53 results about "Mammalian heart" patented technology

The present invention provides methods and devices for closing two overlapping layers of tissue in a mammalian heart, for example a patent foramen ovale (PFO). The closure devices may take a number of different forms and may be retrievable. In some embodiments, the closure devices may be delivered with a catheter capable of puncturing mammalian tissue.

A cardiac assist device synchronization system includes a cardiac assist device and an acoustic or accelerometer sensor that provides a signal input to the cardiac assist device indicative of aortic valve closure. The cardiac assist device is coupled to a mammalian aorta and includes an inflatable chamber and a fluid pump. A fluid conduit is in communication between the chamber and the pump to provide for selective inflation of the chamber. A pump controller triggers the pump in counter-pulsation to a mammalian heart upstream from the aorta. A process for synchronizing a cardiac assist device in counter-pulsation with a left ventricle includes locating an acoustic or accelerometer sensor within a thoracic cavity of a mammal having the assist device coupled to the aorta of the mammal. Through the measurement of an acoustic or acceleration property of an aortic valve of the mammal, and the transmission of aortic valve closure measurement through a controller for the cardiac assist device, counter-pulsatile synchronization for the cardiac assist device is achieved.

Devices and methods for treating heart disease by normalizing elevated blood pressure in the left and right atria of a heart of a mammal are disclosed. Devices may include an adjustable hydraulic diameter shunt portion which can be manually adjusted in vivo. Methods are provided for adjusting the flow rate of the devices in vivo.

Devices and methods for treating heart disease by normalizing elevated blood pressure in the left and right atria of a heart of a mammal are disclosed. Devices may include an adjustable hydraulic diameter shunt portion which can be manually adjusted in vivo. Methods are provided for adjusting the flow rate of the devices in vivo.

A medical simulation model is provided for use in medical training, and having a wall defining a chamber, and having a slit in the wall providing access to the interior of the chamber. A pair of rib-cage members is located within the chamber such that adjacent edges of each member are spaced apart from each other. Resilient biasing elements are connected to each rib-cage member and configured such that adjacent edges of the rib-cage members may be brought into contact with each other, or further spaced-apart, against the action of the resilient biasing elements. A conduit is provided to enable fluid to be introduced into the chamber, and a facsimile of a mammalian heart is located within the chamber.

A method for treating a subject afflicted with a cardiac disorder, in vivo, comprising (i) producing a solution comprising media conditioned from the culture of cells, in vitro, and (ii) administering the solution of step (i) to the subject, thereby treating the cardiac disorder in the subject. Methods for determining whether an agent stimulates or inhibits myocyte proliferation.

Dedifferentiation is a mechanism whereby specialized cells regain properties of their ancestors, including, in the extreme, stemness. We found that highly-purified cardiomyocytes isolated from adult mammalian hearts dedifferentiated rapidly when cultured in mitogen-rich medium. Such myocytes reentered the cell cycle and proliferated, expressing stem cell surface markers such as c-kit and early cardiac transcription factors including GATA and NKx2.5. These myocyte-derived cells (MDC) were capable of re-differentiating into myocytes and endothelial cells. Contrary to prevailing dogma, cardiomyocyte dedifferentiation yields proliferative cells expressing stem cell markers and capable of multilineage differentiation. Cardiomyocyte dedifferentiation is a potential source of endogenous stem cells in the adult heart.

A replacement heart valve structure including a structure of tissue which is an intact, mammalian heart valve that has been harvested and treated to preserve it. A conventional fabric sleeve is typically disposed concentrically around the outside of the tissue structure. A support structure is included to facilitate implanting the heart valve by somewhat increasing the stability of the heart valve structure, but without unduly rigidifying it. An annular sewing cuff may be added adjacent the blood inflow end of the valve structure to facilitate making the annular suture line that is required at that end.

A method for treating cardiac fibrosis resulting from injury of a mammalian heart is described comprising the step of contacting a therapeutically effective amount of relaxin and/or an LGR7 activating agent with cardiac cells following the injury in an amount sufficient to reduce the fibrosis. Also described are methods for protecting the heart following an ischemic event, inhibiting the proliferation of activated fibroblasts and antagonising collagen secretion or deposition in a mammalian heart.

In one embodiment, the present invention is a method of positioning in a mammalian heart of a patient a blood pump including an inflow cannula, a pump housing and an outflow cannula, the method including forming an incision in a low-pressure location on the heart wall; passing the outflow cannula of the blood pump through the incision and into a left ventricle of a heart; positioning a tip of a guidewire into an aorta, distal to an aortic valve; advancing the tip through the aortic valve and into the left ventricle; connecting the tip to the outflow cannula; pulling the blood pump with the guidewire to advance at least a portion of the outflow cannula through the aortic valve and into the aorta; securing the blood pump to the heart, the aorta, or both; disconnecting the tip from the blood pump; and removing the guidewire from the patient.

