OPG (osteoprotegerin) has been suggested to have an important role in atherogenesis and vascular calcification. In the present study, we have investigated serum OPG and RANKL (receptor activator of nuclear factor κB ligand) concentrations in patients with ST elevation AMI (acute myocardial infarction) and established CAD (coronary artery disease). OPG and RANKL were measured in 58 male patients hospitalized in the coronary care unit with ST elevation AMI, in 52 asymptomatic male patients with an established diagnosis of CAD and in 52 healthy male controls. These last two groups were matched with the AMI patients for age and body mass index. OPG was significantly (P<0.05) higher in patients with AMI at 1 h after AMI (8.04±4.86 pmol/l) than in both patients with established CAD (4.92±1.65 pmol/l) and healthy subjects (3.15±1.01 pmol/l). Subjects with established CAD had significantly (P<0.05) increased OPG levels compared with controls. RANKL levels in patients with established CAD (0.02±0.05 pmol/l) and with AMI (0.11±0.4 pmol/l) were significantly (P<0.05) lower compared with controls (0.32±0.35 pmol/l). In the AMI group, OPG decreased significantly (P<0.05) at 1 and 4 weeks after infarction (8.04±4.86 compared with 6.38±3.87 and 6.55±2.6 pmol/l respectively), but OPG levels, either at 1 h or 1–4 weeks after AMI, remained significantly (P<0.05) higher compared with established CAD (4.92±1.65 pmol/l) and controls (3.15±1.01 pmol/l). Our data show for the first time that OPG levels are increased in ST elevation AMI within 1 h of infarction. Whether the increase in OPG is a consequence or a causal factor of plaque destabilization deserves further investigation.

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