Causes of elevated cardiac troponins in the emergency department and their associated mortality

Abstract

Study 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 3^rd 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 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 >99^th %ile of the normal population, as run on the ADVIA Centaur^® platform; Siemens USA, Malvern, PA) during 1 year. Causes of elevated cTn were classified based on the 3^rd Universal Definitions. Comparisons between groups were performed using Χ² and Mann-Whitney U tests.

Results

Of 96,612 ED patients presenting from 5/12-4/13, 13,502 (14%) had cTn measured, of which 1,310 (9.7%) were elevated. Of these, 340 (26.5%, 95% CI, 24.2-29.0) were T1MI, 452 (35.2%, 95% CI, 32.7-37.9) T2MI, 458 (35.7%, 95% CI, 33.1-38.4) multifactorial and 33 (2.5%, 95% CI, 1.8-3.5) due to non-ischemic injury. Non-T1MI patients were slightly older, more likely female, and had higher BUN 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 8-15%] vs. 10% [95% CI 8-12%], 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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