Platelet activation and coronary stent implantation. Effect of antithrombotic therapy.
BACKGROUND
Platelet activation and surface expression of adhesive glycoproteins play a key role in ischemic thrombotic complications after coronary intervention. The purpose of this case-control study was to evaluate the effects of two different antithrombotic regimens on platelet function after coronary Palmaz-Schatz stent implantation.


RESULTS
The study group consisted of 46 "low-risk" patients who were treated with ticlopidine (250 mg BID) and aspirin (100 mg BID) after stenting. The control group was derived from a cohort of 151 patients receiving conventional anticoagulation therapy, including phenprocoumon (target international normalized ratio, 3.5), heparin (activated partial thromboplastin time, 80 to 120 seconds), and aspirin (100 mg BID) after stenting. Criteria for matching were indication for stenting, target vessel, balloon size, inflation pressure, and number of inserted stents. Matches were obtained for 38 patients. Platelet function was evaluated before and daily for 12 days after stenting in venous blood samples with immunologic activation markers. Patients receiving anticoagulation therapy showed a significantly increased surface exposure of LIBS1 (activated fibrinogen receptor; P < .05) and CD62P (P-selectin; P < .001) above prestent values, peaking days 3 to 6 after stenting. In contrast, in patients receiving ticlopidine, expression of LIBS1 decreased (P < .01) and expression of CD62P remained basically unchanged after stenting. Platelet count significantly decreased after stenting in patients treated by anticoagulation (day 3; P < .01), whereas no significant changes were found in the ticlopidine group.


CONCLUSIONS
Significant platelet activation occurs in patients receiving anticoagulation therapy after stenting, while platelet deactivation is found in patients treated with combined antiplatelet therapy. This may contribute to a lowering of the incidence of subacute stent thrombosis.
Gawaz
M
M
First Medizinische Klinik, Technischen Universität München, Germany.
Neumann
F J
FJ
Ott
I
I
May
A
A
Schömig
A
A
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D016022:Case-Control Studies; D003331:Coronary Vessels / Q000601:surgery*; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000378:metabolism; D010644:Phenprocoumon / Q000627:therapeutic use; D015539:Platelet Activation / Q000187:drug effects*; D010976:Platelet Count / Q000187:drug effects; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000378:metabolism; D015607:Stents; D013988:Ticlopidine / Q000627:therapeutic use
D000925:Anticoagulants; D005343:Fibrinolytic Agents; D019007:P-Selectin; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D005340:Fibrinogen; D006493:Heparin; D013988:Ticlopidine; D010644:Phenprocoumon; D001241:Aspirin