Rivaroxaban
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Transient constrictive pericarditis and haemopericardium: case report A 72-year-old man developed haemopericardium leading to transient constrictive pericarditis during treatment with rivaroxaban. The man was diagnosed with atrial fibrillation in November 2013 and underwent successful cardioversion. He was discharged on rivaroxaban [route, dosage and indication not stated]. However, 5 days later, he presented with complaints of orthopnea and exertional dyspnoea. A large circumferential pericardial effusion (haemopericardium) was observed. The man underwent pericardiocentesis. In December 2013, he presented to a pericardial center with complaints of weight gain and exertional dyspnoea on a wheelchair. Physical examination showed bilateral pitting oedema, increased jugular venous pressure to the angle of the jaw, and a pericardial knock. He was diagnosed with a New York Heart Association (NYHA) functional class III heart failure along with concern of constrictive pericarditis and was hospitalised for further management. He had a history of hyperlipidaemia and hypertension, and was a non-smoker. His cardiac MRI showed thick pericardium, residual trace pericardial effusion, prominent diastolic septal bounce, pericardial oedema, respirophasic septal shift, and pericardial enhancement on delayed gadolinium imaging, which suggested acute pericardial inflammation. His pericardial fluid analysis was negative for neoplastic cells and infectious disease. Also, the increased right atrial pressures even after draining the haemopericardium was considered secondary to rivaroxaban therapy. Initially, effusive inflammatory constriction was suspected. Treatment with furosemide and antiinflammatory therapy with colchicine, prednisone and aspirin was initiated. Thereafter, an improvement in shortness of breath and chest pain was noted. A week later, he was discharged. Four months later, a repeat cardiac MRI demonstrated decreased pericardial thickness, oedema, inflammation, and the associated constrictive physiology. The dose of colchicine was reduced and prednisone was tapered slowly. His condition improved and prednisone was discontinued in July 2014. Two months later (in September 2014), he presented with generalised malaise. His cardiac MRI demonstrated increased pericardial thickening, oedema, inflammation, and respirophasic septal shift consistent with returning inflammatory constriction. Hence, he was restarted on prednisone, aspirin and colchicine. During follow-up, an improvement in constrictive physiology was observed on imaging. Then, prednisone was again discontinued in April 2015. Also, all other anti-inflammatory treatment was discontinued in April 2018. In December 2019, he presented with a 2-week history of weight gain and exertional dyspnoea and was diagnosed with NYHA functional class III heart failure. Cardiac MRI showed constrictive pericarditis. He underwent radical pericardiectomy and his symptoms resolved. Pathological examination of the pericardium revealed organised fibrinous pericarditis without granulom
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