Monocyte–platelet aggregates and CD11b expression as markers for thrombogenicity in atrial fibrillation

Pfluecke, Christian; Tarnowski, Daniel; Plichta, Lina; Berndt, K.; Schumacher, Petra B.; Ulbrich, Stefan; Forkmann, Mathias; Christoph, Marian; Poitz, David M.; Wunderlich, Carsten; Strasser, Ruth H.; Ibrahim, Karim

doi:10.1007/s00392-015-0922-4

Cited by 26 publications

(19 citation statements)

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“…Moreover, inflammatory mediators favour to a pro-thrombotic state [16, 17], which may account for the increased risk of thromboembolism and cardiovascular mortality also in this setting. Hence, the relationship between inflammation and cardiovascular events in patients with AHREs deserves further research.…”

Section: Discussionmentioning

confidence: 99%

Inflammation and the risk of atrial high-rate episodes (AHREs) in patients with cardiac implantable electronic devices

Pastori

Miyazawa

et al. 2018

Clin Res Cardiol

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IntroductionAtrial high-rate episodes (AHREs) are associated with an increased risk of developing atrial fibrillation and thromboembolism. The characteristics of ‘real world’ patients developing AHREs are poorly known.MethodsWe included 496 consecutive patients with cardiac implantable electronic devices (CIEDs). Primary endpoint was occurrence of AHREs, defined as > 175 bpm and lasting > 5 min, in a median follow-up of 16.5 (IQR 3.9–38.6) months (1082.4 patient-years). We also tested the predictive value of clinical risk scores for AHREs.ResultsMean age was 68.8 ± 14.0 years, and 35.5% were women; AHREs were recorded in 173 patients [34.7%, 16.0%/year, 95% confidence interval (CI) 13.7–18.6]. Multivariable Cox regression analysis showed that age [hazard ratio (HR) 1.020, 95% CI 1.004–1.035, p = 0.011], prior AF (HR 3.521, 95% CI 2.831–5.206, p < 0.001), white cell count (HR 1.039, 95% CI 1.007–1.072, p = 0.016) and high C reactive protein (CRP; HR 1.039, 95% CI 1.021–2.056, p = 0.038) were independently associated with AHREs. ROC curve analysis showed that the APPLE score (C statistic 0.53, 95% CI 0.48–0.59; p = 0.296) ALARMEc score (C statistic 0.51, 95% CI 0.44–0.57; p = 0.810) were non-significantly associated with AHRE. Similar results were obtained for CHADS2 and CHA2DS2VASc scoreConclusionAHREs are common in CIEDs patients, with age, prior AF, inflammatory markers (high CRP, white cell count) being factors associated with AHREs onset. Clinical risk scores showed limited value for AHREs prediction in this cohort.Electronic supplementary materialThe online version of this article (10.1007/s00392-018-1244-0) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Inflammation and the risk of atrial high-rate episodes (AHREs) in patients with cardiac implantable electronic devices

Pastori

Miyazawa

et al. 2018

Clin Res Cardiol

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“…Edoxaban inhibits platelet aggregation in vitro to a higher degree compared with fondaparinux 25. To further evaluate the effect of apixaban on platelet activity in AF, investigations of other platelet markers are needed 26. In contrast to sCD40L, vWF antigen levels were elevated in a proportion of patients independent of VKA status before randomisation.…”

Section: Discussionmentioning

confidence: 99%

Effect of apixaban compared with warfarin on coagulation markers in atrial fibrillation

