The present invention provides a method for predicting whether a human patient 65 years of age or older is at increased risk for developing heart failure, comprising obtaining the results of an assay that measures levels of NT-proBNP and/or cardiac troponin T in a specimen from the patient wherein an increased NT-proBNP and/or cardiac troponin T level compared to levels in a control indicate an increased risk for developing heart failure.

Disclosed is an isolated binding protein including a cardiac troponin I (cTnI) antigen binding domain, and preparation and a use and the like of the binding protein. The antigen binding domain includes at least one complementarity determining region selected from an amino acid sequence defined in this article, or has at least 80% sequence identity with the complementarity determining region of the amino acid sequence and has KD≤9.96×10.sup.−8 mon affinity with cTnI. The binding protein may be used in the detection field of the cTnI protein.

Disclosed is an isolated binding protein including a cardiac troponin I (cTnI) antigen binding domain, and preparation and a use and the like of the binding protein. The antigen binding domain includes at least one complementarity determining region selected from an amino acid sequence defined in this article, or has at least 80% sequence identity with the complementarity determining region of the amino acid sequence and has KD≤7.51×10.sup.−8 mol/L affinity with cTnI. The binding protein may be used in the detection field of the cTnI.

The present invention relates to a method for predicting the risk of a subject of rapidly progressing to chronic heart failure and/or of hospitalization due to chronic heart failure and/or death. The method is based on the determination of at least one biomarker selected from the group consisting of a BNP-type peptide, IGFBP7 (IGF binding protein 7), a cardiac Troponin, soluble ST2 (sST2), FGF-23 (Fibroblast Growth Factor 23), and Growth Differentiation Factor 15 (GDF-15), in a sample of a subject. The method may further encompass the assessment of the presence or absence of (i) abnormal midwall fractional shortening or (ii) left ventricular hypertrophy. Further envisaged by the present invention are devices adapted to carry out the present invention.

The present invention relates to a method for assessing whether a subject shall be subjected to an imaging based diagnostic assessment. The method is based on the determination of the amount(s) of a cardiac Troponin and/or Fibroblast Growth Factor 23 (FGF-23) in a sample from the subject, and on the comparison of the, thus, determined amount(s) with a reference amount (reference amounts). The present invention also relates to a system for performing an assessment whether a subject shall be subjected to an imaging based diagnostic assessment and to reagents and kits used in performing the methods disclosed herein. Moreover, the present invention is directed to a method for predicting the risk of mortality and/or of a cardiovascular event. Also encompassed is a method for diagnosing an early stage of LVH in a subject having a preserved left ventricular ejection.

Disclosed are a kit for testing myocardial infarction rapidly and a preparation method and use thereof. The kit comprises a strip capable of detecting three markers, namely, human myeloperoxidase (MPO), heart-fatty acid binding protein (FABP3) and cardiac troponin I(cTnI) simultaneously. The strip comprises a sample pad, a conjugate pad, a chromatographic membrane coated with three test lines and a quality control line, and a sample absorption pad. Antibodies of the three markers are all marked on the conjugate pad. The chromatographic membrane has three test lines formed by coating paired antibodies of the three markers respectively, the paired antibodies of the three markers being able to specifically combine with the three markers, respectively. The kit has advantages such as convenient operation, rapid response, high sensitivity and high specificity, point of care test, and economical and practical etc.

The present invention relates to compositions and methods use in designing immunoassay controls. In various aspects, the invention provides synthetic peptides comprising the sequence CPRRPYIL or an analog thereof; ELAGLGFAELQC or an analog thereof; and CDWRKNIDAL or an analog thereof; specific binding reagents that bind to a CPRRPYIL, ELAGLGFAELQC or CDWRKNIDAL peptide; methods of producing such reagents; and assays utilizing such reagents to provide assay controls signals that are unrelated to the measurement of the analyte or analytes of interest in that no reagents used in the analyte assay(s) contribute to the control signal.

A bi-epitope compound of formula I:

##STR00001##

in which: E1 and E2, identical or different, each separately represents a peptide sequence including at least one epitope of an analyte; X and Y, identical or different, each separately represents a linking arm, the carrier molecule is soluble and Z represents an amino acid derivative bearing a thiol function prior to the bonding of same with the carrier molecule. The compound may be contained in a composition, used as a control or standard in an immunoassay and associated method, and/or provided in a kit for implementing an immunoassay.

The present invention relates to a method for detecting heart damage in a patient. The invention also relates to methods for treatment of patients identified as having heart damage. The invention further pertains to methods for evaluating the efficacy of an ongoing therapeutic regimen designated to treat a damaged heart in a patient.

Provided is a means for inhibiting a function of CD69, whereby allowing suppression of an inflammatory response. That is, provided are: a composition for treating an inflammatory disease which includes an antibody that specifically recognizes a myosin regulatory light chain polypeptide (hereinafter abbreviated as Myl), preferably Myl9, Myl12a, and Myl12b, and inhibits a result of an effect of coexistence of Myl with CD69; a method of treating an inflammatory disease, including administering, to a subject diagnosed as having an inflammatory disease, a therapeutically effective amount of the antibody; and a method of identifying a compound that inhibits a result of an effect of coexistence of Myl with CD69, and a method of identifying a candidate compound for treating an inflammatory disease, including selecting a compound that inhibits the result.