An unusual case of non‐infective endocarditis in undiagnosed antiphospholipid syndrome

Abstract

A 57yearold man presented with left facial droop and dysarthria due to a multiterritory ischaemic stroke affecting the right posterior and middle cerebral arteries. His previous history included a segmental pulmonary embolus in the setting of pneumonia. He was not taking any regular medications and denied recreational drug use. There was no relevant family history. He was haemodynamically stable, afebrile and euvolaemic. White cell count was normal at 7.8 × 109/L (reference interval [RI], 4– 12 × 109/L). Creactive protein was mildly elevated at 9 mg/L (RI, < 5 mg/L). On day 1, transthoracic echocardiogram revealed a vegetation on the anterior mitral valve leaflet tip with moderate to severe mitral regurgitation, normal left atrial size and biventricular size and systolic function. Three sets of blood cultures were taken before commencing intravenous ceftriaxone and flucloxacillin. He was transferred to our hospital for surgical consideration. On day 3, transoesophageal echocardiogram confirmed a 2 cm independently mobile lesion on the anterior mitral valve leaflet tip with severe central mitral regurgitation (Box 1). Extended 27day blood cultures remained negative. Routine coagulation studies revealed an elevated activated partial thromboplastin time (aPTT) of 77 seconds (RI, 23– 36 seconds) with normal international normalised ratio (INR). aPTT did not correct with mixing studies. Elevated dilute Russell viper venom time screen ratio of 2.63 (RI, < 1.2) confirmed presence of lupus anticoagulant. Thrombophilia screen confirmed high anticardiolipin IgG > 2024 (RI, < 20) and β2glycoprotein 1 antibody > 6100 (RI, < 20) suggestive of antiphospholipid syndrome. There were no clinical features of systemic lupus erythematosus and autoimmune screen was normal. Computed tomography of the chest, abdomen, and pelvis demonstrated no embolic events or malignancy. A diagnosis of noninfective endocarditis (NIE) due to presumed antiphospholipid syndrome was made. A multidisciplinary consensus opinion involving cardiology, cardiothoracic surgery, infectious diseases, haematology, and stroke teams was made for nonsurgical management with warfarin (target INR, 2– 3). Antibiotics were ceased. He was discharged home on day 10. Anticardiolipin IgG and β2glycoprotein 1 antibody remained elevated at 12 weeks, confirming antiphospholipid syndrome. Repeat transoesophageal echocardiogram at 3 weeks demonstrated significantly reduced mitral valve lesion size with only mild mitral regurgitation (Box 2). The patient continues on lifelong warfarin with no residual stroke symptoms.