Usefulness of Preprocedural Soluble CD40 Ligand for Predicting Restenosis After Percutaneous Coronary Intervention in Patients With Stable Coronary Artery Disease

Türker, Sonay; Güneri, Sema; Akdeniz, Bahri; Özcan, Mehmet Ali; Barış, Nezihi; Badak, Özer; Kırımlı, Önder; Yüksel, Faize

doi:10.1016/j.amjcard.2005.08.024

Cited by 31 publications

(22 citation statements)

References 16 publications

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“…Some additional information about this issue emerges from the study by Cipollone and coworkers [25] and subsequent studies [26], which demonstrated that preprocedural levels of sCD40L are predictive of enhanced inflammatory response and restenosis after PTCA. A mechanistic basis for this clinical study is provided by the work by Urbich et al, who showed that CD40L inhibits endothelial cell migration by increasing production of ROS [27], thus providing a mechanism by which sCD40L generated by thrombosis could promote restenosis.…”

Section: Coronary Artery Diseasementioning

confidence: 96%

CD40/CD40L system and vascular disease

et al. 2007

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Several distinct lines of investigation in the context of atherosclerosis dealing with low-grade inflammation, oxidative stress and platelet activation are now emerging, with CD40/CD40L system as the missing link. CD40 ligand is a transmembrane glycoprotein structurally related to tumour necrosis factor-alpha and more than 95% of the circulating CD40L derives from platelets. CD40L appears as a multiplayer of several cell types in the inflammatory network. The peculiarity of CD40L as an inflammatory mediator derived from platelets expands the functional repertoire of platelets from players of haemostasis and thrombosis to powerful amplifiers of inflammation by promoting the release of cytokines and chemokines, cell activation and cell-cell interactions. The multifunctional role of CD40L, as a simultaneous activator of all these systems, further blurs the intricate relationship between such events both in the physiological systems and the pathological derangement occurring in atherothrombosis.

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Section: Coronary Artery Diseasementioning

confidence: 96%

CD40/CD40L system and vascular disease

et al. 2007

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“…Increased platelet activation is associated with a variety of vascular disorders including acute coronary syndromes, stable coronary artery disease, and restenosis after percutaneous coronary intervention (26,27). Soluble CD40L is a particularly attractive marker for platelet activation because it is shed from the surface of activated platelets, is easily measured, and meaningfully participates in a number of important biologic processes including activation of immunity and thrombosis (28).…”

Section: Discussionmentioning

confidence: 99%

Platelet Activation in Patients with Atherosclerotic Renal Artery Stenosis Undergoing Stent Revascularization

Adlakha

Reed

Brewster

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Soluble CD40 ligand (sCD40L) is a marker of platelet activation; whether platelet activation occurs in the setting of renal artery stenosis and stenting is unknown. Additionally, the effect of embolic protection devices and glycoprotein IIb/IIIa inhibitors on platelet activation during renal artery intervention is unknown.Design, setting, participants, & measurements Plasma levels of sCD40L were measured in healthy controls, patients with atherosclerosis without renal stenosis, and patients with renal artery stenosis before, immediately after, and 24 hours after renal artery stenting.Results Soluble CD40L levels were higher in renal artery stenosis patients than normal controls (347.5 Ϯ 27.0 versus 65.2 Ϯ 1.4 pg/ml, P Ͻ 0.001), but were similar to patients with atherosclerosis without renal artery stenosis. Platelet-rich emboli were captured in 26% (9 of 35) of embolic protection device patients, and in these patients sCD40L was elevated before the procedure. Embolic protection device use was associated with a nonsignificant increase in sCD40L, whereas sCD40L declined with abciximab after the procedure (324.9 Ϯ 42.5 versus 188.7 Ϯ 31.0 pg/ml, P ϭ 0.003) and at 24 hours.Conclusions Atherosclerotic renal artery stenosis is associated with platelet activation, but this appears to be related to atherosclerosis, not renal artery stenosis specifically. Embolization of platelet-rich thrombi is common in renal artery stenting and is inhibited with abciximab.

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“…[13][14][15][16] However, it remains unclear whether and how elevated sCD40L contributes to neointima formation, a prominent feature of restenosis. There are several important findings in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…Cipollone et al 13 reported that preprocedural levels of plasma sCD40L were significantly higher in patients that developed restenosis than in patients with favorable outcomes, and raised sCD40L at baseline was significantly correlated with circulating adhesion molecules (sICAM-1, sVCAM-1, sE-selectin), plasma monocyte chemoattractant protein-1 after PCI, and with lumen loss at 6-month follow-up. Turker et al 14 reported that preprocedural levels of plasma sCD40L were significantly higher and more prolonged in patients with in-stent restenosis compared with patients without in-stent restenosis at 6-month follow-up. In the same study, plasma sCD40L levels were further increased after PCI.…”

mentioning

confidence: 99%

CD40 Ligand Promotes Mac-1 Expression, Leukocyte Recruitment, and Neointima Formation after Vascular Injury

Sanders

Bevard

et al. 2008

The American Journal of Pathology

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High levels of circulating soluble CD40 ligand (sCD40L) are frequently found in patients with hypercholesterolemia, diabetes, ischemic stroke, or acute coronary syndromes, predicting an increased rate of atherosclerotic plaque rupture and restenosis after coronary/carotid interventions. Clinical restenosis is characterized in part by exaggerated neointima formation, but the underlying mechanism remains incompletely understood. This study investigated the role of elevated sCD40L in neointima formation in response to vascular injury in an atherogenic animal model and explored the molecular mechanisms involved. apoE ؊/؊ mice fed a Western diet developed severe hypercholesterolemia, significant hyperglycemia, and high levels of plasma sCD40L. Neointima formation after carotid denudation injury was exaggerated in the apoE ؊/؊ mice. In vivo, blocking CD40L with anti-CD40L monoclonal antibody attenuated the early accumulation of Ly-6G؉ neutrophils and Gr-1 ؉ monocytes (at 3 days) and the late accumulation of Mac-2 ؉ macrophages (at 28 days) in the denudated arteries; it also reduced the exaggerated neointima formation at 28 days. In vitro, recombinant CD40L stimulated platelet P-selectin and neutrophil Mac-1 expression and platelet-neutrophil co-aggregation and adhesive interaction. These effects were abrogated by anti-CD40L or anti-Mac-1 monoclonal antibody. Moreover, recombinant CD40L stimulated neutrophil oxidative burst and release of matrix metalloproteinase-9 in vitro. We conclude that elevated sCD40L promotes platelet-leukocyte activation and recruitment and neointima formation after arterial injury, potentially through enhancement of platelet P-selectin and leukocyte Mac-1 expression and oxidative activity. (Am J

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Usefulness of Preprocedural Soluble CD40 Ligand for Predicting Restenosis After Percutaneous Coronary Intervention in Patients With Stable Coronary Artery Disease

Cited by 31 publications

References 16 publications

CD40/CD40L system and vascular disease

CD40/CD40L system and vascular disease

Platelet Activation in Patients with Atherosclerotic Renal Artery Stenosis Undergoing Stent Revascularization

CD40 Ligand Promotes Mac-1 Expression, Leukocyte Recruitment, and Neointima Formation after Vascular Injury

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