When can I resume anticoagulation in my patient with atrial fibrillation and hemorrhagic stroke?

Optimal timing of resumption of therapeutic anticoagulation (AC) in patients with hemorrhagic stroke or intracranial hemorrhage (ICH) is unclear because of lack of randomized controlled trials, but existing evidence suggests that 4-8 weeks may be reasonable in our patient (1). 

 
The American Heart Association/American Stroke Association 2015 guidelines recommend avoiding AC for at least 4 weeks in patients without mechanical heart valves (class IIB-very weak), while 1 study reported that prediction models of ICH in atrial fibrillation at high risk of thromboembolic event suggest that resumption of AC at 7-8 weeks may be the “sweet spot” when weighing safety against efficacy of AC in this patient population (1-3).

 
Two meta-analyses (1 involving patients with non-lobar ICH, another ICH in patients with nonvalvular atrial fibrillation) found that resumption of AC ranging from 10 to 44 days following ICH may be associated with decrease rates of thromboembolic events without significant change in the rate of repeat ICH (4,5).

 
There are many limitations to the published literature including their retrospective nature, unreported location and size of ICH in many studies, and use of warfarin (not DOACs) as an AC agent (1).

 
Clearly we need randomized controlled trials to answer this important question. In the meantime, a heavy dose of clinical judgement on a case-by-case basis seems appropriate.

Bonus Pearl: Did you know that lobar ICH has high incidence of cerebral amyloid angiopathy and has been associated with higher bleeding rates than has deep ICH (i.e., involving the thalami, basal ganglia, cerebellum, or brainstem) usually due to hypertensive vessel disease (1)? 

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References
1. Gibson D et al. When is it safe to resume anticoagulation in my patient with hemorrhagic stroke. The Hospitalist, February 5, 2019. https://www.the-hospitalist.org/hospitalist/article/193924/neurology/when-it-safe-resume-anticoagulation-my-patient-hemorrhagic/page/0/1
2. Hemphill JC et al. Guidelines for the management of spontaneous intracerebral hemorrhage. Stroke. 2015 Jul;46:2032-60. https://www.ahajournals.org/doi/pdf/10.1161/STR.0000000000000069
3. Pennlert J et al. Optimal timing of anticoagulant treatment after intracerebral hemorrhage in patients with atrial fibrillation. Stroke. 2017 Feb;48:314-20 https://www.ahajournals.org/doi/pdf/10.1161/STROKEAHA.116.014643
4. Murthy SB et al. Restarting anticoagulation therapy after intracranial hemorrhage: A systematic review and meta-analysis. Stroke. 2017 Jun;48:1594-600. https://www.ahajournals.org/doi/full/10.1161/strokeaha.116.016327
5. Biffi A et al. Oral anticoagulation and functional outcome after intracerebral hemorrhage. Ann Neurol. 2017 Nov;82:755-65 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5730065/

When can I resume anticoagulation in my patient with atrial fibrillation and hemorrhagic stroke?

Is there a connection between my patient’s blood type and risk of thromboembolic events?

There seems to be, given the weight of the evidence to date suggesting that non-blood group O may be associated with non-valvular atrial fibrillation (NVAF)-related peripheral cardioembolic complications, myocardial infarction (MI) and ischemic stroke. 1-4

A 2015 retrospective Mayo Clinic study involving patients with NVAF adjusted for CHADS2 score found significantly lower rate of peripheral embolization in those with blood group O compared to those with other blood groups combined (3% vs 2%, O.R. 0.66, 95% CI, 0.5-0.8); rates of cerebral thromboembolic events were not significantly different between the 2 groups, however. 1

A 2008 systematic review and meta-analysis of studies spanning over 45 years reported a significant association between non-O blood group and MI, peripheral vascular disease, cerebral ischemia of arterial origin, and venous thromboembolism.2 Interestingly, the association was not significant for angina pectoris or for MI when only prospective studies were included.  Some studies have reported that the association between VWF and the risk of cardiovascular mortality may be independent of blood group. 5,6

Although the apparent lower risk of thromboembolic conditions in O blood group patients may be due to lower levels of von Willebrand factor (VWF) and factor VIII in this population 1,4, other pathways likely  play a role.7  

As for why the rate of peripheral (but not cerebral) thromboembolic events in NVAP is affected by blood group, it is suggested that, because of their size, larger clots (facilitated by lower VWF levels) may bypass the carotid and vertebral orifices in favor of their continuation downstream to the “peripheral bed”.1

