Chromogenic laboratory assays to measure the factor Xa-inhibiting properties of apixaban—an oral, direct and selective factor Xa inhibitor

Becker, Richard C.; Yang, Hongqiu; Barrett, Yuchen; Mohan, Puneet; Wang, Jessie; Wallentin, Lars; Alexander, John H.

doi:10.1007/s11239-011-0591-8

Cited by 141 publications

(114 citation statements)

References 5 publications

(1 reference statement)

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“…While the PT is in general poorly responsive, the anti-FXa assay proved to be highly correlated and adequately responsive to the apixaban plasma concentrations. 21 The problems of availability and standardization of the anti-FXa assay discussed above for rivaroxaban also apply to apixaban.…”

Section: Apixabanmentioning

confidence: 99%

The laboratory and the direct oral anticoagulants

Tripodi

2013

Blood

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Although direct oral anticoagulants do not need laboratory testing for dose adjustment, there are instances when laboratory measurement of the drug anticoagulant effect may be useful. They include before initiation of treatment, before surgical or invasive procedures, on the occasion of hemorrhagic or thrombotic events, and whenever immediate reversal of anticoagulation is needed. Choice of tests should be primarily based on their prompt availability. Accordingly, the dilute-thrombin or the ecarin clotting times are best suited for dabigatran and the prothrombin time or the anti-FXa for rivaroxaban.

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Section: Apixabanmentioning

confidence: 99%

The laboratory and the direct oral anticoagulants

Tripodi

2013

Blood

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“…Contrasting results have been reported on the correlation between the prolongation of the PT or the APTT and the apixaban concentration (22,23 ). The anti-FXa assay has been evaluated in a substudy of patients treated with apixaban (24 ), and it proved to be highly correlated and adequately responsive to the apixaban concentration in plasma. The problems of availability and standardization of this assay that have already been discussed for rivaroxaban also apply to apixaban.…”

Section: Apixabanmentioning

confidence: 99%

The Laboratory and the New Oral Anticoagulants

Tripodi

2013

Clinical Chemistry

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BACKGROUND:The new oral anticoagulants (NOAs) dabigatran, rivaroxaban, and apixaban have proved effective and safe when used in clinical trials, without a need to adjust the dose in response to laboratory testing. This demonstrated efficacy does not necessarily mean that the laboratory, considered the mainstay for the management of the old anticoagulants, will no longer play a role in treatment with NOAs.CONTENT: Laboratories are involved in the management of anticoagulants in 2 ways. The first, monitoring, implies laboratory testing to assess the drug's effect and to adjust the dosage to maintain anticoagulation within the therapeutic interval. This consideration applies to the old drugs. The second way, measurement, implies laboratory evaluations of drug effect to determine whether patients are under-or overanticoagulated, information that can be useful for decision-making in special circumstances. The latter applies to NOAs.

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“…Initial chromogenic anti-Xa levels had a direct correlation with the results of LMWH assays. 13 Subsequently, in a French study, 3 different anti-Xa assays had a direct correlation with apixaban concentration, whereas prothrombin time and activated partial thromboplastin time did not.…”

Section: Discussionmentioning

confidence: 99%

Plasma Exchange for Urgent Apixaban Reversal in a Case of Hemorrhagic Tamponade after Pacemaker Implantation

Lam¹,

Reyes²,

Seger³

2015

Texas Heart Institute Journal

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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

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Chromogenic laboratory assays to measure the factor Xa-inhibiting properties of apixaban—an oral, direct and selective factor Xa inhibitor

Cited by 141 publications

References 5 publications

The laboratory and the direct oral anticoagulants

The laboratory and the direct oral anticoagulants

The Laboratory and the New Oral Anticoagulants

Plasma Exchange for Urgent Apixaban Reversal in a Case of Hemorrhagic Tamponade after Pacemaker Implantation

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