Drug-induced atrial fibrillation
Cornelis S. van der Hooft, MD*, ,
Jan Heeringa, MD*,
Gerard van Herpen, MD, PhD ,
Jan A. Kors, PhD,
J. Herre Kingma, MD, PhD, and
Bruno H. Ch. Stricker, MB, PhD*,,*
* Pharmaco-epidemiology Unit, Department of Epidemiology & Biostatistics, Erasmus University Medical Center, Rotterdam, the Netherlands
Department of Medical Informatics, Erasmus University Medical Center, Rotterdam, the Netherlands
Inspectorate for Health Care, The Hague, the Netherlands
Department of Clinical Pharmacology, University of Groningen, Groningen, the Netherlands
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Figure 1 Antiarrhythmic drugs have diverse electrophysiologic effects on conduction, refractoriness, and automaticity in the heart. As an example we might consider the simplest form of atrial fibrillation (AF) due to re-entry around one or more obstacles (i.e., scars) that might be found in a patient with AF due to prior myocardial infarction. As a re-entry wave front circulates around an obstacle, it leaves in its wake a region of tissue that is refractory. In order for re-entry to be sustained around such an obstacle, the revolution time (RT) around the circuit must exceed the refractory period (RP) (i.e., RT > RP). Otherwise, the wave front would begin to encounter tissue that was still refractory, thereby preventing or extinguishing the re-entry. If RT < RP, re-entry is not possible, but when a (antiarrhythmic) drug slows conduction velocity more than it prolongs the RP, this drug could initiate re-entry (RT > RP), and the drug would be judged as proarrhythmic (arrow b). If a drug prolongs the RP to a greater degree than it slows conduction velocity, it will prevent re-entry and acts as antiarrhythmic (arrow a).
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