What literature is available describing failure of treatment with DOACs?

Comment by InpharmD Researcher

Failure of DOACs has primarily been documented in case reports. A variety of explanations for suboptimal responses have been discussed, primarily originating around pharmacokinetic and pharmacodynamic differences. One recent analysis based on case reports determined that rivaroxaban has been associated with the greatest number of treatment failures (65.8%), followed by dabigatran (27.8%), apixaban (7.6%), and lastly edoxaban (1.3%). Lower rates of failure associated with apixaban and edoxaban may be due to twice daily dosing and longer half-lives, ranging from 12-17 hours, resulting in a more stable plasma concentration and consistent anticoagulation. Patient populations that may be more susceptible to DOAC treatment failure include patients with renal impairment, hepatic impairment, or extreme body weight, and patients undergoing bariatric surgery due to the complexity of therapeutic management and DOAC dosing in these patients. Additionally, patient compliance, drug-drug interactions, and off-label use may affect likelihood of DOAC success.

Background

A 2021 analysis evaluated patient characteristics and clinical settings where direct oral anticoagulant (DOAC) treatment failure manifests. A total of 51 manuscripts describing 79 patients who exhibited DOAC failure were included for analysis. Patients were more commonly male (51.6%), with a mean age of 52.8 years (range 18 to 88 years). The most common treatment failures were determined to be in patients with antiphospholipid syndrome (APS; 44.3%), atrial fibrillation (30.4%), and deep venous thrombosis (6.3%). Higher failure rates were also observed for rivaroxaban (65.8%), followed by dabigatran (27.8%), apixaban (7.6%), and then edoxaban (1.3%). The most common manifestations of treatment failure were stroke/transient ischemic attack (20.3%), pulmonary embolism (19%), and deep vein thrombosis (19%). Based on this analysis, the authors determined that DOACs have the potential to fail, even in the setting of Food and Drug Administration (FDA) and non-FDA-approved indications. It should be noted that this analysis is strictly based on case reports, and as such, the findings are subject to confounding factors and may vary in clinical practice. [1]

The authors discussed potential mechanisms for failure, thought to be most likely explained by pharmacokinetic and pharmacodynamic properties. Lower failure rates of apixaban and edoxaban may be related to dosing and half-life; rivaroxaban for example has a half-life of 9-13 hours, although it is prescribed at a dose of 20 mg once daily after an initial dosing regimen of 15 mg twice daily. Its relatively fast elimination rate, and high, early peaks of the drug may result in increased risk of bleeding and low troughs, resulting in potentially inadequate anticoagulation. Conversely, apixaban and dabigatran are dosed twice daily with half-lives ranging from 12-17 hours, resulting in a more stable plasma concentration and predictable efficacy. Regarding dabigatran, differences in absorption may be yet another factor contributing to increased risk of failure. The prodrug of dabigatran exhibits limited bioavailability, with stomach and intestinal absorption easily hindered by the lack of acidic conditions. These environmental conditions may be affected by proton pump inhibitors and liver metabolism, for example. Furthermore, DOACs are renally eliminated; elevated renal clearance may decrease efficacy due to rapid elimination, while reduced renal clearance may result in increased risk of bleeding. [1]

Drug-drug interactions may also be a potential culprit, as DOACs are CYP3A4 and P-glycoprotein substrates. Many case reports identified within this review (n= 13 patients) documented patients with concomitant use of a strong CYP inducer, enhancing clearance of the DOAC. Finally, noncompliance with even a single dose of DOAC may be more substantial due to their relatively short half-life, compared to vitamin-K antagonists (VKA), for example, which have a half-life of several days. In the event of a missed VKA dose, the extended half-life allows for a more continuous effect. Alternatively, missing a single dose of a DOAC can lead to inadequate anticoagulation. Notably, many cases of failure documented herein (n= 14) utilized DOAC therapy for APS, an off-label use not supported by robust randomized trials that may complicate ideal drug selection. Among all the cases, some also indicated success when switching to a different DOAC, as reported in 6 cases, with 4 switches being successful due to use of a DOAC with a different mode of action and/or different pharmacokinetic/pharmacodynamic properties. Ultimately, selection of DOAC should be individualized based on patients’ clinical profiles to minimize risk of failure. [1]