Christersson

Wallentin

Andersson

et al. 2018

Heart

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ObjectivesCompare the effect of apixaban and warfarin on coagulation and primary haemostasis biomarkers in atrial fibrillation (AF).MethodsThe biomarker substudy from the Apixaban for Reduction in Stroke and Other Thromboembolic Events in Atrial Fibrillation trial included 4850 patients with AF randomised to treatment with apixaban or warfarin. Sixty per cent of patients used vitamin K antagonist (VKA) within 7 days before randomisation. Prothrombin fragment 1+2 (F1+2), D-dimer, soluble CD40 ligand (sCD40L) and von Willebrand factor (vWF) antigen were analysed at randomisation and after 2 months of study treatment.ResultsIn patients not on VKA treatment at randomisation, F1+2 and D-dimer levels were decreased by 25% and 23%, respectively, with apixaban, and by 59% and 38%, respectively, with warfarin (p<0.0001 for treatment differences for both). In patients on VKA at randomisation, F1+2 and D-dimer levels increased by 41% and 10%, respectively, with apixaban and decreased by 37% and 11%, respectively, with warfarin (p<0.0001 for treatment differences for both). sCD40L levels were slightly increased at 2 months, regardless of VKA or randomised treatment. Apixaban and warfarin also both reduced vWF antigen regardless of VKA treatment. The efficacy (stroke) and safety (bleeding) of apixaban compared with warfarin was similar irrespectively of biomarker levels at 2 months.ConclusionsTreatment with apixaban compared with warfarin for stroke prevention in patients with AF was associated with less reduction in thrombin generation and fibrin turnover. This effect of apixaban could contribute to the clinical results where apixaban was superior to warfarin both in stroke prevention and in reducing bleeding risk.Trial registration numberNCT00412984.

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“…To ascertain whether these statins regulated systemic inflammation in inflammatory arthritis, we assessed the levels of platelet–leukocyte aggregates in peripheral blood from arthritic mice, given the relationship of these heterotypic aggregates and cellular activation with CVD (26, 27). Using flow cytometry, we found that atorvastatin regulated the expression of CD11b on both nonclassic and classic monocytes as well as platelet–monocyte aggregates as measured by a decrease in CD62P ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Leukocytes, including monocytes, are implicated in the propagation of various aspects of CVD (26, 27). Studies investigating the role of different monocyte subsets in atherosclerosis, for example, found elevated classic and nonclassic monocytes in atherosclerotic plaques (33).…”

Section: Discussionmentioning

confidence: 99%

13‐Series resolvins mediate the leukocyte‐platelet actions of atorvastatin and pravastatin in inflammatory arthritis

et al. 2017

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Rheumatoid arthritis is an inflammatory condition characterized by overzealous inflammation that leads to joint damage and is associated with an increased incidence of cardiovascular disease. Statins are frontline therapeutics for patients with cardiovascular disease and exert beneficial actions in rheumatoid arthritis. The mechanism that mediates the beneficial actions of statins in rheumatoid arthritis remains of interest. In the present study, we found that the administration of 2 clinically relevant statins—atorvastatin (0.2 mg/kg) or pravastatin (0.2 mg/kg)—to mice during inflammatory arthritis up-regulated systemic and tissue amounts of a novel family of proresolving mediators, termed 13-series resolvins (RvTs), and significantly reduced joint disease. Of note, administration of simvastatin (0.2 mg/kg) did not significantly up-regulate RvTs or reduce joint inflammation. We also found that atorvastatin and pravastatin each reduced systemic leukocyte activation, including platelet-monocyte aggregates (∼25–60%). These statins decreased neutrophil trafficking to the joint as well as joint monocyte and macrophage numbers. Atorvastatin and pravastatin produced significant reductions (∼30–50%) in expression of CD11b and major histocompatibility complex class II on both monocytes and monocyte-derived macrophages in joints. Administration of an inhibitor to cyclooxygenase-2, the initiating enzyme in the RvT pathway, reversed the protective actions of these statins on both joint and systemic inflammation. Together, these findings provide evidence for the role of RvTs in mediating the protective actions of atorvastatin and pravastatin in reducing local and vascular inflammation, and suggest that RvTs may be useful in measuring the anti-inflammatory actions of statins.—Walker, M. E., Souza, P. R., Colas, R. A., Dalli, J. 13-Series resolvins mediate the leukocyte-platelet actions of atorvastatin and pravastatin in inflammatory arthritis.

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Monocyte–platelet aggregates and CD11b expression as markers for thrombogenicity in atrial fibrillation

Abstract: The content of MPAs and the CD11b expression on monocytes and granulocytes are increased in AF-patients with proven thrombus formation. They seem to be appropriate biomarkers for stratification of thromboembolic risk in patients with AF.

Cited by 26 publications

References 53 publications

Inflammation and the risk of atrial high-rate episodes (AHREs) in patients with cardiac implantable electronic devices

Inflammation and the risk of atrial high-rate episodes (AHREs) in patients with cardiac implantable electronic devices

Effect of apixaban compared with warfarin on coagulation markers in atrial fibrillation

13‐Series resolvins mediate the leukocyte‐platelet actions of atorvastatin and pravastatin in inflammatory arthritis

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