The invention provides methods, compositions, kits, and systems for the sensitive detection of cardiac troponin. Such methods, compositions, kits, and systems are useful in diagnosis, prognosis, and determination of methods of treatment in conditions that involve release of cardiac troponin.

Subject of the present invention are biomarkers and methods for the identification of risk for subsequent cardiovascular event (e.g. coronary heart disease death, non-fatal myocardial infarction, ischemic stroke, hospitalizations for unstable angina pectotis, cardiac arrest) in patients that have experienced an acute coronary syndrome, comprising the detecting the level of NT-proBNP, homocysteine and CRP.

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.

The present invention relates to a method for predicting the prognosis of ischemic disease using an AGE-RAGE-based biomarker. The biomarker can be used as an indicator factor of the clinical severity of ischemic disease, can maximize the efficiency of stem-cell treatment by determination of the optimal timing of the stem-cell treatment on the basis of changes in the biomarker according to the severity of ischemic disease, and can also be used as a useful indicator factor for verifying efficacy after the stem-cell treatment.

Low levels of antibodies reactive with oxidised Cardiolipin (oxCL) in mammals are related to an increased risk of developing cardivacular diseases, auto-immune diseases or inflammatory conditions. High levels can have a protective function and in general there is a negative association between manifestations of these conditions and antibodies against oxCL. Thus, based on their relations methods of monitoring, determining and diagnosing as well as methods of immunisation and therapy of these diseases and conditions are provided.

The invention relates to new antibodies against specific glycosylation sites within the ApoJ protein as well as their application thereof in the diagnosis and prognosis of ischemia and the determination of the risk of a recurrent ischemic event.

The present invention relates to a method of identifying a subject being susceptible to a cardiac intervention based on the determination of GDF-15 in a sample of a subject in need of a cardiac intervention. Moreover, the present invention pertains to a method for predicting the risk of mortality or a further acute cardiovascular event for a subject suffering from a cardiovascular complication based on the determination of GDF-15 and a natriuretic peptide and/or a cardiac troponin in a sample the said subject. Also encompassed by the present invention are devices and kits for carrying out the aforementioned methods.

The invention provides decision tree based systems and methods for estimating the risk of acute coronary syndrome (ACS) in subjects suspect of having ACS. In particular, systems and methods are provided that employ additive decision tree based algorithms to process a subject's initial cardiac troponin I or T (cTnI or cTnT) concentration, a subject's cTnI or cTnT rate of change, and at least one of the following: the subject's age, the subject's gender, the subject's ECG value, the subject's hematology parameter value, to generate an estimate risk of ACS. Such risk stratification allows, for example, patients to be ruled in or rule out with regard to needing urgent treatment.

The present invention is directed to particular monoclonal antibodies and fragments thereof that find use in the detection and isolation of in vitro differentiated cardiomyocytes. In particular, the present invention relates to LSMEM2 biomarkers, including monoclonal antibodies having specificity for cell surface protein LSMEM2 and to methods of using such biomarkers for diagnosis of cardiovascular injury.

The disclosure provides methods for detecting circular endothelial cells (CECs) in a non-enriched blood sample. The present disclosure is based, in part, on the unexpected discovery that CECs can be detected in non-enriched blood samples. The present disclosure is further based, in part, on the discovery that CECs can be detected in non-enriched blood samples by combining the detection of one or more immunofluorescent markers in the nucleated cells of a non-enriched blood sample with an assessment of the morphology of the nucleated cells. The present disclosure is further based, in part, on the discovery that CECs can be detected in non-enriched blood samples by comparing the immunofluorescent marker staining and morphological characteristics of CECs with the immunofluorescent marker staining and morphological characteristics of WBCs. The methods disclosed herein serve to classify human subject in myocardial infarction (MI) patients or healthy controls.