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References

  1. Blustin JM, McBane RD, Mazur M, et al. The association between thromboembolic complications and blood group in patients with atrial fibrillation. Mayo Clin Proc 2015;90;216-23. https://www.sciencedirect.com/science/article/abs/pii/S002561961401043X
  2. Wu O, Bayoumi N, Vickers MA, et al. ABO (H) groups and vascular disease: a systematic review and meta-analysis. J Thromb Haemostasis 2008;6:62-9. https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1538-7836.2007.02818.x
  3. Medalie JH, Levene C, Papier C, et al. Blood groups, myocardial infarction, and angina pectoris among 10,000 adult males. N Engl J Med 1971;285:1348-53. https://www.nejm.org/doi/pdf/10.1056/NEJM197112092852404
  4. Franchini M, Capra F, Targher G, et al. Relationship between ABO blood group and von Willebrand factor levels: from biology to clinical implications. Thrombosis Journal 2007, 5:14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042969/
  5. Meade TW, Cooper JA, Stirling Y, et al. Factor VIII, ABO blood group and the incidence of ischaemic heart disease. Br J Haematol 1994;88:601-7. https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2141.1994.tb05079.x
  6. Jager A, van Hinsbergh VW, Kostense PJ, et al. von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects: the Hoorn Study. Arterioscl Thromb Vasc Biol 1999;19:3071-78. https://www.researchgate.net/publication/12709043_von_Willebrand_Factor_C-Reactive_Protein_and_5-Year_Mortality_in_Diabetic_and_Nondiabetic_Subjects_The_Hoorn_Study
  7. Sode BF, Allin KH, Dahl M, et al. Risk of venous thromboembolism and myocardial infarction associated with factor V Leiden and prothrombin mutations and blood type. CMAJ 2013.DOI:10.1503/cmaj.121636. https://www.ncbi.nlm.nih.gov/pubmed/23382263
Is there a connection between my patient’s blood type and risk of thromboembolic events?

My elderly patient on anticoagulation for non-valvular atrial fibrillation was admitted for evaluation of a fall. Should I discontinue her anticoagulation long term because of potential for intracranial hemorrhage from future falls?

Although there may always be hesitation in resuming anticoagulation (AC) in patients with non-valvular atrial fibrillation (NVAF) and recent fall(s), the weight of the evidence suggests that most patients are still more likely to benefit from AC than be adversely impacted by intracranial hemorrhage.
An often-quoted systematic review article on the risks and benefits of anti-thrombotic (AC or aspirin) therapy in patients with NVAF at risk estimated that persons taking warfarin must fall 295 times in 1 year for warfarin to not be the optimal therapy for reducing the risk of stroke (1). The authors concluded that “a history of and/or the presence of risk factors for falls should not be considered important factors in the decision whether to offer antithrombotic (especially warfarin) therapy to elderly patients with atrial fibrillation”.
In another study involving older adults with NVAF, although a history of falls or documented high risk of falling was associated with a risk of intracranial hemorrhage, this risk did not differ among patients treated with warfarin, aspirin or no antithrombotic therapy (2).
Ultimately, the decision to prescribe AC in patients with NVAF at risk for falls should be made based on shared decision making with patients and caregivers. However, in the absence of absolute contraindications for AC in these patients (eg, intracranial hemorrhage or neurosurgical procedure with high risk for bleeding within the past 30 days, an intracranial neoplasm or vascular abnormality with high risk of bleeding, recurrent life-threatening gastrointestinal or other bleeding events, and severe bleeding disorders), perceived or actual risk of falls by itself should not automatically exempt a patient from receiving AC in NVAF (3).

 

Although much of the data on the relative risk of bleeding against prevention of strokes has been derived from studies involving warfarin, it is reassuring that the risk of intracranial bleed has been lower than that of warfarin for several newer non-vitamin K antagonist direct oral anticoagulants (NOACs or DOACs),  including dabigatran, rivaroxaban, edoxaban and apixaban (4). 

 

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References

1. Man-Son-Hing M, Nichol G, Lau A, et al. Choosing antithrombotic therapy for elderly patiets with atrial fibrillation who are at risk for falls. Arch Intern Med 1999;159:677-685.
2. Gage BF, Birman-Deych E, Kerzner R, et al. Incidence of intracranial hemorrhage in patients with atrial fibrillation who are prone to fall. Am J Med 2005;118:612-617.
3. Hagerty T, Rich MW. Fall risk and anticoagulation for atrial fibrillation in the elderly: a delicate balance. Clev Clin J 2017;84:35-40.

