New pharmacologic approaches to prevent thromboembolism in patients with atrial fibrillation.
Atrial fibrillation (AF) is associated with a 6 fold increased risk for ischemic stroke. Observational studies suggest that one in four to five strokes is due to AF. Depending on the risk profile of an individual patient, the yearly risk for ischemic stroke is between 2% and 14%. AF is accompanied by an increased propensity for atrial clot formation due to a combination of decreased atrial blood flow, increased activity of the platelet/plasmatic coagulation system and prothrombotic changes at the atrial endocardium. This review summarizes the current guidelines for thromboembolic prevention in patients with AF. In many cases, continuous oral anticoagulation therapy (OAT) with vitamin K antagonists (VitKAs) is indicated if AF is accompanied by more than one additional risk factor for thromboembolic complications. However, therapeutic range of VitKAs (Phenprocoumon, Warfarin, and others), the most commonly used oral anticoagulants, is narrow and their use requires regular anticoagulation monitoring. Possibly due to these limitations, about one third of eligible patients are not treated with VitKAs. Furthermore, in many treated patients OAT is not well controlled. Thus, in clinical practice anticoagulation therapy in AF is suboptimal. Therefore, new and more convenient pharmacologic approaches to prevent thromboembolism with i.e. direct thrombin inhibitors (DTI), synthetic polysaccharides (factor Xa Inhibitors), and others are discussed, and their possible future role in the treatment of AF is evaluated.
Hammwöhner
Matthias
M
University Hospital Magdeburg, Division of Cardiology, Magdeburg, Germany.
D'Alessandro
Alessandra
A
Wolfram
Oliver
O
Goette
Andreas
A
D000925:Anticoagulants / Q000009:adverse effects / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D005170:Factor X / Q000037:antagonists & inhibitors / Q000378:metabolism; D006470:Hemorrhage / Q000139:chemically induced; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D017410:Practice Guidelines as Topic; D018570:Risk Assessment; D012307:Risk Factors; D020521:Stroke / Q000209:etiology / Q000517:prevention & control*; D013917:Thrombin / Q000037:antagonists & inhibitors / Q000378:metabolism; D013923:Thromboembolism / Q000150:complications / Q000209:etiology / Q000517:prevention & control*; D014812:Vitamin K / Q000037:antagonists & inhibitors / Q000378:metabolism
D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D014812:Vitamin K; D005170:Factor X; D013917:Thrombin