title: Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes.
abstract: OBJECTIVE
  We sought to assess the mechanism and prognostic value of elevated troponins in patients without acute coronary syndromes (ACS).
  
  
  BACKGROUND
  Cardiac troponins are used as specific markers for the diagnosis of ACS. Recent studies reported a considerable number of critically ill patients without ACS as being troponin-positive, especially patients with sepsis, pulmonary embolism, renal failure, and stroke.
  
  
  METHODS
  We analyzed 58 consecutive, critically ill patients admitted for reasons other than ACS, according to their troponin status. Thirty-day mortality, left ventricular ejection fraction (LVEF), and a panel of inflammatory cytokines were compared between troponin-positive and troponin-negative patients. Relevant coronary artery disease was excluded either by stress echocardiography or autopsy.
  
  
  RESULTS
  Of the 58 critically ill patients, 32 (55%) without evidence of ACS were troponin-positive. Positive troponin levels were associated with higher mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006). Troponin-positive patients had significantly higher median levels of tumor necrosis factor (TNF)-alpha, its soluble receptor, and interleukin (IL)-6. A subgroup of 10 aplastic patients was troponin-negative at study entry. Three became troponin-positive during leukocyte recovery and subsequently died, whereas all the others stayed troponin-negative and survived. Flow-limiting coronary artery disease was not demonstrable at autopsy or stress echocardiography in 72% of troponin-positive patients.
  
  
  CONCLUSIONS
  Elevated troponin is a mortality risk factor for medical intensive care patients admitted for reasons other than ACS. It is associated with decreased left ventricular function and higher levels of TNF-alpha and IL-6.
authors.affiliation: Division of Cardiology, Triemli Hospital, Zurich, Switzerland. peter.ammann@kssg.ch
authors.forename: Peter
authors.initials: P
authors.lastname: Ammann
authors.forename: Marco
authors.initials: M
authors.lastname: Maggiorini
authors.forename: Osmund
authors.initials: O
authors.lastname: Bertel
authors.forename: Edgar
authors.initials: E
authors.lastname: Haenseler
authors.forename: Helen I
authors.initials: HI
authors.lastname: Joller-Jemelka
authors.forename: Erwin
authors.initials: E
authors.lastname: Oechslin
authors.forename: Elisabeth I
authors.initials: EI
authors.lastname: Minder
authors.forename: Hans
authors.initials: H
authors.lastname: Rickli
authors.forename: Thomas
authors.initials: T
authors.lastname: Fehr
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000453:epidemiology*; D016638:Critical Illness / Q000401:mortality; D016207:Cytokines / Q000378:metabolism; D025401:Echocardiography, Stress; D005260:Female; D016905:Gram-Negative Bacterial Infections / Q000097:blood / Q000401:mortality; D016908:Gram-Positive Bacterial Infections / Q000097:blood / Q000401:mortality; D006801:Humans; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000502:physiology; D012307:Risk Factors; D012772:Shock, Septic / Q000097:blood / Q000401:mortality; D013318:Stroke Volume / Q000502:physiology; D016019:Survival Analysis; D013577:Syndrome; D013997:Time Factors; D014336:Troponin / Q000097:blood*
chemical_list: D015415:Biomarkers; D016207:Cytokines; D014336:Troponin