Discontinuous propagation of the cardiac impulse and arrhythmogenesis.

Abstract

SummaryThe complex discontinuous architecture of cardiac tissue induces a number of interactions between the cellular properties of the myocardium that affect impulse propagation:1. Slow (< 10 cm/sec) conduction velocities in the myocardium can only be achieved by discontinuous conduction. In the more continuous type of conduction, as occurring during inhibition of INa, conduction block occurs at velocities of approximately 20 cm/sec.2. If the discontinuity reaches a critical degree, Ica, L is needed to propagate the cardiac impulse. This situation may occur during cell‐to‐cell uncoupling and at sites of local tissue discontinuities.3. The conduction phenomena occurring at tissue discontinuities, such as pivoting points, isthmus, and abrupt tissue expansions are markedly influenced by the underlying properties of the cellular network. Electrical uncoupling at the cellular level can reduce the effect of the discontinuities to produce conduction block and reverse unidirectional block to bidirectional conduction. By contrast, reduction of INa increases the probability of unidirectional block at such sites. Since activation of INa may become rate‐dependent at high rates and in depolarized tissue, this predicts an instability in activation patterns during a tachycardia.Do the above considerations really predict arrhythmogensis? It is obvious that increasing the degree of structural discontinuity creates a substrate for reentrant arrhythmias. However, with the exception of the demonstration of spiral wave initation in vitro,5 no direct effects of tissue discontinuities on arrhythmia initiation have been demonstrated so far. Furthermore, pathologies associated with an increased degree of structural discontinuities, such as a hypertrophy and failure, also show an increased propensity to triggered arrhythmias, and initiation of ventricular tachcardias from small foci has been observed in whole hearts. These complexities make it difficult to extrapolate findings of experimental and theoretical work at the cellular level directly to whole hearts and human pathologies where several mechanisms for initiation and maintenance of tachycardias may coexist.