A 27-year-old male professional rugby player was admitted to his local district general hospital with a 2-day history of chest tightness and breathlessness. He had no other significant past medical history and was not taking any regular medications. He admitted to regularly taking cocaine and performance-enhancing steroids. He was haemodynamically stable with normal saturation. The main findings on physical examination were an irregularly irregular pulse and bibasal crackles. His admission electrocardiogram (ECG) showed AF and his chest X-ray findings were in keeping with pulmonary oedema. Initial bloods tests were within normal range. Transthoracic echocardiogram (TTE) revealed bi-atrial dilatation and a moderately dilated left ventricle (left ventricular end diastolic diameter 7 cm) with mild concentric left ventricular (LV) hypertrophy with an ejection fraction (EF) 35–40%. He was acutely managed with intravenous diuretics and initiated on evidence-based heart failure medications including beta-blockers and angiotensin-converting enzyme inhibitors. In view of his drug history, a working diagnosis of drug-induced dilated cardiomyopathy (DCM) was made. Once stabilized, he was discharged on bisoprolol 2.5 mg and ramipril 2.5 mg. In anticipation of a direct current cardioversion (DCCV), he was started on rivaroxaban 20 mg. He was counselled not to participate in any competitive sports. To further investigate his cardiomyopathy, he underwent an outpatient coronary angiogram which revealed unobstructed coronary arteries. In addition, a cardiac magnetic resonance (CMR) confirmed a dilated left ventricle with globally impaired systolic function and a calculated EF of 37%. There was no evidence of scarring or fibrosis on delayed enhancement images. He was unable to maintain sinus rhythm following DCCV and relapsed back into persistent AF. His CHA2DS2-VASc score was 1 (LV dysfunction) which does not strictly mandate anticoagulation; however, he made an informed decision to continue rivaroxaban. On a follow-up TTE performed 3 months later, LV systolic function remained unchanged. His ramipril was increased and he was initiated on eplerenone. Left ventricular function gradually improved on optimal medical therapy and, at 8 months of follow-up, had returned to near-normal (EF 50–55%). He remained in AF and experienced a brief episode of left arm weakness and paraesthesia suggestive of a transient ischaemic attack (TIA) despite being compliant with anticoagulation. As his CHA2DS2-VASc score increased to 3 (TIA, LV dysfunction) he now had a clear indication for anticoagulation. Connective tissue disorders, syphilis, and Fabry disease screening were negative. At 1-year follow-up, he was asymptomatic (New York Heart Association 1) but remained in AF and continued to participate in competitive rugby, whilst on oral anticoagulation despite counselling regarding the high bleeding risk. He was reluctant to terminate his professional rugby career prematurely and sought alternative stroke prevention strategies that obviated the need for continuous anticoagulation. He was referred to a Tertiary Cardiology Centre for further management of his AF and consideration of a left atrial appendage occlusion (LAAO) device. A 27 mm Watchman Flx (Boston Scientific, MA, USA) device was successfully deployed under general anaesthetic in the left atrial appendage with a good seal and no leaks (, ). He was discharged home on a 6-week course of aspirin and clopidogrel therapy with a follow-up transoesophageal echocardiogram to assess LAAO device position and guide cessation of antiplatelet strategy.