Conductive bridges in cardiac tissue: a beneficial role or an arrhythmogenic substrate?

Abstract

For many years, propagation of excitation in cardiac tissue was considered to occur in a homogeneous electrical syncytium. This view has permitted the application of concepts and quantitative relationships developed originally by Hodgkin and Huxley to describe action-potential propagation in the continuous structure of the nerve axon.1 The properties of action-potential conduction were associated with membrane properties alone, while effects of the myocardial architecture were, for the most part, ignored. The microscopic anatomical structure of the myocardium as an assembly of discrete cells separated by a periodic intercalated disk structure was established in the 1950s, followed in later years by the identification of gap junctions as specialized structures for electrical communication between cardiac cells.2–5 The pioneering work of Madison Spach and coworkers in the early 1980s6,7 directed attention to the effects of structural discontinuities on action-potential propagation in the heart. Spach’s experiments revealed electrical properties of cardiac tissue that could not be explained on the basis of the theory that describes conduction of excitation in a continuous medium (the so-called continuous cable theory). For example, the maximum rate of action-potential depolarization, (dV/dt)max, was observed to increase as propagation velocity decreased with wider angles of propagation relative to the myocardial fiber axis. This inverse relationship between (dV/dt)max and velocity is in sharp contrast to the direct relation between these parameters, which is a hallmark of conduction in continuous structures. Thus, conduction in cardiac tissue is discontinuous and its properties are influenced profoundly by the myocardial architecture. The theory of discontinuous conduction predicts the experimentally observed differences from continuous conduction and …