Aspects of trace element status have previously been investigated as possible contributory factors to atherosclerosis. In this present study a more comprehensive approach has been taken, looking at the relationship between dietary macro- and micronutrient intake, serum concentrations of zinc and copper, and markers of inflammation in dyslipidaemic patients with or without established coronary artery disease (CAD) and healthy controls, so that a clearer understanding of the potential relationship between copper and zinc status and coronary disease may be ascertained. Dyslipidaemic patients (n = 238) were recruited from the local General Hospital in Guildford, UK. Fifty-five of these patients had established CAD. Control subjects (n = 135) were recruited from among employees at the local University and Hospital. A validated food frequency questionnaire was used for estimating the dietary intake of zinc and copper. Serum copper, copper/caeruloplasmin ratio, zinc/copper ratio, and C-reactive protein (CRP) were significantly different in the patient groups compared to controls [serum copper: 17.20 +/- 0.2 v 15.91 +/- 0.29 micromol/L, p < 0.001; copper/caeruloplasmin ratio: 111.37 +/- 2.18 v 100.63 +/- 2.93 micromol/g, p < 0.01; zinc/copper ratio: 0.85 +/- 0.01 v 0.90 +/- 0.01, p < 0.05; and CRP: 1.25 (0.42-3.26) v 0.58 (0.17-1.42) mg/L, p < 0.001]. Dietary protein, total fat, starch, fibre, monounsaturated fat, zinc, and zinc/copper ratio were also significantly higher in the patients compared to controls. Patients with established CAD had significantly higher serum CRP (p < 0.05) and lower serum zinc (p < 0.01) and zinc/copper ratio (p < 0.01) compared to both patients without CAD and healthy controls. Significant differences in copper and zinc status, dietary intake and markers of inflammation were observed in patients with dyslipidaemia, with or without established CAD, compared with control subjects. Differences in serum CRP, copper and caeruloplasmin may be related to a heightened state of inflammation. The imbalance in zinc/copper metabolism may either contribute to the CAD risk or be a consequence of an acute phase response.