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HIGH-sensitivity troponin assays are effective in accelerating the diagnosis or exclusion of acute coronary syndrome and cutting emergency department stays, according to Victorian research published in the MJA. (1)
Professor Hans Schneider, director of pathology at The Alfred Hospital, Melbourne, told MJA InSight the introduction of the new high-sensitivity cardiac troponin (hscTn) assays had improved the diagnosis of acute coronary syndrome (ACS).
“They are better assays and I think, over time, all hospitals will move to them”, Professor Schneider said.
“When you put the assay in the right clinical pathway, you should be able to send patients home earlier from the emergency department”, he said, adding that The Alfred Hospital was attempting to reduce its emergency department (ED) short-stay time from 6 to 3 hours for patients at low risk of acute myocardial infarction.
The MJA research included 12 360 patients with suspected ACS presenting to Geelong Hospital ED before and after the changeover to hscTn assays, and found that the test was associated with more rapid diagnosis and less time in the ED.
“A higher proportion of patients had coronary angiographies after the changeover, but there was no significant change in rates of invasive treatment or inhospital mortality”, the researchers wrote.
In an accompanying editorial, Professor Derek Chew, of the department of cardiovascular medicine at Flinders Medical Centre, and Brisbane emergency physician Dr Louise Cullen, wrote that while the troponin assays offered improved patient outcomes by reducing the chance of missing myocardial infarction, they could also increase the “investigative burden” for patients with raised troponin from other causes. (2)
They said diagnostic innovation needed to be used in conjunction with “more effective clinical practice” by clinicians who fully understood the diagnostic tests they were using.
“This will require more robust protocols for risk quantification before troponin tests are requested, coupled with pathways for very early discharge and possibly investigations in ambulatory care settings”, they wrote.
Professor Con Aroney, interventional cardiologist at Queensland Cardiology and associate professor of medicine at the University of Queensland, told MJA InSight the shorter evaluation periods associated with hscTn assays would result in cost savings and would “definitely” become more widely available.
Professor Aroney said it was hoped this new accelerated pathway would be addressed in a revision of the ACS guidelines, currently being considered by the Heart Foundation and the Cardiac Society of Australia and New Zealand.
“The new ACS guidelines, which should be updated in the next 6 months, hopefully will address this issue more fully and come up with an official Australian guideline with regard to this accelerated pathway”, he said.
Professor Schneider said it was important to put patient assessment ahead of the test results. However, he said clinicians also needed to be conscious of the frequency of atypical presentations.
“I have seen quite a few [atypical presentations]. You have very elderly people who have an infarct and don’t have much pain. So it’s not always that easy.”
He said hscTn assays were very effective in excluding ACS. “If somebody has had chest pain for a period of time and you do the test and the test is negative, you are pretty sure that they won’t have acute coronary syndrome.”
A “For debate” article in the same issue of the MJA explored the use of troponin testing in general practice. (3)
The authors wrote that while hospitalisation should be the “default option” for patients with ACS symptoms, a single troponin test in primary care could exclude the possibility of acute myocardial infarction in asymptomatic low-risk patients whose symptoms resolved at least 12 hours prior.
Professor Aroney told MJA InSight these recommendations were valid and should be considered by the guideline committee.
Professor Schneider said an ED was the best place for a patient with chest pain and suspected ACS. However, in rural and regional areas point-of-care troponin testing was playing a key role in diagnosis in schemes such as South Australia’s Integrated Cardiovascular Clinical Network, he said. (4)
“These point-of-care assays are less sensitive but they still showed significant decreases in mortality in SA by having the right clinical pathways, so, in my opinion, the test in itself cannot supplant the clinical care of patients”, he said.
1. MJA 2014: 201: 158-161
2. MJA 2014; 201: 125-126
3. MJA 2014; 201: 155-157
4. MJA 2014; 200: 157-160
“The clinical pathways used remain critical for its use.” says Hans Schneider. That would work well if the clinical guidelines channelled the right people into the testing pathways, and didn’t encourage excessive admission and invasive testing. The test can be complicated by the ”oculo-stent reflex” where the operator sees a narrowing and stents it, even if there is no AMI, or no proof that the narrowing was associated with a chest pain episode. And yet, we know that stenting in non_AMI ACS does not improve outcome. What incentive is there for cardiologists to avoid invasive testing and pursue medical therapy?
The introduction of high sensitivity assays for troponin (be it I or T) allows better precision and accuracy in the identification of patients with AMI. The first generation of troponin assays identified additional patients not recognised by CKMB who had an increased risk of dying of AMI ( Med J Aust. 2001 Feb 19;174(4):170-3.). Subsequent improvement of the assays helped to identify additional patients at risk (Clin Chem. 2006 Feb;52(2):298-300). The assay used by Yip et al. (Med J Aust 2014; 201 (3): 158-161) is not considered to be a highly sensitive troponin assay (https://www.aacc.org/publications/clin_chem/Documents/030109Jaffe.pdf; Eur Heart J (2012) doi: 10.1093/eurheartj/ehs154; J Am Heart Assoc. 2014; 3: e000403). The Siemens Vista assay used is a contemporary troponin assay, similar to the one used at the Alfred in Melbourne from 2004 until July 2013, when it moved to a high sensitivity assay. Current high sensitivity troponin assays are able to measure troponin values in more than 50% of normal subjects, they frequently have different reference intervals for males and females and measure values in the low ng/L range.
The comments of CC and Sue are valid since troponin elevation is not automatically a sign of AMI but indicates myocardial damage, but not the cause of it. The clinical pathways used remain critical for its use.
CC is right. The actual study in the MJA found that people spent less time in ED, but MORE people got invasive testing without an increase in AMI diagnosis or outcome benefit. Want to reduce health care costs? DOn’t misapply a test to a low prevalence population, and don’t misinterpret the pathophysiology. Raised troponin is a marker for myocaridal cell strain, not necessarily acute coronary artery occlusion. We need critical thinking before we apply tools, and more tools than just hammers.
whilst the Professor praises the value of high sensitivity troponins, he appears to ignore the low specificity of this test, and the huge risk of overinvestigation of patients who frequently have raised troponins for reasons other than AMI. Quite frankly the high sensitivity troponins have created a lot of frustration for staff in Emergency department settings.