A 2020 review discussing common clinical challenges with use of DOACs indicates comorbidities that may affect DOAC pharmacokinetics include renal insufficiency, hepatic impairment, and extreme body weights due to their potential to alter the DOAC elimination rate and increase the risk of thromboembolic or bleeding events. All DOACs therapies are eliminated by the kidneys to varying degrees, and thus, alterations in renal clearance must be taken into account when dosing these agents. Dabigatran is the most renally eliminated (80%), followed by edoxaban (50%), rivaroxaban (35%), apixaban (27%), and betrixaban (11%). Due to the variation in DOAC levels that may occur in patients with renal impairment, it is important to renally dose DOACs appropriately as recent studies suggest that up to 32% of patients experience inappropriate DOAC dosing, with the most common form being subtherapeutic dosing due to renal insufficiency. Inappropriate dosing of DOACs can carry consequences, including increased risk for thrombotic and bleeding complications resulting from subtherapeutic and supratherapeutic dosing, respectively. [2]

Similar to patients with renal impairment, patients with hepatic impairment are also at increased risk of bleeding complications and thrombotic events during DOAC administration, as alterations in hepatic function affect DOAC biotransformation to varying extents. Apixaban is the most reliant on hepatic metabolism for drug elimination, accounting for 75% of its elimination pathway, followed by rivaroxaban (65%), edoxaban (50%), dabigatran (20%), and betrixaban (18%). As there is no proficient monitoring parameter to assess for safety, patients with hepatic dysfunction may not be ideal candidates for DOACs. All DOACs can be considered in patients with mild hepatic impairment without any dose adjustment, but with lack of available data, the optimal anticoagulation strategy for this patient population remains unclear. [2]

As for patients with hepatic impairment, optimal anticoagulation strategy and DOAC dosing have not been established for patients with extreme body weights. Recently, concerns have arisen that use of DOACs in patients with extreme body weight may be impacted by physiological changes that affect clearance of the medication, leading to adverse outcomes and limited data to guide prescribers. Based on pharmacokinetic changes, fixed DOAC doses may lead to decreased drug exposures in obese patients and increased drug exposures in underweight patients. Despite subgroup analyses and meta-analyses of data from DOAC clinical trials revealing no difference in efficacy or safety outcomes in obese patients, extreme-body-weight populations have been underrepresented in clinical trials. An analysis conducted by the International Society on Thrombosis and Haemostasis (ISTH) suggests that DOACs are safe in patients ≤ 120 kg at standard doses but are not recommended in patients > 120 kg. [2]

Patients with low body weight (<60 kg) also represent a population in which measuring renal function plays a vital role in assessing use of DOACs, as renal function is commonly overestimated due to lower muscle mass. Low-body-weight patients typically present with comorbid conditions that predispose them to adverse outcomes (i.e., elderly age, frailty, and renal impairment). Overall, pharmacokinetic data suggest extreme body weights affect DOAC disposition, but published data has not adequately confirmed this. While the patient populations mentioned within this review have not explicitly observed increased DOAC failure rates, the complexity of therapeutic management and DOAC dosing in these patients, potentially leading to altered levels, presents potential situations in which DOAC failure may be more likely to occur. [2]

Another 2020 review provides additional insight into certain special populations where DOAC efficacy may become altered. As gastrointestinal surgery alters the absorptive surface, DOAC drug absorption may be affected, leading to greater variability in anticoagulant drug levels. However, the evidence for use in this population is noted to be extremely limited. Bariatric surgery or extensive bowel surgery may also directly alter anticoagulant levels. Additional studies have also observed inter-individual differences between patients despite receiving the same DOAC regimen. These findings are concerning, as DOAC level assessment is not commonly performed. Even if abnormal absorption is identified, individual-based dosing of DOACs is not commonly practiced. [3]

