Short Attention Span Summary
What is the significance of an elevated troponin? In this retrospective look, about 25% were type 1 MI (plaque rupture + thrombus), 35% type 2 MI (supply-demand mismatch), 36% multifactorial, and 2.5% non-ischemic cardiac injury. Does it matter that a patient has an elevated troponin? Yes, those with non-type 1 MI had the same mortality as those with type 1 MI, around 10-11%. An elevated troponin is a marker for badness and for increased mortality, whether due to classic MI from plaque rupture or for another reason.
Acad Emerg Med. 2016 Jun 20. doi: 10.1111/acem.13033. [Epub ahead of print]
Causes of elevated cardiac troponins in the emergency department and their associated mortality.
Meigher S1, Thode HC1, Peacock WF2, Bock JL3, Gruberg L4, Singer AJ1.
1Departments of Emergency Medicine, Stony Brook University, Stony Brook, NY.
2Department of Emergency Medicine, Baylor College of Medicine, Houston, TX.
3Department of Clinical Pathology, Stony Brook University, Stony Brook, NY.
4Department of Cardiology, Stony Brook University, Stony Brook, NY.
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 3rd 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.
We performed a structured, retrospective review of all consecutive adult ED patients with elevated troponin I (defined as >99th %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 3rd Universal Definitions. Comparisons between groups were performed using Χ2 and Mann-Whitney U tests.
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).
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. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
PMID: 27320126 [PubMed – as supplied by publisher]