Troponin: An update
I have been working with troponin since it came to this country several years ago. Most of my experience has been with troponin I (cTnI). When cTnI first was released to the laboratories the cut-off was set at 0.4. Then it dropped to 0.2 and now it has been lowered by some laboratories even further. These newer variations have pros and cons as you have seen. For example, there are reports of measurable cTn following a marathon.
"The increase in early diagnostic sensitivity of hs-cTn assays for ACS comes at the cost of a reduced ACS specificity, because more patients with other causes of acute or chronic myocardial injury without overt myocardial ischemia are detected than with previous cTn assays."
These newer assays detect low levels of cTn in apparently healthy people. "In addition, the sensitive assays detect more cTn positive patients who do not have a final diagnosis of ACS. It is unknown if such mild elevations in cTn detected by sensitive assays are of clinical concern. What is certain is that AMI remains a clinical not a biochemical diagnosis and interpretation of cTn concentrations should be made according to the clinical context." It has been demonstrated that the newer assays are better able (using the area under the ROC curve) to identify AMI in patients with existing CAD compared to the ‘standard' cTn.
A diagnostic accuracy study of patients presenting to the emergency department (ED) with symptoms of ACS was performed. Troponin was measured at 0, 2 and 6h post-presentation. AMI was made by 2 cardiologists and incorporated the 0 and 6h troponin values measured by a sensitive troponin assay. There was no significant difference in the diagnostic accuracy of early versus late biomarker strategies when used with the current risk stratification processes. Incorporation of a significant delta did not improve the stratification at 2h post-presentation."
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