References:

[1] Kajy M, Mathew A, Ramappa P. Treatment Failures of Direct Oral Anticoagulants. Am J Ther. 2021;28(1):e87-e95. doi:10.1097/MJT.0000000000001083
[2] Chen A, Stecker E, A Warden B. Direct Oral Anticoagulant Use: A Practical Guide to Common Clinical Challenges. J Am Heart Assoc. 2020;9(13):e017559. doi:10.1161/JAHA.120.017559
[3] Toorop MMA, Lijfering WM, Scheres LJJ. The relationship between DOAC levels and clinical outcomes: The measures tell the tale. J Thromb Haemost. 2020;18(12):3163-3168. doi:10.1111/jth.15104

Literature Review

A search of the published medical literature revealed 4 studies investigating the researchable question:

What literature is available describing failure of treatment with DOACs?

Level of evidence

D - Case reports or unreliable data  Read more→



Please see Tables 1-4 for your response.


 

Possible Rivaroxaban Failure During the Postpartum Period

Design

 Case study

Case presentation

A 35-year-old postpartum woman who presented to the emergency department with complaints of tachycardia, intermittent chest pain, headache, and paresthesias 5 days after starting rivaroxaban 15 mg BID for DVT was diagnosed with a new multiple segmental PE. As a source of thrombosis embolization or extension, no triggering reason, including noncompliance, was found.

She was still experiencing postpartum bleeding per vagina, which had increased in quantity after starting rivaroxaban, and she was passing clots when she arrived at the ED. She denied having a fever, chills, weakness, shortness of breath, dizziness, or vision abnormalities. She denied any thrombosis, pregnancy loss, stillbirth, or hospitalizations other than for deliveries. The patient had stopped breastfeeding a week before. She denied using tobacco, alcohol, or illegal drugs.

The patient was hospitalized, a heparin infusion was started to treat the PE, and the rivaroxaban was stopped. The following day, she was switched to enoxaparin 1 mg/kg (90 mg) subcutaneously every 12 hours, bridged to warfarin, and discharged home on the overlapping regimen with close monitoring by the pharmacist-managed outpatient Anticoagulation Management Service.

Study Author Conclusions

To our knowledge, this is the first case report of potential failure associated with rivaroxaban therapy in the postpartum period, possibly due to pharmacokinetic alterations seen in the postpartum period contributing to decreased drug exposure, yielding reduced anticoagulant efficacy. Clinicians should carefully weigh the risks and benefits of DOAC therapy in postpartum patients or other special populations requiring anticoagulation therapy. This report also highlights the need for further research identifying the impact of pharmacokinetic changes induced by special populations and the need to develop monitoring assays for such clinical situations.
References:

Rudd KM, Winans AR, Panneerselvam N. Possible Rivaroxaban Failure during the Postpartum Period. Pharmacotherapy. 2015;35(11):e164-e168. doi:10.1002/phar.1662

 

A Case Report of Recurrent Transient Ischaemic Attacks on Dabigatran for Atrial Fibrillation: Real-world Insight Into Treatment Failure

Design

 Case study

Case presentation

This is the case of a 51-year-old male with atrial fibrillation (AF) and transient ischemic attacks on therapeutic doses of dabigatran. The patient had a past medical history of rapid atrial flutter and underwent direct cardioconversion (DCCV) in 2015 and was placed on sotalol 40 mg BID and apixaban 5 mg BID. He required atrial flutter ablation in 2016 but still needed to repeat DCCV for recurrent AF.

He was in asymptomatic rapid AF with failed DCCV in September 2018. His apixaban was changed to dabigatran 150 mg b.i.d. while being considered for AF ablation due to the availability of a reversal medication and lower bleeding risk, as indicated by the cardiac electrophysiologist. At presentation, his medication box indicated 100% compliance, and his admission coagulation testing revealed a modestly extended activated partial thromboplastin time and thrombin time (TT).

