Cardiac Marker Test Kit

Cardiac markers are mainly used to diagnose myocardial cell injury. cTnI and cTnT play a major role in regulating cardiac striated muscle contraction and are specific and sensitive markers of myocardial injury. Lipoprotein-associated phospholipase A2(LP-PLA2) is a vascular-specific marker of inflammation. Cardiac type fatty acid binding protein (H-FABP) is a key fatty acid carrier protein, which is  the most promising marker of myocardial injury.

Products Details

Chemiluminescent Solution(General Items)

Series

Product Name

Product Name

Cardiac Marker

Troponin I

cTnI

Creatine Kinase Isoenzyme-MB

CK-MB

Myohemoglobin

Myo

Growth Stimulating Factor 2

ST2

Lipoprotein-associated Phospholipase A2

LP-PLA2

D-Dimer

D-Dimer

Heart-type Fatty Acid-binding Protein

H-FABP

S100-β Protein

S100-β

Brain Natriuretic Peptide

BNP

N-Terminal pro-Brain Natriuretic Peptide

NT-proBNP

Cardiac markers are mainly used to diagnose myocardial cell injury. cTnI and cTnT play a major role in regulating cardiac striated muscle contraction and are specific and sensitive markers of myocardial injury. Myoglobin exists in myocardial and skeletal muscles, and released into the bloodstream when skeletal muscle and myocardial damage (acute myocardial infarction (mi), excessive movement and muscle disease, In acute myocardial infarction, the serum myoglobin concentration deviated from the normal value within 2-3 hours of the initial period of heartache due to myocardial tissue disorder, and reached the highest value within 6-9 hours, and returned to the normal value around 24 hours later. Ck-MB is one of the three isomers of Creatine Kinase (CK), the other two are CK-BB and CK-MM. The MB type mainly exists in cardiomyocytes, so CK-MB has high specificity for myocardium. In Acute Myocardial Infarction (AMI), it is secreted into the blood. Ck-MB rises 4-6 hours after the onset of myocardial infarction, peaks at 24 hours, and returns to normal within 3 days. Lipoprotein-associated phospholipase A2(LP-PLA2) is a vascular-specific marker of inflammation. It has been found that LP-PLA2 is an independent risk factor for coronary heart disease and ischemic stroke. Recently approved by the US FDA to predict the risk of coronary heart disease and ischemic stroke, LP-PLA2 levels are linearly logarithmic associated with coronary heart disease and vascular death. D-dimer is a specific degradation product of fibrin monomer crosslinked by activator XIII and hydrolyzed by fibrinolytic enzyme, which is a specific marker of fibrinolytic process. During acute myocardial infarction, plasma levels of DD are significantly elevated. S100 protein also called central nervous specific protein as biochemical markers of brain damage in brain injury after a certain amount of time, but also closely related to brain damage degree and the prognosis and, better stability, its density detection helps the clinical judgment of nerve tissue lesion size, treatment effect and judge the prognosis, etc. Cardiac type fatty acid binding protein (H-FABP) is a key fatty acid carrier protein. It is highly cardio-specific (that is, expressed primarily in cardiac tissue), but is also expressed at low concentrations in tissues other than the heart. After the onset of myocardial ischemic injury, H-FABP may be detected in the blood as early as 1 to 3 hours after the onset of chest pain, peak at 6 to 8 hours and return to normal plasma levels within 24 to 30 hours. It is the most promising marker of myocardial injury, and the high level of plasma H-FABP can be detected in the early stage of acute myocardial infarction (0-3 h), and its release is essentially dependent on myocardial ischemia injury. PreproBNP is synthesized in cardiomyocytes and transformed into a precursor molecule called proBNP. ProBNP is then decomposed into physiologically active BNP, and the degradation fragment NT-probNP. The European Heart Society guidelines for heart failure recommend BNP and NT-proBNP as molecular markers for preliminary diagnostic detection of heart failure. ST2 is a cardiac protein produced by cardiomyocytes under biomechanical stress. Excessive sST2 in serum can make the myocardium lack adequate IL-33 protection during mechanical stress injury, resulting in myocardial remodeling and cardiac dysfunction. The continuous increase of ST2 level reflects the continuous progress of myocardial fibrosis and remodeling, and the intensification of the pathological process of heart failure. ST2 is used for the clinical evaluation of patients with acute and chronic HF, so as to guide the treatment of HF.The determination of ST2 in combination with BNP or nT-probNP may improve the accuracy of evaluating the prognosis of heart failure.

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