Troponin, A Predictor of Mortality in Methadone Exposure: An Observational Prospective Study
Open Access
- 20 April 2021
- journal article
- research article
- Published by Wolters Kluwer Health in Journal of the American Heart Association
- Vol. 10 (8) , e018899
Abstract
Background: Methadone poisoning/overdose is a global public health problem. We aimed to determine whether methadone poisoning increased cardiac troponin and whether high‐sensitivity cardiac troponin I (hs‐cTnI) levels predicted the need for intensive care unit admission, intubation, and mortality. Methods and Results: This observational, prospective single‐center study was done at Loghman‐Hakim Hospital (Tehran, Iran) from June 2018 until February 2019. Patients aged >14 years admitted with a diagnosis of methadone exposure were included. Patients were excluded if they had coexisting conditions associated with elevated hs‐cTnI levels. An ECG and hs‐cTnI levels were obtained on emergency department presentation. Patients were followed up on their need for intubation, intensive care unit admission, and in‐hospital mortality. Of 245 included patients (186 [75.9%] men; median age, 33 years), most referred to loss of consciousness (210 cases, 89%). Nineteen (7.7%) patients had hs‐cTnI levels of >0.1 ng/mL (positive), and 41 (16.7%) had borderline levels of 0.019 to 0.1 ng/mL. Twenty‐three (9.3%) cases were admitted to the intensive care unit, 21 (8.5%) needed intubation, and 5 (2%) died during hospitalization. An hs‐cTnI cutoff value of 0.019 ng/mL independently predicted mortality. For optimal concomitant sensitivity and specificity, receiver operating characteristic curve analysis was conducted and showed that hs‐cTnI had an independent significant association with mortality, with a cutoff value of 0.0365 ng/mL (odds ratio, 38.1; 95% CI, 2.3–641.9; P 0.019 ng/mL, and particularly >0.0365 ng/mL, of hs‐cTnI predicted mortality in our sample. Future studies should measure troponin levels in methadone maintenance treatment clients to assess the risk of myocardial injury from long‐term exposure.Keywords
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