IOHEXOL, PLATELET ACTIVATION AND THROMBOSIS II - IOHEXOL-INDUCED PLATELET SECRETION DOES NOT AFFECT COLLAGEN-INDUCED OR TISSUE-FACTOR-INDUCED THROMBUS FORMATION IN BLOOD THAT IS ANTICOAGULATED WITH HEPARIN ANDASPIRIN

Background: There is a dispute about the potential effects of radiogra phic contrast media (CM) on thrombogenesis. The nonionic CM iohexol tr iggers platelet beta-thromboglobulin (beta-TG) secretion, and thus may activate the platelets and promote thrombosis. We addressed this topi c in a study employing a human model of arterial thrombus formation in the presence of aspirin and heparin. This was a follow-up to our init ial study (on thrombus formation in native blood) which did not includ e antithrombotic drugs. The nonionic CM iohexol (monomer) and iodixano l (dimer) and the ionic CM ioxaglate (dimer) were compared. Methods an d Results: Thrombus formation was triggered by a surface rich in eithe r collagen or tissue factor, positioned in a parallel-plate perfusion chamber device at an arterial wall shear rate of 2600 s(-1). Blood fro m healthy volunteers, following ingestion of 1 g aspirin, was mixed wi th 40 vol% CM and 2.0 IU/ml heparin and passed over the surfaces. Thro mbus formation in the presence of either CM showed no difference, desp ite the fact that iohexol triggered a pronounced platelet beta-TG secr etion; iodixanol or ioxaglate were virtually inert. Conclusion: There was no association between iohexol-induced beta-TG secretion and throm bus formation on collagen (platelet-driven) or on tissue factor (throm bin-driven) in the presence of a standard antithrombotic regimen of as pirin and heparin as used in the clinic. The notion of a thrombotic ri sk due to platelet activation by iohexol was thus not substantiated by this study.