Atrial fibrillation (AF) is the most common cardiac arrhythmia [1] and a major cause of thromboembolic events [2]. In non-valvular AF, nearly all thrombi originate in the left atrial appendage (LAA) [3], where impaired contraction and blood stasis promote clot formation. To mitigate this risk, current clinical guidelines [4] recommend long-term anticoagulant therapy. However, patient-specific haemodynamic response to these drugs and their optimal posology remains difficult to quantify. Among direct oral anticoagulants, rivaroxaban, a direct factor Xa inhibitor, is one of the most commonly prescribed [5]. In this work, a mono-physics fluid–structure interaction (FSI) model [6] based on smoothed particle hydrodynamics (SPH) is employed to investigate thrombus formation and dissolution in a patient-specific LAA morphology. AF conditions were modelled in the absence and in the presence of rivaroxaban therapy. The adopted thrombus model converts fluid particles into a solid phase by introducing spring links when specific biochemical/hydrodynamic conditions are met. Thrombus dynamics are captured through the transport and interactions of key coagulation factors, platelets, and fibrinolytic species. Specifically, the model includes factor X/Xa, prothrombin, thrombin, antithrombin, fibrinogen, fibrin, three platelet types (resting, activated, bound), and fibrinolytic components such as tissue plasminogen activator (t-PA), plasminogen, plasmin, and antiplasmin. Furthermore, rivaroxaban is explicitly modelled as a species, enabling assessment of different drug dosages. By integrating coagulation kinetics, fibrinolysis, and anticoagulant transport, this model captures the complex interactions driving thrombus formation and lysis. This approach provides a mechanistic tool for patient-specific assessment of thromboembolic risk and tuning of anticoagulation therapy, offering insight into the interplay between arrhythmic haemodynamic, pharmacological intervention, and fibrinolytic activity.