[Antithrombotic therapy in acute coronary syndromes].
Inhibition of coagulation is a key therapeutic principle in acute coronary syndromes (ACS). A plethora of substances is used in daily clinical practice to prevent thrombocyte aggregation, i.e. primary haemostasis, as well as activation of the coagulation cascade. Prevention of thrombocyte aggregation is accomplished by inhibiting thromboxane synthesis by acetyl salicylic acid, blockade of the ADP receptor, and by inhibition of the glycoprotein IIb/IIIa-receptor. Inhibition of the plasmatic coagulation in the setting of acute coronary syndromes is primarily achieved by the use of unfractionated or low-molecular weight heparins. Beyond this, several next-generation substances such as the novel, potent ADP receptor antagonist prasurgel or the selective direct thrombin- and factor Xa-antagonists are being developed and are investigated in clinical trials. It remains to be determined which place these novel substances will take in the armentarium of anticoagulants in acute coronary syndromes, and whether they will be employed in the majority of ACS-patients or just in certain sub-populations (e.g., in patients with a high or a low bleeding risk, in the presence of aspirin- or clopidogrel resistance etc.). The current review summarizes the mode of action as well as the clinical use of currently employed anticoagulants in acute coronary syndromes.
Herzkreislaufzentrum, Klinik für Kardiologie, UniversitätsSpital Zürich und Kardiovaskuläre Forschung, Institut für Physiologie, Universität Zürich.
Jan
J
Steffel
Thomas F
TF
Lüscher
D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000378:metabolism*; D005343:Fibrinolytic Agents / Q000008:administration & dosage* / Q000009:adverse effects / Q000493:pharmacokinetics*; D006321:Heart / Q000187:drug effects*; D006801:Humans; D008955:Models, Cardiovascular; D009206:Myocardium / Q000378:metabolism*
D005343:Fibrinolytic Agents