4. Lopez RD, Guimaraes PO, Kolls BJ, et al. Intracranial hemorrhage in patietns with atrial fibrillation receiving anticoagulation therapy. Blood 2017;129:2980-87. 

My elderly patient on anticoagulation for non-valvular atrial fibrillation was admitted for evaluation of a fall. Should I discontinue her anticoagulation long term because of potential for intracranial hemorrhage from future falls?

Should my patient with non-valvular atrial fibrillation on hemodialysis be anticoagulated?

Whether patients with end-stage kidney disease (ESKD) and non-valvular atrial fibrillation (AF) benefit from anticoagulation is a matter of controversy. 1,3 Although there may be some suggestion of benefit of warfarin for stroke prevention in this patient population, 2 there is also a higher concern for bleeding. 4-6 An increased risk of stroke among patients with ESKD and AF on warfarin has also been reported. 7

A 2018 Kidney Disease:Improving Global Outcomes (KDIGO) Controversies Conference concluded that there is “insufficient high-quality evidence” to recommend anticoagulation for prevention of stroke in patients with ESKD and atrial fibrillation. 8

However, the 2014 American College of Cardiology (ACC)/American Heart Association (AHA)/ Heart Rhythm (HRS) guideline states that it is reasonable to consider warfarin therapy in patients with ESKD and non-valvular AF with CHA2DS2 -VASc score of 2 or greater (Class IIa recommendation, level of evidence B).8 Of interest, the FDA recently approved the use of a direct oral anticoagulant (DOAC), apixaban, in ESKD potentially providing an alternative to the use of warfarin when anticoagulation is considered.10

Perhaps the decision to anticoagulate patients with ESKD for atrial fibrillation is best made on a case-by-case basis taking into account a variety of factors, including the risk of thromboembolic event, the risk of bleeding complications as well as patient preference.

References

1. Genovesi S, Vincenti A, Rossi E, et al. Atrial fibrillation and morbidity and mortality in a cohort of long-term hemodialysis patients. Am J Kidney Dis 2008;51:255-62. https://www.ncbi.nlm.nih.gov/pubmed/18215703

2. Olesen JB, Lip GY, Kamper AL, et al. Stroke and bleeding in atrial fibrillation with chronic kidney disease. N Engl J Med 2012;367:625-35. https://www.ncbi.nlm.nih.gov/pubmed/22894575

3. Shah M, Avgil TM, Jackevicius CA, et al. Warfarin use and the risk for stroke and bleeding in patients with atrial fibrillation undergoing dialysis. Circulation2014;129:1196-203. https://www.ncbi.nlm.nih.gov/pubmed/24452752

4. Elliott MJ, Zimmerman D, Holden RM. Warfarin anticoagulation in hemodialysis patients: a systematic review of bleeding rates. Am J Kidney Dis 2007;50:433-40. https://www.ncbi.nlm.nih.gov/pubmed/17720522

5. Holden RM, Harman GJ, Wang M, Holland D, Day AG. Major bleeding in hemodialysis patients. Clin J Am Soc Nephrol 2008;3:105-10. https://www.ncbi.nlm.nih.gov/pubmed/18003768

6. Wizemann V, Tong L, Satayathum S, et al. Atrial fibrillation in hemodialysis patients: clinical features and associations with anticoagulant therapy. Kidney Int 2010;77:1098-106. https://www.ncbi.nlm.nih.gov/pubmed/20054291

7. Chan KE, Lazarus JM, Thadhani R, Hakim RM. Warfarin use associates with increased risk for stroke in hemodialysis patients with atrial fibrillation. J Am Soc Nephrol2009;20:2223-33. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754104/

8. Turakhia MP, Blankestijn PJ, Carrero J, et al. Chronic kidney disease and arrythias: conclusions from a Kidney Disease:Improving Global Outcomes (KDIGO) Controversies Conference. Eur Heart J, ehy060. Published 07 March 2018. https://www.ncbi.nlm.nih.gov/pubmed/29522134

9. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Circulation 2014;130:2071-104. http://circ.ahajournals.org/content/130/23/2071 

10. Moll S. Use of direct oral anticoagulants in patients on hemodialysis. Diffusion, October 11, 2017. http://www.hematology.org/Thehematologist/Diffusion/7794.aspx 

Contributed by Brad Lander, MD, Mass General Hospital, Boston, MA.

