title: Clinical significance of troponin elevations in acute decompensated diabetes without clinical acute coronary syndrome.
abstract: BACKGROUND
  Elevation of cardiac troponin has been documented in multiple settings without acute coronary syndrome. However, its impact on long-term cardiac outcomes in the context of acute decompensated diabetes remains to be explored.
  
  
  METHODS
  We performed a retrospective analysis of 872 patients admitted to Temple University Hospital from 2004-2009 with DKA or HHS. Patients were included if they had cardiac troponin I (cTnI) measured within 24 hours of hospital admission, had no evidence of acute coronary syndrome and had a follow up period of at least 18 months. Of the 264 patients who met the criteria, we reviewed the baseline patient characteristics, admission labs, EKGs and major adverse cardiovascular events during the follow up period. Patients were categorized into two groups with normal and elevated levels of cardiac enzymes. The composite end point of the study was the occurrence of a major cardiovascular event (MACE) during the follow up period and was compared between the two groups.
  
  
  RESULTS
  Of 264 patients, 24 patients were found to have elevated cTnI. Compared to patients with normal cardiac enzymes, there was a significant increase in incidence of MACE in patients with elevated cTnI. In a regression analysis, which included prior history of CAD, HTN and ESRD, the only variable that independently predicted MACE was an elevation in cTnI (p = 0.044). Patients with elevated CK-MB had increased lengths of hospitalization compared to the other group (p < 0.001).
  
  
  CONCLUSIONS
  Elevated cardiac troponin I in patients admitted with decompensated diabetes and without evidence of acute coronary syndrome, strongly correlate with a later major cardiovascular event. Thus, elevated troponin I during metabolic abnormalities identify a group of patients at an increased risk for poor long-term outcomes. Whether these patients may benefit from early detection, risk stratification and preventive interventions remains to be investigated.
authors.affiliation: Cardiology Section, Temple University School of Medicine, PA, USA.
authors.forename: Anthony
authors.initials: A
authors.lastname: Eubanks
authors.forename: Farhan
authors.initials: F
authors.lastname: Raza
authors.forename: Mohamad
authors.initials: M
authors.lastname: Alkhouli
authors.forename: April N
authors.initials: AN
authors.lastname: Glenn
authors.forename: Carol
authors.initials: C
authors.lastname: Homko
authors.forename: Abul
authors.initials: A
authors.lastname: Kashem
authors.forename: Alfred
authors.initials: A
authors.lastname: Bove
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood; D000328:Adult; D015415:Biomarkers / Q000097:blood; D048909:Diabetes Complications / Q000097:blood*; D005260:Female; D006801:Humans; D007662:Ketosis / Q000097:blood* / Q000150:complications; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D019210:Troponin I / Q000097:blood*; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D019210:Troponin I