The present invention relates to a method for identifying whether or not it may be appropriate to administer to a subject a therapy for alleviating any potential consequences which may arise due to the subject having an atrial fibrillation (AF), the method comprising detecting, in a sample of fluid from the subject, a level of ccl21 and/or ddit4 expression and determining whether or not it may be appropriate to administer to the subject a therapy for alleviating any consequences which may arise due to the subject having AF, based upon the ccl21 and/or ddit4 expression level detected. Also provided are an anticoagulant or other AF therapy and a method of administering an anticoagulant drug or another AF therapy.

The present invention relates to a method for identifying whether or not it may be appropriate to administer to a subject a therapy for alleviating any potential consequences which may arise due to the subject having an atrial fibrillation (AF), the method comprising detecting, in a sample of fluid from the subject, a level of ccl21 and/or ddit4 expression and determining whether or not it may be appropriate to administer to the subject a therapy for alleviating any consequences which may arise due to the subject having AF, based upon the ccl21 and/or ddit4 expression level detected. Also provided are an anticoagulant or other AF therapy and a method of administering an anticoagulant drug or another AF therapy.

This invention relates to a diagnostic test measuring circulating HU proteins or gene transcripts in a blood sample to assess arrhythmic risk in heart failure patients. The invention addresses this need and features a diagnostic/prognostic test for measuring circulating HU levels in a sample to assess arrhythmic risk in heart failure patients, alternatively, to determine the risk of SCD. The methods described herein represent a non-invasive (or minimally invasive) test assay. The methods described herein may also include computing a level of an SCN5A variant, or cardiac transcription factors MESP1 (mesoderm posterior posterior protein 1), or MEF2C (myocyte enhancer factor-2), or any combination thereof.

Described herein are methods for evaluating a cardiac preparation. The methods involve providing at least one sample comprising one or more cardiac cells, pacing the one or more cardiac cells at two or more fixed rates; and measuring a fixed response of the one or more cardiac cells at each of the two or more fixed rates. Also described herein are methods for evaluating the cardiac effect of a compound. The methods involve providing at least one sample comprising one or more cardiac cells; contacting each sample with the compound; pacing the one or more cardiac cells at two or more fixed rates; and measuring a fixed response of the one or more cardiac cells to the compound at each of the two or more fixed rates.

T cell surface marker, CRTH2, is a target for treating Postural Orthostatic Tachycardia Syndrome, a hemodynamic abnormality. Targeting CRTH2 permits control of disease symptoms in POTS, for which no FDA approved treatment is currently available. Cell surface expression on certain T cell subsets characterizes the syndrome. Cell surface expression can be conveniently determined in plasma samples using flow cytometry.

Provided herein are methods that include (i) determining a level of soluble ST2 in a biological sample from a subject, (i) comparing the level of soluble ST2 in the biological sample to a reference level of soluble ST2 (e.g., a level of soluble ST2 in the subject at an earlier time point), and (iii) selecting, implanting, replacing, or reprogramming an implanted cardiac device, e.g., an ICD, CRT, or CRT-D device, for a subject having an elevated level of soluble ST2 in the biological sample compared to the reference level of soluble ST2, or selecting a subject for participation in, or stratifying a subject participating in, a clinical study of a treatment for reducing the risk of a ventricular tachyarrhythmia (VTA) event. Also provided are methods for evaluating the risk of a VTA event in a subject. Also provided are kits for performing any of these methods.

Among the various aspects of the present disclosure is the provision of a method of detection, treatment, and monitoring of cardiovascular disease or a foot wound by detection of a novel biomarker, Fatty Acid Synthase (FAS). Briefly, therefore, the present disclosure is directed to methods that allow for improved, noninvasive, and reliable diagnosis of these conditions, particularly in subjects suffering from Type 2 Diabetes (T2D).

Methods of determining whether specific drugs or patients carry an increased risk of causing or developing, respectively, long QT syndrome or Torsades de Pointes and methods of treating such patients.

The present invention relates to a method for diagnosing atrial fibrillation in a subject, said method comprising the steps of a) determining the amount of total NT-proBNP in sample from the subject, b) determining the amount of unglycosylated NT-proBNP in a sample from the subject, c) calculating a score of the amounts determined in steps a) and b), d) comparing the calculated score with a reference score, and e) diagnosing atrial fibrillation in a subject.

Various embodiments are described herein for creating a 3D human heart model for modelling arrythmias, wherein the method comprises seeding a structure with a mixture of human cardiomyocytes, cardiac fibroblasts and a fibrin mixture to form cardiac tissue; applying a plating media for settlement and compaction of the cardiac tissue; and adding an arrhythmogenic media to the cardiac tissue, where the arrhythmogenic media comprises methyl-beta cyclodextrin for disrupting calcium signaling.