Increased Neutrophil-Platelet Adhesion in Patients With Unstable Angina

Ott, I.; Neumann, Franz‐Josef; Gawaz, Meinrad; Schmitt, Manfred; Schömig, Albert

doi:10.1161/01.cir.94.6.1239

Cited by 370 publications

(270 citation statements)

References 39 publications

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“…The importance of neutrophil-platelet adhesive interactions has been noted in the circulation of patients with unstable angina 50 and after coronary angioplasty. 51 Recently, it has been shown that blockade of the selectins with an analogue of sLe x reduced intimal hyperplasia after balloon injury in rabbits.…”

Section: Discussionmentioning

confidence: 99%

Selectin Blockade Reduces Neutrophil Interaction With Platelets at the Site of Deep Arterial Injury by Angioplasty in Pigs

Merhi

Provost

Chauvet

et al. 1999

ATVB

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Abstract-The adhesion of neutrophils to damaged arterial surfaces is increased in the presence of platelets by a mechanism implicating platelet P-selectin. Such interactions may enhance thrombus formation and the vascular response to injury. In this study, we investigated the effects of a selectin blocker (CY-1503), an analogue of sialyl Lewis x , on platelet and neutrophil interactions after arterial injury produced by angioplasty in pigs.51 Cr-platelet deposition and 111In-neutrophil adhesion were quantified on intact, mildly and deeply injured carotid arterial segments, produced by balloon dilation, in control (saline, nϭ8) and treated (CY-1503, 15 mg/kg IV, nϭ7) pigs. The hematological parameters, the aggregation of whole blood in response to adenosine diphosphate, and the activating clotting time, as well as the heart rate and mean arterial blood pressure, were similar among groups and were not influenced significantly by CY-1503. The level of platelet and neutrophil adhesion increased significantly with the severity of arterial injury but was not influenced by CY-1503 on intact and mildly injured arterial segments. However, at the site of deep arterial injury, CY-1503 treatment was associated with a 58% reduction (PϽ0.01) in neutrophil adhesion, from 446.7Ϯ72.6ϫ10 3

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Section: Discussionmentioning

confidence: 99%

Selectin Blockade Reduces Neutrophil Interaction With Platelets at the Site of Deep Arterial Injury by Angioplasty in Pigs

Merhi

Provost

Chauvet

et al. 1999

ATVB

View full text Add to dashboard Cite

show abstract

“…For example, studies with un-separated leukocyte populations reveal a significant increase in platelet-leukocyte complexes in allergic mice and in human asthmatics (Pitchford et al, 2003(Pitchford et al, , 2005. Similar processes occur in patients with COPD (Ferroni et al, 2000), atherosclerosis (Arber et al, 1991;Ott et al, 1996;Neumann et al, 1997;Sarma et al, 2002;Huo et al, 2003) and RA (Joseph et al, 2001;Bunescu et al, 2004). In this regard, experimental models of disease have provided evidence for a requirement of platelets in pulmonary eosinophil and lymphocyte recruitment in rabbits, guineapigs and mice in models of allergic inflammation (LellouchTubiana et al, 1988;Coyle et al, 1990;Pitchford et al, 2003Pitchford et al, , 2005; and neutrophil and monocyte recruitment in atherosclerosis (Arber et al, 1991;Neumann et al, 1997;Hayward et al, 1999) and RA (Schmitt-Sody et al, 2005).…”

Section: Leukocyte Recruitment and Activation: Influence Of Plateletsmentioning

confidence: 97%

“…These studies suggest a participation of platelets in the inflammatory responses as well as the recognized events leading to thrombus formation. Platelet binding to leukocytes occurs during acute coronary events, and these heterotypic aggregates are formed as a result of activation by inflammatory mediators (Arber et al, 1991;Ott et al, 1996) and are largely bound via P-selectin/P-selectin glycoprotein ligand-1 (PSGL-1) interactions (Sarma et al, 2002). It is worth noting that an increased expression of CD40L occurs on the surface of platelets in acute coronary syndromes (Garlichs et al, 2001), although the significance of this is not yet known, it reveals another mechanism whereby platelets may further stimulate the inflammatory response during atherosclerosis.…”

Section: Platelet Activation In Atherosclerosismentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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“…The presence of increased leukocyte-platelet binding has been shown in patients with acute coronary syndromes (25). Adhesion of platelets to circulating myeloid leukocytes in vitro and in vivo is related to platelet activation (26).…”

Section: Myocardial Infarction; Mpv Mean Platelet Volume; Wbc Whitmentioning

confidence: 99%

Relationship of admission hematological indexes with myocardial reperfusion abnormalities in acute ST segment elevation myocardial infarction patients treated with primary percutaneous coronary interventions

Maden¹,

Kacmaz²,

Selçuk³

et al. 2009

Canadian Journal of Cardiology

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Increased Neutrophil-Platelet Adhesion in Patients With Unstable Angina

Abstract: Thus, this study demonstrates that increased neutrophil-platelet adhesion may contribute to neutrophil activation in unstable angina.

Cited by 370 publications

References 39 publications

Selectin Blockade Reduces Neutrophil Interaction With Platelets at the Site of Deep Arterial Injury by Angioplasty in Pigs

Selectin Blockade Reduces Neutrophil Interaction With Platelets at the Site of Deep Arterial Injury by Angioplasty in Pigs

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Relationship of admission hematological indexes with myocardial reperfusion abnormalities in acute ST segment elevation myocardial infarction patients treated with primary percutaneous coronary interventions

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