acenocoumarol and Endocarditis

Prosthetic valve thrombosis (PVT) represents a serious and potentially lethal complication. It can be attributed more frequently to inadequate anticoagulant therapy. We present a case of acute aortic mechanical valve thrombosis six months after implantation. The patient discontinued oral anticoagulation after being discharged following the primary operation. Two days after reinitiating warfarin as an outpatient, he developed acute valve thrombosis presenting with symptoms and signs of cardiac failure. He was managed with intravenous thrombolysis with a recombinant plasminogen activator which resulted in immediate resolution of thrombus and clinical improvement. A paradox procoagulant effect of warfarin is evident on the first one or two days after initiation of therapy. A 'bridging' protocol with unfractionated or low molecular weight heparin (LMWH) should be considered, according to recently published guidelines, until warfarin reaches therapeutic levels and exerts an antithrombotic effect.

Topics: Acenocoumarol; Acute Disease; Adult; Anticoagulants; Aortic Valve Insufficiency; Endocarditis; Fibrinolytic Agents; Heart Valve Prosthesis; Heart Valve Prosthesis Implantation; Heparin; Humans; Male; Medication Adherence; Tenecteplase; Thrombolytic Therapy; Thrombosis; Tissue Plasminogen Activator; Treatment Outcome; Warfarin

A 73-year-old woman with endocarditis was treated with flucloxacillin and rifampicin. She already used the anticoagulant acenocoumarol because of a recent heart valve replacement. After starting rifampicin therapy the sensitivity for the acenocoumarol was reduced. The international normalised ratio (INR) did not exceed 2.0, while values of 2.5-3.5 were required. Increase of the daily dose of acenocoumarol with a factor 6 compared to the dose which resulted in a therapeutic INR before hospitalisation, proved insufficient to obtain a therapeutic INR during long-term rifampicin therapy. 21 days after rifampicin discontinuation the INR finally responded to high coumarin dosages. The breakdown of coumarins in the liver is increased by rifampicin due to induction of several isoenzymes of the cytochrome P450-system. This case illustrates that sensitivity to coumarins can be decreased profoundly even after discontinuation of rifampicin therapy. INR should be monitored closely not only at the start and discontinuation of rifampicin therapy, but also during the weeks after discontinuation of rifampicin treatment.

Topics: Acenocoumarol; Aged; Anti-Bacterial Agents; Anticoagulants; Dose-Response Relationship, Drug; Drug Interactions; Endocarditis; Female; Heart Valve Prosthesis; Humans; International Normalized Ratio; Liver; Rifampin; Time Factors