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  • Open Access

Elevated Troponin T levels in patients with and without renal dysfunction in a general intensive care unit

  • 1 and
  • 1
Critical Care20048 (Suppl 1) :P81

https://doi.org/10.1186/cc2548

  • Published:

Keywords

  • Intensive Care Unit
  • Acute Coronary Syndrome
  • Renal Dysfunction
  • Cardiac Myocyte
  • Cardiac Troponin

Myocardial dysfunction is common in critically ill patients. The diagnosis of an acute coronary syndrome has been revolutionised by the protein isomer, cardiac Troponin T (cTnT). In the nonintensive care setting early recognition of patients with elevated cTnT and the instigation of appropriate treatment has been shown to reduce the risk of death and myocardial infarction. Concern has been raised about the prognostic value of cTnT in patients with renal dysfunction as troponin is renally excreted.

Methods

A retrospective audit was carried out on 180 consecutive admissions to a general (noncardiothoracic) intensive care unit (ICU) to establish the incidence of raised cTnT (cTnT > 0.1 ng/ml) in patients with and without renal dysfunction. Renal dysfunction was defined as Creatinine > 120 μmol/l. Results expressed as median (minimum–maximum).

Results

Of 180 admissions, 62 patients (39 males, age 69 years [34–85 years]) had an elevated cTnT > 0.1 ng/ml during their time on the ICU. The length of stay was 5.5 days for patients with a raised cTnT and 3 days for patients with a normal cTnT (P < 0.003). The primary diagnosis for admission was cardiac in six patients, respiratory in 14 patients, general medical in 18 patients, vascular surgery in nine patients and general surgical in 15 patients. Of these 32/62 (51.6%) died while on the ICU compared with 24/118 (20.3%) of those with a normal cTnT (P < 0.001). In 70.9% of cases the raised cTnT occurred within the first 72 hours of admission.

The outcome and cTnT of patients with and without renal dysfunction are presented in Table 1. There was no correlation between renal function and cTnT level (r = -0.06). There was no significant difference in outcome between raised cTnT patients with and without renal dysfunction.

Table 1

 

Renal impairment

Normal renal function

 

Alive

Dead

Alive

Dead

Total number of patients

19

20

11

8

cTnT (ng/ml) (minimum–maximum)

0.4 (0.14–2.17)

0.31 (0.12–12.2)

0.35 (0.12–7.1)

0.35 (0.11–3.74)

Conclusion

Elevated markers of cardiac myocyte damage are common in critically ill patients and are associated with an increased mortality rate. This effect is seen irrespective of renal function.

Authors’ Affiliations

(1)
James Cook University Hospital, Middlesbrough, UK

Copyright

© BioMed Central Ltd. 2004

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