PLATELET RESPONSE TO VASCULAR-SURGERY - A PRELIMINARY-STUDY ON THE EFFECT OF ASPIRIN AND HEPARIN

Patients with peripheral arterial disease (PAD) demonstrate high cardi ovascular mortality, which is further increased after arterial reconst ruction. Enhanced platelet reactivity has been postulated for these pa tients. The effect of surgery and of periprocedural aspirin and hepari n therapy on platelet reactivity was assessed with the Stagnation Poin t Flow Adhesio-Aggregometer (SPAA). The platelet adhesivity and aggreg ability of 44 PAD patients was quantitated perioperatively. Aspirin wa s administered during the entire course, low molecular weight heparin (LMWH) preoperatively and as of the fourth postoperative (pOP) day and unfractionated heparin (UH) upon surgery and three days thereafter. A group of 15 aspirin-free general surgical patients receiving LMWH and with no evidence of PAD served as controls. Plasma fibrinogen levels and platelet count were determined. The heparin-induced platelet activ ation (HIPA) assay for detection of heparin-associated thrombocytopeni a (HAT) antibodies was also performed. Baseline values of SPAA-measure d platelet reactivity (p < 0.001) and plasma fibrinogen (p < 0.01) wer e higher for patients as compared to controls and increased markedly a fter surgery. In the PAD group maximum platelet activation and fibrino gen levels coincided with a marked drop in platelet count and were con comitant to administration of unfractionated heparin. Thereby, a drop in platelet count of > 30% was observed in 25 patients (57%). The HIPA test verified HAT antibodies in 3 (12%) of these patients, two of whi ch suffered postoperative thrombosis. In the control group significant pOP increases were noted only for plasma fibrinogen. Changes in plate let count and reactivity were minimal and nonsignificant. No thrombosi s occurred and no HAT antibodies were detected. In PAD patients, concu rrent to pathologically enhanced baseline platelet function, surgical intervention resulted in a further increase in platelet reactivity in spite of aspirin therapy. UH may have promoted this hyperreactivity, a s indicated by the concomitant decrease in platelet count with the coi ncidence of postoperative thrombosis and the presence of HAT antibodie s. In the absence of PAD platelets participate insignificantly in the pOP acute phase reaction hallmarked by an increase in plasma fibrinoge n.