We report the case of an 82-year-old A pixaban is a novel oral anticoagulant (NOAC) that is used to prevent stroke in patients who have nonvalvular atrial fibrillation (AF). This drug has predictable therapeutic levels that do not require laboratory monitoring; however, there is no specific antidote to reverse its toxicity.1,2 We present a case of hemorrhagic pericarditis and cardiac tamponade after pacemaker implantation in a patient who was taking apixaban because of AF. Novel therapy and subsequent treatment are discussed.
Case ReportAn 82-year-old man with sick sinus syndrome and paroxysmal AF presented at our catheterization laboratory from the clinic, with near-syncope and bradycardia (CHADS 2 score, 2 of 6). On 24-hour Holter monitoring, the predominant result was sinus rhythm. An echocardiogram revealed a normal left ventricular ejection fraction (>0.60), grade II (pseudonormal) diastolic dysfunction, no significant valvular regurgitation, and normal pulmonary artery pressures. A dual-chamber permanent pacemaker was implanted to treat the patient's brady-tachy syndrome and because ventricular pacing revealed pacemaker syndrome (hypotension that results from ventricular pacing due to the absence of the atrial kick that normally increases stroke volume during atrioventricular synchrony). During the procedure, the atrial lead was repositioned. One day postoperatively, the patient was discharged from the hospital after undergoing chest radiography (with normal findings), device interrogation, and incision evaluation. Because of his stroke risk, he was prescribed apixaban (5 mg twice/d) at discharge. He had normal renal function (Table I) and a body weight of 172 lb.During the week after pacemaker implantation, the patient developed fatigue, a low-grade fever (99.2 °F), nausea, moderate pleuritic chest pain, and a productive cough with clear sputum. He was readmitted to the hospital. His blood pressure had decreased from 130/77 mmHg after pacemaker implantation to 100/68 mmHg upon readmission, when he was taking no antihypertensive medications. Physical examination revealed an irregular, tachycardic rhythm (100-130 beats/min), and distended neck veins; auscultation yielded diminished bibasilar breath sounds but no quiet heart sounds. Laboratory data revealed acute kidney injury (Table I) and a substantially elevated erythrocyte sedimentation rate and fibrinogen level. The patient's platelet count and coagulation times were normal; his hemoglobin level had decreased from 15 g/dL after pacemaker implantation to 12 g/dL on readmission. He was taken to the cardiac intensive care unit, where he remained hemodynamically stable.Computed axial tomograms (CT) of the chest (Fig. 1) were not conclusive for right ventricular free-wall perforation, although a moderate-to-large circumferential pericardial effusion of 1.7 cm was detected; its Hounsfield density suggested the presence of Case Reports