Published Online
on July 21, 2003

A more recent version of this article appeared on August 5, 2003

This Article Full Text (PDF) All Versions of this Article: 108/5/536    most recent 01.CIR.0000081774.31064.62v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Heitzer, T. Articles by Munzel, T. Search for Related Content PubMed PubMed Citation Articles by Heitzer, T. Articles by Munzel, T. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Medline Plus Health Information Coronary Artery Disease Hazardous Substances DB L-TYROSINE NITRIC OXIDE Related Collections Platelets

Submitted on March 18, 2003
Revised on May 8, 2003
Accepted on May 9, 2003

Platelet Glycoprotein IIb/IIIa Receptor Blockade Improves Vascular Nitric Oxide Bioavailability in Patients With Coronary Artery Disease

Thomas Heitzer MD^*, Isabel Ollmann BS, Katharina Köke BS, Thomas Meinertz MD, and Thomas Munzel MD

From the Universitätsklinikum Hamburg-Eppendorf, Medizinische Klinik III, Kardiologie und Angiologie, Hamburg, Germany.

^* To whom correspondence should be addressed. E-mail: heitzer{at}uke.uni-hamburg.de.

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 N^G-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.

Key words: coronary artery disease • platelets • endothelial dysfunction • nitric oxide

This article has been cited by other articles:

				M. P. Ruiz-Torres, M. Griera, A. Chamorro, M. L. Diez-Marques, D. Rodriguez-Puyol, and M. Rodriguez-Puyol Tirofiban increases soluble guanylate cyclase in rat vascular walls: pharmacological and pathophysiological consequences Cardiovasc Res, April 1, 2009; 82(1): 125 - 132. [Abstract] [Full Text] [PDF]

				S. R. Steinhubl, J. J. Badimon, D. L. Bhatt, J.-M. Herbert, and T. F. Luscher Clinical evidence for anti-inflammatory effects of antiplatelet therapy in patients with atherothrombotic disease Vascular Medicine, May 1, 2007; 12(2): 113 - 122. [Abstract] [PDF]

				A. Lerman, D. R. Holmes, J. Herrmann, and B. J. Gersh Microcirculatory dysfunction in ST-elevation myocardial infarction: cause, consequence, or both? Eur. Heart J., April 1, 2007; 28(7): 788 - 797. [Abstract] [Full Text] [PDF]

				Y-J Yang, J-L Zhao, S-J You, Y-J Wu, Z-C Jing, W-X Yang, L Meng, Y-W Wang, and R-L Gao Different effects of tirofiban and aspirin plus clopidogrel on myocardial no-reflow in a mini-swine model of acute myocardial infarction and reperfusion Heart, August 1, 2006; 92(8): 1131 - 1137. [Abstract] [Full Text] [PDF]

				T. Heitzer, V. Rudolph, E. Schwedhelm, M. Karstens, K. Sydow, M. Ortak, P. Tschentscher, T. Meinertz, R. Boger, and S. Baldus Clopidogrel Improves Systemic Endothelial Nitric Oxide Bioavailability in Patients With Coronary Artery Disease: Evidence for Antioxidant and Antiinflammatory Effects Arterioscler Thromb Vasc Biol, July 1, 2006; 26(7): 1648 - 1652. [Abstract] [Full Text] [PDF]

				J. Herrmann Peri-procedural myocardial injury: 2005 update Eur. Heart J., December 1, 2005; 26(23): 2493 - 2519. [Abstract] [Full Text] [PDF]

				P. C. Williams, M. J. Coffey, B. Coles, S. Sanchez, J. D. Morrow, J. R. Cockcroft, M. J. Lewis, and V. B. O'Donnell In vivo aspirin supplementation inhibits nitric oxide consumption by human platelets Blood, October 15, 2005; 106(8): 2737 - 2743. [Abstract] [Full Text] [PDF]

				L. B. Mime, S. Arnhold, J. H. Fischer, K. Addicks, E. R. d. Vivie, G. Bennink, and M. Suedkamp Pharmacologic cerebral capillary blood flow improvement after deep hypothermic circulatory arrest: An intravital fluorescence microscopy study in pigs J. Thorac. Cardiovasc. Surg., September 1, 2005; 130(3): 670 - 676. [Abstract] [Full Text] [PDF]

				S. Fichtlscherer, S. Breuer, and A. M. Zeiher Prognostic Value of Systemic Endothelial Dysfunction in Patients With Acute Coronary Syndromes: Further Evidence for the Existence of the "Vulnerable" Patient Circulation, October 5, 2004; 110(14): 1926 - 1932. [Abstract] [Full Text] [PDF]