Abstract

Abstract Introduction Direct oral anticoagulants (DOACs), as substrates of cytochrome P450 and / or P–glycoprotein (P–gp), are susceptible to drug–drug interactions (DDI) by both inducers and inhibitors. Awareness of this aspect is essential when choosing a DOAC, to avoid exposing the patient to an increased risk of bleeding or cardioembolicism. Description We report the clinical case of a 41–year–old woman with a history of iron deficiency anemia and primary hypertrophic cardiomyopathy (HCM), who came to our emergency room for an episode of atrial fibrillation with high ventricular rate (HR 140 bpm), datable (<48h) and haemodynamically well tolerated. She was therefore subjected to pharmacological cardioversion with amiodarone, which was found to be effective. Subsequently, she was subjected to interrogation of the defibrillator (ICD), of which the patient was a carrier in primary prevention, with the finding of numerous episodes of AF, lasting up to several hours, paucisymptomatic. An antiarrhythmic prophylaxis with amiodarone and anticoagulant therapy with edoxaban was therefore recommended at discharge. In the following two months, in conjunction with the menstrual cycle, the patient had access to emergency room for metrorrhagia with the need for blood transfusion due to severe anemia (Hb 6 gr / dl). The gynecological tests were negative and she was entrusted to the cardiologist for the management of the therapy. Reassessed on an outpatient basis, given the impossibility of changing antiarrhythmic drugs, as amiodarone is the only molecule recommended for rhythm control in patients with this type of cardiomyopathy, and given the possible interaction between edoxaban and amiodarone (+ 40% plasma DOAC levels ), it was decided to shift to another DOAC: rivaroxaban 20 mg (less interference). In the following twelve months the patient no longer had acute anemia phenomena, the hemoglobin values remained stable and upon interrogation of the ICD device there were no arrhythmic events. Comment We have described this case to underline how the possible pharmacokinetic interactions between DOACs and antiarrhythmic drugs are of fundamental importance in daily clinical practice, especially when there are non–reversible causes that increase the risk of bleeding. In this case, the therapy shift vs a DOAC with a documented lower DDI interaction was found to be conclusive.

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