137 results about "Post myocardial infarction" patented technology

A composition for promoting repair of damaged tissues, being a cross-linked alginate solution, which can be maintained in liquid form indefinitely (under constant conditions) and only gels in vivo. This cross-linked alginate solution is an ideal material to be used for tissue repair. Injection of said material into cardiac tissue post-myocardial infarct induced tissue regeneration. The invention provides such injectable solution, as well as compositions and method of preparation thereof. The invention also provides various methods and uses of the cross-linked alginate solution, for cardiac tissue regeneration, induction of neo-vascularization, enhancing SDF-1 expression and guiding stem cell chemotaxis, among others. A kit for tissue repair is also provided.

A noninvasive or minimally invasive treatment of infarct areas of the heart with High Intensity Focused Ultrasound (HIFU) emitted without respect to the timing or phase of the cardiac cycle, intended to remodel cardiac tissue by inducing angiogenesis and / or the formation of myocytes to improve cardiac function.

A cardiac rhythm management (CRM) system provides for post-myocardial infarction (MI) therapy with closed-loop control using one or more ultrasound transducers sensing one or more ultrasound signals indicative of cardiac dimensions. Cardiac size parameters are produced using the one or more ultrasound signals to represent, for example, cardiac chamber diameter, cardiac chamber volume, cardiac wall thickness, infarct size, and degree of change in any of these parameters over time or between measurements. In various embodiments, such cardiac size parameters provide for titration, safety check, and acute optimization of the post-MI therapy.

The present invention relates to the identification of miRNAs that are involved in heart failure and the process of post-myocardial infarction remodeling in heart tissue. Modulation of these identified miRNAs as a treatment for myocardial infarction, cardiac remodelling, and heart failure is described.

Compositions, methods of manufacture and methods of treatment for post-myocardial infarction are herein disclosed. In some embodiments, the composition includes at least two components. In one embodiment, a first component can include a first functionalized polymer and a substance having at least one cell adhesion site combined in a first buffer at a pH of approximately 6.5. A second component can include a second buffer in a pH of between about 7.5 and 9.0. A second functionalized polymer can be included in the first or second component. In some embodiments, the composition can include at least one cell type and / or at least one growth factor. In some embodiments, the composition(s) of the present invention can be delivered by a dual bore injection device to a treatment area, such as a post-myocardial infarct region.

The invention provides methods for reducing the incidence and / or severity and / or delaying the onset of heart dysfunction / failure and improving overall survival through the use of remote ischemic per-conditioning and post-conditioning.

Methods and compositions for treating post-myocardial infarction damage are herein disclosed. In some embodiments, a carrier with a treatment agent may be fabricated. The carrier can be formulated from a bioerodable, sustained-release substance. The resultant loaded carrier may then be suspended in at least one component of a two-component matrix system for simultaneous delivery to a post-myocardial infarction treatment area.

Methods and compositions for treating post-myocardial infarction damage are herein disclosed. In some embodiments, a carrier with a treatment agent may be fabricated. The carrier can be formulated from a bioerodable, sustained-release substance. The resultant loaded carrier may then be suspended in at least one component of a two-component matrix system for simultaneous delivery to a post-myocardial infarction treatment area.

The invention relates to a method for preparing a chitosan-silk fibroin composite nano-fiber multifunctional patch for promoting myocardial tissue regeneration and monitoring stem cells. The method comprises the following steps: preparing a cellulose nano-fiber basal plate by an electrostatic spinning technology; alternately assembling positively charged chitosan (CS) and negatively charged silk fibroin (SF) to the surface of nano-fibers layer by layer by adopting a layer-by-layer assembly technique, and assembling 5.5-10.5 layers to form a CS-SF composite nano-fiber membrane; and planting seed cells of adipose tissue-derived stromal cells or cardiac progenitor cells labeled by green fluorescent protein and firefly luciferase on the surface of the CS-SF composite nano-fiber membrane, preparing the patch by three-dimensional co-culture. The patch has excellent biocompatibility, can be used as a cell vector, has an effect of resisting oxidative stress to improve the survival rate and treatment efficiency of stem cells, and is capable of evaluating the number, distribution and function states of transplanted stem cells, effectively preventing occurrence of post-myocardial infarction heart failure and reducing the death rate of ischemic cardiomyopathy.

A method of treating chronic post-myocardial infarction including helical needle transendocardial delivery of autologous bone marrow (ABM) mononuclear cells around regions of hypo or akinesia in chronic post-myocardial infarction (MI) patients. The treatment is safe and improves ejection fraction (EF).

The invention relates to application of E1A-simulated gene cellular repressor (CREG) protein, in particular to application of CREG protein or active fragment thereof in preparation of drug used for preventing and / or treating acute myocardial infarction, heart failure after acute myocardial infarction and / or ventricular remodeling after the same. The invention further relates to application of recombinant vector or recombinant cell expressing the CREG protein or the active fragment thereof in preparation of the drug used for preventing and / or treating acute myocardial infarction, heart failure after acute myocardial infarction and / or ventricular remodeling after the same.

