Bivalirudin decreases NO bioavailability by vascular immobilization of myeloperoxidase

RUDOLPH V, RUDOLPH TK, SCHOPFER FJ, BONACCI G, LAU D, SZÖCS K, KLINKE A, MEINERTZ T, FREEMAN BA, BALDUS S.

AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS

Año: 2008 vol. 327 p. 324 - 324

ivalirudin, a direct thrombin inhibitor, has emerged as an important alternative to heparin in patients undergoing percutaneous coronary intervention. However, it remains elusive if potentially adverse extracoagulant properties are responsible for the fact that its favorable effects in clinical studies are mainly driven by a reduction in bleeding events. The aim of the current study was to determine the effects and mechanisms of acute treatment with bivalirudin in comparison to heparin on NO bioavailability, an important factor for the pathogenesis of ischemic events. In particular, we studied the interaction between bivalirudin and myeloperoxidase (MPO), a leukocyte-derived enzyme that consumes endothelial-derived nitric oxide (NO), modifies a variety of biological targets, and thus affects the integrity of the vessel wall. In patients undergoing elective percutaneous coronary intervention, bivalirudin, in contrast to heparin, exhibited a significant decrease in plasma MPO levels (p