32 results about "Acute mi" patented technology

A method for differentiating acute myocardial infarction (AMI) from other ECG abnormalities. The method is performed by modeling selected ECG confounders that tend to obscure AMI evidence in the ECG waveform, and by purging a subject's ECG waveform of the effect(s) of these confounders through linking selected confounder models with an appropriate, computer-implementable purge algorithm.

The invention relates to a non-invasive attached telemetering electrocardiographic recording method having an ultra-long record period and an ultra-high storage capacity. By using the method, characteristic values of electrocardiographic waves can be safely, stably and clearly acquired under the natural physiological state of a human body within a long period (more than 15 days), microvolt-level measurements of T-wave alternans can be acquired, and the collection, processing and high-capacity storage of electrocardiographic waves can be completed; and multiple electrocardiographic recording pasters can be used to realize the simultaneous recording of multi-channel body surface electrocardiograms, and a computer data processing and analysis system can complete the data monitoring and analysis, image display, data storage and printing and output of the recorded signals and realize the networking transmission of the electrocardiosignals. The clinical indications of the device include: symptoms related to suspected arrhythmia; determination of arrhythmia property, and completion of reasonably evaluating anti-arrhythmia treatment and monitoring myocardial ischemia; evaluation of anemic heart disease treatment measures; instructions to acute myocardial infarction patients before leaving hospital and during convalescence; and installation, detection and function assessment of sudden cardiac death and heart pacemakers.

A combination therapy for the treatment of acute myocardial infarction comprises administering a combination of a thrombolytic agent and levosimendan or a pharmaceutically acceptable salt thereof to a patient. The combination synergistically reduces mortality of patients with acute myocardial infarction.

The invention relates to markers for acute myocardial infarction (AMI), particularly markers that may be used in the rapid and accurate diagnosis of AMI or reinfarction. A method of diagnosing cardiac injury comprising identifying an elevated concentration of cardiac myosin binding protein C (cMyBP-C) or a fragment thereof or myosin regulatory light chain 2 (MLC2) or a fragment thereof in a sample obtained from a subject.

The invention is a method for treating a heart disease, in particular acute myocardial infarction (AMI) in a subject comprising the step of administering to the subject a Tjp1 inhibitor, wherein administration of said Tjp1 inhibitor promotes cardiomyocyte proliferation. The invention further includes use of Tjp1 inhibitor in the manufacture of a medicament for a heart disease, a patch, and a nucleic acid encoding a Tjp1 inhibitor. In a particular embodiment, the Tjp1 inhibitor is a nucleic acid, i.e. an siRNA or shRNA of Tjp1. The invention also includes administration of said Tjp1 inhibitor in combination with Neuregulin-1 (NRG1), Fibroblast growth factor (FGF), Vascular endothelial growth factor (VEGF) or Follistatin-like 1 (Fst1) and wherein said inhibitor is delivered in an adeno-associated virus of serotype 9 (AAV 9).

A diagnostic method for determining prognosis of a myocardial infarcted patient, wherein the amounts of FXIII protein are determined on the day of myocardial infarction (t0) and at least on the following three days (t1 to t3), wherein a lowering of FXIII amount on any one of t0 to t3 below a threshold value is indicative of an increased risk of poor prognosis.

Methods and apparatuses, including devices and systems, for remote and detection and/or diagnosis of acute myocardial infarction (AMI). In particular, described herein are handheld and adhesive devices having an electrode configuration capable of recording three orthogonal ECG lead signals in an orientation-specific manner, and transmitting these signals to a processor. The processor may be remote or local, and it may automatically or semi-automatically detect AMI, atrial fibrillation or other heart disorders based on the analyses of the deviation of the recorded 3 cardiac signals with respect to previously stored baseline recordings.

An objective of the present invention is to provide methods of testing for acute ischemic diseases using active hepcidin as an indicator, methods for determining the timing to administer an agent for treating the disease, and kits for these methods.

To accomplish the above-mentioned objective, the present inventors analyzed the serum proteome patterns characteristic of acute myocardial infarction patients using SELDI-TOF-MS. As a result, it was found that hepcidin-20 has a very high correlation with acute myocardial infarction. Furthermore, the present inventors discovered that at the time of disease onset, the blood concentration of hepcidin-20 rises sharply in particular, and shows high levels within six hours, especially four hours of onset. The present invention enables early diagnosis of acute ischemic diseases.

