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Rapid, complete, uniform activation of all atrial tissue is important for rhythm stability. Typical flutter, the most common among atrial tachycardias, has anisotropic conduction at the terminal crest as an essential part of its mechanism
Normal heart activation is characterised by regular alternation between depolarisation/repolarisation and rest. Activation originates in the right atrium, around the sinus node area, and spreads until the atria are completely activated. Once activation is complete atrial tissue is refractory and a period of rest necessarily precedes the next activation cycle. This sequence is caused by pacemaker cells with discharge rates that respond to neural and humoral stimuli, thus allowing adaptation of heart function to physiologic demands. However, this normal sequence is not so simple to sustain, as demonstrated by the frequent appearance of re-entrant tachycardias.
Rapid, complete, uniform activation of all atrial tissue is important for rhythm stability. Preferential conduction pathways have been long recognised in the atria,1–3 despite the absence of bundles of specialised conduction akin to the His-Purkinje network of the ventricles.4 James and Sherf5 attributed the faster conduction along the terminal crest and Bachmann’s bundle to the presence of specialised cells; however, present day thinking explains this by the anisotropic properties of atrial myocardium.
In cardiac electrophysiology “anisotropy” refers to changes in conduction dependent on the anatomic orientation of myocardial fibres. According to the cable theory, conduction velocity depends on myocardial action potential upstroke—that is, the velocity of intracellular voltage change from negative to positive at the time of depolarisation.6 A decrease in the rate of depolarisation would cause conduction slowing as, for example, when antiarrhythmic drugs block the fast sodium (Na+) channel. But a new …