Abciximab therapy post elective coronary artery stenting does not prevent a troponin rise mediated by increased levels of platelet P-selectin and platelet-monocyte aggregates

Abstract number: P1769

Connor D. E., Joseph J. E., Baron D. W., Muller D. W., Roy P., Wilson S. W., Ma D. D. F.

St Vincents Hospital, Australia

Coronary artery stenting is used to treat atherosclerosis and all patients routinely receive aspirin and clopidogrel. Whilst the platelet glycoprotein IIb/IIIa antagonist abciximab may also be used, its benefit is less clear. We hypothesized that stenting would result in increased platelet activation and platelet-monocyte aggregates, and that use of abciximab may not necessarily limit subsequent cardiac ischemic damage. 27 patients undergoing elective stenting for stable angina were studied. Blood samples for platelet activation analysis were obtained from the coronary artery pre and post stenting. Platelet activation was determined by whole blood flow cytometric analysis of platelet CD62p, CD63 and PAC-1 expression and platelet-leukocyte complex formation. Troponin (TnI) levels were measured in peripheral blood samples taken 18-h post procedure and were the primary endpoint. All patients received aspirin and clopidogrel, whilst abciximab was given according to the cardiologist's discretion. A total of 15 patients received abciximab. A significant positive correlation was found between percentage increase (post compared to prestent) in CD62p expression and TnI levels (P = 0.005). There was a similar trend with percentage increase in platelet-monocyte aggregates, although this just failed to reach statistical significance (P = 0.08). A positive correlation was found between percentage increase in CD62p expression and percentage increase in platelet-monocyte aggregates (P = 0.013). Patients with an increase in CD62p expression had higher median TnI levels than those with no increase (3.1 and 0.4, respectively, P = 0.05). Patients with increased platelet-monocyte complexes demonstrated significantly higher median TnI levels compared to those with no increase (3.1 and 0.4, respectively, P = 0.04). There was no significant difference in median TnI levels between patients who received abciximab compared to those who did not (1.5 vs. 1.7 µg mL^-1, P = 0.75), and there were no significant differences in poststent levels of platelet activation markers between abciximab and nonabciximab patients. We conclude that increased platelet activation post stenting (namely increased platelet CD62p and platelet-monocyte aggregates) is associated with increased TnI levels, and that abciximab (which has its major effect on platelet GP IIb/IIIa) may be of little additional benefit for those patients who demonstrate such platelet activation. We continue to recruit patients and will also examine 30-day clinical event rate.