Causes of Elevated Cardiac Troponins in the Emergency Department and Their Associated Mortality
Stephen Meigher1, Henry C Thode1, W Frank Peacock2
1Department of Emergency Medicine, Stony Brook University, Stony Brook, NY.
Insights
Elevated cardiac troponins (cTn) often indicate myocardial damage. Nearly 75% of these elevations are not Type 1 myocardial infarction (T1MI), yet carry similar in-hospital mortality risks as T1MI.
Area of Science:
- Cardiology
- Emergency Medicine
- Biomarkers
Background:
- Cardiac troponins (cTn) are sensitive indicators of myocardial injury.
- Elevated cTn levels necessitate etiological determination, as per the third universal definition of myocardial infarction (MI).
- Distinguishing between Type 1 MI (T1MI) and other causes of cTn elevation is crucial for patient management.
Purpose of the Study:
- To investigate the causes of elevated cTn in an emergency department (ED) setting.
- To compare the characteristics and in-hospital mortality of patients with T1MI versus non-T1MI (including Type 2 MI, multifactorial, and non-ischemic causes).
Main Methods:
- Retrospective review of adult ED patients with elevated troponin I over one year.
- Classification of elevated cTn causes based on the third universal MI definition.
- Statistical comparisons (chi-square, Mann-Whitney U) of patient demographics, comorbidities, cardiac risk factors, and mortality between T1MI and non-T1MI groups.
Main Results:
- Of 13,502 patients with cTn measured, 1,310 (9.7%) had elevated levels.
- Non-T1MI causes accounted for approximately 75% of elevated cTn (T2MI: 35.2%, multifactorial: 35.7%, non-ischemic: 2.5%).
- In-hospital mortality was high and similar for both T1MI (11%) and non-T1MI (10%) groups.
Conclusions:
- The majority of elevated cardiac troponin in the ED are not due to Type 1 Myocardial Infarction.
- Non-T1MI etiologies, encompassing Type 2 MI, multifactorial causes, and non-ischemic injury, are prevalent.
- Patients with non-T1MI share similar high in-hospital mortality rates as those with T1MI, underscoring the need for thorough etiological investigation.
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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