Objectives: To analyse the relation between serum glucose concentration and hospital outcome across the whole spectrum of acute coronary syndromes. Methods: This was a prospective cohort study of 2127 patients presenting with acute coronary syndromes. The patients were stratified into quartile groups (Q1 to Q4) defined by serum glucose concentrations of 5.8, 7.2, and 10.0 mmol/l. The relation between quartile group and major in-hospital complications was analysed. Results: The proportion of patients with acute myocardial infarction increased incrementally across the quartile groups, from 21.4% in Q1 to 47.9% in Q4 (p < 0.0001). The trend for frequency of in-hospital major complications was similar, particularly left ventricular failure (LVF) (Q1 6.4%, Q4 25.2%, p < 0.0001) and cardiac death (Q1 0.7%, Q4 6.1%, p < 0.0001). The relations were linear, each glucose quartile increment being associated with an odds ratio of 1.46 (95% confidence interval (CI) 1.27 to 1.70) for LVF and 1.52 (95% CI 1.17 to 1.97) for cardiac death. Although complication rates were higher for a discharge diagnosis of acute myocardial infarction than for unstable angina, there was no evidence that the effects of serum glucose concentration were different for the two groups, there being no significant interaction with discharge diagnosis in the associations between glucose quartile and LVF (p = 0.69) or cardiac death (p = 0.17). Similarly there was no significant interaction with diabetic status in the associations between glucose quartile and LVF (p = 0.08) or cardiac death (p = 0.09). Conclusion: Admission glycaemia stratified patients with acute coronary syndromes according to their risk of in-hospital LVF and cardiac mortality. There was no detectable glycaemic threshold for these adverse effects. The prognostic correlates of admission glycaemia were unaffected by diabetic status and did not differ significantly between patients with acute myocardial infarction and those with unstable angina.

The association between CRP and cardiac events in patients with unstable angina is influenced by pretreatment with aspirin. Modification of the acute-phase inflammatory responses to myocardial injury is the major mechanism of this interaction.

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These results indicate that impaired renal function will have little effect on the plasma concentrations of lamotrigine achieved for a given dosing regimen.

We conclude that ACE inhibition reduces troponin release in non-ST-elevation ACS. This is likely to be mediated by the beneficial effects of treatment on vascular reactivity and the coagulation system.

Aiiirs T h e aim of this study was to compare the pharmacokinetics of the antiepileptic agent, lamotrigine, in patients with chronic renal failure and healthy volunteers. Methods Non-compartmental pharmacohnetics of a single oral dose (200 nig) of the anti-epileptic agent, lamotrigine, and its main metabolite, lamotrigine N'glucuronide, were determined for 10 patients with chronic renal failure of mean estimated creatinine clearance 18 ml ininand a control group of 11 healthy volunteers, matched for age and gender. ResultsFor lamotrigine, there were no significant differences in Cmas, frnZ, AUC, t+,z, C L / F and amount excreted in urine although ttz tended to be longer for the renal failure group with a mean (fs.d.) of 35.9f 10.7 h us 2 7 . 8 k 4 . 3 h for the control group. For the renal failure group, Vz/F was 18% higher (95% C1 1% to 39%) compared with controls and CL, was reduced to 61% (95% C1 46% to 80%) of the control group value. For lamotrigine glucuronide, C,m,, was increased 4-fold (95% C1 3.1 to 5.3) and A U C 7.8-fold (95% C1 6.0 to 10.1) in the renal failure group compared with controls. CL, was approximately %fold lower and apparent tt was increased by 53% (95% C1 27% to 84%). Concentrations of an N2-methylated cardo-active metabolite, previously observed in dogs, were below the limit of detection (2 ng r n -l ) of the ASTED/h.p.l.c. assay in the renal failure group as well as controls. Conc-hsiorzs These results indicate that impaired renal function will have little effect on the plasma concentrations of lamotrigine achieved for a given dosing regimen.

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