109 results about "Left Ventricle Remodeling" patented technology

Methods and systems for closing an opening or defect in tissue, closing a lumen or tubular structure, cinching or remodeling a cavity or repairing a valve preferably utilizing a purse string or elastic device. The preferred devices and methods are directed toward catheter-based percutaneous, transvascular techniques used to facilitate placement of the devices within lumens, such as blood vessels, or on or within the heart to perform structural defect repair, such as valvular or ventricular remodeling. In some methods, the catheter is positioned within the right ventricle, wherein the myocardial wall or left ventricle may be accessed through the septal wall to position a device configured to permit reshaping of the ventricle. The device may include a line or a plurality of anchors interconnected by a line. In one arrangement, the line is a coiled member.

Methods of and devices for restoring the normal geometry of a heart, including but not limited to the structures supporting the atrioventricular valves. The techniques and devices described herein operate on the principle of displacement, both active and passive, to reverse cardiac remodeling and limit ischemic atrioventricular valve regurgitation.

Methods and systems for closing an opening or defect in tissue, closing a lumen or tubular structure, cinching or remodeling a cavity or repairing a valve preferably utilizing a purse string or elastic device. The preferred devices and methods are directed toward catheter-based percutaneous, transvascular techniques used to facilitate placement of the devices within lumens, such as blood vessels, or on or within the heart to perform structural defect repair, such as valvular or ventricular remodeling. In some methods, the catheter is positioned within the right ventricle, wherein the myocardial wall or left ventricle may be accessed through the septal wall to position a device configured to permit reshaping of the ventricle. The device may include a line or a plurality of anchors interconnected by a line. In one arrangement, the line is a coiled member.

This is a support device that prevents, reduces, and delays remodeling of diseased cardiac tissue, and also decreases the impact of such remodeling on collateral tissue is disclosed. The invention further reinforces abnormal tissue regions to prevent over-expansion of the tissue due to increased afterload and excessive wall tension. As a result, the support device prevents phenomenon such as systolic stretch from occurring and propagating. The support structure maintains and restores diastolic compliance, wall motion, and ejection fraction to preserve heart functionality. As such, the support device prevents and treats cardiomyopathy and congestive heart failure.

An apparatus and method for assessing myocardial wall stress is disclosed. The method may be used in conjunction with electro-stimulatory therapy for preventing or reversing ventricular remodeling. In such therapy, one or more stimulatory pulses are delivered to the heart such that a stressed region of the myocardium is pre-excited relative to other regions, thereby subjecting the stressed region to a lessened preload and afterload during systole. The unloading of the stressed myocardium over time effects reversal of undesirable ventricular remodeling.

The present invention provides a drug for at least one of prevention and treatment of cardiac failure capable of suppressing cardiac depression and the onset of cardiac failure in ventricular remodeling, and a method for screening the drug. The drug for at least one of prevention and treatment of cardiac failure of the present invention contains a compound that inhibits a functional expression of ASK1 protein in a cardiomyocyte as an active ingredient, and a method for screening a drug for at least one of prevention and treatment of cardiac failure of the present invention includes selecting a medicinal component for at least one of prevention and treatment of cardiac failure from a drug candidate compound by using inhibition of a functional expression of ASK1 protein as an indication. As shown in FIG. 1, if ASK1 protein is removed, for example, the ventricle dilation can be attenuated in ventricular remodeling after myocardial infarction, pressure loading, or the like, which makes it possible to prevent and treat cardiac failure.

An apparatus and method for reversing ventricular remodeling with electro-stimulatory therapy. A ventricle is paced by delivering one or more stimulatory pulses in a manner such that a stressed region of the myocardium is pre-excited relative to other regions in order to subject the stressed region to a lessened preload and afterload during systole. The unloading of the stressed myocardium over time effects reversal of undesirable ventricular remodeling.

An apparatus and method for reversing ventricular remodeling with electro-stimulatory therapy. A ventricle is paced by delivering one or more stimulatory pulses in a manner such that a stressed region of the myocardium is pre-excited relative to other regions in order to subject the stressed region to a lessened preload and afterload during systole. The unloading of the stressed myocardium over time effects reversal of undesirable ventricular remodeling.

The invention discloses a medical cardiac tamponade object and relates to the field of medical instruments. The medical cardiac tamponade object comprises a supporting frame and a base. The supporting frame is composed of a plurality of developing units, a plurality of fixing tips, a plurality of umbrella-rib-shaped sectional rods and a plurality of cambered surfaces. Every two adjacent umbrella-rib-shaped sectional rods are connected through one cambered surface to form the inverted-umbrella-shaped supporting frame, wherein the umbrella periphery of the supporting frame is turned outwards with the outward-turning angle ranging from 0 degree to 90 degrees. One end of each umbrella-rib-shaped sectional rod is connected with one corresponding fixing tip erected on the umbrella periphery of the supporting frame. Each fixing tip is provided with one developing unit. All the umbrella-rib-shaped sectional rods and all the fixing tips are coated with polymer separation films respectively. The bottom of the supporting frame is connected with the base. The bottom of the base is a plane. Being in the inverted umbrella shape, the medical cardiac tamponade object can effectively reduce the ventricular volume and reduce ventricular tension, thereby improving ventricular remodeling and cardiac functions of a patient.

