Investigational Anti–Atrial Fibrillation Pharmacology and Mechanisms by Which Antiarrhythmics Terminate the Arrhythmia: Where Are We in 2020?
| Autor: | Alexander Burashnikov |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Drug medicine.medical_specialty reentry Refractory Period Electrophysiological media_common.quotation_subject Action Potentials 030204 cardiovascular system & hematology 03 medical and health sciences 0302 clinical medicine Heart Conduction System Heart Rate Internal medicine Atrial Fibrillation medicine Potassium Channel Blockers Atrial effective refractory period Animals Humans media_common Pharmacology Extramural Mechanism (biology) business.industry Atrial fibrillation Reentry medicine.disease 030104 developmental biology Drugs in the Pipeline - Invited Review Article Cardiology antiarrhythmics Cardiology and Cardiovascular Medicine business arrhythmias Anti-Arrhythmia Agents sodium channel Sodium Channel Blockers |
| Zdroj: | Journal of Cardiovascular Pharmacology |
| ISSN: | 1533-4023 0160-2446 |
| Popis: | Antiarrhythmic drugs remain the mainstay therapy for patients with atrial fibrillation (AF). A major disadvantage of the currently available anti-AF agents is the risk of induction of ventricular proarrhythmias. Aiming to reduce this risk, several atrial-specific or -selective ion channel block approaches have been introduced for AF suppression, but only the atrial-selective inhibition of the sodium channel has been demonstrated to be valid in both experimental and clinical studies. Among the other pharmacological anti-AF approaches, “upstream therapy” has been prominent but largely disappointing, and pulmonary delivery of anti-AF drugs seems to be promising. Major contradictions exist in the literature about the electrophysiological mechanisms of AF (ie, reentry or focal?) and the mechanisms by which anti-AF drugs terminate AF, making the search for novel anti-AF approaches largely empirical. Drug-induced termination of AF may or may not be associated with prolongation of the atrial effective refractory period. Anti-AF drug research has been largely based on the “suppress reentry” ideology; however, results of the AF mapping studies increasingly indicate that nonreentrant mechanism(s) plays an important role in the maintenance of AF. Also, the analysis of anti-AF drug-induced electrophysiological alterations during AF, conducted in the current study, leans toward the focal source as the prime mechanism of AF maintenance. More effort should be placed on the investigation of pharmacological suppression of the focal mechanisms. |
| Databáze: | OpenAIRE |
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