Increased coronary arterial release of interleukin-1 receptor antagonist and soluble CD40 ligand indicative of inflammation associated with culprit coronary plaques

Inflammatory and vasoactive factors in the aspirate from the culprit coronary artery of patients with acute myocardial infarction

“…CRP has been found in atherosclerotic plaques, and therefore it is not only considered a marker of inflammation, but also an active mediator of the disease [17 -19]. However, recent reports could not confirm increased CRP concentration in the culprit coronary artery compared to the concentration in the peripheral blood [6,12]. Our results also show that the CRP level in the culprit coronary artery did not differ from that in the systemic blood.…”

“…There are currently, however, few data regarding the presence of various soluble vasoactive, inflammatory or thrombotic substances in the culprit vessel and their role in the development of the no-reflow phenomenon and myocardial malperfusion. Kabbani et al [11] reported enhanced platelet and thrombin reactivity and Aggarwal et al [12] found increased interleukin-1 receptor antagonist and soluble CD40 ligand levels in coronary ostial blood of patients with acute coronary syndrome. In a recent report, Maier et al [6] also found locally increased levels of inflammatory markers such as IL-6 and serum amyloid A at the site of ruptured plaque in patients with AMI.…”

Systemic Inflammation After Drug-Eluting Stent Placement

“…The local tissue concentration of drug from a coated stent exceeds that in the blood by up to 300,000-fold [21], and our results suggest that the local antiinflammatory properties of DES do not lead to a reduction in the systemic inflammatory state. We have previously shown that the concentrations of cytokines in blood from a culprit artery are reflective of the intensity of the systemic inflammatory state before coronary stenting [22]. Thus, the robust systemic inflammation seen after implantation of a DES may be triggered, at least in part, by enhanced local production of upstream cytokines despite the presence of stents coated with potentially anti-inflammatory drugs.…”

Osteoprotegerin is not associated with angiographic coronary calcification

“…Our first finding is that platelet-mediated inflammation as represented by levels of sCD40L is inversely related to the development of CLC. Levels of sCD40L were previously demonstrated to be elevated in patients with unstable coronary syndromes [19,20] and were associated with culprit coronary plaques [21]. The observation that patients with CLC have lower concentrations of sCD40L is consistent with such plaques having lower risk of thrombosis and rupture.…”