Biomarkers in acute coronary syndrome 4

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Biomarkers in acute coronary syndrome 4

Biomarkers in acute coronary syndrome 4:

Why Troponins Are The “Gold Standard”

cTn-I (cardiac troponin-I) has a thirteen-fold greater concentration in cardiac muscle than CK-MB and it is found only in cardiac muscle. Moreover, it is not expressed in response to skeletal muscle injury. Antibodies to cTn-I do not appear to cross-react with skeletal muscle Troponin I.

With the advent of high sensitivity troponin estimation and delta troponin for early rule in early rule out strategy in the emergency department, it has become the number one and gold standard in the assessment of acute coronary syndrome. Elevation of troponin has to be correlated with clinical and other parameters for a diagnosis of myocardial infarction. Other causes of troponin elevation as in chronic kidney disease have now been grouped under Myocardial Injury, which has equally bad prognosis compared to myocardial infarction, though not amenable to treatment modalities like reperfusion.

B-Type Natriuretic Peptide (BNP)

B-Type Natriuretic Peptide (BNP) is found in the cardiac ventricles and released in response to stretch and increased volume in the ventricle. BNP levels are related to the left ventricular end-diastolic pressure and the New York Heart Association (NYHA) class of heart failure.

ANP (Atrial Natriuretic Peptide) has its primary origin in the cardiac atria and is released in response to atrial distension. BNP (B-type Natriuretic Peptide – originally found in the brain) has its primary source in the ventricular myocardium and is released in response to ventricular overload. CNP (C-type Natriuretic Peptide) has its origin in the endothelium and is released in response to endothelial stress.

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