Abstract 16204: Circulating Levels of sTREM-1 and Mortality in Patients With an Acute Myocardial Infarction
Background and Aim: Acute myocardial infarction triggers an inflammatory cascade and activation of innate immune responses that lead to deleterious cardiac remodeling. The Triggering Receptor Expressed on Myeloid cells-1 (TREM-1) is a receptor expressed by neutrophils and monocytes. TREM-1 engagement has been shown to amplify the production of pro-inflammatory cytokines and chemokines as well as stimulating rapid neutrophil degranulation and oxidative burst. We investigated the relationship between plasma levels of the soluble form of TREM1 (sTREM1) and mortality following AMI.
Methods: We used data from 1015 patients enrolled in FAST-MI 2005 and replicate the measurements among 1293 patients enrolled in FAST-MI 2010, 2 nationwide surveys (NCT00673036,NCT01237418) conducted five years apart with a similar methodology and including during a one-month period all patients admitted for AMI with symptom onset ≤ 48 hours .
Results: Plasma levels of sTREM-1 at admission were related to higher risk of death after 2 years of follow up. The impact of sTREM-1 remained significant after adjustment for cardiovascular risk factors, hospital management including reperfusion therapy, recommended drug therapies, and C reactive protein. The adjusted HR of death at 2 years associated with an increase of 1 pg/mL of sTREM-1 was 2.22 (CI 95%=1.69-2.93, p< 0.0001). The risk of death was also associated with increasing tertiles of circulating sTREM-1 concentrations (H= 1.65 (0.87-3.10) and 3.11(1.72-5.64) in the second and third tertiles respectively, compared with the lowest tertile (P < 0.0001). The relationship between high plasma levels of sTREM-1 and increased mortality at 1 year was also replicated in FAST-MI 2010 (figure).
Conclusion: Circulating levels of sTREM-1 are associated with a higher risk of death in AMI patients. Whether inhibiting TREM-1 pathway in AMI setting would result in improving outcome needs further evaluation.
Author Disclosures: H. Ait Oufella: None. S. Gibot: None. N. Danchin: Research Grant; Significant; Astra zeneca, Daichi-Sankyo, Eli Lilly, GSK, MSD, Novartis, Sanofi. Speakers Bureau; Modest; Boehringer, Eli Lilly, MSD, NovoNordisk, Pfizer, Sanofi, servier, The Medco. Speakers Bureau; Significant; Astra Zeneca. M. Derive: None. S. kotti: None. J. lemarie: None. P. Ohlmann: None. A. Heitz: None. J. joffre: None. J. Darchis: None. A. Tedgui: None. Z. mallat: None. T. Simon: Research Grant; Significant; Astra Zeneca, Daichi, Lily, GSK, MSD, novaetis. Honoraria; Modest; sanofi, MSD, lilly, Bayer. Consultant/Advisory Board; Modest; Astra zeneca.
- © 2014 by American Heart Association, Inc.