scholarly journals Running after Activated Clotting Time Values in Patients Receiving Direct Oral Anticoagulants: A Potentially Dangerous Race. Results from a Prospective Study in Atrial Fibrillation Catheter Ablation Procedures

2021 ◽  
Vol 10 (18) ◽  
pp. 4240
Author(s):  
Karim Benali ◽  
Julien Verain ◽  
Nefissa Hammache ◽  
Charles Guenancia ◽  
Darren Hooks ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Catheter Ablation ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Clotting Time ◽  
Af Ablation ◽  
Activated Clotting Time ◽  
Real Increase ◽  
A Prospective Study ◽  
The Relationship

Background: Activated Clotting Time (ACT) guided heparinization is the gold standard for titrating unfractionated heparin (UFH) administration during atrial fibrillation (AF) ablation procedures. The current ACT target (300 s) is based on studies in patients receiving a vitamin K antagonist (VKA). Several studies have shown that in patients receiving Direct Oral Anticoagulants (DOACs), the correlation between ACT values and UFH delivered dose is weak. Objective: To assess the relationship between ACT and real heparin anticoagulant effect measured by anti-Xa activity in patients receiving different anticoagulant treatments. Methods: Patients referred for AF catheter ablation in our centre were prospectively included depending on their anticoagulant type. Results: 113 patients were included, receiving rivaroxaban (n = 30), apixaban (n = 30), dabigatran (n = 30), and VKA (n = 23). To meet target ACT, a higher UFH dose was required in DOAC than VKA patients (14,077.8 IU vs. 9565.2 IU, p < 0.001), leading to a longer time to achieve target ACT (46.5 min vs. 27.3 min, p = 0.001). The correlation of ACT and anti-Xa activity was tighter in the VKA group (Spearman correlation ρ = 0.53), compared to the DOAC group (ρ = 0.19). Despite lower ACT values in the DOAC group, this group demonstrated a higher mean anti-Xa activity compared to the VKA group (1.56 ± 0.39 vs. 1.14 ± 0.36; p = 0.002). Conclusion: Use of a conventional ACT threshold at 300 s during AF ablation procedures leads to a significant increase in UFH administration in patients treated with DOACs. This increase corresponds more likely to an overdosing than a real increase in UFH requirement.

scholarly journals Activated Clotting Time Monitoring during Atrial Fibrillation Catheter Ablation: Does the Anticoagulant Matter?

2020 ◽  
Vol 9 (2) ◽  
pp. 350 ◽  
Author(s):  
Anne-Céline Martin ◽  
Maeva Kyheng ◽  
Vincent Foissaud ◽  
Alain Duhamel ◽  
Eloi Marijon ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Catheter Ablation ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Vitamin K Antagonist ◽  
Strongly Correlated ◽  
Clotting Time ◽  
Response Curves ◽  
Activated Clotting Time

Atrial fibrillation (AF) catheter ablation is performed in patients receiving direct oral anticoagulants (DOACs) with intra-procedural unfractionated heparin (UFH) administration to achieve activated clotting time (ACT) at 300 s, as for vitamin K antagonist (VKA). We determined whether ACT monitoring might be transposed from VKA to DOAC-treated patients. Blood was taken from 124 patients receiving uninterrupted dabigatran, rivaroxaban, apixaban, or VKA or being untreated. DOAC concentration or INR (VKA) were measured. ACT was determined at baseline, and after spiking with UFH doses equivalent to 1000, 2500, 5000 and 10000 IU in vivo. At baseline, anticoagulants prolonged ACT differently, ACT was longer with dabigatran and shorter with apixaban despite similar concentrations. ACT strongly correlated with INR and dabigatran concentration, but not with apixaban or rivaroxaban concentrations. Moreover, UFH effects on ACT prolongation depended on the anticoagulant: dose-response curves in samples with VKA and dabigatran were parallel whereas ACT prolongation in response to UFH was significantly smaller with rivaroxaban and especially apixaban. Therefore, UFH to achieve ACT at 300 s might be transposed from VKA to uninterrupted dabigatran-treated patients but not to patients receiving FXa-inhibitors, especially apixaban. Targeting 300 s might expose to UFH overdosing and bleeding, questioning the current anticoagulation strategy.

scholarly journals Management of Intraprocedural Anticoagulation in Patients on Non-Vitamin K Antagonist Oral Anticoagulants Undergoing Catheter Ablation for Atrial Fibrillation

