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Causes of Elevated Cardiac Troponins in the Emergency Department and Their Associated Mortality.
Academic Emergency Medicine 2016 November
OBJECTIVE: Cardiac troponins (cTn) are structural components of myocardial cells and are expressed almost exclusively in the heart. Elevated cTn levels indicate myocardial cell damage/death but not reflect the underlying etiology. The third universal definition of myocardial infarction (MI) differentiates MI into various types. Type 1 (T1MI) is due to plaque rupture with thrombus, while type 2 (T2MI) is a result of a supply:demand mismatch. Non-MI cTn elevations are also common. We determined the causes of elevated cTn in a tertiary care emergency department (ED) and the associated in-hospital mortality.
METHODS: We performed a structured, retrospective review of all consecutive adult ED patients with elevated troponin I (defined as > 99th percentile of the normal population, as run on the ADVIA Centaur platform; Siemens USA) during 1 year. Causes of elevated cTn were classified based on the third universal definitions. Comparisons between groups were performed using chi-square and Mann-Whitney U-tests.
RESULTS: Of 96,612 ED patients presenting from May 2012 to April 2013, a total of 13,502 (14%) had cTn measured, of which 1,310 (9.7%) were elevated. Of these, 340 (26.5%, 95% confidence interval [CI], 24.2% to 29.0%) were T1MI, 452 (35.2%, 95% CI = 32.7% to 37.9%) T2MI, 458 (35.7%, 95% CI = 33.1% to 38.4%) multifactorial, and 33 (2.5%, 95% CI = 1.8% to 3.5%) due to nonischemic injury. Non-T1MI patients were slightly older, more likely female, and had higher blood urea nitrogen and creatinine. Comorbidities were more common in non-T1MI while cardiac risk factors were more common in T1MI. Non-T1MI patients were less likely to have diagnostic ECGs and had lower initial and subsequent cTn levels. In-hospital mortality rates were similarly high for T1MI and non-T1MI (11% [95% CI = 8% to 15%] vs. 10% [95% CI = 8% to 12%], p = 0.48).
CONCLUSIONS: Of all ED patients with elevated cTn, ~75% have a non-T1MI. The mortality of patients with non-T1MI is similar to the mortality in patients with T1MI.
METHODS: We performed a structured, retrospective review of all consecutive adult ED patients with elevated troponin I (defined as > 99th percentile of the normal population, as run on the ADVIA Centaur platform; Siemens USA) during 1 year. Causes of elevated cTn were classified based on the third universal definitions. Comparisons between groups were performed using chi-square and Mann-Whitney U-tests.
RESULTS: Of 96,612 ED patients presenting from May 2012 to April 2013, a total of 13,502 (14%) had cTn measured, of which 1,310 (9.7%) were elevated. Of these, 340 (26.5%, 95% confidence interval [CI], 24.2% to 29.0%) were T1MI, 452 (35.2%, 95% CI = 32.7% to 37.9%) T2MI, 458 (35.7%, 95% CI = 33.1% to 38.4%) multifactorial, and 33 (2.5%, 95% CI = 1.8% to 3.5%) due to nonischemic injury. Non-T1MI patients were slightly older, more likely female, and had higher blood urea nitrogen and creatinine. Comorbidities were more common in non-T1MI while cardiac risk factors were more common in T1MI. Non-T1MI patients were less likely to have diagnostic ECGs and had lower initial and subsequent cTn levels. In-hospital mortality rates were similarly high for T1MI and non-T1MI (11% [95% CI = 8% to 15%] vs. 10% [95% CI = 8% to 12%], p = 0.48).
CONCLUSIONS: Of all ED patients with elevated cTn, ~75% have a non-T1MI. The mortality of patients with non-T1MI is similar to the mortality in patients with T1MI.
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