Background This study tested the hypothesis that serum concentrations of high-sensitivity C-reactive protein (hs-CRP) and soluble CD40 ligand (sCD40L) significantly reflect serial changes in patients with unstable angina, and thus the serum concentrations of these inflammatory biomarkers may be good candidates for predicting late restenosis after coronary stenting. Methods and ResultsThe circulating concentrations of sCD40L and hs-CRP were prospectively measured (both pre-procedure, and on days 21, 90, and 180 after the procedure) in 77 consecutive patients with unstable angina undergoing coronary stenting. These inflammatory mediators were also evaluated in 30 healthy volunteers. The serum concentrations of sCD40L and hs-CRP were significantly higher pre-procedure in study patients than in normal control subjects (all p values <0.0001). These inflammatory markers then declined to a substantially lower concentration by day 21 (all p values <0.05). Circulating concentrations of hs-CRP in each patient then differed little from each other afterwards. However, the sCD40L concentration was once again raised significantly on days 90 and 180 as compared to day 21 (both p values <0.05). This study found no significant link between raised circulating concentrations of sCD40L and hs-CRP and late restenosis. Conclusions Circulating concentrations of sCD40L and hs-CRP were significantly increased in unstable angina patients pre-procedure and declined substantially thereafter. However, the circulating concentrations of these 2 inflammatory mediators were not useful in predicting late restenosis following coronary stenting. (Circ J 2005; 69: 890 -895)

The reduction of myocardial Na,K-ATPase in CHF is limited to the alpha 3 isoform. Furthermore, because similar changes in myocardial ouabain-binding sites and Na,K-ATPase alpha 3 isoform were produced by chronic norepinephrine infusion, the decrease in the Na,K-ATPase in CHF is most likely mediated via excess sympathetic stimulation.

revious studies have demonstrated that combined therapy with aspirin and ticlopidine can synergically inhibit platelet reactivity, and thus substantially reduce the incidence of early ischemic events following coronary artery stenting. 1-3 However, acute or subacute stent thrombosis still occurs in up to 1-2% of patients, especially soon after stent implantation, 1,2 and it has been suggested that this phenomenon is caused by the delayed onset of the antiplatelet effect of ticlopidine. 4 Clopidogrel, a new thienopyridine derivative that is chemically related to ticlopidine, blocks platelet activation by selectively and irreversibly inhibiting the binding of adenosine diphosphate (ADP) to its receptor on platelets, and subsequently inhibiting the ADP-dependent activation of the Gp IIb-IIIa complex, the major receptor for fibrinogen binding on platelet surface. 5 Some recent studies have shown that clopidogrel, particularly as a loading dose of 300 mg, can rapidly and significantly inhibit platelet aggregation in both healthy subjects and patients with atherosclerotic disease, even after just 2 h. 6-8 Thus, such a loading dose, followed by daily doses of 75 mg, has become one of the most popular regimens for patients after coronary stenting in our clinical practice. However, a more recent study has demonstrated that the conventional loading dose in patients with unstable angina (UA) undergoing coronary stenting inhibited no more than 40% of ADP (20 g) induced platelet aggregation within the first 4 h, whereas a loading dose of 600 mg of clopidogrel more substantially inhibited ADP (20 g) induced platelet aggregation. 4 These findings 4,6-8 raise suspicions regarding which dose regimen is most suitable for patients, particularly those with acute coronary syndrome (ACS) and platelet hyperreactivity who are undergoing coronary stenting.The ADP stimulation test, a physiologic assay that can provide information regarding platelet aggregation ability, is well established in various clinical settings. 4,[6][7][8] However, the CD62p expression test using flow cytometry, which can provide essential information on platelet activation, has not been fully investigated in patients with UA or other clinical settings. Furthermore, data are not available regarding the serial changes in platelet activation after a loading dose of 300 mg of clopidogrel therapy, followed by daily doses of 75 mg, in the clinical setting of UA. This is very important for physicians in their daily clinical practice, because platelet activation is a hallmark of ACS, 9-11 and formed the basis of the present study. Background Platelet activation is crucial in the development of acute or subacute stent thrombosis following implantation. This study investigated whether a conventional regimen comprising a loading dose of 300 mg of clopidogrel, followed by daily doses of 75 mg, could significantly suppress platelet activation in patients with unstable angina (UA) undergoing coronary stenting. Methods and ResultsPlatelet activation (expressed by CD62p) was ser...

Many studies have found that systemic inflammation plays an important role in the pathogenesis of atrial fibrillation (AF). Gout is a chronic systemic inflammatory disorder, but little evidence exists regarding whether the risk of AF is increased in patients with gout. The National Health Insurance Research Database in Taiwan was used in this study, and gout was defined as the occurrence of at least one episode of an acute gout attack requiring medical treatment. A total of 63264 gout and 63264 age- and gender-matched patients were included as the study population. The Cox model was used to evaluate the risk of AF in patients with gout. Patients with gout experienced a greater frequency of co-morbidities compared to patients without gout. The cumulative incidences of AF were 4.61% and 3.04% in patients with and without gout, respectively (log-rank test, P < 0.001). After adjusting for co-morbidities and prescription medication use, gout was found to be associated with AF [hazard ratio (HR), 1.38]. Moreover, the HR for AF decreased with increasing age in our study. Gout was found to be associated with an increased risk of developing AF after adjusting for potential confounders.