The AJC in March 1959

Abstract

The March 1959 issue of The American Journal of Cardiology was an extremely exciting issue that was almost entirely dedicated to arrhythmias. Many topics were included with regard to the mechanisms of a variety of arrhythmias, a clinical description of several important arrhythmias, including those caused by digitalis intoxication, bidirectional tachycardia and reciprocal rhythms, and the therapy for them. Several articles discussed proposed mechanisms for a variety of arrhythmias. These reports reveal the great ingenuity of investigators who had nothing more than a surface ECG from which to deduce the intricate mechanisms of these arrhythmias. Many issues are not settled even today despite further development and refinement of microelectrode and voltage-clamping techniques, experimental animal models, computerized activation mapping, and human investigation using programmed stimulation and endocardial catheter recording. Two articles in the symposium, 1 by Fox entitled, “The Mechanisms of Atria1 Fibrillation and Flutter” and the other by Scherf and Schott entitled, “Mechanism of Origin of Ectopic Beats,” dealt with explanations of the mechanisms of atria1 flutter/fibrillation and the mechanisms for ventricular ectopic beats. Both studies had lengthy discussions and the authors used skilled reasoning to try to prove that these arrhythmias were due to ectopic impulse formation and not reentry. Many of the mechanisms currently being evaluated, including triggered activity due to oscillatory afterpotentials, abnormal ectopic impulse formation and reentry, were discussed by these investigators. The main reason reentry was discarded was that at the time there were no data that suggested that an impulse could conduct slowly enough to allow the reentrant circuit to exist in a small amount of ventricular or atria1 tissue. Experimental evidence for oscillatory afterpotentials and relation of preceding cycle length to the extra beats, be they atria1 or ventricular, led these investigators to conclude that the extra beats arose by the triggering “automatic foci,” the characteristics of which could have been due to afterpotentials. We now know from the extremely fine work of Wit, Cranefield, Hoffman and Spach and their colleagues that slow conduction can occur in the presence of high potassium levels, a physiologic consequence of ischemia, in either normal or diseased tissue due to varying degrees of uniform or heterogeneous anisotropy, and due to cells manifesting the slow inward current.1-5 Thus, the main criticisms of these authors militating against reentry as a mechanism were re-