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Introduction: Pentraxin-3 (PTX3) is an acute-phase reactant that shares structural and functional homology with C-reactive protein (CRP). However, unlike CRP, which is synthesized mainly in the liver, PTX3 is produced at the site of inflammation. It has been suggested that PTX3 plays the same role in the periphery that CRP does in circulation. PTX3 may represent a rapid marker of local inflammation., Methods: Fifty-one patients with stable coronary artery disease (CAD) were enrolled. Blood samples were collected on admission. Plasma concentration of PTX3 and high-sensitivity CRP (hsCRP) were determined., Results: Median PTX3 concentration was 0.92 μmol/L (0.58-1.40). Median hsCRP concentration was 0.90 mg/L (0.75-1.10). There was a positive correlation between PTX3 and total cholesterol (R=0.34; P=0.01), PTX3 and LDL cholesterol (R=0.35; P=0.01), and PTX3 and hsCRP (R=0.46; P = 0.0005). We found no correlation between hsCRP and all laboratory parameters. We found higher PTX3 concentrations in patients with Canadian Cardiovascular Society (CCS) functional class 3 (compared to CCS functional class 2) and in patients taking nitrates. Lower PTX3 concentrations were reported in patients taking calcium channel blockers (amlodipine). hsCRP concentrations remained similar among these subgroups of patients., Conclusions: PTX3 is a marker of clinically more advanced CAD (CCS2 vs CCS3; nitrates vs no nitrates). PTX3 is also associated with other cardiovascular risk factors (total cholesterol, LDL cholesterol, and hsCRP). PTX3 may be a potential early marker of cardiovascular risk before the increase of systemic markers like hsCRP.

Background: Dual antiplatelet therapy (aspirin plus clopidogrel) is recommended in patients undergoing percutaneous coronary intervention (PCI). Treatment with proton pump inhibitors (PPIs) decreases bleeding rate. Alarming reports have been made that PPIs may decrease the antiplatelet activity of clopidogrel. We sought to determine whether levels of interleukin-6 (IL-6) and transforming growth factor-β1 (TGF-β1) might help distinguish individuals at risk for adverse events., Methods: Thirty-eight patients on aspirin and clopidogrel were enrolled and divided into two groups: group 1 [patients receiving omeprazole (n = 18)] and group 2 [patients not receiving omeprazole (n = 20)]. Patients underwent PCI and were scheduled for twelve-month clinical follow-up. The major, adverse cardiac and cerebrovascular events (MACCE) include death, re-hospitalization for acute coronary syndromes, and stroke., Results: Median concentrations of IL-6 were higher in group 1 at 4.7 pg/mL, in comparison with group 2, 1.65 pg/mL (p = 0.003). Median concentrations of TGF-β1 were similar in both groups (p = 0.5). Patients in group 1 had a significantly higher leukocyte count [103/mm3] (median 7.5 vs 6.5; p = 0.04). There were no deaths during follow-up. The incidence of myocardial infarction was higher in group 1 (33.4% vs 5.0%; p = 0.03). MACCE at twelve months were more frequent in group 1 (55.6% vs 20.0%; p = 0.02). The cut-off value to predict MACCEs for IL-6 was > 3.6 pg/mL (sensitivity 64%, specificity 88%, positive predictive value 75%, negative predictive value 81%)., Interpretation: We show here that concomitant omeprazole use is associated with an increased inflammatory reaction. Drug interactions may reduce the anti-inflammatory effect of clopidogrel. This mechanism maybe responsible for an increased risk of non-fatal, cardiovascular events, following stent placement.

Background: Contrast media are being widely applied for both diagnostic and therapeutic purposes. This has resulted in increasing incidence of contrast-induced nephropathy (CIN)., Methods: We aimed to investigate the value of baseline serum IL-6 concentrations in predicting CIN before the rise of serum creatinine (SCr) in patients undergoing percutaneous coronary intervention. Seventy four Caucasian patients were enrolled. CIN was defined as an increase in SCr concentration of more than 44 micromol/L, or a 25% increase above baseline within 48 hours after contrast administration., Results: CIN developed in 16 out of 74 patients (21.6%). The median concentration of IL-6 was 3.2 pg/mL. The median IL-6 concentration on admission was lower in patients who subsequently did not develop CIN (2.7 pg/mL versus 8.3 pg/mL, p < 0.0001). Receiver operating characteristics analysis showed a high diagnostic value of baseline SCr and IL-6. The cut-off value to predict CIN for IL-6 was over 4.0 pg/mL (sensitivity 88%, specificity 76%, PPV 50%, NPV 96%). Multivariate logistic regression analysis revealed three independent predictors of CIN: IL-6 (OR 1.43; 95%CI: 1.17-1.76), serum creatinine (OR 1.79; 95%CI: 1.1-3.39), and ejection fraction (OR 0.86; 95%CI: 0.50-0.95)., Conclusions: Increased concentrations of IL-6 on admission are associated with subsequent CIN. Our study proposes that IL-6 be added to the list of potential markers that could be used, along with renal function parameters, in clinical practice.

Background: The efficacy of percutaneous coronary intervention (PCI) is limited by the need for repeat revascularization resulting from restenosis. The restenosis rate after treatment for in-stent restenosis (recurrent restenosis) is high (> 30%). Numerous studies have suggested the predictive value of interleukin 6 (IL-6) and transforming growth factor beta1 (TGF-beta1)., Methods: We sought to determine whether serum levels of IL-6 and TGF-beta1 could help identify individuals with recurrent restenosis. Thirty seven patients with a history of stent implantation were enrolled and divided into three groups: (1) patients with a current, first restenosis (n = 9); (2) patients with current restenosis and at least one prior restenosis (recurrent restenosis) (n = 11), and (3) patients with a history of restenosis, but without current restenosis (n = 17)., Results: The baseline profile was similar in all three groups. The median (25th-75th percentile) concentrations of IL-6 were: group 1 - 2.8 (1.4-5.5); group 2 - 2.6 (0.6-8.6); group 3 - 2.4 (0.9-4.7) p = 0.69 and TGF-beta1: group 1 - 3.6 (0.2-14.4); group 2 - 4.2 (1.8-57.6); group 3 - 6.6 (2.8-30.0) p = 0.57. Moreover we found no correlation, either between diameter stenosis and IL-6 (R = 0.10; p = 0.38) or TGF-beta1 (R = 0.10; p = 0.57). Both IL-6 (AUC 0.59 p = 0.4 and AUC 0.51 p = 0.9) and TGF-beta1 (AUC 0.64 p = 0.2 and AUC 0.50 p = 0.9) failed to provide significant results in receiver-operating characteristic analysis., Conclusion: We report that there is no association between the severity of diameter stenosis (restenosis) and IL-6 or TGF-beta1 concentrations. Our findings might suggest that levels of IL-6 and TGF-beta1 have no predictive value for identifying patients with recurrent restenosis.