Electrical activity of human atrial fibres at frequencies corresponding to atrial flutter

• Published in: Cardiovascular research Vol. 23; no. 2; pp. 159 - 168
• Main Authors: LAURIBE, PHILIPPE, DENIS, ESCANDE, NOTTIN, REMY, CORABOEUF, EDOUARD
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.02.1989
• Subjects: Action Potentials - drug effects; anti-arrhythmic drugs; atrial flutter; Atrial Flutter - physiopathology; Biological and medical sciences; Calcium Channel Blockers - pharmacology; Culture Techniques; Electrophysiology; Fundamental and applied biological sciences. Psychology; Heart; Heart - physiopathology; Heart Atria - physiopathology; high frequencies; human atrial cells; Humans; Microelectrodes; Ouabain - pharmacology; Sodium Channels - drug effects; Vertebrates: cardiovascular system; Heart; Human; Atrium; Calcium; Sodium; Membrane transport; Electrophysiology; Action potential; Circulatory system; Atrial flutter
• ISSN: 0008-6363; 1755-3245
• DOI: 10.1093/cvr/23.2.159

Little information is available about rate dependent changes in electrical activity of human myocardial cells. We therefore studied, in vitro, the electrical activity of adult human atrial fibres driven at frequencies near that of atrial flutter by means of the standard microelectrode technique. Thirty two atrial samples exhibiting “normal” responses with fast upstroke were selected. At very high frequencies, the action potential (AP) upstroke arose from the repolarisation phase of the preceding AP in spite of marked frequency induced shortening of the plateau. As the stimulation rate was progressively increased, the take off potential (TOP) was less and less negative and the maximal rate of depolarisation (Vmax) decreased. Moreover, in most preparations, a clear alternation between two types of action potentials occurred. Calcium channel inhibitors cobalt (5 mM) or diltiazem (5.10−6 M) shortened AP duration, increased Vmax and markedly reduced alternation. Sodium channel inhibitors, tetrodotoxin (7.5 10−6 M) or lignocaine (10−5 M) shortened AP duration and induced a transient increase in Vmax. Ouabain (10−6 M) prolonged AP duration, decreased Vmax, enhanced alternation and finally suppressed the 1:1 capture of the atrial tissue. Our results show that, at high driving rates corresponding to the frequencies of atrial flutter, slight variations in action potential duration induced by drugs are associated with marked concomitant variations in Vmax and probably with consequent modifications of the conduction velocity.