Should my patient with non-valvular atrial fibrillation on hemodialysis be anticoagulated?

In my patient on oral anticoagulation about to undergo coronary stenting, will triple therapy (an oral anticoagulant plus two antiplatelet agents) be necessary or can I get away with double therapy (an oral anticoagulant plus a single antiplatelet agent)?

 

Patients with atrial fibrillation (AF) who need percutaneous coronary intervention (PCI) after acute coronary syndrome or for stable angina pose a treatment challenge as oral anticoagulants (OACs) and dual antiplatelet therapy (DAPT) are often used concurrently to decrease the risk of systemic thromboembolism and stent thrombosis. However, “triple therapy”, including aspirin, a P2Y12 inhibitor, and an OAC (eg, warfarin or a direct oral anticoagulant-DOAC), also increases the risk of bleeding, necessitating several recent landmark trials to better address the subject.

Two modest-sized RCTs (WOEST and ISAR-TRIPLE) reported that when compared to triple therapy (DAPT plus warfarin), double therapy (single antiplatelet agent plus INR-targeted warfarin) is associated with reduced risk of bleeding complications without an increased risk of thrombotic events. 1,2

Two larger RCTs, PIONEER AF-PCI and RE-DUAL PCI, studied rivaroxaban and dabigatran, respectively, in patients with non-valvular AF undergoing PCI and found a reduction in bleeding events in patients receiving double therapy (single antiplatelet agent plus DOAC) compared to triple therapy (DAPT plus warfarin), without an increased risk of thrombotic complications. 3,4

Collectively, these studies suggest that it may be safe to treat patients with increased risk of bleeding with double therapy (even immediately following PCI) without an increase in thrombotic events. If triple therapy is elected, duration should be minimized, clopidogrel should be preferred over more potent P2Y12 inhibitors, and a PPI should be considered.

 

References:

  1. Dewilde WJ, Oirbans T, Verheugt FW, et al. Use of clopidogrel with or without aspirin in patients taking oral anticoagulant therapy and undergoing percutaneous coronary intervention: an open-label, randomised, controlled trial. Lancet. 2013;381:1107-15. https://www.ncbi.nlm.nih.gov/pubmed/23415013
  2. Fiedler KA, Maeng M, Mehilli J, et al. Duration of triple therapy in patients requiring oral anticoagulation after drug-eluting stent Implantation: The ISAR-TRIPLE Trial. J Am Coll Cardiol. 2015;65:1619-29. https://www.ncbi.nlm.nih.gov/pubmed/25908066
  3. Gibson CM, Mehran R, Bode C, et al. Prevention of bleeding in patients with atrial fibrillation undergoing PCI. N Engl J Med. 2016;375:2423-2434. http://www.nejm.org/doi/pdf/10.1056/NEJMoa1611594
  4. Cannon CP, Bhatt DL, Oldgren J, et al. Dual antithrombotic therapy with dabigatran after PCI in atrial fibrillation. N Engl J Med. Published online, Aug, 27, 2017. http://www.nejm.org/doi/pdf/10.1056/NEJMoa1708454

 

Contributed by Amulya Nagarur, MD, Mass General Hospital, Boston, MA

In my patient on oral anticoagulation about to undergo coronary stenting, will triple therapy (an oral anticoagulant plus two antiplatelet agents) be necessary or can I get away with double therapy (an oral anticoagulant plus a single antiplatelet agent)?

Is my patient with aortic stenosis and no atrial fibrillation at higher risk of a cerebrovascular accident?

Several lines of evidence suggests that even in the absence of atrial fibrillation, patients with aortic stenosis (AS) may be at higher risk of a cerebrovascular accident (CVA).

A population-based study from Mayo Clinic examining the risk of cerebrovascular events (primarliy ischemic strokes or transient ischemic attacks) among patients with valvular heart disease reported severe aortic stenosis (study defined as mean pressure gradient >30 mm Hg) as a predictor of cerebrovascular event, independent from atrial fibrillation or age and at rates similar to those of mitral stenosis 1.  Similarly, the simvastatin and ezetimibe in AS study involving patients with mild-to-moderate AS not prescribed oral anticoagulation found that CHA2DS2-VASc was a major predictor of stroke, independent of atrial fibrillation or aortic valve replacement2. Thromboembolic CVA has also been reported in the setting of calcified bicuspid aortic valve with moderate-severe AS3.