Circulation ◽  
2018 ◽  
Vol 138 (6) ◽  
pp. 627-633 ◽  
Author(s):  
Anne-Céline Martin ◽  
Anne Godier ◽  
Kumar Narayanan ◽  
David M. Smadja ◽  
Eloi Marijon
Keyword(s):  
Atrial Fibrillation ◽  
Catheter Ablation ◽  
Unfractionated Heparin ◽  
Vitamin K ◽  
Vitamin K Antagonists ◽  
Oral Anticoagulants ◽  
Vitamin K Antagonist ◽  
Clotting Time ◽  
Anticoagulation Management ◽  
Activated Clotting Time

Catheter ablation has gained a prominent role in the management of atrial fibrillation (AF), with recent data providing positive evidence on hard outcomes, including hospitalization and mortality. Ablation, however, exposes the patient to a rather unique situation, combining risks for both major bleeding and thromboembolic events. In this setting, the critical importance of rigorous anticoagulation during the procedure has been underlined, and the latest international guidelines now recommend performing AF catheter ablation with uninterrupted non-vitamin K antagonist oral anticoagulants (NOACs) and concomitant administration of unfractionated heparin adjusted to achieve and maintain a target activated clotting time of ≥300 seconds. Whereas observational studies and randomized controlled trials support the safety and efficacy of uninterrupted NOAC strategy for AF catheter ablation, recent experiences have questioned this point, showing a greater unfractionated heparin requirement in NOAC-treated patients compared with vitamin K antagonists–treated patients to achieve the target activated clotting time. Important gaps in evidence regarding optimal intraprocedural anticoagulation management need to be acknowledged. A thorough appreciation of the physiology of anticoagulation during AF catheter ablation and the relevant differences between vitamin K antagonists and NOACs is required, while also understanding the limitations of activated clotting time measurement with regard to accurate intraprocedural anticogulation monitoring. This review aims to provide a critical look at this relatively ignored aspect of AF catheter ablation, especially pitfalls in NOAC monitoring, and to identify gaps in knowledge that need to be addressed in the near future.

Direct Oral Anticoagulants in the Setting of Catheter Ablation of Atrial Fibrillation: State of art

2020 ◽  
pp. 100622 ◽  
Author(s):  
Giuseppe Coppola ◽  
Egle Corrado ◽  
Mirko Luparelli ◽  
Girolamo Manno ◽  
Antonino Mignano ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Catheter Ablation ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
State Of Art

scholarly journals Activated clotting time monitoring during atrial fibrillation catheter ablation: Does the anticoagulant matter?

2020 ◽  
Vol 12 (2-4) ◽  
pp. 204
Author(s):  
A.C. Martin ◽  
M. Kyheng ◽  
V. Foissaud ◽  
A. Duhamel ◽  
E. Marijon ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Catheter Ablation ◽  
Clotting Time ◽  
Activated Clotting Time

scholarly journals Acute Kidney Injury due to Anticoagulant-Related Nephropathy : A Suggestion for Therapy

2020 ◽  
Vol 2020 ◽  
pp. 1-5 ◽  
Author(s):  
Letizia Zeni ◽  
Chiara Manenti ◽  
Simona Fisogni ◽  
Vincenzo Terlizzi ◽  
Federica Verzeletti ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Oral Anticoagulants ◽  
Direct Oral Anticoagulants ◽  
Kidney Injury ◽  
Cast Nephropathy ◽  
Anca Associated Vasculitis ◽  
A Prospective Study ◽  
The Relationship ◽  
Gross Haematuria ◽  
Strong Suspicion

The relationship between kidneys and anticoagulation is complex, especially after introduction of the direct oral anticoagulants (DOAC). It is recently growing evidence of an anticoagulant-related nephropathy (ARN), a form of acute kidney injury caused by excessive anticoagulation. The pathogenesis of kidney damage in this setting is multifactorial, and nowadays, there is no established treatment. We describe a case of ARN, admitted to our Nephrology Unit with a strong suspicion of ANCA-associated vasculitis due to gross haematuria and haemoptysis; the patient was being given dabigatran. Renal biopsy excluded ANCA-associated vasculitis and diagnosed a red blood cell cast nephropathy superimposed to an underlying IgA nephropathy. Several mechanisms are possibly responsible for kidney injury in ARN: tubular obstruction, cytotoxicity of heme-containing molecules and free iron, and activation of proinflammatory/profibrotic cytokines. Therefore, the patient was given a multilevel strategy of treatment. A combination of reversal of coagulopathy (i.e., withdrawal of dabigatran and infusion of its specific antidote) along with administration of fluids, sodium bicarbonate, steroids, and mannitol resulted in conservative management of AKI and fast recovery of renal function. This observation could suggest a prospective study aiming to find the best therapy of ARN.

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