Key result
High-sensitivity cardiac troponin I levels >0.0365 ng/mL independently predicted mortality in patients admitted for methadone exposure (OR 38.1; 95% CI 2.3-641.9; P<0.001).
Why the study?
Methadone poisoning is a global public health problem, but whether it increases cardiac troponin and whether hs-cTnI levels predict ICU admission, intubation, and mortality was unknown.
Does high-sensitivity cardiac troponin I (hs-cTnI) predict the need for intensive care unit admission, intubation, and mortality in patients with methadone exposure?
Observational (n=245)
No
Does high-sensitivity cardiac troponin I (hs-cTnI) predict the need for intensive care unit admission, intubation, and mortality in patients with methadone exposure?
Odds Ratio: 38.1 (95% CI 2.3–641.9)
p-value: p=<0.001
Elevated high-sensitivity cardiac troponin I levels independently predict in-hospital mortality in patients presenting with methadone poisoning.
hs-cTnI elevation in methadone poisoning may predict mortality; hypothesis-generating for troponin-guided risk stratification in toxicology.
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 <0.001). Conclusions Methadone exposure/toxicity is a newly identified cause of elevated hs‐cTnI. Values >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.
No takes yet. Share an insight, caveat, or question.
Sheibani et al. (2021) conducted an observational in Methadone exposure (n=245). High-sensitivity cardiac troponin I (hs-cTnI) >0.0365 ng/mL vs. Lower hs-cTnI levels was evaluated on Mortality (OR 38.1, 95% CI 2.3-641.9, p=<0.001). High-sensitivity cardiac troponin I levels >0.0365 ng/mL independently predicted mortality in patients admitted for methadone exposure (OR 38.1; 95% CI 2.3-641.9; P<0.001).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: