Implementation of a Sensitive Troponin I Assay and Risk of Recurrent Myocardial Infarction and Death in Patients With Suspected Acute Coronary Syndrome
Does use of a high-sensitivity troponin I assay lead to improved clinical outcomes in patients with suspected acute coronary syndrome (ACS)?
Patients admitted with suspected ACS before (n = 1,038 during the validation phase) and after (n = 1,054 during the implementation phase) lowering the threshold of detection for myocardial necrosis from 0.20-0.05 ng/ml with a sensitive troponin I assay were stratified into three groups (<0.05 ng/ml, 0.05-0.19 ng/ml, and ≥0.20 ng/ml). During the validation phase, only concentrations above the original diagnostic threshold of 0.20 ng/ml were reported to clinicians. The primary endpoint was event-free survival (recurrent myocardial infarction [MI] and death) at 1 year in patients grouped by plasma troponin concentrations.
Plasma troponin concentrations were <0.05 ng/ml in 1,340 patients (64%), 0.05-0.19 ng/ml in 170 patients (8%), and 0.20 ng/ml or more in 582 patients (28%). During the validation phase, 39% of patients with plasma troponin concentrations of 0.05-0.19 ng/ml were dead or had recurrent MI at 1 year compared with 7% and 24% of those patients with troponin concentrations of <0.05 ng/ml (p < 0.001) or 0.20 ng/ml or more (p = 0.007), respectively. During the implementation phase, lowering the diagnostic threshold to 0.05 ng/ml was associated with a lower risk of death and recurrent MI (from 39% to 21%) in patients with troponin concentrations of 0.05-0.19 ng/ml (odds ratio, 0.42; p = 0.01).
The authors concluded that in patients with suspected ACS, implementation of a sensitive troponin assay increased the diagnosis of MI and identified patients at high risk of recurrent MI and death.
The use of troponins over creatine kinase-myocardial band for the diagnosis of MI has improved management of patients with suspected ACS and raises the issue as to whether even more sensitive assays will lead to further improvements in care. The current study indicates that a significant number of patients presenting with chest pain have evidence of myocyte injury not detected by current troponin thresholds. These patients were detected by increasing the sensitivity of the troponin assay. Importantly, this study suggests that this increased detection rate leads to improved patient management and clinical outcomes. Additional investigations on this important topic are needed.
Keywords: Myocardial Infarction, Acute Coronary Syndrome, Biological Markers, Chest Pain, Troponin I, Creatine Kinase, MB Form
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