Ionic contrast agent-mediated endothelial injury causes increased platelet deposition to vascular surfaces.

Contrast agent-mediated endothelial injury may be clinically relevant to the development of acute thrombosis after coronary interventions. We sought to investigate the extent to which contrast agents increase platelet deposition by measuring deposition of indium-111 radiolabeled platelets in an isolated perfused rabbit carotid artery model. Carotid artery segments were perfused at physiologic temperature, pressure, and shear. Vessels were subjected to angioplasty or no angioplasty before exposure to either buffer, diatrizoate (high osmolal/ionic), ioxaglate (low osmolal/ionic), or ioversol (low osmolal/nonionic). Subsequent deposition of indium-111 radiolabeled platelets was quantified. In vessels without balloon angioplasty, platelet deposition (platelets/cm2) was 110,000 +/- 95,000 for buffer perfused vessels, 280,000 +/- 210,000 for vessels perfused with diatrizoate, 290,000 +/- 160,000 for vessels perfused with ioxaglate, and 130,000 +/- 98,000 for vessels perfused with ioversol. After balloon angioplasty, platelet deposition was 1,300,000 +/- 590,000 for buffer controls, 1,800,000 +/- 320,000 for diatrizoate-perfused vessels, 1,500,000 +/- 450,000 for ioxaglate-perfused vessels, and 1,000,000 +/- 180,000 for ioversol-perfused vessels. In vessels without balloon angioplasty, diatrizoate and ioxaglate increased platelet deposition 2.5-fold and 2.6-fold, respectively, relative to buffer-perfused vessels (p < 0.05 and p < 0.01), whereas no increase was seen with ioversol. After balloon angioplasty, diatrizoate increased platelet deposition 1.4-fold over control (p < 0.05), whereas ioxaglate and ioversol showed no statistically significant increase. We conclude that ionic contrast media may cause more endothelial injury and associated localized platelet deposition than nonionic contrast media. These findings may be relevant to coronary interventions, specifically with regard to acute closure and chronic restenosis.