The present invention relates to method of reversing left ventricle remodeling by combined administration of therapeutically effective amounts ranolazine and at least one co-remodeling agent, which may be an ACE inhibitor, an ARB, or a beta-blocker. The method finds utility in the treatment of heart failure. This invention also relates to pharmaceutical formulations that are suitable for such combined administration.

The invention discloses an application of a traditional Chinese medicine composition in the preparation of a medicine for treating dilated cardiomyopathy. The traditional Chinese medicine composition of the invention achieves the aim of treating dilated cardiomyopathy by improving the heart function effectively and improving the ventricular remodeling to a certain extent.

An apparatus and method for reversing ventricular remodeling with electro-stimulatory therapy. A ventricle is paced by delivering one or more stimulatory pulses in a manner such that a stressed region of the myocardium is pre-excited relative to other regions in order to subject the stressed region to a lessened preload and afterload during systole. The unloading of the stressed myocardium over time effects reversal of undesirable ventricular remodeling.

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.

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.

Methods, devices, kits and compositions to treat a myocardial infarction. In one embodiment, the method includes the prevention of remodeling of the infarct zone of the ventricle using a combination of therapies. The method may include the introduction of structurally reinforcing agents. In other embodiments, agents may be introduced into a ventricle to increase compliance of the ventricle. The prevention of remodeling may include the prevention of thinning of the ventricular infarct zone. Another embodiment includes the reversing or prevention of ventricular remodeling with electro-stimulatory therapy. The unloading of the stressed myocardium over time effects reversal of undesirable ventricular remodeling. These therapies may be combined with structurally reinforcing therapies. In other embodiments, the structurally reinforcing component may be accompanied by other therapeutic agents. These agents may include but are not limited to pro-fibroblastic and angiogenic agents.

The invention belongs to the traditional Chinese pharmaceutics field, and relates to an application of traditional Chinese medicine radix scrophulariae to the preparation of a drug for preventing and curing cardiac hypertrophy, hypertrophic cardiomyopathy and chronic heart failure. The invention researches the effect of the cardiac hypertrophy and ventricle reconstruction model of a plurality of mice and rats on the traditional Chinese medicine radix scrophulariae. The experimental results show that the radix scrophulariae water or the alcohol abstracts has evident function for preventing the cardiac hypertrophy, the ventricular remodeling and the chronic heart failure caused by various reasons, the mechanism is obviously related with the excessive activation of the neuroendocrine system such as a suppressing renin-angiotensin-aldosterone system and is related with the functions of blood pressure reduction, heart beat slowing and hemodynamics improvement. The figwort can be used for preparing the drug for preventing the diseases of cardiac hypertrophy, hypertrophic cardiomyopathy and chronic heart failure and for reducing the possibility of the incidence rate of arrhythmia and the sudden death of patients with cardiac hypertrophy, hypertrophic cardiomyopathy and chronic heart failure.

The invention provides methods for (a) reducing mortality associated with heart failure; (b) improving oxygen consumption; (c) treating heart failure; (d) treating hypertension; (e) improving the quality of life in a heart failure patient; (f) inhibiting left ventricular remodeling; (g) reducing hospitalizations related to heart failure; (h) improving exercise tolerance; (j) increasing left ventricular ejection fraction; (k) decreasing levels of B-type natriuretic protein; (l) treating renovascular diseases; (m) treating end-stage renal diseases; (n) reducing cardiomegaly; (o) treating diseases resulting from oxidative stress; (p) treating endothelial dysfunctions; (q) treating diseases caused by endothelial dysfunctions; or (r) treating cardiovascular diseases; in a patient in need thereof, wherein the patient has a Arg389Arg polymorphism and / or a Gly389Gly polymorphism in the beta 1 adrenergic receptor gene, comprising administering to the patient (i) at least one antioxidant compound or a pharmaceutically acceptable salt thereof; (ii) at least one nitric oxide enhancing compound; and (iii) optionally the best current therapy for the treatment of cardiovascular diseases. In one embodiment the antioxidant is a hydralazine compound or a pharmaceutically acceptable salt thereof and the nitric oxide enhancing compound is isosorbide dinitrate and / or isosorbide mononitrate.

