All troponins are not created equal
S Jossi1, S L Gordon, M A Legge
1Department of Clinical Chemistry, North Shore Hospital, Takapuna, Auckland, New Zealand.
Insights
Different troponin assays show poor agreement in classifying results, leading to significant variations in diagnosing acute coronary syndromes. Clinicians must consider the clinical context over assay-specific normal ranges.
Area of Science:
- Cardiology
- Clinical Chemistry
- Biomarker Analysis
Background:
- Troponin assays are crucial for diagnosing acute coronary syndromes (ACS).
- Clinical decisions rely on categorizing troponin results as positive or negative.
- Variability between troponin assays may impact patient diagnosis and management.
Purpose of the Study:
- To evaluate the categorical agreement between four different troponin assays.
- To assess the impact of assay variability on the classification of troponin results.
Main Methods:
- Analysis of 60 blood samples using three troponin I assays (Centaur, Architect, i-STAT) and one troponin T assay (Roche Elecys).
- Determination of upper reference limits based on a 10% coefficient of variation.
- Assessment of continuous agreement using Pearson's correlation and categorical agreement using Cohen's kappa.
Main Results:
- Continuous agreement between assays was generally good (Pearson's r = 0.871-0.995).
- Categorical agreement varied from poor (kappa = 0.37-0.48) to good (kappa = 0.68).
- The percentage of positive results ranged from 37% to 72%, a nearly twofold variation.
Conclusions:
- Significant variations exist in the proportion of positive results among different troponin assays.
- This variability may lead to missed diagnoses or false positives, affecting ACS management.
- Clinical judgment and context are essential when interpreting troponin results, rather than relying solely on local assay normal ranges.
Abstract:
Troponin measurement is central to the management and risk stratification of acute coronary syndromes. Decisions are made by categorizing troponin as positive or negative. We sought to evaluate categorical agreement between four troponin assays. Sixty blood samples were analysed by three troponin I assays (Centaur, Architect and point-of-care i-STAT) and one troponin T (TnT) assay (Roche Elecys). The upper reference limit was taken as the lowest value with a coefficient of variation of 10% or less. Continuous agreement between assays was good (Pearson's correlation coefficient 0.871-0.995). Categorical agreement assessed by Cohen's kappa varied from poor (between Architect and Centaur kappa = 0.37, and between TnT and Centaur kappa = 0.48) to good (between Architect and i-STAT kappa = 0.68, and between TnT and i-STAT kappa = 0.68). Percentage of positive results varied almost twofold, from 37% for the Centaur to 72% for the Architect. Comparison of four troponin assays showed up to twofold variations in the proportion of positive results. This implies that either a large proportion of troponin-positive diagnoses are missed by some assays or the assays with higher positivity are generating large numbers of false positives. Clinicians should evaluate troponin results in the clinical context and not base decisions solely on the 'normal range' of their local troponin assay.
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