title: Future prospects of antiarrhythmic treatment based on experimental studies.
abstract: Based on recent experimental studies, a number of speculations about future developments are made regarding the treatment of atrial fibrillation, the problem of proarrhythmia in patients with heart failure, and the treatment of ventricular tachycardia developing during the first 6 weeks following the onset of myocardial infarction. Rapid atrial pacing, or atrial fibrillation, leads to a shortening of the atrial refractory period which persists for a long time following cardioversion. This 'cardiac memory', which also exists on the ventricular level, favours re-induction of atrial fibrillation because the wavelength for re-entry is reduced. Future development of drugs that would prolong the atrial action potential after prolonged periods of atrial fibrillation would increase the success of cardioversion. Although atrial fibrillation is probably most often caused by multiple wavelet re-entry, recent studies show that in some instances a small stable re-entrant circuit is responsible for the arrhythmia. If catheter mapping could reliably localize such a circuit, catheter ablation may be a new therapeutic option. Drug treatment for atrial fibrillation carries a high risk for mortality in patients with heart failure. The arrhythmogenic mechanisms in heart failure are poorly understood, even though there are indications for an increased likelihood of triggered arrhythmias based on delayed afterdepolarizations. Further research in this area is required, particularly where it concerns the response of the (prolonged) action potential in failing hearts to K(+) channel blocking agents. Mortality in patients developing their first attack of ventricular tachycardia within 6 weeks after the onset of myocardial infarction is almost twice that of patients who have their first tachycardia later. Action potential characteristics of ventricular cells overlying an infarct are abnormal during the first weeks of infarct healing, and return to normal after 2 months. It would be worthwhile to study the response to anti-arrhythmic drugs in such cells, in the hope of finding drugs that would increase their refractory periods. Eventually, this could lead to different forms of drug treatment in ventricular tachycardia during the first 6 to 8 weeks following infarction as compared to tachycardias in later stages.
authors.affiliation: Department of Clinical and Experimental Cardiology, University of Amsterdam, The Netherlands.
authors.forename: M J
authors.initials: MJ
authors.lastname: Janse
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000209:etiology / Q000628:therapy*; D017115:Catheter Ablation; D006801:Humans; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000628:therapy*
chemical_list: D000889:Anti-Arrhythmia Agents