Most rural hospitals reliant on POC troponin

Wednesday, April 17th, 2019 | Rory | No Comments

Miller R, Stokes T, Nixon G. Point-of-care troponin use in New Zealand rural hospitals: a national survey. New Zealand Medical Journal. 2019;132(1493):13.

Not a great surprise: most rural hospitals do not have timely access to the same troponin assays that metropolitan hospitals rely on, instead reliant on less sensitive point-of-care troponin. A significant number of NSTEMI maybe missed using POC troponin at the manufacturer’s cut-off and we have an observational study underway evaluating a pathway that will limit these missed AMI.(1,2) This pathway has been shown to be effective in a pilot run in a low-risk primary care population.(3) There is also hope as discussed previously that a new high precision point-of-care assay will bring rural chest pain assessment in line with urban hospitals.(4)

“The results of this survey reinforce the importance of considering the context and resources of all New Zealand hospitals when making recommendations at a national level, such as the adoption of ADPs. Failure to do so can confuse clinical practice in our small rural hospitals that have access to fewer resources and risks exacerbating existing inequities.”

Abstract

AIMS: Accelerated diagnostic chest pain pathways (ADP) have become standard of care in urban emergency departments. It is, however, unknown how widely they are used in New Zealand’s rural hospitals because ADP require immediate access to contemporary or high-sensitivity troponin (hs-Tn). We aimed to determine for rural hospitals the troponin assay being used, if they were using an ADP and if they had access to on-site exercise tolerance testing (ETT).

METHODS: An online survey was sent to 27 rural hospitals providing acute care in New Zealand.

RESULTS: Most rural hospitals (23/27, 85%) responded to the survey. Most (17/23, 74%) used point-of- care cardiac troponin (POC-cTn) and the majority of these hospitals (15/17, 88%) were reliant on this assay 24-hours per day. All hospitals that had timely access to hs-Tn (8/23, 35%) used an ADP but only a minority (4/17, 24%) of hospitals using POC-cTn used an ADP. Only a minority of the larger rural hospitals (7/23, 30%) had access to on-site ETT.

CONCLUSIONS: Most New Zealand rural hospitals rely on POC-cTn to assess chest pain and are not using an ADP. There are limited data available to support this approach in rural settings especially with patients who are not low-risk.

References

1. Miller R, Nixon G. The assessment of acute chest pain in New Zealand rural hospitals utilising point-of-care troponin. Journal of Primary Health Care. 2018;10(1):90–2.

2. Schneider HG, Ablitt P, Taylor J. Improved sensitivity of point of care troponin I values using reporting to below the 99th percentile of normals. Clinical Biochemistry. 2013 Aug;46(12):979–82.

3. Norman T, Devlin G, Than M, George P, Young J, Egan G, et al. Measured Implementation of an Accelerated Chest Pain Diagnostic Pathway in Primary Care. Heart, Lung and Circulation. 2018 Jan;27:S4–5.

4. Pickering JW, Young JM, George PM, Watson AS, Aldous SJ, Troughton RW, et al. Validity of a Novel Point-of-Care Troponin Assay for Single-Test Rule-Out of Acute Myocardial Infarction. JAMA Cardiology. 2018 Oct;

A nearly High Sens point-of-care Troponin: potential equity for rural hospitals?

Friday, October 19th, 2018 | Rory | 2 Comments

Pickering JW, Young JM, George PM, et al. Validity of a Novel Point-of-Care Troponin Assay for Single-Test Rule-Out of Acute Myocardial Infarction. JAMA Cardiol. Published online October 17, 2018. doi:10.1001/jamacardio.2018.3368

Second troponin paper for the day:

A first look at a new POC assay from Abbott by a group well known for their work in chest pain assessment. This preliminary study performed in Christchurch ED (urban population) shows a single test (used in a laboratory) on presentation (that takes 15minutes to run) effectively excludes Type 1 myocardial infarction in low-risk patients – with the same Sens/NPV as a laboratory based . Need to wait to see real world performance but promising for rural GP and hospitals reliant on point-of-care troponin when assessing chest pain. Not calling it high-sens yet… Semantics

Open access

https://jamanetwork.com/journals/jamacardiology/fullarticle/2705683

High-STEACS: making a difference?

