Thromb Haemostasis
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Multicenter Study
Persistent enhanced platelet activation in patients with acute myocardial infarction and coronary microvascular obstruction: clinical implications.
About 30% of patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing recanalisation of the infarct-related coronary artery do not achieve valid myocardial reperfusion (no-reflow phenomenon or coronary microvascular obstruction [MVO]). The mechanisms of MVO are incompletely understood. In this study we investigated the role platelet activation in the pathogenesis of coronary MVO in STEMI patients. ⋯ Platelet receptor expression, platelet receptor conformational change for fibrinogen binding availability and MPA formation were increased in STEMI patients with MVO compared to both STEMI patients with MR and stable CAD patients, both on admission and at one-month follow-up (p<0.05 for all). Among STEMI patients, platelet activation is greater in those who display coronary MVO, compared to those with MR, after successful PCI, both on admission and one month after STEMI, suggesting that enhanced platelet activation might be involved in the pathogenesis of MVO. The persistence of enhanced platelet activation despite double classical anti-platelet therapy suggests that new anti-platelet strategies should be considered in patients with coronary MVO.
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Intracranial haemorrhage (ICH), which affects up to 1% of patients on oral anticoagulation per year, is the most feared and devastating complication of this treatment. After such an event, it is unclear whether anticoagulant therapy should be resumed. Such a decision hinges upon the assessment of the competing risks of haematoma growth or recurrent ICH and thromboembolic events. ⋯ Patients with deep hemispheric ICH and a baseline risk of ischemic stroke >6.5% per year, that corresponds to CHADS2≥ 4 or CHA2DS2-VASc ≥ 5, may receive net benefit from restarting anticoagulation. To date, a reasonable recommendation regarding time to resumption of anticoagulation therapy would be after 10 weeks. Available data regarding the role of magnetic resonance imaging in assessing the risks of both ICH and warfarin-related ICH do not support the use of this test for excluding anticoagulation in patients with atrial fibrillation.
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Circulating microparticles play a pro-inflammatory and procoagulant detrimental role in the vascular dysfunction of septic shock. It was the objective of this study to investigate mechanisms by which a pharmacological modulation of microparticles could affect vascular dysfunction in a rat model of septic shock. Septic or sham rats were treated by activated protein C (aPC) and resuscitated during 4 hours. ⋯ In inoculated naïve recipients, microparticles from aPC-treated septic rats prompted reduced NF-κB and cyclooxygenase-2 arterial activation, blunted the generation of pro-inflammatory iNOS and secondarily increased platelet and endothelial microparticles. In conclusion, in this septic shock model, increased circulating levels of procoagulant microparticles led to negative haemodynamic outcomes. Pharmacological treatment by aPC modified the cell origin and levels of circulating microparticles, thereby limiting vascular inflammation and favouring haemodynamic improvement.
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Reversal of anticoagulation is recommended to correct the international normalised ratio (INR) for patients with intracranial haemorrhage (ICH) associated with vitamin K antagonists (VKA). However, the validity of such treatment is debated. We sought to identify, prospectively, the prognostic effect of VKA-ICH treatment in a cohort of patients (n=71; median age 78 years, range 20-89; 52% males). ⋯ Baseline NIHSS predicted mortality (OR: 1.18; 95%CI: 1.09-1.27), independence (OR: 0.83; 95%CI: 0.74-0.94) and neurological recovery (NIHSS 0-1) (OR: 0.83; 95%CI: 0.73-0.95). The data indicate that VKA-ICH had a poor prognosis. Treatment and INR correction did not appear to affect outcomes.
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Randomized Controlled Trial Comparative Study Clinical Trial
Comparison of the CHADS2, CHA2DS2-VASc and HAS-BLED scores for the prediction of clinically relevant bleeding in anticoagulated patients with atrial fibrillation: the AMADEUS trial.
Many of the risk factors for stroke in atrial fibrillation (AF) are also important risk factors for bleeding. Wetested the hypothesis that the CHADS2 and CHA2DS2-VASc scores (used for stroke risk assessment) could be used to predict serious bleeding, and that these scores would compare well against the HAS-BLED score, which is a specific risk score designed for bleeding risk assessment. From the AMADEUS trial, we focused on the trial's primary safety outcome for serious bleeding, which was "any clinically relevant bleeding". ⋯ The HAS-BLED score also demonstrated significant NRI for the outcome of "any clinically relevant bleeding" when compared with CHADS2 (p=0.001) and CHA2DS2-VASc (p=0.04). In conclusion, the HAS-BLED score demonstrated significant discriminatory performance for "any clinically relevant bleeding" in anticoagulated patients with AF, whilst the CHADS2 and CHA2DS2-VASc scores did not. Bleeding risk assessment should be made using a specific bleeding risk score such as HAS-BLED, and the stroke risk scores such as CHADS2 or CHA2DS2-VASc scores should not be used.