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Platelet Activation Markers (platelet + activation_marker)
Selected AbstractsPlatelet hyperactivity in clinical depression and the beneficial effect of antidepressant drug treatment: how strong is the evidence?ACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2004R. Von Känel Objective:, Platelet hyperactivity is thought to contribute to the increased coronary artery disease (CAD) risk in depression. This study reviewed the evidence for hyperactive platelets and for effects of antidepressant drug treatment on platelet ,stickiness' in clinical depression. Method:, By means of PubMed electronic library search, 34 studies in English were identified (1983,2003) and critically reviewed. Results:, In depression, flow cytometry studies allowing detection of subtle platelet activation states consistently found at least one platelet activation marker to be increased, while the bulk of platelet aggregation studies did not suggest increased platelet aggregability. Platelets seem to be more activated in depressed patients with CAD than in depressed individuals without CAD. The selective serotonin reuptake inhibitors normalized platelet hyperactivity in four studies. Conclusion:, Data on platelet activity in depression are inconclusive. To resolve this issue and its clinical implications, studies in larger sample sizes controlling for confounders of platelet functioning and prospectively designed are needed. [source] The effects of maximal treadmill graded exercise testing on haemorheological, haemodynamic and flow cytometry platelet markers in patients with systolic or diastolic heart failureEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2008I. Chung ABSTRACT Background, Acute exercise has been associated with activation of thrombosis, and this risk may be accentuated in patients with heart failure. Given the relation of platelets to atherothrombosis, we tested the hypothesis that acute exercise would adversely affect platelet indices and platelet activation markers in patients with systolic and diastolic heart failure. Materials and methods, We studied 20 patients with systolic heart failure (17 men, 3 women; mean age 64 ± 10 years, all with ejection fraction (EF) , 40%) and 20 patients with diastolic heart failure (14 men, 6 women; mean age 64 ± 8 years, mean EF = 66%) who were exercised to maximal intensity, who were compared to 13 healthy controls (6 men, 7 women; mean age 60 ± 4 years, mean EF = 73%). We measured platelet indices (platelet volume, mass and component) and platelet activation markers (platelet-bound CD62P%G, CD63%G and CD40L%G using flow cytometry, as well as plasma sCD40L and soluble P-selectin (sP-sel) levels). Results, Baseline Mean Platelet Volume (MPV), sP-sel, CD40L%G and CD63%G levels were significantly higher in patients with systolic and diastolic heart failure, when compared with controls. The mean exercise duration and VO2 peak in patients with systolic and diastolic heart failure were not significantly different, but lower than that seen in healthy controls. Following exercise, mean haematocrit, CD62P%G, and CD63%G significantly increased in all three subject groups (all P < 0·05). The proportional change in CD62P%G and CD63%G were not significantly different between healthy controls and heart failure patients (P > 0·05). Conclusion, Acute maximal graded exercise increases platelet activation markers, with no disproportionate differences between heart failure patients and healthy controls, despite the former group having a lower exercise tolerance and VO2 peak. [source] Effects of Helicobacter pylori Eradication on Platelet Activation and Disease Recurrence in Patients with Acute Coronary SyndromesHELICOBACTER, Issue 6 2004J. Ignasi Elizalde ABSTRACT Background., Platelet activation is consistently observed in animal models of Helicobacter pylori infection and could help to explain the alleged epidemiological association between H. pylori and coronary heart disease. Materials and Methods., Ninety-two patients with recent acute coronary syndromes were enrolled. Helicobacter pylori -positive patients were randomized to receive a 7-day course of omeprazole, amoxycillin and metronidazole or placebos. Two months later, H. pylori status was reassessed and baseline parameters, including soluble P-selectin and platelet surface expression of CD62P, CD63 and CD41, were measured again. Patients were followed-up for 1 year or until death or readmission. Results., No baseline differences were observed between H. pylori -positive and -negative cases. Among H. pylori -positive patients, 18 received placebo and 31 received active medication resulting in eradication in 21 cases. No differences were observed in inflammatory parameters or platelet activation markers between patients with persistent or resolved H. pylori infection. However, coronary events recurred at 6 and 12 months, respectively, in 35% and 55% of patients with persisting H. pylori infection compared with 10% and 25% of patients in whom H. pylori was either absent or eradicated (p = .01). Only final H. pylori status [RR 3.07 (95% CI 1.35,98)] and number of coronary risk factors [RR 2.58 (95% CI 1.51,4.41)] were independent predictors of recurrence. Conclusions., Infection with H. pylori does not induce significant platelet activation in patients treated for coronary disease. Helicobacter pylori -infected patients, however, may have an increased risk of recurrence of coronary events. [source] Platelet Activation Markers in Patients With Heart Assist DeviceARTIFICIAL ORGANS, Issue 4 2005Oliver Dewald Abstract:, Clinical use of heart assist devices is often associated with thromboembolic complications. We hypothesized that platelets may be activated in patients receiving assist devices and examined expression of the platelet activation markers CD62, CD63, and thrombospondin using flow cytometry in eight patients with Novacor left ventricular assist system (LVAS) or Berlin Heart. Patients with end-stage heart failure had elevated expression of platelet activation markers before insertion of the assist device. While CD62 (P < 0.05) and thrombospondin expression (n.s.) decreased by the 14th postoperative day, the CD63 expression remained elevated (n.s.). A good correlation was found between CD62 and thrombospondin expression (r = 0.72). Bleeding time ex vivo indicated platelet dysfunction during the first 4 weeks after implantation. No relation between expression of platelet activation markers and bleeding time ex vivo were found. In conclusion, expression of the platelet activation markers CD62, CD63, and thrombospondin is increased in patients with end-stage heart failure before device placement and shows prolonged elevation during the assist period. Future studies in larger patient populations are necessary to identify new and specific markers of platelet activation in this clinical setting. [source] | ||||||||||