Why the study?
Does combined antiplatelet therapy with aspirin and ticlopidine after intracoronary stent placement affect platelet, leukocyte, and endothelial cell activation in patients with coronary artery disease?
Does combined antiplatelet therapy with aspirin and ticlopidine after intracoronary stent placement affect platelet, leukocyte, and endothelial cell activation in patients with coronary artery disease?
Combined antiplatelet therapy with aspirin and ticlopidine after coronary stenting is associated with significant platelet and leukocyte deactivation, despite concurrent endothelial cell activation.
Supports differential activation effects of dual antiplatelet therapy post-stenting; hypothesis-generating and requires prospective validation before clinical consideration.
Activated platelets and leukocytes have been demonstrated to play a role in the development of stent thrombosis, and coronary angioplasty has been shown to result in activation of platelets, leukocytes, and endothelial cells. We aimed to evaluate the effects of intracoronary stent placement and aspirin plus ticlopidine treatment on platelets, leukocytes, and endothelial cells via observing the serial changes in the circulating soluble forms of adhesion molecules in 54 patients with coronary artery disease, who had elective coronary angioplasty and stent implantation for a single lesion of the left anterior descending artery. After stent placement, intravenous heparin infusion was administered only for 24 hours, and aspirin plus ticlopidine treatment was applied for 1 month. Venous blood samples were drawn before stent placement, and repeated 24 and 48 hours after the procedure. Patients were excluded if they had had recent cardiovascular events or any illness that might influence platelet, leukocyte, and endothelial cell function. The plasma level of sL-selectin was significantly decreased 48 hours after coronary stenting (636+/-110 ng/mL vs 567+/-93 ng/mL; P = 0.001, respectively). Likewise, the plasma level of sP-selectin was also decreased significantly 48 hours after the procedure (260+/-61 ng/mL vs 233+/-83 ng/mL, P = 0.01). The sE-selectin level was found to be significantly increased 24 hours (31+/-9 ng/mL vs 39+/-12 ng/mL, P = 0.0001) and 48hours(31+/-9 ng/mL vs 42+/-15 ng/mL, P = 0.001) after coronary stenting. The results of our study suggest that significant platelet and leukocyte deactivation take place in patients treated with combined antiplatelet therapy after stenting; endothelial cell activation also occurs during this treatment.
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Atalar et al. (2001) studied this question.
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