Abstract
Time for primary review 34 days. In their classic studies published in 1964, Han, Moe and co-workers [1,2] established an association between nonuniform recovery of excitability and lowered fibrillation threshold. They concluded that “those agencies known to favour the development of ventricular fibrillation were found to increase the temporal dispersion of recovery of excitability, whether the average refractory period was reduced … or increased…. The results emphasise the importance of nonuniformity of excitability and conduction velocity during the relative refractory period in the induction of turbulent impulse propagation.” The purpose of this review is to describe the basis of dispersion in recovery of excitability in the ventricle and its association with arrhythmogenesis. Ventricular tachyarrhythmias are readily generated not only in acute ischaemia/infarction but also in hearts that have undergone remodelling following myocardial infarction [3–5]. Life-threatening arrhythmias are commonly seen in patients with previous myocardial infarction in the absence of new ischaemic events, as evidenced by the ability to initiate sustained ventricular tachycardia by programmed stimulation [6]. The risk of ventricular arrhythmias and sudden death in heart failure is inversely proportional to the left ventricular ejection fraction [7]. However, the Veterans Heart Failure Trial and other studies suggest that the proportion of deaths that are sudden is higher in patients with less severe LV dysfunction [8]. Such individuals are less likely to die from pump failure, hence they are at greater relative (but not absolute) risk of sudden death in comparison with patients with advanced heart failure. The classical prerequisites for the development of reentry are the presence of a potential circuit around an anatomical obstacle, unidirectional block, and sufficiently slow conduction to enable recovery of excitability in time for reexcitation by the depolarizing wavefront [9]. A feature of this type of reentry is the presence … * Corresponding author. Tel.: +44-141-211-4722; fax: +44-141-552-4683 stuart.cobbe{at}clinmed.gla.ac.uk
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