SEQ IDNO.1 and SEQ ID NO.2. The cardiac hypertrophy refers to a pathophysiological process which is caused by overloading of a heart due to genetic factors, hypertension, myocardial infarction, valve diseases and the like and mainly takes thickening of ventricular muscles and narrowing of ventricular cavities as main characteristics. The invention also relates to an application of a complex loaded withthe hsa-miR-15a-5p/hsa-miR-16-5p in preparing a medicament for treating cardiac hypertrophy, wherein the complex is a CHO-PGEA-nucleic acid complex.

The invention relates to a guide steel wire for the hybrid therapy of a muscular ventricular septal defect and a positioning and conveying device of the guide steel wire. The positioning and conveyingdevice comprises a detecting sheathing canal, the guide steel wire and a steel wire ring part catcher. The detecting sheathing canal is hollow and has an obtuse head part. The head end of the guide steel wire is bent into a water-drop-shaped ring part. The steel wire ring part catcher is composed of a handle and a ring hook. The ring hook is located at the position, close to the top end, in the handle. The positioning and conveying device has the advantages that the L-shaped detecting sheathing canal with the obtuse head part conveniently conducts detection on the muscular ventricular septaldefect at the deep part of a ventricular cavity from a ventriculus dexter; the guide steel wire can directly arrive at and penetrate through the muscular ventricular septal defect along a canal cavityof the detecting sheathing canal, and through the design of the water-drop-shaped ring of the head part, it is avoided that the head end of the guide steel wire enters a ventriculus sinister and accidentally injures a ventricular wall or valve tissue; the top end of the steel wire ring part catcher is obtuse, and the accidental injuries caused to valves, chordae tendineae, musculi papillares andventricular walls when the guide steel wire goes deep into the ventriculus sinister are reduced; the ring part of the guide steel wire can be conveniently caught by the ring hook, the guide steel wireis pulled out of a heart to be fixed, and a stable steel wire guide route is established.

The invention discloses an electrode guide wire shaping device of a cardiac pacemaker in the technical field of cardiac pacemaker implantation, and the electrode guide wire shaping device comprises a guide clamping seat, clamping columns, a clamping block and a lifting column, the vertical side wall is a cambered surface, and the multiple clamping columns are sequentially and uniformly arranged at the top of the guide clamping seat in an arc shape; the vertical side wall of one side of each clamping column protrudes out of the inner arc surface of the guide clamping seat, the electrode guide wire can be clamped at a specific angle through a specific shape, the electrode guide wire is drawn and shaped under the clamping of the specific radian, stable deformation at a set angle is formed, the radian of the guide clamping seat can be changed, and the clamping effect is good. Adjustment is carried out according to the size and the shape of a ventricular cavity of a patient, so that the shaping radian of the guide wire is changed, the deformation and the angle of the electrode guide wire are more suitable for the size, the angle and the like of the ventricular cavity of the corresponding patient, meanwhile, shaping of the electrode guide wire is more convenient, the shaping angle is more stable, and the success rate is higher.