135 results about "Post myocardial infarction" patented technology

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.

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.

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.

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.

The invention discloses an application of an LncRNA XLOC_057528 inhibitor to preparation of medicines for promoting blood vessel regeneration. Overexpression and silence of lncRNA XLOC_057528 confirmthat lncRNA XLOC_057528 can influence expression of a p53 gene and protein to human umbilical vein endothelial cells, and besides, confirm that the lncRNA XLOC_057528 participates in promotion of proliferation of the human umbilical vein endothelial cells, restraining of apoptosis of the human umbilical vein endothelial cells, and restraining of canaliculization of the human umbilical vein endothelial cells, and further confirm that the lncRNA XLOC_057528 can participate in restraining of blood vessel regeneration after miocardial infarction. Therefore, the lncRNA XLOC_057528 inhibitor can beused for preparing the medicines for promoting blood vessel regeneration, and particularly the lncRNA XLOC_057528 inhibitor can be used for preparing the medicines for promoting blood vessel regeneration after miocardial infarction.