Methods of reducing sepsis or cardiogenic shock in patients experiencing myocardial injury are described. More specifically, this disclosure relates to the administration of a C5-C9 terminal complement inhibitor to patients who have had coronary artery bypass grafting or an acute myocardial infarction thereby reducing the incidence of sepsis.

The invention discloses a research method of MS-275 acting on acute myocardial ischemia reperfusion injury. The research method comprises the following steps: step I, performing ligation of an anterior descending branch of a left coronary artery of an SD male bandicoot to construct a bandicoot acute MI/RI model; step II, observing the action of the MS-275 in an MI/RI acute stage of the bandicoot;and step III, discussing a molecular mechanism of the MS-275 on bandicoot MI/RI protection action. According to the research, through constructing the bandicoot acute MI/RI model and combination within vivo and vitro experiments, the following research objectives are achieved: (1) observing the acetylation level of histone, and expression of HDAC1 and microRNA-210(miR-210) in cardiac muscle tissue of the bandicoot at the MI/RI acute stage; (2) confirming that the MS-275, a novel HDACI type selective depressant, has protection action on MI/RI of the bandicoot and influence on the acetylation level of the histone and expression of HDAC1 and miR-210 in tissue of a myocardial infarction region of the bandicoot subjected to myocardial ischemia reperfusion; and (3) disclosing a specific molecular mechanism that the MS-275 improves MI/RI of the bandicoot from the angle of miRNA epigenetic regulation, and providing an important theory and experiment basis for MI/RI treatment with HDACi.

The invention provides a device for detecting diagnostic blood markers as early as half an hour upon an acute myocardial infarction symptoms onset.

Disclosed herein are uses of a polypeptide comprising NIMoEsh to treat a disease or condition associated with acute myocardial infarction (AMI) in a subject in need thereof, of a polypeptide comprising NIMoEsh to restore heart function after AMI in a subject in need thereof, of a polypeptide comprising NIMoEsh to reduce or prevent AMI-induced heart function loss in a subject in need thereof, of a polypeptide comprising NIMoEsh to reduce AMI-induced heart tissue infarct in a subject in need thereof, and of a polypeptide comprising NIMoEsh to protect cardiomyocytes against AMI-induced function loss in a subject in need thereof. Disclosed also herein are methods by which such treating, restoring, reducing or preventing, reducing, and/or protecting may be done, and a polypeptide comprising NIMoEsh for use in such treating, restoring, reducing or preventing, reducing, and/or protecting.

Various systems, devices, and methods are disclosed herein for healing acute myocardial infarction (AMI) patients using a heart, pump controlled in a maimer that maximizes mechanical unloading of the left ventricle in the presence of cardiovascular instability and minimizes myocardial oxygen consumption (MVO2) and consequentially infarct size to prevent the development of subsequent heart failure. In a closed feedback system, the system can include a sensor configured to generate an output used to measure or calculate a left ventricular systolic pressure (LSVP) within the left ventricle of a heart and a controller coupled to a heart, pump. The controller can be configured to measure or calculate the LVSP based on the output of the sensor and to control an operation of the heart pump to maximize mechanical unloading of the left ventricle based on the measured or calculated LVSP.

The present invention relates to a method of providing cardiac protection to a subject having undergone myocardial infarction, the method comprising administering to the subject a therapeutically effective amount of a granzyme B inhibitor. The inventor proves that after acute MI occurs in a mouse, CD8 + T lymphocytes are rapidly collected and activated in ischemic heart tissue, granzyme B is released, and myocardial cell apoptosis and myocardial function deterioration are caused. The depletion of antibody-mediated (CD8 + T lymphocytes) CD8 + T lymphocytes reduces the content of granzyme B in cardiac muscle and apoptosis and inflammatory responses. The mAb-mediated CD8 depletion will limit myocardial damage and improve cardiac function. These effects are reproduced in mice that are deficient in CD8 + T cell selective granzyme B. Granzyme B is also produced by other cell types, such as NK cells. Overall granzyme B deletion (GzmB-/-mouse) can reduce apoptosis in cardiac muscle, reduce local pro-inflammatory markers and ultimately limit infarction area after MI. The inventor also proves that the increase of the circulation level of granzyme B in an acute MI patient indicates that the mortality risk is increased during one-year follow-up visit. This work reveals the previously unexpected pathogenic effect of granzyme B following acute ischemia and identifies a new therapeutic target for this destructive condition.