This week DEMTEd took a look at troponins and chest pain workup using ‘accelerated diagnostic protocols’.
Chest pain assessment and troponin testing: the status quo
As of 2011, our guidelines in working up patients with possible acute coronary syndromes rely upon clinical assessment augmented with consecutive electrocardiograph and troponin assays.
The algorithm specifies a high sensitivity troponin, which is pretty controversial and impractical for those of us who can’t get them.
The timeline is also cumbersome in practice – we typically admit 4-6 patients a day to our short stay unit to work up possible ACS with intermediate risk as per the guidelines.
The troponin in chest pain assessment
In the session today Dr Louise Cullen spent some time talking about the nuts and bolts of troponin testing. Here are some of the key points as I saw them:
- Troponin is released by myocardium in response to injury. It doesn’t come in any appreciable quantity from anywhere else.
- Troponin I and Troponin T are released from myocardium in equal amounts, but what happens after that may differ – some is free, some form complexes with other substances which are variably detected by different assays, and it may be that troponin T has a longer clearance t½ . This accounts for the differences in reference ranges between assays.
- The normal range has been generally defined by the 99th percentile, which means that of an unselected population, you might expect to see 1% of people having a troponin ‘elevated’ – by definition.
- The term ‘high-sensitivity’ troponin has (in practice for us in Oz) referred to a Roche assay for Troponin T (such as the test in current private practice). Unlike older troponin assays, most people have a troponin T above the detection limit of the test. So it generally returns a number, not just a “negative”. Interpreting that number when it is not very high has been problematic. Interestingly in the states the ‘high-sensitivity’ troponin assays have not been in general use – they are not FDA approved. And of course at an institutional level Qld Health does not provide a hs troponin yet.There is a new high sensitivity troponin I assay which seems likely to percolate into our practice in the medium term. It’s worth mentioning as it seems to be as sensitive and considerably more specific that the hs-TnT that we are currently using, on the figures we were shown today, for ACS.
- The definition of MI has evolved. The cardiologists have categorised MI into 5 different types, only one of which is the pathophysiology I was probably supposed to learn in medical school (plaque rupture/thrombosis).The presence of an elevated biomarker (troponin) alone is not enough – to call it a Type I MI, for example, you need consistent symptoms, ECG changes and/or echo evidence.
- The above doesn’t change the fact that an elevated troponin confers a mortality risk in the person that has it, whether it’s due to ACS or not.
Of course, we mainly use a troponin in the context of working up a patient with undifferentiated chest pain. The ‘rule out’.
Accelerated Diagnostic Protocols for chest pain presentations
The assessment process detailed in the guidelines does confer a considerable cost burden to our patients (who are trapped in hospital) and to our health care system (providing the care and the tests).
In my patter to patients on presentation, I tell ‘em that we can rule out an MI with the ECG/blood tests and that we are looking at their future risk of a heart attack with the next test – in our institution a stress ECG.
Of course, once you get a 6 hour troponin back and start the final leg of your assessment, you’re looking at a length of stay of at least 8 hours, and often overnight depending on how you go about arranging.
The articles linked below describe an accelerated diagnostic protocol with (in one) high sensitivity troponin testing. The numbers and the process are pretty attractive and probably represent the next evolution of our practice. A TIMI score of 1 or less, no new ischaemic changes on ECG and normal hs-TnI at 0 and 2 hrs identifies a significant proportion of patients with a low risk of MACE (<1%) who don’t look to need further testing.
By way of references check out a couple of papers on accelerated protocols (the future?) and the 2011 guideline summary (the past):
2-Hour Accelerated Diagnostic Protocol to Assess Patients With Chest Pain Symptoms Using Contemporary Troponins as the Only Biomarker