Patients with increased hs-cTnT at admission and a typical presentation of ACS but without an absolute δ change ≥7ng/L are usually found to have UAP with hs-cTnT increases due to underlying chronic cardiac damage. (In the case a previous MI of the anterior wall)
With the use of absolute δ changes, a rise and/or fall of at least 9.2 ng/L for a population consisting of patients with ACS and non-ACS conditions, or 6.9 ng/L for an ACS population seems to be more adequate than relative δ changes for ruling out AMI.1
The present results suggest that clinical assessment, ECG analysis and serial measurement of hs-TnT in serum showing lack of rise or fall in its kinetic activity indicating chronic myocardial injury.
|
|||||||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||||||
|
|||||||||||||||||||||||||||||||||||||
|
Diagnosis
Unstable angina
(and heart failure following a previous anterior wall infarction)
Typical angina pectoris, although an elevated cTnT-hs level was found at admission. In order to distinguish between acute and a chronic cTnT-hs elevation; troponin levels must be monitored with serial testing. The changes in troponin levels are below 50 % (<7 ng/L). In this case the small changes in concentration are indicative of chronic myocardial damage. This is consistent with the magnetic resonance imaging (MRI), indicating a previous myocardial infarction of the anterior wall.
Conclusion
There is no rise or fall in cTnT-hs values needed for AMI diagnosis.
