Vipin Bhayana <[log in to unmask]> enquired about the Abbott AxSYM
Troponin I assay.
This is the predominant method used for Troponin I in Australia. From the
last EQA report 40 out of 61 labs doing I's are using the AxSYM method. As
with many others, we use it because we already have the AxSYM platform and
the scientists are familar with it and and can offer a 24 hour service with
minimal change. Therefore the assay may be the best (or not) but we did not
choose it for its analytical quality.
However regarding quality the precision around the decision points is not
great and careful sample handling (eg re-centrifugation) can avoid some
analytical false positives.
Regarding cuttoffs, we are guided very heavily by the literature, and there
has been remarkably little peer-reviewed data using the AxSYM so far.
Abbott are getting there and the best source of information is the package
insert.
So: we use their disease-free reference interval of </= 0.5 ug/L (most
walking-well are well below this) and a diagnostic cuttoff for AMI of 2.0
ug/L. The unanswered question to me at present is what level is significant
with regard to Minor Mycardial Damage (MMD) with associated poor prognosis
in the UAP patient group? None of the Abbott data addresses this problem.
Causes of elevated troponin (>0.5 ug/L) on the AxSYM then can be due to:
AMI (usually above 2.0 ug/L, can reach several hundred ug/L); MMD -
indicating the need for inpatient management (obviously moving the cuttoff
up from 0.5 ug/L will improve specificity for coronary disease / cardiac
event prediction but at a loss of sensitivity - I have seen little data eg
ROC curve on the Abbott assay for this - Hans, please publish soon!); renal
failure (5% above 1.2 ug/L - Abbott); Skeletal muscle damage (5% above 1.0
ug/L - Abbott); cardiac bypass surgery (gross elevations peak 3-6 hours
post-op - in-house data); peri/myocarditis; cardiac trauma; other cardiac
procedures (eg stenting).
Experience at at least one Hospital in Sydney was to discontinue the use of
the assay due to too many "false-positives" leading to overcrowding of
coronary care beds. Abbott have raised the cuttoff from 0.4 to 0.5 since
then and the hospitals troubles were probably exacerbated by the well-known
episode of quality problems with the assay. I think (unsubstantiated
opinion) that a cuttoff of about 0.6-0.8 ug/L would give a suitable balance.
As an aside I hope to see vast improvements in TnI assays in the near
future. The Dade Stratus method shows an order of magnitude improvement in
precision and this looks like it will allow much better patient
stratification in the troublesome range (Clin Chem 1999;10:1789-96).
These are my opinions and should be treated as such. I would be interested
in any other thoughts on cuttoffs for different troponin assays.
Best wishes,
Graham Jones
Staff Specialist in Chemical Pathology
St Vincent's Hospital, Sydney
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