title: Pharmacokinetic evaluation of  rivaroxaban  for the treatment of acute coronary syndromes.
abstract: BACKGROUND
  Arterial and venous thrombotic states, including myocardial infarction (MI), stroke and deep vein thrombosis with subsequent pulmonary embolism, are a significant cause of cardiovascular mortality and morbidity. Factor Xa (FXa) plays a pivotal role in thrombus formation. Its inhibition following acute coronary syndromes (ACS) blocks amplification of thrombin generation and subsequent clot formation, resulting in a risk reduction in recurrent MI, stroke and death. For this reason, a predictable form of oral anticoagulation continues to be an ongoing need. Rivaroxaban , the first oral FXa inhibitor, acts by direct inhibition of FXa and does not require an antithrombin cofactor for its activity.
  
  
  METHODS
  This paper describes the pharmacokinetics (PK) of low-dose rivaroxaban tested in patients with ACS. Age, gender, renal function and body weight have no clinically significant effects on the PK of the drug in treatment of ACS. Caution should be maintained during co-administration of strong CYP3A4 inducers and inhibitors. Among patients with moderate and severe hepatic impairment and in those with associated coagulopathies, rivaroxaban however is contraindicated.
  
  
  CONCLUSIONS
  The mortality benefit with low-dose rivaroxaban in ACS patients was first demonstrated in ATLAS ACS2 TIMI-51 trial. With its rapid oral bioavailability, predictable PK, low drug-drug interaction and no need for monitoring, the use of low-dose rivaroxaban in addition to dual antiplatelet therapy offers an appealing new option in improving outcomes following ACS in the modern era of novel oral FXa inhibitors.
authors.affiliation: Harvard Medical School, Beth Israel Deaconess Medical Center, Cardiovascular Division, Department of Medicine, Boston, MA 02115, USA.
authors.forename: Lakshmi
authors.initials: L
authors.lastname: Gopalakrishnan
authors.forename: Varun
authors.initials: V
authors.lastname: Kumar
authors.forename: Payal
authors.initials: P
authors.lastname: Kohli
authors.forename: Priyamvada
authors.initials: P
authors.lastname: Singh
authors.forename: Ujjwal
authors.initials: U
authors.lastname: Rastogi
authors.forename: C Michael
authors.initials: CM
authors.lastname: Gibson
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D000284:Administration, Oral; D001780:Blood Coagulation Tests; D017322:Clinical Trials, Phase II as Topic; D017326:Clinical Trials, Phase III as Topic; D004353:Drug Evaluation, Preclinical; D004347:Drug Interactions; D015951:Factor Xa / Q000378:metabolism; D065427:Factor Xa Inhibitors; D006207:Half-Life; D006801:Humans; D009025:Morpholines / Q000493:pharmacokinetics* / Q000494:pharmacology*; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology; D011655:Pulmonary Embolism / Q000188:drug therapy; D016032:Randomized Controlled Trials as Topic; D000069552:Rivaroxaban; D020521:Stroke / Q000188:drug therapy / Q000503:physiopathology; D013876:Thiophenes / Q000493:pharmacokinetics* / Q000494:pharmacology*; D013917:Thrombin / Q000037:antagonists & inhibitors / Q000378:metabolism; D013927:Thrombosis / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D065427:Factor Xa Inhibitors; D009025:Morpholines; D013876:Thiophenes; D000069552:Rivaroxaban; D013917:Thrombin; D015951:Factor Xa