Coagulation studies performed at admission revealed a moderately extended activated partial thromboplastin time (APTT) of 38 s (range 25-37 s) and TT of 83.7 s (range 14-20 s). The TT suggested that dabigatran could be present, but only at subtherapeutic levels. Levels were undetectable by Hemoclot assay (Hyphen Biomed) on STA-R analyzer (Stago) after four further monitored doses of dabigatran 150 mg b.i.d. (40 ng/mL). With the apparent failure of therapy, anticoagulation was switched to apixaban 5 mg b.i.d., resulting in peak levels of 299 ng/mL (on target range: 91-321 ng/mL). At his most recent check-up, he had no further neurological episodes.

Study Author Conclusions

There are a number of isolated case reports of DOAC failure in stroke prophylaxis and management has simply involved switching to another DOAC or warfarin. This case is unique as we have discovered undetectable levels of dabigatran, providing a mechanism for failure.
References:

Huynh R, Anderson S, Chen VM, Yeoh T. A case report of recurrent transient ischaemic attacks on dabigatran for atrial fibrillation: real-world insight into treatment failure. Eur Heart J Case Rep. 2020;4(2):1-4. Published 2020 Mar 3. doi:10.1093/ehjcr/ytaa041

 

Treatment Failure of Cerebral Venous Thrombosis With Rivaroxaban: A Case Report and Narrative Review

Design

 Case Report

Case presentation

The case of a 47-year-old East Asian man weighing 79 kg is presented hereafter. He had a past medical history of poorly managed type 2 diabetes, with a glycated hemoglobin (Hb A1C) of 10.5%. Furthermore, the patient reported a brain operation 12 years before his presentation to the hospital, but could not produce records of the procedure's specifics.

He presented with complaints of dizziness and an unsteady gait in February 2020. He also experienced two episodes of generalized tonic-clonic seizures in the ER, which were managed with IV lorazepam. An immediate CT scan revealed a left temporal venous hemorrhagic infarction caused by thrombosis of the left sigmoid and transverse sinuses, as well as the vein of Labbe. It also revealed surrounding perilesional edema with mass effect as effacement of the overlaying cortical sulci, compression of the ipsilateral lateral ventricle, and partial effacement of the left ambient cistern. An initial thrombophilia screen revealed normal antithrombin III, factor V Leiden, and protein S levels. Protein C activity, on the other hand, was mildly reduced, with a value of 60%.

The patient had a left-sided decompressive craniectomy and was started on heparin infusion, which was later changed to enoxaparin at a therapeutic dose. The anticoagulation was changed from enoxaparin to dabigatran at a dose of 150 mg orally twice daily on March 13, 2020, in accordance with the findings of the RE-SPECT CVT study. The attending medical team planned to anticoagulant the patient with dabigatran for six months and then examine the patient's clinical condition at the end of that time. If clinically stable, protein C activity would be measured again two weeks after anticoagulation was stopped, as the initially discovered low protein C activity could be related to the acute condition.

Before moving the patient to a long-term hospital, an MRI head was performed, which revealed indications of re-canalization of the cerebral venous sinuses. As the patient got agitated, he was transferred to a long-term nasogastric tube (NGT), which was implanted to ease medicine administration. Dabigatran was later discontinued because the capsules must not be opened, and hence, dabigatran cannot be supplied via NGT. Rivaroxaban, which can be crushed and delivered through NGT, was introduced at a dose of 20 mg orally daily on March 15, 2020.

The patient was symptom-free until June 29, when he became increasingly agitated, despite the fact that he had no seizure or other new focal neurological symptoms. An intracranial CT venogram was performed, which revealed a previously unknown filling defect in the left sigmoid sinus, indicating a new cerebral vein thrombosis (CVT). An accidental left temporal abscess was also discovered on MRI. Because this abscess was small in size and the patient was afebrile with normal inflammatory markers (white blood cells, C-reactive protein, lactic acid, and procalcitonin were all within normal ranges), and he had no new neurological deficit, the infectious diseases consultant and neurosurgery consultant suggested IV antibiotics as treatment for it rather than surgical intervention, which was later proven to be effective in his case. The recurrence of new CVT despite complete anticoagulation with rivaroxaban was deemed a therapeutic failure, and dabigatran was reintroduced orally on July 3, 2020.

