21 results about "Proarrhythmia" patented technology

A method for determining a location of an arrhythmogenic focus 632 in or near a heart 101 includes positioning a locator assembly 100 in the heart 101, the locator assembly 100 including a plurality of electrodes 102 for receiving electrical signals from the heart 101, generating a first signal array 733 from the electrical signals received by the plurality of electrodes 102 to determine an actual location of the arrhythmogenic focus 632, artificially stimulating the heart 101 based on the actual location determined by the first signal array 733 to generate a second signal array 735, and ascertaining the actual location of the arrhythmogenic focus 632 by comparing the first signal array 733 to the second signal array 735. In some embodiments, the locator assembly 100 includes a plurality of bipolar electrodes 102.

A method includes applying pacing to ventricle of heart of patient from multiple electrode locations over circumference of multi-electrode catheter area. Cardiac signals are received in response to the pacing. A correlation algorithm is applied to the received signals to calculate a plurality of correlations among the received signals. Based on calculated correlations, the area is checked if it includes an arrhythmogenic location identified with predefined sufficient spatial resolution. If the resolution is insufficient, sub-area to pace is defined. Subsequent pacing is applied to ventricle from multiple electrode locations over a circumference of the sub-area. Subsequent cardiac signals are received in response to the subsequent pacing. Subsequent correlations among the subsequent received signals are calculated. Based on the subsequent correlations, it is ascertained whether the arrhythmogenic location is found in the sub-area. If an arrhythmogenic location is found with sufficient spatial resolution, the identified arrhythmogenic location is indicated to user.

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).

Disclosed is a method of identifying a subject who has or is predisposed to cardiac arrhythmia, the method comprising: a. obtaining a sample from the subject; and b. testing nucleic acid from the sample for the presence or absence of an allele at a single nucleotide polymorphism (SNP) which is CYP2J2*7; wherein the presence of the allele indicates that the subject has or is predisposed to cardiac arrhythmia.

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.

The invention relates to identification of ventricular tachycardia (VT) targets by selective pacing. A method includes applying pacing to a ventricle of a heart of a patient from a plurality of electrode locations on a circumference of a multi-electrode catheter region. A cardiac signal is received in response to the pacing. A correlation algorithm is applied to the received signals to calculate a plurality of correlations between the received signals. Based on the calculated correlation, it is checked whether the region includes an arrhythmic location identified at a predefined sufficient spatial resolution. If the resolution is insufficient, the sub-region to be paced is defined. Subsequent pacing is applied to the ventricle from a plurality of electrode locations on the circumference of the sub-region. A subsequent cardiac signal is received in response to the subsequent pacing. A subsequent correlation between the subsequently received signals is calculated. Based on the subsequent correlations, it is determined whether to find the arrhythmic location in the sub-region. If an arrhythmic location is found with sufficient spatial resolution, the identified arrhythmic location is indicated to the user.

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.

Systems are provided for generating data representing electromagnetic states of a heart for medical, scientific, research, and / or engineering purposes. The systems generate the data based on source configurations such as dimensions of, and scar or fibrosis or pro-arrhythmic substrate location within, a heart and a computational model of the electromagnetic output of the heart. The systems may dynamically generate the source configurations to provide representative source configurations that may be found in a population. For each source configuration of the electromagnetic source, the systems run a simulation of the functioning of the heart to generate modeled electromagnetic output (e.g., an electromagnetic mesh for each simulation step with a voltage at each point of the electromagnetic mesh) for that source configuration. The systems may generate a cardiogram for each source configuration from the modeled electromagnetic output of that source configuration for use in predicting the source location of an arrhythmia.

Disclosed 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 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 are methods for determining the cardiotoxicity and / or proarrhythmic effect of a drug compound in vitro using such cell constructs.

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.

The invention discloses application of a carbon monoxide donor CORM2 in preparation of a medicine for treating heart injury caused by myocardial infarction, and belongs to the technical field of biology. The medicine provided by the invention comprises an effective amount of CORM2 and pharmaceutically acceptable auxiliary materials, wherein the pharmaceutically acceptable auxiliary materials comprise a filler, a diluent, an adhesive, a disintegrating agent and an emulsifier; the medicine containing CORM2 can improve the symptoms of myocardial conduction time prolonging, conduction dispersion increasing, heart rate slowing and the like of myocardial infarction patients, can relieve mRNA level rising of TNF-alpha, IL-1beta and IL-6 caused by myocardial infarction at the same time, can obviously relieve inflammatory response, caused by myocardial infarction, in myocardial tissue of mice, and has a good application prospect. The invention has important clinical guiding significance for treating arrhythmia caused by myocardial infarction, and provides a new way for exploring the development of low-toxicity and high-efficiency anti-arrhythmia drugs.

The present invention provides a drug for treating arrhythmogenic cardiomyopathy that has, as an active ingredient, a gene therapy drug used for delivering a normal gene corresponding to a gene having a gene mutation to myocardial cells of a patient with arrhythmogenic cardiomyopathy caused by a gene mutation, such that a normal protein is caused to be expressed. The present invention also provides pluripotent stem cells established from cells of a patient with arrhythmogenic cardiomyopathy caused by a mutation of a plakophilin-2 gene or a desmoglein-2 gene.

Described herein are methods, devices and systems for classifying an R-wave detection as a false R-wave detection due to T-wave oversensing (TWO) or P-wave oversensing (PWO), by determining whether at least one of first TWO or PWO temporal criteria or second TWO or PWO temporal criteria are met for R-wave detections in a window leading up to an arrhythmic episode detection, and based on an extent of the R-wave detections classified as being false R-wave detections due to TWO or PWO selectively preventing or aborting delivery of therapy intended to treat the arrhythmic episode, selectively preventing transmission by the IMD to an external device of data corresponding to the arrhythmic episode that can be used for diagnostic purposes, or selectively adjusting at least one parameter of the R-wave detection threshold that can be used by the IMD for detecting further R-waves and thereby detecting a further arrhythmic episode.

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.

To provide a method for evaluation of electrical propagation in the heart.SOLUTION: A method includes applying pacing to ventricle of heart of patient from multiple electrode locations over circumference of multi-electrode catheter area. Cardiac signals are received in response to the pacing. A correlation algorithm is applied to the received signals to calculate a plurality of correlations among the received signals. Based on calculated correlations, the area is checked if it includes an arrhythmogenic location identified with predefined sufficient spatial resolution. If the resolution is insufficient, sub-area to pace is defined. Subsequent pacing is applied to ventricle from multiple electrode locations over a circumference of the sub-area. Subsequent cardiac signals are received in response to the subsequent pacing. Subsequent correlations among the subsequent received signals are calculated. Based on the subsequent correlations, it is ascertained whether the arrhythmogenic location is found in the sub-area. If an arrhythmogenic location is found with sufficient spatial resolution, the identified arrhythmogenic location is indicated to user.SELECTED DRAWING: Figure 1

To provide more effective therapies for patients with arrhythmogenic right ventricular cardiomyopathy, and to provide therapies that target the underlying structural nature of the disease.SOLUTION: Provided is a vector for use in a method for treating a structural cardiovascular disease or condition in a subject in need thereof, the method including administering the vector to the subject, the vector encoding a connexin 43 polypeptide sequence operably linked to a promoter that is active in myocardial tissue, and administration of an effective amount of the vector resulting in increased connexin 43 levels in at least a part of the subject's heart.SELECTED DRAWING: None

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.