Clinically Important Drug–Drug Interactions Between Antiarrhythmic Drugs and Anticoagulants

Konieczny, Kaja M.; Dorian, Paul

doi:10.19102/icrm.2019.100304

Cited by 12 publications

(14 citation statements)

References 13 publications

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“…128 Quinidine is also a weak inhibitor of CYP3A4 and INR should be monitored more frequently when quinidine is initiated in the setting of chronic warfarin use. 14,147…”

Section: Oral Anticoagulants and Antiarrhythmic Drugsmentioning

confidence: 99%

“…1 This increase in plasma concentration can be tempered by administering dronedarone 2 hours after DOAC administration, but this combination should generally be avoided with all DOACs. 128,147 While a study reported no clinically significant elevation in INR in patients taking warfarin who were initiated on dronedarone, a moderate CYP3A4 inhibitor, cases of dronedarone-associated increases in INR have been reported. 148,149…”

Section: Oral Anticoagulants and Antiarrhythmic Drugsmentioning

confidence: 99%

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Drug Interactions Affecting Oral Anticoagulant Use

Mar

Gopinathannair

Gengler

et al. 2022

Circ: Arrhythmia and Electrophysiology

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Oral anticoagulants (OACs) are medications commonly used in patients with atrial fibrillation and other cardiovascular conditions. Both warfarin and direct oral anticoagulants are susceptible to drug-drug interactions (DDIs). DDIs are an important cause of adverse drug reactions and exact a large toll on the health care system. DDI for warfarin mainly involve moderate to strong inhibitors/inducers of cytochrome P450 (CYP) 2C9, which is responsible for the elimination of the more potent S-isomer of warfarin. However, inhibitor/inducers of CYP3A4 and CYP1A2 may also cause DDI with warfarin. Recognition of these precipitating agents along with increased frequency of monitoring when these agents are initiated or discontinued will minimize the impact of warfarin DDI. Direct oral anticoagulants are mainly affected by medications strongly affecting the permeability glycoprotein (P-gp), and to a lesser extent, strong CYP3A4 inhibitors/inducers. Dabigatran and edoxaban are affected by P-gp modulation. Strong inducers of CYP3A4 or P-gp should be avoided in all patients taking direct oral anticoagulant unless previously proven to be otherwise safe. Simultaneous strong CYP3A4 and P-gp inhibitors should be avoided in patients taking apixaban and rivaroxaban. Concomitant antiplatelet/anticoagulant use confers additive risk for bleeding, but their combination is unavoidable in many cases. Minimizing duration of concomitant anticoagulant/antiplatelet therapy as indicated by evidence-based clinical guidelines is the best way to reduce the risk of bleeding.

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“…128 Quinidine is also a weak inhibitor of CYP3A4 and INR should be monitored more frequently when quinidine is initiated in the setting of chronic warfarin use. 14,147…”

Section: Oral Anticoagulants and Antiarrhythmic Drugsmentioning

confidence: 99%

Section: Oral Anticoagulants and Antiarrhythmic Drugsmentioning

confidence: 99%

Drug Interactions Affecting Oral Anticoagulant Use

Mar

Gopinathannair

Gengler

et al. 2022

Circ: Arrhythmia and Electrophysiology

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“…64 Amiodarone can also increase plasma dabigatran and rivaroxaban concentrations, especially in patients with kidney disease. 163–165…”

Section: P-glycoproteinmentioning

confidence: 99%

Drug Interactions Affecting Antiarrhythmic Drug Use

Mar

Horbal

Chung

et al. 2022

Circ: Arrhythmia and Electrophysiology

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Antiarrhythmic drugs (AAD) play an important role in the management of arrhythmias. Drug interactions involving AAD are common in clinical practice. As AADs have a narrow therapeutic window, both pharmacokinetic as well as pharmacodynamic interactions involving AAD can result in serious adverse drug reactions ranging from arrhythmia recurrence, failure of device-based therapy, and heart failure, to death. Pharmacokinetic drug interactions frequently involve the inhibition of key metabolic pathways, resulting in accumulation of a substrate drug. Additionally, over the past 2 decades, the P-gp (permeability glycoprotein) has been increasingly cited as a significant source of drug interactions. Pharmacodynamic drug interactions involving AADs commonly involve additive QT prolongation. Amiodarone, quinidine, and dofetilide are AADs with numerous and clinically significant drug interactions. Recent studies have also demonstrated increased morbidity and mortality with the use of digoxin and other AAD which interact with P-gp. QT prolongation is an important pharmacodynamic interaction involving mainly Vaughan-Williams class III AAD as many commonly used drug classes, such as macrolide antibiotics, fluoroquinolone antibiotics, antipsychotics, and antiemetics prolong the QT interval. Whenever possible, serious drug-drug interactions involving AAD should be avoided. If unavoidable, patients will require closer monitoring and the concomitant use of interacting agents should be minimized. Increasing awareness of drug interactions among clinicians will significantly improve patient safety for patients with arrhythmias.

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“…После всасывания ПОАК попадают в центральное кровообращение и подвергаются различным степеням метаболизма через систему печеночного цитохрома P450 3A4 и выводятся с различной скоростью с мочой и стулом [18]. [20]. Соталол не метаболизируется и вместо этого элиминируется нормальными почками без изменений [21].…”

Section: транспортная система P-gp (гликопротеины проницаемости или белок множественной лекарственной резистентности)unclassified

Safety and interaction of direct oral anticoagulants with antiarrhythmic drugs

Tatarsky

Kazyonnova

2021

Russ J Cardiol

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The use of direct oral anticoagulants minimized the risks associated with vitamin K antagonist (warfarin) therapy. Currently, direct oral anticoagulants have priority over warfarin for the prevention of thromboembolic events in patients with atrial fibrillation and a number of other conditions requiring anticoagulant therapy. Direct oral anticoagulants along with antiarrhythmic therapy are the accepted strategy for atrial fibrillation treatment. At the same time, the effect of drug-drug interactions (DDI) between direct oral anticoagulants and antiarrhythmic drugs, which have common points of metabolic application, has not been fully elucidated. In order to provide effective and safe anticoagulant and antiarrhythmic therapy in patients with AF, it is important to understand the mechanisms and severity of DDI of direct oral anticoagulants and antiarrhythmic agents. This review discusses the issues of DDI of direct oral anticoagulants and antiarrhythmic drugs used to treat atrial fibrillation.

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Clinically Important Drug–Drug Interactions Between Antiarrhythmic Drugs and Anticoagulants

Cited by 12 publications

References 13 publications

Drug Interactions Affecting Oral Anticoagulant Use

Drug Interactions Affecting Oral Anticoagulant Use

Drug Interactions Affecting Antiarrhythmic Drug Use

Safety and interaction of direct oral anticoagulants with antiarrhythmic drugs

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