Potential factors increasing the risk of CVA in AS include calcium embolization from the valve and increased microthrombus formation on the valve which may be present in 53% of stenotic aortic valves3,4.  In addition, severe AS may be a marker for other conditions that increase risk of CVA, such as atherosclerosis or prothrombotic tendencies1.

References

  1. Petty GW, Khandheria BK, Whisant JP. Predictors of cerebrovascular event and death among patients with valvular heart disease: A population-based study. Stroke 2000;31:2628-2635. http://stroke.ahajournals.org/content/strokeaha/31/11/2628.full.pdf
  2. Greve AM, Dalsgaard M, Bang CN, et al. Stroke in patients with aortic stenosis: The simvastatin and ezetimibe in aortic stenosis study. Stroke 2014;45:1939-1946. http://stroke.ahajournals.org/content/strokeaha/45/7/1939.full.pdf
  3. Mahajan N, Khetarpal V, Alfonso L. Stroke secondary to calcific bicuspid aortic valve: Case report and literature review. J Cardiol 2009;54:158-61. https://www.ncbi.nlm.nih.gov/pubmed/19632538
  4. Pleet AB, Massey EW, Vengrow ME. TIA, stroke, and the bicuspid aortic valve. Neurology 1981;31:1540-2. https://www.ncbi.nlm.nih.gov/pubmed/7198207 
Is my patient with aortic stenosis and no atrial fibrillation at higher risk of a cerebrovascular accident?

Which is more effective in managing rapid ventricular rate in atrial fibrillation, diltiazem or metoprolol?

Overall, diltiazem may be more effective than metoprolol in the acute management of AFib with RVR without increased side effects based on a few small but randomized double-blind studies.

A systematic review1 based on 2 trials2,3 comparing IV diltiazem with IV metroprolol in patients with atrial fibrillation seen in emergency departments has reported better acute rate control with IV diltiazem (RR 1.8 [95% CI, 1.2-1.6]).  In these studies, the onset of rate control was faster and the percentage decrease in ventricular rate at each time point was higher with IV diltiazem.  In general, 0.25 mg/kg of IV diltiazem (max 25 mg) and 0.15 mg/kg of IV metoprolol (max 10 mg) were used.

Exclusion criteria in these studies included severe congestive heart failure, hypotension, acute coronary syndrome, and use of either class of drugs within the past five days.

References

  1. Martindale JL, deSouza IS, Silverberg M et al.. Beta-blockers versus calcium channel blockers for acute rate control of atrial fibrillation with rapid ventricular response: a systematic review. Eur J Emerg Med 2015;22: 150-154. https://www.ncbi.nlm.nih.gov/pubmed/25564459
  2. Demircan C, Cikriklar H, Engindeniz Z, et al. Comparison of the effectiveness of intravenous diltiazem and metoprolol in the management of rapid ventricular rate in atrial fibrillation. Emerg Med J 2005;22: 411-414. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1726824/pdf/v022p00411.pdf 
  3. Fromm C, Suan SJ, Cohen V, et al. Diltizem vs metoprolol in the management of atrial fibrillation or flutter with rapid ventricular rate in the emergency department. J Emerg Med 2015;49:175-82. https://www.ncbi.nlm.nih.gov/pubmed/25913166

Contributed by William L. Hwang, MD, Mass General Hospital, Boston, MA.

Which is more effective in managing rapid ventricular rate in atrial fibrillation, diltiazem or metoprolol?

My patient with atrial fibrillation (AF) with a CHA2DS2-VASc score ≥2 is not a candidate for anticoagulation due to excessive bleeding risk. Does high-dose aspirin provide an effective alternative for stroke prevention in this setting?

 The SPAF (Stroke Prevention in Atrial Fibrillation) trial1 found a 42% reduction in overall risk of stroke with daily aspirin (325 mg). However, critics note that no benefit was observed among patients > 75 y or those with severe stroke.

7 other studies on the topic failed to confirm reduction in the risk of stroke at a range of aspirin doses (25mg bid-1,300mg qd) 2. These studies reported that aspirin is associated with a 19% reduction in stroke incidence (similar to patients with vascular disease), with a 95% CI that crosses zero (-1% to 35%), raising doubts about its actual benefit in AF3. For secondary prevention, aspirin was associated with a 2.5% reduction in the annual risk of stroke. However, these results were influenced by the only trial with a favorable outcome, SPAF-14.

In short, even at higher doses, aspirin may not be the answer for stroke prevention in patients with AF.

