Antiplatelet use and glycaemic control in noncardiac critically ill patients with elevated Troponin T levels

In the nonintensive care setting recognition of patients with elevated Troponin T (cTnT) and the instigation of appropriate treatment, including antiplatelet agents and glycaemic control, reduces the risk of death and myocardial infarction [1]. In a surgical intensive care unit (ICU) (62% cardiothoracic) intensive insulin therapy reduces morbidity and mortality among critically ill patients [2].

Aims/methods

A retrospective audit was performed on 180 consecutive admissions to a general (noncardiothoracic) ICU to establish the incidence of raised cTnT (cTnT > 0.1 ng/ml) and treatment prescribed. The outcome measures were antiplatelet use, glycaemic control and all-cause mortality during the ICU admission. The unit protocol stated an insulin infusion should be commenced if blood glucose (BM) > 11.1 mmol/l.

Results

The incidence of cardiac myocyte damage, diagnosed by an elevated cTnT, was 62/180 (33%) with an associated all-cause mortality rate of 32/62 patients (51.6%) vs 24/118 patients (20.3%) in cTnT normal patients (P < 0.001). The median length of admission was 5.5 days for patients with a raised cTnT and 3 days for patients with a normal cTnT (P < 0.003). In 70.9% of cases, the raised cTnT occurred within the first 72 hours of admission to the ICU. Of those patients with an elevated cTnT, 10 patients were already on aspirin, two on clopidogrel and 14 had clear contraindications to antiplatelet therapy. Four patients (6%) were prescribed aspirin and 31 eligible patients (50%) did not receive antiplatelet therapy.

In patients with an elevated cTnT, 60/62 sets of notes were assessed for glycaemic control. In these patients 38/60 (63.3%) had BM > 11.1 mmol/l and 59/60 (98.3%) had BM > 6.1 mmol/l. A past history of impaired glucose tolerance/diabetes mellitus was present in 12/38 (31.6%) of patients with an elevated BM >11.1 mmol/l. Insulin therapy was not commenced in 6/38 patients with BM > 11.1 mmol/l. In 19/32 (59.4%) of patients prescribed insulin there was a delay in infusion commencement (median 3.5 hours, range 1–9 hours). Hypoglycaemia (BM < 2.2 mmol/l) was documented in 3/32 patients receiving insulin. The mortality rate was high in all patients with a raised BM (BM 6.1–11.1 mmol/l, mortality 12/21 (57.1%) vs 20/38 (52.6%) for BM > 11.1 mmol/l; NS). The one patient without an elevated BM survived.

Conclusions

Elevated markers of cardiac myocyte damage are common in critically ill patients and are associated with an increased mortality rate. The use of antiplatelet agents and optimisation of glycaemic control in this group might reduce morbidity and mortality. The aetiology of raised cTnT in the critically ill and specific treatment outcomes requires further investigation.