Methods and compositions for treating post-myocardial infarction damage are herein disclosed. In some embodiments, a carrier with a treatment agent may be fabricated. The carrier can be formulated from a bioerodable, sustained-release substance. The resultant loaded carrier may then be suspended in at least one component of a two-component matrix system for simultaneous delivery to a post-myocardial infarction treatment area.

Certain embodiments of the present invention provide systems and methods for ablating non-viable cardiac tissue. In an embodiment, the method may include locating non-viable cardiac tissue utilizing an electronic medical image. The method may also include locating non-viable cardiac tissue utilizing an ultrasound unit, wherein a contrast agent is used to characterize the non-viable cardiac tissue. The method may also include guiding a catheter to the location of the non-viable cardiac tissue according to the imaging of the ultrasound unit. The method may also include ablating the non-viable cardiac tissue. The ablating of the non-viable cardiac tissue may include cauterizing the non-viable cardiac tissue, cyroablating the non-viable cardiac tissue, or include radiofrequency ablation. The method may also include attempting to locate the non-viable cardiac tissue utilizing an electronic medical image after ablating the non-viable cardiac tissue.

The invention discloses the application of a Chinese traditional medicinal combination in preparing the medicaments used for curing myocardial infarction. The Chinese traditional medicinal combination inhibits the activity of matrix metalloproteinase, the damage to the heart support structure, the progressive ventricular dilatation, and the change of gene phenotype of the heavy chain of myosin of the cardiac muscle during the reversion of the restructuring of the cardiac muscle, thus inhibiting the restructuring of the cardiac muscle after myocardial infarction, improving the function of heart after myocardial infarction so that sufferers of myocardial infarction benefit from the Chinese traditional medicinal combination clinically, or the prognoses of myocardial infarction is improved.

The invention discloses an active-oxygen-responsive degradable polyurethane heart patch for myocardial infarction repair and a preparation method thereof. The heart patch comprises a cast membrane, an electrospun fibrous membrane and a porous membrane, and polyurethane is active-oxygen-responsive degradable polyurethane containing thioketal bonds. The invention also provides a method for preparing the heart patch. The preparation method is simple and is convenient to operate, active-oxygen polyurethane films with different pore sizes and porosities can be prepared as required, and the active-oxygen polyurethane films have good mechanical properties, oxidation resistance, degradability and biocompatibility. Under the condition that functional cells or factors are not added into the polyurethane patch, cardiac functions can be effectively recovered after myocardial infarction, and the left ventricle remodeling and fibrosis degree after myocardial infarction can be inhibited; and after the cells or active factors are added, the treatment effect can be further improved. The active-oxygen-responsive degradable elastic polyurethane heart patch disclosed by the invention is simple in preparation method and has a good application prospect.

The invention discloses an application of LncRNA XLOC_075168 to preparation of medicines for promoting angiogenesis. Overexpressing and silencing of lncRNA XLOC_075168 confirm that the lncRNA XLOC_075168 can influence the expression of an ATG7 gene and protein in human umbilical vein endothelial cells, also confirm that the lncRNA XLOC_075168 participates in promoting the proliferation of the human umbilical vein endothelial cells, restraining the apoptosis of the human umbilical vein endothelial cells and promoting the canaliculization of the human umbilical vein endothelial cells, and further illustrate that the lncRNA XLOC_075168 can possibly participate in promoting the angiogenesis after miocardial infarction. Therefore, the lncRNA XLOC_075168 or a reagent for promoting expression ofthe lncRNA XLOC_075168 can be used for preparing medicines for promoting angiogenesis and can particularly be used for preparing medicines for promoting angiogenesis after miocardial infarction.

The invention relates to the combination of inhibitors of phosphodiesterase 1 (PDE1) and inhibitors of Neprilysin (NEP) useful for the treatment of certain cardiovascular diseases or related disorders, e.g., hypertension, congestive heart disease, and post-myocardial infarction. In another embodiment, the invention relates to the combination of inhibitors of PDE1 and inhibitors of NEP for the treatment of diseases or disorders characterized by disruption of or damage to various cGMP / PKG mediated pathways in the cardiovascular system (e.g., in cardiac tissue or in arterial smooth muscle).

The present invention relates to pharmaceutical uses of a Na<+>-coupled HCO3< > transporter (NBC1) N-cyano amide sulfide inhibitor S0859, and provides uses of a Na<+>-coupled HCO3< > transporter (NBC1) N-cyano amide sulfide inhibitor S0859 in preparation of heart failure treating drugs. According to the present invention, the results prove that the inhibitor S0859 can regulate the intracellular calcium ion homeostasis after myocardial infarction, improve ventricular remodeling, and inhibit intracellular calcium overload so as to inhibit ventricular remodeling, such that the invention can provide a new heart failure treating drug so as to effectively delay heart failure and ventricular remodeling caused by myocardial infarction.

