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Troponin I ELISA

Troponin I ELISA
ber: TnI HU-LB01                                    
Description: Tr
Sample Type: Serum                        
Sample Size: 50 µl                                        
Available Sizes: 96 Wells                      
Range: 1-50 ng/ml
Sensitivity: 1.0 ng/ml
Incubation: 1 hour(s) 20 minutes (s)
Protocol: Troponin I ELISA
Regulatory Status: RUO 
Product Distribution: Worldwide    

Troponin I ELISA is intended for the quantitative determination of cardiac troponin I in human Serum. Measurement of troponin I values are useful in the evaluation of acute myocardial infarction (AMI).
Troponin-I ELISA is a Enzyme Immunoassay  for the quantitative determination of cardiac troponin-I (cTnI) in human serum or plasma . Troponin-I values are used to assist in the diagnosis of myocardial infarction (MI) and in the risk stratification of patients with acute coronary syndromes (including unstable angina and non-ST elevation) with respect to relative risk of mortality, myocardial infarction, or increased probability of ischemic events. Troponin-I (TnI) is a regulatory subunit of the troponin complex associated with the actin thin filament within muscle cells. TnI, in conjunction with troponin-C and troponin-T, plays an integral role in the regulation of muscle contraction. Three distinct tissue specific isoforms of TnI have been identified from skeletal and cardiac muscles. The cardiac isoform exhibits only 60% similarity with the skeletal muscle isoforms and contains additional amino acids at the N-terminus; cTnI has a molecular weight of approximately 24,000 daltons. Clinical studies have demonstrated the release of cTnI into the blood stream within hours following acute myocardial infarctions (AMI) or ischemic damage. Elevated levels of cTnI (above the values established for non-AMI specimens) are detectable in serum within 4 to 6 hours after the onset of chest pain, reach peak concentrations in approximately 8 to 28 hours, and remain elevated for 3 to 10 days following AMI. The temporal pattern of cTnI release following an infarction thus extends across the diagnostic windows of both creatine kinase-MB (CK-MB) and lactate dehydrogenase (LD). The clinical utility of cTnI measurements for the assessment of myocardial damage has been demonstrated in several clinical studies indicating improved cardiac specificity of cTnI over CK-MB. The high specificity of cTnI measurements is beneficial in identifying cardiac injury for clinical conditions involving skeletal muscle injury resulting from surgery, trauma, extensive exercise, or muscular disease. The World Health Organization (WHO) criteria for defining AMI are the presence of two of the following three elements: unequivocal ECG changes, unequivocal serum cardiac enzyme changes, and prolonged chest pain.

The Joint European Society of Cardiology/American College of Cardiology Committee current guideline redefines MI and supports the use of cTnI as a preferred marker for myocardial injury. Their definition of MI is a typical
rise and gradual fall of cardiac troponin (or more rapid fall of CK-MB) with at least one of the following: ischemic symptoms, pathological Q waves on electrocardiogram (ECG), ischemic ECG changes, or coronary artery intervention. Serial sampling is recommended to detect the temporal rise and fall of troponin levels characteristic of MI. An elevated troponin alone is not sufficient to make the diagnosis of myocardial infarction.

Other markers such as CK-MB and myoglobin can be used in conjunction with troponin-I results in aiding the diagnosis of MI.

Several major studies have shown that cTnI is also useful as a predictor of cardiac risk in patients with unstable angina. Previous studies showed that during 30-day follow-up, patients with acute coronary syndromes(Including unstable angina) were at greater risk of progressing to MI if cTnI is elevated.  Thus, cTnI can play an important role in identifying patients with acute coronary syndromes who are at greater risk for cardiac events.