Early Interleukin-1 Receptor Antagonist Elevation in Patients with Acute Myocardial Infarction

Giuseppe Parti, Andrea D'Ambrosio, Simona Mega, Gabriele Giorgi, Enrico Maria Zardi, Domenico Maria Zardi, Giordano Dicuonzo, Aldo Dobrina, Germano Di Sciascio

Risultato della ricerca: Contributo su rivistaArticolo in rivistapeer review

Abstract

OBJECTIVES: We sought to evaluate interleukin-1 receptor antagonist (IL-1Ra) levels in patients with ST-segment elevation acute myocardial infarction (AMI) upon emergency department (ED) admission in order to assess the sensitivity of such a determination by comparison with common markers of myocardial necrosis. BACKGROUND: Inflammatory markers are elevated in patients with unstable coronary syndromes, but IL-1Ra levels during the early phases of AMI have not been previously investigated. METHODS: Levels of IL-1Ra were measured in 44 consecutive patients with AMI and compared with creatine kinase (CK), CK-MB, troponin I, myoglobin, and C-reactive protein (CRP). RESULTS: Upon admission, 82% of patients had elevated (>230 pg/ml) IL-1Ra levels, compared with 41% of patients with raised CK (p = 0.001), CK-MB (45%, p = 0.002), troponin I (57%, p = 0.027), myoglobin (48%, p = 0.004), and CRP (57%, p = 0.019) levels. The IL-1Ra values were significantly higher in patients with heralded AMI than in those without pre-infarction angina (671 vs. 320 pg/ml, p = 0.013). The sensitivity of IL-1Ra determination increased to 86% when chest pain duration was S3 h and to 91% if heralded infarction occurred. CONCLUSIONS: Our study indicates that, unlike markers of necrosis, an increase of IL-1Ra levels occurs early in patients with AMI, is more significant in those with heralded infarction and symptom onset ≤3 h, and precedes the release of markers of necrosis. Thus, IL-1Ra determination may be an important early adjuvant toward the diagnosis of AMI in the ED.

Lingua originaleInglese
pagine (da-a)35-38
Numero di pagine4
RivistaJournal of the American College of Cardiology
Volume43
Numero di pubblicazione1
DOI
Stato di pubblicazionePubblicato - 7 gen 2004
Pubblicato esternamente

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