Study Author Conclusions

Our case report adds to the uncertainty regarding the use of DOACs in the treatment of CVT. In the absence of well-designed multi-center randomized controlled trials, no strong recommendation can be made in favor of or against the use of DOACs in this patient population.
References:

Mohamed M, Musa M, Fadul A, Abdallah I, Najim M, Saeed A. Treatment Failure of Cerebral Venous Thrombosis With Rivaroxaban: A Case Report and Narrative Review. Cureus. 2022;14(4):e23778. Published 2022 Apr 3. doi:10.7759/cureus.23778

 

Management of venous thromboembolism in patients experiencing direct oral anticoagulant treatment failure: a single-center review of practice and outcomes

Design

Retrospective chart review

N= 54

Objective

To characterize direct oral anticoagulant (DOAC) treatment failures and to rationalize subsequent anticoagulation strategies

Study Groups

DOAC failure (N= 54)

Inclusion Criteria

Consecutive patients treated for venous thromboembolism and experiencing a DOAC treatment failure

Exclusion Criteria

N/A

Methods

Patient and treatment characteristics were retrospectively collected from medical records, including the subsequent and final anticoagulation treatments after initial DOAC failure. Suboptimal response to initial treatment was defined as persistent symptoms of the original deep vein thrombosis (DVT), despite 4 to 6 weeks of anticoagulation.

Duration

DOAC failure: September 2014 to May 2018

Median follow-up: 34 months

Outcome Measures

Management strategies following initial DOAC failure

Baseline Characteristics

 

DOAC failure (N= 54)

 

Age, years (range)

56 (23 to 89)  

Female

44%  

Time from initiation to DOAC failure, days (range)

40 (3 to 1,055)  

Acute VTE treatment

67%  

Acute event at presentation, n

DVT

Pulmonary embolism (PE)

Concurrent DVT and PE


32

3

1

 

Secondary VTE prevention

33%

 

Thrombotic risk factors

Anti-phospholipid syndrome

Cancer


6%

9%

 

Non-resolution of original VTE

56%

 

New breakthrough of thrombosis

44%  

Anticoagulant at time of treatment failure

Apixaban 5 mg twice daily

Apixaban 2.5 mg twice daily

Rivaroxaban 20 mg once daily

 

57%

11%

28%

 

Results

Endpoint

DOAC failure (N= 54)

 

Initial management with LMWH

Median time on parenteral anticoagulation, days (range)

69% (37 of 54)

52 (14 to 472)

 

Switched back to oral anticoagulation after LMWH

VKA

DOAC

84% (31 of 37)

19%

81%

 

Taking DOAC at 34 months follow-up

Switched back to anticoagulation regimen that was initially failed, n

Switched back to same anticoagulant at higher dose, n

61% (33 of 54)

7

3

 

On long-term DOAC therapy or completed treatment at the end of follow-up

72%

 

Adverse Events

N/A

Study Author Conclusions

In the absence of evidence or guidelines, brief rescue of anticoagulation with parenteral therapy can be an effective strategy when treatment with a DOAC fails.

InpharmD Researcher Critique

While this study provides further insight into potential treatment management of DOAC failures, randomized controlled trials evaluating the safety and efficacy of parenteral anticoagulation following DOAC failure are needed to determine whether it is an appropriate management strategy.



References:

McIlroy G, Smith N, Lokare A, Beale K, Kartsios C. Management of venous thromboembolism in patients experiencing direct oral anticoagulant treatment failure: a single-center review of practice and outcomes. J Thromb Thrombolysis. 2020;49(3):441-445. doi:10.1007/s11239-020-02042-6