Direct oral anticoagulation and severe obesity – One size fits all?

Figures

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  Fig. 1. DOAC are candidate master inhibitors of the inflammation/thrombosis/atrial cardiomyopathy axis in obesity. The causes and consequences of atrial fibrillation (AF) are closely linked to a prothrombotic state, sterile inflammation and an atrial cardiomyopathy that encompasses structural, mechanical and functional remodeling of the atrial myocardium. The same constellation of deleterious changes is associated with obesity, a major driver of AF. The direct oral anticoagulants (DOAC) may represent master inhibitors of this pathological interaction. The inhibitory targets of DOAC, the coagulation factors thrombin and activated factor X (FXa), promote clot formation and the activation, aggregation and degranulation of platelets, culminating in thromboembolism and stroke. Via protease-activated receptors (PAR), thrombin and FXa also trigger coagulation-independent inflammatory, structural and functional alterations in adipose tissue, blood cells and the heart and vasculature, thereby supporting the inflammatory atrial cardiomyopathy that provides a vulnerable substrate for AF. By disabling this thromboinflammatory interplay, DOAC may suppress both the evolution and the thrombotic…