Abstract
Background: The pathway linking inflammation and thrombosis has been extensively studied. Experimental data support that arterial thrombosis also induces a detectable inflammatory response, which in turn, activates prothrombotic pathways closing a vicious circle that interconnects inflammation and thrombosis. Aim: We designed this study to investigate the causes of inflammatory markers increase after coronary angioplasty. Methods: We analyzed the interrelationship of thrombotic and inflammatory markers and the effect of blocking thrombus formation on the inflammatory response in 50 patients undergoing high thrombotic risk coronary angioplasty. The relationship of platelet number to soluble CD40 Ligand, Interleukin-6 and C-reactive protein blood levels was studied. Half of the study population was treated with standard antithrombotic drugs and the other half with the standard therapy plus platelet GP IIb-IIIa receptor inhibitor Eptifibatide. Results: There was a clear correlation between basal platelet count and sCD40L basal levels, post-angioplasty sCD40L increase and post-angioplasty IL-6 levels and post-angioplasty IL-6 levels with post-angioplasty CRP levels. Postangioplasty CRP, IL-6 and sCD40L blood levels were influenced by GP IIb-IIIa treatment in patients with angiographic thrombus. Conclusion: Platelet aggregation induces a proinflammatory response which is blocked by a GP IIb-IIIa inhibitor agent, particularly in patients with patent angiographic thrombus.
Highlights
Atherosclerosis is a chronic inflammatory disease [1]
The Thrombosis-Inflammation Link We propose a sequence of events that links intra-arterial thrombosis and inflammation which is: Platelet activation/aggregation→CD40L expression/ sCD40L release→IL-6 production→CRP production
We found that in non-treated patients: 1) There is a linear relationship between platelet number and sCD40L concentration, between sCD40L post-angioplasty increase and IL-6 postangioplasty concentration, and between IL-6 post-angioplasty concentration and CRP post-angioplasty concentration; 2) A GP IIb-IIIa inhibitor blocked CRP and IL-6 increase in patients with angiographic thrombus, and preserved sCD40L consumption in all patients
Summary
It is generally accepted that the chronic and subtle increase in blood levels of several inflammatory markers, such as CRP or IL-6, reflects the underlying inflammatory process which affects the arterial wall [2]. Intra-arterial thrombus formation, which is a pathophysiological landmark of ACS, can induce a pro-inflammatory reaction, and is a more plausible cause for the increase in inflammatory markers than the “systemic inflammatory burst” [6]. Many studies give support to the hypothesis that platelet activation/aggregation—by means of CD40L and sCD40L activity—may induce a pro-inflammatory cytokine response [7,8,9,10,11]. Postangioplasty CRP, IL-6 and sCD40L blood levels were influenced by GP IIb-IIIa treatment in patients with angiographic thrombus. Conclusion: Platelet aggregation induces a pro-inflammatory response which is blocked by a GP IIb-IIIa inhibitor agent, in patients with patent angiographic thrombus
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