(Circulation. 1996;94:1206-1208.)
© 1996 American Heart Association, Inc.
Articles |
Association of Neutrophils With Platelet Aggregates in Unstable Angina
Should We Alter Therapy?
the Department of Medicine, Pathology and Biochemistry, DeBakey Heart Center, Baylor College of Medicine, and The Methodist Hospital, Houston, Tex.
Correspondence to Mark L. Entman, MD, Baylor College of Medicine, Department of Medicine, Section of Cardiovascular Sciences, One Baylor Plaza, Houston, TX 77030. E-mail: mentman@bcm.tmc.edu.
Key Words: Editorials • blood cells • platelets • angina
 |
Introduction |
|---|
In this issue of Circulation, Dr Ott and his colleagues1 have convincingly demonstrated evidence for increased neutrophil-platelet interaction associated with unstable angina not seen in patients with stable angina. Although such interactions have been suggested previously, as duly referenced by the authors, the work by Ott and coworkers has defined these observations and characterized some of the cellular changes in neutrophils consequent to this interaction that are potentially important in consideration of their pathophysiological significance. We intend to provide an alternative perspective to the scholarly discussion provided by Ott and colleagues. We wish to address the potential of these findings as a diagnostic and prognostic tool and as a part of the pathophysiology of unstable angina and to discuss the potential therapeutic implications.
|
Platelet-Neutrophil Interaction as a Diagnostic and Prognostic Tool |
|---|
The major finding of the study by Ott et al1 is the evidence of augmented platelet-neutrophil interaction in the circulating venous blood of patients with unstable angina. They consider the mechanism of this adhesion and its potential relationship to the pathophysiological process, which is, at least theoretically, occurring on a labile plaque in the coronary circulation. However, activated neutrophils and neutrophil-platelet aggregates will certainly be cleared rapidly from the circulation by both the spleen and the lung. Because the complexes are both rapidly cleared and not likely to be stable (see below), this measurement offers a potential way of following the ongoing metastable interaction. It would be of interest to measure the rate at which these aggregates disappeared as a function of classic treatment approaches to
This article has been cited by other articles:
 |
|
 |
|
  M R Ray, S Mukherjee, S Roychoudhury, P Bhattacharya, M Banerjee, S Siddique, S Chakraborty, and T Lahiri Platelet activation, upregulation of CD11b/CD18 expression on leukocytes and increase in circulating leukocyte-platelet aggregates in Indian women chronically exposed to biomass smoke Human and Experimental Toxicology, November 1, 2006; 25(11): 627 - 635. [Abstract] [PDF]
|
|
|
|
 |
|
 T. Khreiss, L. Jozsef, L. A. Potempa, and J. G. Filep Opposing Effects of C-Reactive Protein Isoforms on Shear-Induced Neutrophil-Platelet Adhesion and Neutrophil Aggregation in Whole Blood Circulation, October 26, 2004; 110(17): 2713 - 2720. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. J. T. McCarty, N. Tien, B. S. Bochner, and K. Konstantopoulos Exogenous eosinophil activation converts PSGL-1-dependent binding to CD18-dependent stable adhesion to platelets in shear flow Am J Physiol Cell Physiol, May 1, 2003; 284(5): C1223 - C1234. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Neelamegham, A. D. Taylor, H. Shankaran, C. W. Smith, and S. I. Simon Shear and Time-Dependent Changes in Mac-1, LFA-1, and ICAM-3 Binding Regulate Neutrophil Homotypic Adhesion J. Immunol., April 1, 2000; 164(7): 3798 - 3805. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.Y. Jeremy, G.D. Angelini, M. Khan, D.P. Mikhailidis, R.J. Morgan, C.S. Thompson, K.R. Bruckdorfer, and K.M. Naseem Platelets, oxidant stress and erectile dysfunction: an hypothesis Cardiovasc Res, April 1, 2000; 46(1): 50 - 54. [Full Text] [PDF]
|
|
|
|
|
|
J. Y. Jeremy, D. Rowe, A. M. Emsley, and A. C. Newby Nitric oxide and the proliferation of vascular smooth muscle cells Cardiovasc Res, August 15, 1999; 43(3): 580 - 594. [Full Text] [PDF]
|
|
|
|
 |
|
 H. Ikeda, T. Ueyama, T. Murohara, H. Yasukawa, N. Haramaki, H. Eguchi, A. Katoh, Y. Takajo, I. Onitsuka, T. Ueno, et al. Adhesive Interaction Between P-Selectin and Sialyl Lewisx Plays an Important Role in Recurrent Coronary Arterial Thrombosis in Dogs Arterioscler Thromb Vasc Biol, April 1, 1999; 19(4): 1083 - 1090. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Irani, Y. Pham, L. D. Coleman, C. Roos, G. E. Cooke, A. Miodovnik, N. Karim, C. C. Wilhide, P. F. Bray, and P. J. Goldschmidt-Clermont Priming of Platelet {alpha}IIbß3 by Oxidants Is Associated With Tyrosine Phosphorylation of ß3 Arterioscler Thromb Vasc Biol, November 1, 1998; 18(11): 1698 - 1706. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Minamino, M. Kitakaze, S. Sanada, H. Asanuama, T. Kurotobi, Y. Koretsune, M. Fukunami, T. Kuzuya, N. Hoki, and M. Hori Increased Expression of P-Selectin on Platelets Is a Risk Factor for Silent Cerebral Infarction in Patients With Atrial Fibrillation : Role of Nitric Oxide Circulation, October 27, 1998; 98(17): 1721 - 1727. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Konstantopoulos, S. Neelamegham, A. R. Burns, E. Hentzen, G. S. Kansas, K. R. Snapp, E. L. Berg, J. D. Hellums, C. W. Smith, L. V. McIntire, et al. Venous Levels of Shear Support Neutrophil-Platelet Adhesion and Neutrophil Aggregation in Blood via P-Selectin and ß2-Integrin Circulation, September 1, 1998; 98(9): 873 - 882. [Abstract] [Full Text] [PDF]
|
|