Soluble CD40 ligand release in patients with stable coronary artery disease during elective stent implantation: effect of drug-eluting stent over bare metal stent

OZET P coronary intervention (PCI) itself, which is used in the treatment of coronary artery disease (CAD), has an evident platelet-activating effect resulting in poor outcomes.[1,2] CD40 ligand (CD40L) is an established marker of platelet aggregation that plays an important role in thrombosis and plaque destabilization.[3,4] The soluble form of CD40, soluble CD40L (sCD40L), is released after platelet stimulation[5,6] and induces tissue factor expression on monocytes[7] and endothelial cells,[8] accelerating the inflammatory process and promoting coagulation. Mechanical endothelial injury is speculated as a reason for this early post-procedural elevation in CD40L levels.[9,10] Delayed arterial healing and impaired endothelial function are also suggested as possible mechanisms of adverse cardiac events following drug-eluting stent (DES) implantation.[11,12] However, the effect(s) of DES implantation on sCD40L levels in patients with stable CAD are not clear. In the present study, we investigated the impact of DES or bare metal stent (BMS) implantation on sCD40L release and outcomes in patients with stable CAD. PATIENTS AND METHODS Eighty-nine consecutive patients with stable CAD undergoing successful one or multivessel stent replacement were prospectively recruited. Successful procedure was defined as <20% residual stenosis, no procedural complications (dissection, abrupt vessel closure, side branch occlusion, no-reflow phenomenon, intracoronary thrombus, or distal embolization) and presence of Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow. Death, myocardial infarction (MI) and urgent operation requirement were defined as clinical procedural complications.[13] A detailed history was obtained and thorough physical examination performed before the procedure. Patients with acute coronary syndrome, type C lesions in coronary arteries, renal failure, infectious diseases or inflammatory states, malignancy, and procedural failure were not included in the study. Simultaneous DESand BMSimplanted patients were also excluded. All patients were given clopidogrel 300 mg loading dose 24 hours before the procedure and 75 mg/day maintenance, acetylsalicylic acid 300 mg/day, statins, and appropriate anti-hypertensive management. DES or BMS implantation was decided by the operator based on the lesion characteristics and the patient’s clinical history. DESs, when used in appropriate patients, were sirolimusand paclitaxel-eluting stents. Patients were followed for one year following procedures for possible adverse cardiac events determined as death, MI and revascularization. Coronary angioplasty was performed according to a standard Judkins technique through a femoral approach. All patients were administered 100 IU/kg of unfractionated heparin intravenously. Stent implantation was performed with at least nominal balloon inflation pressure. Preand post-dilatation procedures were also performed if necessary. Total size and length of implanted stents and preand post-dilatation procedures were recorded for each patient, for possible impact on sCD40L release. Blood samples were drawn from all patients, just before and 2 hours after the procedure. Tubes were centrifuged at 3500 rpm for 10 minutes. Plasma samples were stored at -20 °C until analyses. Samples were analyzed with commercially available Quantikine Human CD40 Ligand Immunoassay system (RD SPSS Inc; Chicago, Illinois, USA). The obtained data were presented as mean ± SD, checked for normal distribution by Kolmogorov-Smirnov test and compared with unpaired Student t-test when the distribution appeared normal. Nonparametric test (Mann-Whitney U test) was used when there was non-normal distribution. Categorical data between two or more groups were compared by the χ2 test. The correlations of continuous variables were analyzed by Pearson and ordinal variables by Spearman correlation analysis. Delta Turk Kardiyol Dern Ars 676