More Musing About the Inter-relationships of Atrial Fibrillation and Atrial Flutter and Their Clinical Implications

Abstract

The inter-relationship between atrial fibrillation (AF) and atrial flutter (AFL) has long been recognized both in patients and in animal models.1 There are 2 important aspects of this inter-relationship relevant to the article by Mohanty et al.2 First is the fact that AF virtually always precedes the onset of classical cavotricuspid isthmus (CTI)–dependent AFL, and second, the development of classical CTI AFL requires the development or presence of a line of block in the right atrium between the venae cavae.1 The first aspect probably was initially recognized by Sir Thomas Lewis,3 who, in studies in the normal canine heart, burst paced the right atrium, and obtained mostly transient AF, but sometimes sustained AFL. Lewis mapped the AFL and concluded that AFL was because of re-entry around the great veins (ie, the superior and inferior vena cavae). This conclusion became well accepted. The second aspect was addressed by Rosenblueth and Garcia Ramos,4 who postulated that the reason it was so difficult for Lewis et al to induce AFL was because there was short circuiting of the AFL reentrant circuit by conduction across the atria in the region between the vena cavae (from the left atrium or to the right atrium or vice versa) making the reentrant circuit impossible to sustain. Therefore, in studies in the canine heart (1947), they created conduction block between the vena cavae, either with a crush lesion (permanent block) or by painting cocaine on the atrial epicardium in the intercaval region (transient block), and, with burst atrial pacing, easily induced AFL. The latter occurred consistently in the presence of the crush lesion, but only transiently with the use of cocaine, as the effects of the cocaine wore off. Over the years, many more studies further advanced these 2 aspects of AFL. Almost …