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Cardiovascular Research 2001 50(1):10-23; doi:10.1016/S0008-6363(01)00197-3
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Dispersion of ventricular repolarization and refractory period

Francis L Burton and Stuart M Cobbe*

Department of Medical Cardiology, Glasgow Royal Infirmary, 10, Alexandra Parade, Glasgow G31 2ER, Scotland, UK

* Corresponding author. Tel.: +44-141-211-4722; fax: +44-141-552-4683 stuart.cobbe@clinmed.gla.ac.uk

Received 25 August 2000; accepted 27 December 2000

KEYWORDS Arrhythmia (mechanisms); Hypertrophy; Infarction; Repolarization; Ventricular arrhythmias

The first 150 words of the full text of this article appear below.


   1 Introduction
 
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 . . . [Full Text of this Article]


   2 Conditions for reentry
 

   3 Action potential duration, repolarization time and refractory period
 

   4 Measurement of repolarization time and refractory period
 
4.1 Measurement of repolarization time
4.1.1 Intracellular recording
4.1.2 Optical mapping
4.1.3 Monophasic action potential recording
4.1.4 Activation–recovery intervals
4.1.5 Projection of repolarization to the body surface
4.2 Measurement of refractory period
4.2.1 Extrastimulus technique
4.2.2 Ventricular fibrillation intervals

   5 Estimation of dispersion
 
5.1 Global dispersion
5.2 Local dispersion

   6 Physiological dispersion of APD
 
6.1 Heterogeneity of cell types: transmural dispersion
6.2 Base–apex dispersion
6.3 Interventricular dispersion
6.4 Role of intercellular coupling
6.5 Differences in autonomic response
6.6 Restitution

   7 Changes in dispersion associated with acute myocardial ischaemia
 
7.1 Heterogeneity of metabolic changes in ischaemia
7.2 Action potential duration
7.3 Refractory period

   8 Changes in dispersion associated with myocardial infarction and hypertrophy
 
8.1 Subacute (healing) phase
8.2 Chronic (healed) phase
8.3 Effect of ventricular dilatation
8.4 Sympathetic innervation
8.5 Gap junction remodelling

   9 Is increased dispersion of repolarization time arrhythmogenic?
 

   10 Conclusion
 

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