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 a device and method for manufacturing an isolating layer in cardiac tamping. The device comprises an assembly device, an umbrella-shaped framework structure, an isolating membrane and reinforcing ribs. The assembly device comprises an upper cover, a lower cover and a plurality of locating bolts. The umbrella-shaped framework structure comprises a plurality of umbrella-rib-shaped joint rods. One ends of the umbrella-rib-shaped joint rods are evenly distributed in the peripheral direction of a base cylinder. The other ends of the umbrella-rib-shaped joint rods extend outwards in a radial mode to form a cone. The isolating membrane covers the inner surface or outer surface of the cone formed by the umbrella-rib-shaped joint rods. The reinforcing ribs are arranged between the umbrella-rib-shaped joint rods and the isolating membrane. The high-molecular isolating membrane and the umbrella-shaped framework structure are combined to form the umbrella-shaped isolating layer by heating, pressing and fusing the high-molecular reinforcing ribs. The cardiac tamping effectively isolates the ventricular volume via the isolating layer, and therefore the ventricular volume is effectively reduced, the ventricular tension is reduced, and then ventricular remodeling and the cardiac function of patients are improved.

A method for treating a heart valve involves introducing a delivery catheter into a target ventricle of a heart, the delivery catheter having a coil device disposed at least partially therein, deploying a distal end of the coil device from the delivery catheter, navigating the distal end of the coil device behind a plurality of trabeculae carneae features associated with an inner wall of the ventricle to form one or more coils, and tightening the one or more coils to reduce a diameter of the target ventricle.

The invention belongs to the pharmaceutical field of traditional Chinese medicine, relating to application of phenylpropanoid component-Angoroside C in traditional Chinese medicine of radix scrophulariae to preparing a medicament for preventing and treating myocardial hypertrophy, ventricular remodeling and congestive heart failure. The function of the Angoroside C is researched by utilizing a rat ventricle reconstruction model caused by abdominal aortic coarctation. Experimental results show that the Angoroside C improves symptoms of myocardial hypertrophy and ventricular remodeling and biological functions of myocardium through inhibiting related stimulating and mediated factors resulting in myocardial hypertrophy and ventricular remodeling. The Angoroside C has obvious inhibiting effects on cardiomyocyte hypertrophy and interstitial collagen remodeling, can balance myocardial collagen fiber metabolism, can be used for preparing the medicament for preventing and treating myocardial hypertrophy and ventricular remodeling and can further prevent or delay occurrence and development of heart failure and reduce the incidence rate of arrhythmia, heart failure and sudden death of a patient suffering from myocardial hypertrophy and ventricular remodeling. Furthermore, the invention discloses a novel process for extracting and separating the Angoroside C from radix scrophulariae.

A biologically engineered stent for treating patients suffering from acute myocardial infarction / ischemia. The stent is inserted in a vessel upstream to and proximal the damaged muscle / ischemic area. The stent elutes Stromal Derived Factor (SDF1) / CXCR4 complex and / or Vascular Endothelial Growth Factor (VEGF) to attract autologous stem cell for the repair of damaged myocardium or tissues and inducing vascularization (creation of collateral vessels) to the ischemic area. The SDF1 / CXCR4 acts as a homing mechanism for stem cells. Stem cell mobilizing agents such as Gm-CSF, GCSF and Plerixafor, as a CXCR4 blocker, may be added systemically to assist in stem mobilization. A protocol consisting of multiple doses of Gm-CSF or GCSF may be given in order to mobilize stem cells from the patient. Optionally, stem cells may be injected into the patient. The treatment stimulates repair and improves survival of damaged myocardium and prevents ventricular remodeling.

The invention discloses application of chaetocin in preparation of drugs for preventing and treating hypoxic pulmonary hypertension. Test researches show that when the chaetocin is used for preparingthe drugs for preventing and treating hypoxic pulmonary hypertension, pulmonary arterial pressure can be reduced remarkably, pulmonary vascular remodeling caused by chronic hypoxia is improved, pressure load of the ventriculus dexter is relieved, cardiac hypertrophy and ventricular remodeling are improved, heart failure is delayed, it shows great effect of preventing and treating hypoxic pulmonaryhypertension, in an experiment process, obvious adverse reactions are not seen, and the drugs are expected to be developed into a new-generation safe and effective drug for preventing and treating pulmonary hypertension.

The invention relates to a prognosis model for evaluating tumor immunotherapy related myocarditis based on sST2 and application thereof, and belongs to the technical field of biomedical detection. Theinvention provides a model for evaluating prognosis of tumor immunotherapy related myocarditis based on sST2. Immune myocarditis is a few but severe adverse reaction in tumor immunotherapy, and sST2is a novel heart marker and participates in the process of cardiac dysfunction caused by cardiac hypertrophy, myocardial fibrosis, ventricular remodeling and the like. The invention provides an sST2-based model for evaluating tumor immunotherapy related myocarditis prognosis, which is beneficial to providing reference information for disease prognosis of immunotherapy related myocarditis patientsso as to assist in clinically formulating a reasonable diagnosis and treatment scheme.

The object of the present invention is to provide a pharmaceutical composition for treating non-ischemic heart failure caused by exacerbation of cardiomyopathy. The long-term administration of a colony-stimulating factor ameliorates progressive myocardial fibrosis, left ventricular remodeling and heart failure.