Key result
Among adult emergency department patients with elevated cardiac troponins, non-Type 1 MI accounted for ~75% of cases and had similar in-hospital mortality to Type 1 MI (10% vs. 11%; p=0.48).
Why the study?
Does the etiology of elevated cardiac troponin (Type 1 MI vs non-Type 1 MI) affect in-hospital mortality in adult emergency department patients?
Observational (n=1,310)
No
Does the etiology of elevated cardiac troponin (Type 1 MI vs non-Type 1 MI) affect in-hospital mortality in adult emergency department patients?
Absolute Event Rate: 10% vs 11%
p-value: p=0.48
In emergency department patients with elevated troponin, non-Type 1 MI is the cause in approximately 75% of cases and is associated with an in-hospital mortality rate comparable to Type 1 MI.
Most ED troponin elevations are non-Type 1 MI with comparable mortality; leaves open whether etiology-specific strategies alter outcomes.
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.
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Meigher et al. (2016) conducted an observational in Elevated cardiac troponins (n=1,310). Non-Type 1 Myocardial Infarction (non-T1MI) vs. Type 1 Myocardial Infarction (T1MI) was evaluated on In-hospital mortality (p=0.48). Among adult emergency department patients with elevated cardiac troponins, non-Type 1 MI accounted for ~75% of cases and had similar in-hospital mortality to Type 1 MI (10% vs. 11%; p=0.48).
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