The online version of this article (doi:10.1186/1475-2840-11-154) contains supplementary material, which is available to authorized users.
None of the authors have competing interests to disclose.
AE worked to collect data, research background articles, and draft the initial version of the manuscript. FR worked to collect data, research background articles and provide key editorial input for subsequent drafts of the manuscript. MA initiated the experimental design, researched background articles, interpreted EKGs, provided key editorial input for subsequent drafts of the manuscript. AG worked to edit the collected data, provide key editorial input for subsequent drafts, and played a key role in analyzing the study results and was very active in drafting the initial discussion section. HK provided key insight into the final outcomes, study design, editorial review and final version of the manuscript. AK worked throughout all stages of the study to provide key insight regarding the study outcomes, interpreting data, researching background articles and validation of statistical analysis. AB served as the principal investigator and worked in all stages of the study including statistical analysis, editorial review, and provided key insight regarding interpretation of the data. All contributions from authors involved were essential in the development of the manuscript. All authors read and approved the final manuscript.
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.
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.
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).
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.
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- Clinical significance of troponin elevations in acute decompensated diabetes without clinical acute coronary syndrome
April N Glenn
- BioMed Central
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