Soluble CD40 ligand is an early initiator of inflammation after coronary intervention

Abstract

Background 

This prospective study evaluated the early increase in markers of inflammation after coronary stenting, and the predictors of early rise. Elevation of markers of inflammation after percutaneous coronary intervention correlates with an increased risk of adverse events. The role of soluble CD40 ligand (sCD40L) as a potential initiator of inflammation after stenting has not been described.

Methods 

Seventy-five patients were treated with heparin alone (n=25), or randomized to adjuvant treatment with eptifibatide (n=26) or abciximab (n=24) during stenting. Systemic blood was obtained before coronary stenting and at 10 min after stenting. C-reactive protein (CRP), interleukin (IL)-6, IL-1 receptor antagonist and sCD40L were determined by enzyme liberated immunosorbent assay.

Results 

sCD40L exhibited the greatest relative rise (35%, P=0.01 compared to concentrations before intervention) in the first 10 min after stenting. In a logistic regression model, an early increase in the concentration of sCD40L was predicted by baseline laboratory values (white blood count and sCD40L level before stenting) and procedural characteristics (number of stents and glycoprotein IIb-IIIa inhibitor assignment).

Conclusions 

In conclusion, a systemic inflammatory response is detectable 10 min after coronary stent placement. The early increase in sCD40L suggests a possible role for this marker in the initiation of inflammation after coronary stenting.

In Brief

In this prospective study of 75 patients undergoing coronary stenting, a systemic inflammatory response was evident within 10 min of coronary stenting. Soluble CD40 ligand had the greatest relative rise in the first 10 min after stenting suggesting a possible role for this cytokine in the initiation of the inflammatory response; predictors of this early rise included preprocedural white blood count, preprocedural soluble CD40 ligand level, use of multiple stents and randomization to eptifibatide.