Abstract
Catheter Ablation Versus Antiarrhythmic Medication in Patients with Atrial Fibrillation: a Propensity-Matched Analysis Based on a German Claims Data Set
Highlights
Despite significant advances in antithrombotic therapy in recent years, thromboembolic conditions such as myocardial infarction, ischemic stroke, venous thrombosis, and pulmonary embolism remain major causes of death and morbidity in developed countries [1]
This study investigated the safety, pharmacokinetics, and effect on biomarkers for thrombosis of CS1, a new advanced controlled release formulation of sodium valproate designed to produce optimum valproic acid concentrations during the early morning hours, when concentrations of plasminogen activator inhibitor (PAI)-1 and the risk of thrombotic events is highest
The principle behind the CS1 controlled-release formulations, described above was to achieve a peak concentration of valproic acid at a median of 12 hours after dosing and a trough concentration during the day which is half of the peak concentrations during the night and early morning. With this specific pharmacokinetic profile, it is expected that drug concentration-related AEs will be minimized, whereas the antithrombotic efficacy should be enhanced. This is in contrast to the therapeutic use of valproic acid in the treatment of epilepsy, where a stable plasma concentration higher than the peak concentration in this study, over 24 hours is the target for successful treatment [32]
Summary
Despite significant advances in antithrombotic therapy in recent years, thromboembolic conditions such as myocardial infarction, ischemic stroke, venous thrombosis, and pulmonary embolism remain major causes of death and morbidity in developed countries [1]. The extent of thrombosis in an individual reflects a balance between coagulation and fibrinolytic activity in the blood vessels. All current antithrombotic therapies focus on inhibiting the coagulation cascade, platelet function, or both, but dosing is often suboptimal because of the need to prevent dosedependent bleeding complications [2]. There remains a need for novel strategies to prevent thrombotic disease without increasing the risk of bleeding. Impaired fibrinolysis [3,4], due to either decreased production and depleted storage of tissue plasminogen activator (t-PA) or increased expression of the principal inhibitor of fibrinolysis, plasminogen activator inhibitor-1 (PAI-1) , has been reported in large studies in patients with coronary heart disease (CHD) or cardiovascular risk factors such as hypertension, obesity and/or smoking [5,6,7,8,9]
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