BACKGROUND: Platelet glycoprotein IIb/IIIa receptor blockade not only enhances epicardial flow but also improves microvascular perfusion. Inhibition of abnormal platelet-endothelial interactions may contribute to this beneficial effect. The present study was designed to determine whether glycoprotein IIb/IIIa receptor blockade influences endothelial vasomotor function and NO bioactivity in patients with coronary artery disease. METHODS AND RESULTS: Forty patients with symptomatic coronary artery stenosis were studied before planned percutaneous coronary intervention. By using venous occlusion plethysmography, endothelium-dependent and -independent vasodilation was determined by measuring forearm blood flow responses to acetylcholine with and without NG-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside. Vascular function tests were repeated during glycoprotein IIb/IIIa receptor blockade by tirofiban in 27 patients and by eptifibatide in 13 patients. A subgroup of 10 patients was retested 6 hours after stopping infusion of tirofiban. Glycoprotein IIb/IIIa receptor blockade by both substances improved acetylcholine-induced vasodilation and L-NMMA responses. Six hours after withdrawal of tirofiban infusion, the beneficial effects were not evident. Sodium nitroprusside-induced vasodilation was not changed by glycoprotein IIb/IIIa receptor blockade. CONCLUSIONS: These findings support the concept that abnormal platelet-endothelial interactions contribute to endothelial dysfunction and impaired NO bioactivity in patients with symptomatic coronary artery disease.
BACKGROUND: Platelet glycoprotein IIb/IIIa receptor blockade not only enhances epicardial flow but also improves microvascular perfusion. Inhibition of abnormal platelet-endothelial interactions may contribute to this beneficial effect. The present study was designed to determine whether glycoprotein IIb/IIIa receptor blockade influences endothelial vasomotor function and NO bioactivity in patients with coronary artery disease. METHODS AND RESULTS: Forty patients with symptomatic coronary artery stenosis were studied before planned percutaneous coronary intervention. By using venous occlusion plethysmography, endothelium-dependent and -independent vasodilation was determined by measuring forearm blood flow responses to acetylcholine with and without NG-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside. Vascular function tests were repeated during glycoprotein IIb/IIIa receptor blockade by tirofiban in 27 patients and by eptifibatide in 13 patients. A subgroup of 10 patients was retested 6 hours after stopping infusion of tirofiban. Glycoprotein IIb/IIIa receptor blockade by both substances improved acetylcholine-induced vasodilation and L-NMMA responses. Six hours after withdrawal of tirofiban infusion, the beneficial effects were not evident. Sodium nitroprusside-induced vasodilation was not changed by glycoprotein IIb/IIIa receptor blockade. CONCLUSIONS: These findings support the concept that abnormal platelet-endothelial interactions contribute to endothelial dysfunction and impaired NO bioactivity in patients with symptomatic coronary artery disease.
Authors: Mir Abolfazl Ostad; Eva Nick; Vitor Paixao-Gatinho; Boris Schnorbus; Robert Schiewe; Peter Tschentscher; Thomas Munzel; Ascan Warnholtz Journal: Clin Res Cardiol Date: 2010-07-21 Impact factor: 5.460
Authors: Sheryl Martin-Schild; Hashem Shaltoni; Anitha T Abraham; Andrew D Barreto; Hen Hallevi; Nicole R Gonzales; James C Grotta; Sean I Savitz Journal: Cerebrovasc Dis Date: 2009-10-16 Impact factor: 2.762
Authors: Payal C Desai; Julia E Brittain; Susan K Jones; Adam McDonald; Douglas R Wilson; Rosalie Dominik; Nigel S Key; Leslie V Parise; Kenneth I Ataga Journal: Thromb Res Date: 2013-08-08 Impact factor: 3.944