The invention discloses application of an inhibitor of LncRNA XLOC_110286 in preparation of medicine for promoting angiogenesis. It is confirmed that the LncRNA XLOC_110286 is involved in inhabitationof proliferation of human umbilical vein endothelial cells through overexpression and silence of the LncRNA XLOC_110286, apoptosis of the human umbilical vein endothelial cells are promoted, migration of the human umbilical vein endothelial cells is inhibited, formation of human umbilical vein endothelial cell canaliculi is inhabited, and it is further stated that the LncRNA XLOC_110286 may has the inhibiting effect on angiogenesis after infarct. Thus, the inhibitor of the LncRNA XLOC_110286 can be used for preparation of the medicines for promoting angiogenesis. Specifically, the inhibitor of the LncRNA XLOC_110286 can be used for preparation of medicine for promoting angiogenesis after myocardial infarction.

The present invention involves the use of transcription factors including Tbx5, Mef2C, Hand2, myocardin and Gata4 to reprogram cardiac fibroblasts into cardiomyocytes, both in vitro and in vivo. Such methods find particular use in the treatment of patients post-myocardial infarction to prevent or limit scarring and to promote myocardial repair.

The present disclosure describes the role for miR-322(424) / 503 in the differentiation of cardiac precursor cells. Thus, the use of these molecules in the programming of resident stem / progenitor cells into cardiomyocytes, both in vitro and in vivo. Such methods find particular use in the treatment of patients post-myocardial infarction to prevent or limit scarring and to promote myocardial repair.

There is provided the use of a GALR2-specific agonist in the preparation of a medicament for the prevention or treatment of brain injury, damage or disease, wherein the brain injury or damage is caused by one of: embolic, thrombotic or haemorrhagic stroke; direct or indirect trauma or surgery to the brain or spinal cord; ischaemic or embolic damage to the brain during cardiopulmonary bypass surgery or renai dialysis; reperfusion brain damage following myocardial infarction; brain disease; chemical damage as the result of excess alcohol consumption or administration of chemotherapy agents for cancer treatment; radiation damage; or immunological damage as the result of bacterial or virai infection. The brain disease may be one of Alzheimer's Disease, Parkinson's Disease, Multiple Sclerosis or variant Creutzfeld Jacob Disease.

The invention is directed to methods for diagnosing reperfusion / non-reperfusion hemorrhage and predicting cardiac arrhythmias and sudden cardiac death in subjects comprising using imaging techniques to detect regional iron oxide deposition. The invention also provides treatment methods for subject at increased risk of sudden cardiac death.

The invention discloses an application of a medicine of anthropogenic adiponectin spherical fragment in curing diabetic-anemic cardiopathy. A gene sequence of the anthropogenic adiponectin spherical fragment obtained by the invention absolutely accords with a known gene sequence, and compared with the full-length adiponectin, the hydrolyzed anthropogenic adiponectin spherical fragment has stronger biological activity, fast reaction after dosage, good bioavailability and better clinic application prospect, especially when the diabetes patient receives a recanalization treatment after a myocardial infarction, the anemically myocardial damage of the diabetes patients can be eased by the exogenetic dosage.

The invention discloses application of EMD638683 in protection of the heart suffering from acute myocardial infarction. The invention provides application of EMD638683 in preparation of products having the following functions: 1) prevention and / or treatment of myocardial infarction of animals; 2) prevention and / or treatment of heart failure caused by myocardial infarction of animals; and 3) inhibition of the expression of SGK1 protein in cardiac muscle tissue after myocardial infarction of animals. Experimental results of the invention prove that EMD638683 has treatment effect on mice with myocardial infarction, and experimental data is provided for clinical application of EMD638683 in treatment of myocardial infarction. The EMD638683 is of important theoretical significance to research on and development of medicines used for preventing and treating heart failure caused by myocardial infarction and has good application prospects.

The present invention relates to compounds of Formula (Ia) and pharmaceutical compositions thereof that modulate the activity of the beta-3 adrenergic receptor. Compounds of the present invention and pharmaceutical compositions thereof are directed to methods useful in the treatment of a beta-3 adrenergic receptor-mediated disorder, such as, heart failure; cardiac performance in heart failure; mortality, reinfarction, and / or hospitalization in connection with heart failure; acute heart failure; acute decompensated heart failure; congestive heart failure; severe congestive heart failure; organ damage associated with heart failure (e.g., kidney damage or failure, heart valve problems, heart rhythm problems, and / or liver damage); heart failure due to left ventricular dysfunction; heart failure with normal ejection fraction; cardiovascular mortality following myocardial infarction; cardiovascular mortality in patients with left ventricular failure or left ventricular dysfunction; left ventricular failure; left ventricular dysfunction; class II heart failure using the New York Heart Association (NYHA) classification system; class III heart failure using the New York Heart Association (NYHA) classification system; class IV heart failure using the New York Heart Association (NYHA) classification system; LVEF<40% by radionuclide ventriculography; LVEF≤35% by echocardiography or ventricular contrast angiography; and conditions related thereto.