10 results about "Proarrhythmia" patented technology

Arrhythmogenic cardiomyopathy (ACM) is a familial heart disease characterized by progressive myocardial fibrofatty infiltration. Compositions in the treatment of fibrofatty accumulation and its pathogenesis in ACM include activators of glycosphingolipid (GSL) glycosyltransferase, β-1,4-galactosyltransferase- V (β-1,4-GalT-V).

An example method includes storing reconstructed electrophysiological data sets for at least two baseline time intervals and at least one modulation time interval. The electrophysiological data sets are representative of electrophysiological signals reconstructed at locations across a respective surface of interest within a patient's body based on non-invasively measured electrophysiological signals for respective time intervals. The modulation time interval can overlap with modulating an arrhythmia or arrhythmogenic activity. The method can also include computing dominant frequency maps from the electrophysiological signals reconstructed for at least two baseline data sets and the at least one modulation data set. The method can also include analyzing the dominant frequency maps to determine an indication of dominant frequency stability across at least a portion of the surface of interest.

To provide methods for forming mature cardiomyocytes.SOLUTION: Disclosed herein are methods of using a cell-derived extracellular matrix derived in-vitro from cells isolated from amniotic fluid (AFC-ECM) for the maturation of immature cardiomyocytes derived from human induced pluripotent stem cells (immature hiPSC-CMs) in culture, forming mature cardiomyocytes. Also disclosed herein is a cell construct comprising a monolayer of these mature cardiomyocytes on an AFC-ECM useful for cardiotoxicity and / or proarrhythmic screening assays of drug compounds. Also disclosed herein are methods for determining the cardiotoxicity and / or proarrhythmic effect of a drug compound in vitro using such cell constructs.SELECTED DRAWING: None

A medical probe can include electrodes for ablation and sensing proximity to tissue and / or monitoring electrical signals within the cardiovascular system to identify aberrant conductive tissue sites that are responsible for an arrhythmia. The electrodes can be oriented on an end effector assembly, such as a basket assembly, such that one side of an electrode is positioned to contact tissue and the opposite side is inhibited from contacting tissue. To enable both efficient delivery of energy as well as high sensitivity for ECG sensing an impedance reducing coating can be positioned on the tissue contacting side and an impedance increasing coating can be applied on the opposite side. The impedance increasing coating of an IRE electrode can be thin enough to allow energy to be delivered through the coating during ablation. An RF electrode an have sufficient mass to carry electrical energy for thermal ablation.

The present invention relates to compositions, methods, and devices for preventing irregular electromechanical waves in the myocardium that lead to pathological conditions as arrhythmia. In particular, the invention relates to compositions and methods to increase the conductivity of the myocardium to restore an impairment of the electrical conduction system of the heart. To that end substances with high conductivity, as carbon nanotube suspensions or metal nanowire suspensions, are injected in the myocardium at closely adjacent locations on circular or open lines or are introduced in patches of cardiomyocytes that are subsequently placed on the myocardium.

A locator assembly (100) for determining a location of an arrhythmogenic foci (632) in or near a heart (101). The locator assembly (100) having a longitudinal axis (100a) and a circumference (100c). The locator assembly (100) includes a device body (112) and a plurality of components that are coupled to the device body (112). The plurality of components are distributed about the longitudinal axis (100a) and the circumference (100c). The device body (112) is movable between (i) a contracted state wherein the device (112) body is contracted, and (ii) an expanded state wherein the device body (112) is expanded outwardly from the contracted state so that the device body (112) has an increased circumference (100c).

The present application relates to the technical field of genetic engineering, in particular to a kind of gene medicine for treating PNPLA2 mutation arrhythmogenic cardiomyopathy and its preparation method and application.The effective component of gene medicine provided in the present application includes shuttle plasmid;The shuttle plasmid includes AAV9 carrier and PNPLA2 gene.The present application delivers normal PNPLA2 gene by AAV9 carrier, repairs the lipid metabolism disorder caused by mutation, reduces the fat deposition in myocardium, and then improves the pathological changes of ACM.By restoring the function of PNPLA2 gene, the process of myocardial fibrosis can be effectively inhibited, and the heart function can be improved.The present application uses myocardial specific promoter cTnT to ensure that PNPLA2 gene is only expressed in myocardium, so as to improve the targeting of gene therapy, and avoid the side effects caused by systemic expression.This strategy can effectively reduce the side effects of gene therapy, and ensure the accuracy and safety of treatment.

Provided herein are methods and compositions for plakophilin-2 gene therapy for treating heart diseases such as arrhythmogenic right ventricular cardiomyopathy (ARVC) or arrhythmogenic cardiomyopathy (ACM).

This invention provides a method for treating or preventing human cardiomyopathy. [Solution] A method for treating or preventing cardiomyopathy in a human subject, comprising delivering a therapeutic dose of a gene therapy vector to cardiomyocytes of the human subject, wherein the gene therapy vector comprises a nucleic acid sequence encoding placofilin-2 (PKP2) or a functional variant thereof.

This disclosure relates, in general terms, to methods and agents for treating arrhythmogenic cardiomyopathy (ACM). More specifically, this disclosure relates to the use of CD14 antagonist antigen-binding molecules for treating ACM, including mitigation or inhibition of the development of undesirable cardiac remodeling and improvement of cardiac function, including improvement of ventricular and atrial function, in patients with ACM.