1. Oxygen-derived free radicals have been implicated in reperfusion injury after thrombolytic therapy in acute myocardial infarction. To test the hypothesis that diabetic patients may have increased oxidative stress which may lead to increased reperfusion damage and thereby contribute to a poorer outcome in these patients, we measured two indices of free-radical activity, diene conjugate molar ratios as an index of lipid isomerization and thiobarbituric acid-reactive material as an index of lipid peroxidation, in 66 non-diabetic and 26 diabetic patients admitted with acute myocardial infarction who received thrombolytic therapy and in whom reperfusion was assessed using early time to peak creatine kinase-MB isoenzyme release.
2. Baseline diene conjugate molar ratios or thiobarbituric acid-reactivity did not differ significantly between diabetic and non-diabetic patients (1.97 + 0.98 versus 2.16 + 1.34; not significant and 2.10 + 0.60 versus 1.99 + 0.73 μmol/l; not significant). In patients with enzymic evidence of reperfusion (i.e. time to peak enzyme release ≦12h) diene conjugate molar ratios peaked at 6 h compared with 12 h in those with unsuccessful reperfusion (i.e. time to peak enzyme release >12 h). In patients with unstable angina the maximum increase in the diene conjugate molar ratios was significantly less than in patients with acute myocardial infarction (6.80 + 12.3 versus 15.82 + 22.55%; P = 0.035). There was a significant fall in thiobarbituric acid-reactivity at 24 h in patients with enzymic evidence of reperfusion (P = 0.017). There were no major differences in these rises and falls between diabetic and non-diabetic patients.
3. These findings suggest the free-radical activity as assessed by diene conjugate molar ratios was increased after myocardial infarction, but the increase was not significantly different in diabetic and non-diabetic patients. Early peaking of free-radical activity was associated with enzymic evidence of reperfusion.