Un abstract de un artículo a publicarse en Academic Emergency Medicine, sobre la significancia de las troponinas elevadas en el Servicio de Emergencia (Urgencias).
Los autores concluyen que aproximadamente el 75% de todos los pacientes con troponinas cardíacas elevadas en Urgencias no tienen infarto miocárdico tipo 1. Sin embargo la mortalidad de los pacientes sin IM tipo 1 es similar a la de los pacientes con IM tipo 1.
Analizando e n profundidad, me parece que hay un sesgo, porque en el grupo non-T1MI tambien hay MI, es decir, infartos miocárdicos agudos, pero de los de tipo 2. Un 35% que pesan mucho y por ello la mortalidad es similar. Es verdad que también hay un 35% de elevación de trapo niña de causa «multifactorial», pero es que más de un tercio de los pacientes con troponina I elevada tienen un IM tipo 2.
http://www.ncbi.nlm.nih.gov/pubmed/27320126
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 S, Thode HC, Peacock WF, Bock JL, Gruberg L4, Singer AJ.
Author information
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 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.
METHODS:
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.
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. This article is protected by copyright. All rights reserved.
