title: Trauma-induced secondary cardiac injury is associated with hyperacute elevations in inflammatory cytokines.
abstract: BACKGROUND
  Clinical evidence supports the existence of a trauma-induced secondary cardiac injury. Experimental research suggests inflammation as a possible mechanism. The study aimed to determine if there was an early association between inflammation and secondary cardiac injury in trauma patients.
  
  
  METHODS
  A cohort study of critically injured patients between January 2008 and January 2010 was undertaken. Levels of the cardiac biomarkers troponin I and heart-specific fatty acid-binding protein and the cytokines tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-1β, and IL-8 were measured on admission to hospital, and again at 24 and 72 h. Participants were reviewed for adverse cardiac events (ACEs) and in-hospital mortality.
  
  
  RESULTS
  Of 135 patients recruited, 18 (13%) had an ACE. Patients with ACEs had higher admission plasma levels of TNF-α (5.4 vs. 3.8 pg/mL; P = 0.03), IL-6 (140 vs. 58.9 pg/mL, P = 0.009), and IL-8 (19.3 vs. 9.1 pg/mL, P = 0.03) compared with those without events. Hour 24 cytokines were not associated with events, but IL-8 (14.5 vs. 5.8 pg/mL; P = 0.01) and IL-1β (0.55 vs. 0.19 pg/mL; P = 0.04) were higher in patients with ACEs at 72 hours. Admission IL-6 was independently associated with heart-specific fatty acid-binding protein increase (P < 0.05). Patients who presented with an elevated troponin I combined with either an elevated TNF-α (relative risk [RR], 11.0; 95% confidence interval [CI], 1.8-66.9; P = 0.015), elevated IL-6 (RR, 17.3; 95% CI, 2.9-101.4; P = 0.001), or elevated IL-8 (RR, 15.0; 95% CI, 3.1-72.9; P = 0.008) were at the highest risk of in-hospital death when compared with individuals with normal biomarker and cytokine values.
  
  
  CONCLUSIONS
  There is an association between hyperacute elevations in inflammatory cytokines with cardiac injury and ACEs in critically injured patients. Biomarker evidence of cardiac injury and inflammation on admission is associated with a higher risk of in-hospital death.
authors: Centre for Trauma Sciences, Barts and the London School of Medicine & Dentistry, Queen Mary, UK. HenryDe-Ath@doctors.org.uk.
authors: Henry D
authors: HD
authors: De'Ath
authors: Joanna
authors: J
authors: Manson
authors: Ross
authors: R
authors: Davenport
authors: Simon
authors: S
authors: Glasgow
authors: Ian
authors: I
authors: Renfrew
authors: L Ceri
authors: LC
authors: Davies
authors: Rakesh
authors: R
authors: Uppal
authors: Karim
authors: K
authors: Brohi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood*; D016207:Cytokines / Q000097:blood*; D050556:Fatty Acid-Binding Proteins / Q000097:blood; D005260:Female; D006335:Heart Injuries / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D006801:Humans; D007375:Interleukin-1 / Q000097:blood; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D019210:Troponin I / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014947:Wounds and Injuries / Q000097:blood / Q000150:complications* / Q000276:immunology*; D055815:Young Adult
chemical_list: D015415:Biomarkers; D016207:Cytokines; D050556:Fatty Acid-Binding Proteins; D007375:Interleukin-1; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha