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Management of Atrial Fibrillation in Patients with Heart Failure
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Panagiotis Korantzopoulos, Aris Bechlioulis
Pharmacological therapy of AF aims at rate and/or rhythm control, with the goal of hemodynamic and clinical improvement. Rate control is particularly important in cases of fast ventricular response. Adequate ventricular rate control increases diastolic LV filling and reduces risk of further deterioration due to arrhythmia-induced cardiomyopathy. However, the latter risk is not completely abolished, as the irregularity of the underlying rhythm may still have a significant impact on LV function. On the other hand, effective long-term rhythm control is not feasible in most cases. Pharmacologic therapies, such as antiarrhythmic drugs, have limited efficacy in the maintenance of sinus rhythm in HF. Moreover, the safety profile and the side effects of antiarrhythmic agents, especially in frail HF patients who have several comorbidities, limit their widespread use. Apart from ion channel blocking drugs, agents with favorable hemodynamic, antifibrotic, or other pleiotropic effects may have a role in a rhythm control strategy. Optimal medical therapy of HF per se may be quite effective in reducing AF burden, especially agents that inhibit the renin-angiotensin-aldosterone system, which have been shown to reduce the incidence of AF in HFrEF when administered in optimal doses,74 although no such benefit was shown in HFpEF patients.74 Furthermore, aldosterone receptor antagonists may be effective in AF prevention, especially in the HFrEF setting.75
Basic pharmacology of cardiac drugs
Published in John Edward Boland, David W. M. Muller, Interventional Cardiology and Cardiac Catheterisation, 2019
Whatever its basic mechanism (or mechanisms) of action, it is a very useful antiarrhythmic agent with demonstrated effectiveness in the therapy and prophylaxis of most types of arrhythmia. It is particularly effective in the treatment of atrial fibrillation, supraventricular arrhythmias associated with Wolff–Parkinson–White Syndrome, ventricular arrhythmias complicating hypertrophic cardiomyopathy (which responds poorly to beta-blocking agents or calcium antagonists) and refractory, recurrent ventricular tachycardia and fibrillation. In the latter life-threatening situation, amiodarone has proved effective in large numbers of patients whose condition had failed to respond to a series of other established and experimental drugs.
Therapy of acute myocardial infarction
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Joshua M. Stolker, Michael W. Rich
Treatment of atrial fibrillation includes correcting any reversible abnormalities (e.g., hypokalemia), controlling the ventricular rate, and restoring sinus rhythm in patients with hemodynamic compromise. In patients who are hemodynamically stable, rate control with β-blockers or rate-lowering calcium channel blockers (i.e., diltiazem or verapamil) is appropriate. In most cases, IV heparin to maintain the aPTT in the range of 50–70 seconds is also indicated. Although effective rate control often results in spontaneous conversion to sinus rhythm, if new-onset atrial fibrillation persists longer than 24 hours, pharmacological or electrical cardioversion should be considered. Antiarrhythmic agents commonly used in the cardioversion of recent-onset atrial fibrillation include amiodarone or sotalol. These agents are negatively inotropic and should be used with caution in the presence of significant left ventricular dysfunction. In patients who exhibit hypotension, severe HF, or organ hypoperfusion attributable to atrial fibrillation, immediate electrical cardioversion is the treatment of choice (16). Patients with persistent or chronic atrial fibrillation should receive long-term antithrombotic therapy with warfarin or a direct oral anticoagulant (dabigatran, rivaroxaban, apixaban, edoxaban) (204).
Keeping a balance in chronic lymphocytic leukemia (CLL) patients taking ibrutinib: ibrutinib-associated adverse events and their management based on drug interactions
Published in Expert Review of Hematology, 2021
Hee Jeong Cho, Dong Won Baek, Juhyung Kim, Jung Min Lee, Joon Ho Moon, Sang Kyun Sohn
As mentioned above, most medications used for rate and rhythm control potentially alter the exposures of ibrutinib and AF drugs. To minimize toxicities associated with drug-drug interactions, it is necessary to choose the medications that show less interactions with ibrutinib. With regard to the rate control of AF, beta-blockers with no known drug interactions are recommended as first-line therapy [37]. Digoxin could be an alternative option in cases where beta-blockers are not applicable. However, as digoxin interacts with p-glycoprotein, it should be taken at least six hours apart from ibrutinib, a p-glycoprotein inhibitor [37,78]. Antiarrhythmic agents such as amiodarone should be used cautiously because of their possible drug interactions with ibrutinib. According to an ibrutinib-associated AF management algorithm published by cardiologists, hemodynamically unstable patients need antiarrhythmic management, and in case of stable patients who can tolerate anticoagulants, electrical or chemical cardioversion may be considered for rhythm control [37].
Current pharmacotherapeutic strategies for cardiac arrhythmias in heart failure
Published in Expert Opinion on Pharmacotherapy, 2020
Ashish Correa, Yogita Rochlani, Wilbert S. Aronow
Cardiac arrhythmias are frequently seen in patients with HF. These rhythm disturbances can be related to the underlying pathology that causes the HF (such as atrial myopathy, ischemic cardiomyopathy, and scar related arrhythmia). Conversely, the arrhythmia itself can precipitate HF, such as with tachycardia-mediated cardiomyopathy. Regardless of the etiology, arrhythmias often lead to worsening of HF and are the leading cause of death in this patient population. It is important to treat these arrhythmias to control symptoms, slow disease progression and prevent sudden death. Management depends on the type of arrhythmia (atrial or ventricular), the stage of HF and other comorbidities. Antiarrhythmic agents are often used along with device therapy and catheter ablation. However, antiarrhythmic agents come with their own problems, such as proarrhythmic and negative inotropic effects. The knowledge of cardiac arrhythmias seen in HF patients and their evidence-based pharmacologic management strategies are important for physicians caring for these patients.
The potassium channel blocker, dalfampridine diminishes ouabain-induced arrhythmia in isolated rat atria
Published in Archives of Physiology and Biochemistry, 2019
Nahid Ghebleh Zadeh, Gholamhassan Vaezi, Azam Bakhtiarian, Zahra Mousavi, Abdolhossein Shiravi, Vahid Nikoui
Potassium (K+) channels are the main type of ion channel and are distributed in all living organisms (Littleton and Ganetzky 2000). These channels make potassium-selective pores that located inside cell membranes. Moreover, these channels are localized on various cell types and regulate numerous cellular functions (Schmitt et al. 2014). These channels also control the repolarization of atrial action potentials (Schmitt et al. 2014). It is well-known that prolongation of cardiac action potential and effective refractory period prevents cardiac arrhythmias, particularly in short action potential conditions. Recent investigations are focused on discovering the antiarrhythmic agents the prolong action potentials without proarrhythmic adverse effects. As well as sodium channel blockers, potassium channel blockers also exert antiarrhythmic properties (Gerlach 2003). Based on Vaughan-Williams classification scheme, potassium channel blockers are class III antiarrhythmic agents. These agents block the potassium channels, which mediate phase 3 of repolarization. Consequently, blockade of these channels delays repolarization, which prolongs both action potential duration and effective refractory period (Singh and Ahmed 1994, Dorian 2000).