 References

  1. Stroke Prevention in Atrial Fibrillation Study. Final results. Circulation 1991;84, 527–39.
  2. January CT, Wann LS, Alpert  JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation  2014;130, e199–e267.
  3. European Heart Rhythm Association et al. Guidelines for the management of atrial fibrillation: the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology (ESC). Europace  2010; 12, 1360–420.
  4. Sabir IN, Matthews GDK,  Huang, CL-H. Antithrombotic therapy in atrial fibrillation: aspirin is rarely the right choice. Postgrad Med J 2013; 89, 346–51.

 

Contributed by Jacqueline Boehme, M.D., Medical Resident, Mass General Hospital

My patient with atrial fibrillation (AF) with a CHA2DS2-VASc score ≥2 is not a candidate for anticoagulation due to excessive bleeding risk. Does high-dose aspirin provide an effective alternative for stroke prevention in this setting?

Does electroconvulsive therapy (ECT) pose a risk of embolic stroke in patients with atrial fibrillation (AF)?

Acute embolic stroke in the setting of AF without anticoagulation after ECT has been reported in a single case report in the absence of conversion to normal sinus rhythm (1). Several cases of episodic or persistent conversion to normal sinus rhythm (NSR) in patients with AF undergoing ECT have also been reported (in the absence of embolic stroke), leading some to recommend anticoagulation therapy in such patients (2), though no firm data exist.

The mechanism by which ECT promotes cardioversion from AF to NSR is unclear as direct electrical influence of ECT on the heart is thought to be negligible (1). Arrhythmias such as atrial flutter and AF have also been reported after ECT (1). Curiously, ECT is associated with increased 5- hydroxytryptamine (5- HT2)-receptor densities of platelets in patients with depression which may enhance platelet reactivity and increase the risk of embolic stroke (3) even in the absence of cardioversion.

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References

  1. Suzuki H, Takano T, Tominaga M, et al. Acute embolic stroke in a patient with atrial fibrillation after electroconvulsive therapy. J Cardiol Cases 2010; e12-e14. https://www.sciencedirect.com/science/article/pii/S1878540910000113
  2. Petrides G, Fink M. Atrial fibrillation, anticoagulation, electroconvulsive therapy. Convulsive Therapy 1996;12:91-98. https://journals.lww.com/ectjournal/Abstract/1996/06000/Atrial_Fibrillation,_Anticoagulation,_and.4.aspx
  3. Stain-Malmgren R, Tham A, Ǻberg-Wistedt A. Increased platelet 5-HT2 receptor binding after electroconvulsive therapy in depression. J ECT 1998;14:15-24. https://europepmc.org/abstract/med/9661089
Does electroconvulsive therapy (ECT) pose a risk of embolic stroke in patients with atrial fibrillation (AF)?

How should I choose between the novel oral anticoagulants (NOACs)?

Although warfarin has long been the standard treatment for venous thromboembolism (VTE) and thomboprophylaxis in atrial fibrillation (AF), the need for its frequent monitoring, potential drug interactions, and narrow therapeutic window made it far from ideal. Since 2009, NOACs have become viable alternative agents owing to their more predictable and safer pharmacological profiles. NOACs include several direct factor Xa inhibitors (apixaban, rivaroxaban, edoxaban) and a direct thrombin inhibitor (dabigatran). Approved indications include: (1) thromboprophylaxis in nonvalvular AF; (2) treatment of deep venous thrombosis or pulmonary embolism; and (3) primary prevention of postoperative VTE. 

Compared to warfarin, NOACs are associated with a reduced risk of intracranial hemorrhage, and in the case of apixaban, lower risk of gastrointestinal bleeding; rivaroxaban and edoxaban have been associated with a higher risk of gastrointestinal bleeding.   Apixaban is also the only NOAC whose dose can be safely reduced in chronic kidney disease, including those on hemodialysis. 

References

 

1. Baber U, Mastoris I, and Mehran R. Balancing ischaemia and bleeding risks with novel oral anticoagulants. Nat Rev Cardiol 2014;11:693-703.  https://www.ncbi.nlm.nih.gov/pubmed/25367652 

2. Ansell JE. Universal, class-specific, and drug-specific reversal agents for the new oral anticoagulants. J Thromb Thrombolysis 2016;41:248-52. https://www.ncbi.nlm.nih.gov/pubmed/26449414

 

Contributed by William L. Hwang, MD, Mass General Hospital, Boston, MA

How should I choose between the novel oral anticoagulants (NOACs)?