The present disclosure relates to a method and a device for treating heart failure by normalizing elevated blood pressure in the left and right atria of a heart of a mammal. The present disclosure includes methods for creating and maintaining an opening in the atrial septum. Tools for making an opening and enlarging the opening are also disclosed. Use of the techniques and tools described herein prolongs the patency of an intra-atrial pressure relief opening.

The present invention provides methods of identifying an incidence of ischemia in mammalian tissue, particularly mammalian heart tissue. Further, a method of reducing apoptosis in mammalian tissue, preferably heat tissue, is provided. These methods involve measuring and comparing the gene expression levels of both apoptosis-specific eIF-5A and proliferating eIF-5A and correlating an incidence of ischemia when the expression level of apoptosis-specific eIF-5a is higher than proliferating eIF-5A. In the method of reducing apoptosis in mammalian tissue, there is provided an agent that inhibits expression of apoptosis-specific eIF-5A. Preferred agents are antisense oligonucleotides to human apoptosis-specific eIF-5A.

The present invention is in the fields of lipid metabolism and dietary supplementation and provides methods and compositions to improve heart health of a mammal by orally administering stearidonic acid and related compounds to the mammal. The improved heart health is evidenced by the enrichment of cardiac tissue with eicosapentaenoic acid (20:5, ω3) and docosapentaenoic acid (22:5, ω3) following the administration. Also provided are methods for promoting a stearidonic acid containing product by advertising its heart health benefits.

The invention relates to pharmaceutical compositions comprising 5-Methoxytryptamine or a salt thereof for the prevention and/or treatment of mammalian cardiac tissue damage. 5-Methoxytryptamine and the salts thereof act as free radical scavengers in the prevention and/or treatment of mammalian cardiac tissue damage mediated by free oxygen radicals.

The invention relates to new compositions comprising an aldosterone antagonist according to a particular posology for the treatment of heart failure in non-human mammal animals.

Methods and materials for high-resolution three-dimensional imaging of mammalian tissues, such as heart and intestine, are described. Both methods of tissue preparation for imaging and methods of imaging are described, as well as kits comprising materials and media for use in the methods.

The present invention finds that PI3-K inhibitor and MAPK inhibitor can obviously improve heart failure cardiac function of mammal, also finds that the combined application of PI3-K inhibitor, MAPK inhibitor and medicine rh NRG for curing heart failure of mammal can obviously improve heart failure cardiac function of mammal, they have synergistic action. Said invention also provides a method for preventing, curing and delaying heart disease of mammal by using PI3-k inhibitor and MAPK inhibitor and it's composite.

This intention relates to new compounds and their pharmaceutical use, and to the pharmaceutical use of known compounds, which compounds inhibit certain transmembrane potassium currents in the atrium of the heart of a mammal without significantly affecting other ion channels, for the treatment of heart disease particularly atrial fibrillation. The invention also relates to pharmaceutical compositions comprising such compounds.

There is provided piezoelectric devices for restoring normal contraction rhythms of a heart, or for pacing a heart, comprising a housing, a piezoelectric generator seated within the housing and having first and second electrical conductors wherein the first conductor is connected to an electrically conducting portion of the housing, an electrically conductive skin contact electrode wherein the electrode is electrically insulated from the conducting portion of the housing and is connection with the second conductor, and an actuator for actuating the piezoelectric generator to generate an electrical current in response to stimuli from a user. There is further provided methods for restoring normal contraction rhythms of a heart in cardiac arrest, or for pacing a heart, comprising the administering an electric shock from a piezoelectric device to the chest area of a mammal proximal the heart. The use of a piezoelectric device for such functions is also provided.

A method, system and device for monitoring and treating conditions of a mammalian heart, among which may include bradyarrhythmias, tachyarrhythmias and heart failure, the device being configured as a pacemaker that harvests energy as it implements the pacemaker functions to treat and monitor conditions of the heart. The pacemaker has a case, electrical circuitry sealed within the case, an electrode that is electrically coupled to the electrical circuitry, and embodiments may include a microelectromechanical system (MEMS) for harvesting and converting the kinematic energy of the heart into electrical energy. Embodiments provide receivers at locations of the heart which sense heart activity and are controlled with pacing circuitry to deliver electrical impulses at locations and time intervals to replicate the contractions of a normal functioning heart. Further embodiments provide a multi-part pacemaker where case-connectable electrode part may be implanted separately from the case part.