Friday, October 19th, 2018 | Rory | No Comments

Shah ASV, Anand A, Strachan FE, Ferry AV, Lee KK, Chapman AR, et al. High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: a stepped-wedge, cluster-randomised controlled trial. The Lancet. 2018 Sep;392(10151):919–28.

Large trial that showed no difference in patient outcomes (mortality, major adverse cardiac events) despite an increase in the number of patients re-classified as having NSTEMI with the high-sens assay compared to a contemporary troponin assay. These patients were older and female (a lower cutoff is used in the high-sens but not the contemporary assay for females).

These Scottish hospitals used the troponin in a different way to that used in most NZ urban hospitals, where there is an accelerated chest pain pathway, which limits external validity. The sites tested at 0hrs and 6–12hrs.

Some NZ rural hospitals use high-sens troponin but most use a point-of-care assay. Few if any use a contemporary troponin, but this is still being reported in community laboratories. It is unclear what this means for those using the point-of-care test.

I think that it is becoming clear that the value of the high-sensitivity troponin assay is in allowing an earlier, rather than a better risk assessment.

deeper analysis at The Bottom Line

Summary

Background High-sensitivity cardiac troponin assays permit use of lower thresholds for the diagnosis of myocardial infarction, but whether this improves clinical outcomes is unknown. We aimed to determine whether the introduction of a high-sensitivity cardiac troponin I (hs-cTnI) assay with a sex-specific 99th centile diagnostic threshold would reduce subsequent myocardial infarction or cardiovascular death in patients with suspected acute coronary syndrome.

Methods In this stepped-wedge, cluster-randomised controlled trial across ten secondary or tertiary care hospitals in Scotland, we evaluated the implementation of an hs-cTnI assay in consecutive patients who had been admitted to the hospitals’ emergency departments with suspected acute coronary syndrome. Patients were eligible for inclusion if they presented with suspected acute coronary syndrome and had paired cardiac troponin measurements from the standard care and trial assays. During a validation phase of 6–12 months, results from the hs-cTnI assay were concealed from the attending clinician, and a contemporary cardiac troponin I (cTnI) assay was used to guide care. Hospitals were randomly allocated to early (n=5 hospitals) or late (n=5 hospitals) implementation, in which the high- sensitivity assay and sex-specific 99th centile diagnostic threshold was introduced immediately after the 6-month validation phase or was deferred for a further 6 months. Patients reclassified by the high-sensitivity assay were defined as those with an increased hs-cTnI concentration in whom cTnI concentrations were below the diagnostic threshold on the contemporary assay. The primary outcome was subsequent myocardial infarction or death from cardiovascular causes at 1 year after initial presentation. Outcomes were compared in patients reclassified by the high-sensitivity assay before and after its implementation by use of an adjusted generalised linear mixed model. This trial is registered with ClinicalTrials.gov, number NCT01852123.

Findings Between June 10, 2013, and March 3, 2016, we enrolled 48282 consecutive patients (61 [SD 17] years, 47% women) of whom 10360 (21%) patients had cTnI concentrations greater than those of the 99th centile of the normal range of values, who were identified by the contemporary assay or the high-sensitivity assay. The high- sensitivity assay reclassified 1771 (17%) of 10 360 patients with myocardial injury or infarction who were not identified by the contemporary assay. In those reclassified, subsequent myocardial infarction or cardiovascular death within 1 year occurred in 105 (15%) of 720 patients in the validation phase and 131 (12%) of 1051 patients in the implementation phase (adjusted odds ratio for implementation vs validation phase 1·10, 95% CI 0·75 to 1·61; p=0·620).

Interpretation Use of a high-sensitivity assay prompted reclassification of 1771 (17%) of 10 360 patients with myocardial injury or infarction, but was not associated with a lower subsequent incidence of myocardial infarction or cardiovascular death at 1 year. Our findings question whether the diagnostic threshold for myocardial infarction should be based on the 99th centile derived from a normal reference population.