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Review
. 2002 Apr 30;99(9):5755-6.
doi: 10.1073/pnas.102171699.

Unraveling the genetics and mechanisms of cardiac arrhythmia

Affiliations
Review

Unraveling the genetics and mechanisms of cardiac arrhythmia

Denis Noble. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Figure 1
Figure 1
Simulation of the spread of the electrical activation wavefront in an anatomically detailed cardiac model (17). The wavefront (shown here in red, with the endocardial surface of the ventricle in blue) is generated by ionic current flowing through sodium channels. As each cell becomes excited it passes current to neighboring cells. The speed of conduction depends on the intensity of the sodium current. Earliest activation occurs at the left ventricular endocardial surface near the apex (Left). Activation then spreads in an endocardial-to-epicardial direction (outward) and from apex toward the base of the heart (upward, Center frames). The activation sequence is strongly influenced by the fibrous-sheet architecture of the myocardium, as illustrated by the nonuniform transmission of excitation. In normal conduction, as in this simulation, the wavefront dies out as it reaches the top (base) of the ventricle, because the conduction is so rapid that the wavefront cannot encounter any more cells to excite. Computer modeling on this whole-organ level with equations based on channel protein properties could form the basis of reconstructing arrhythmias generated by mutations of the cardiac sodium channel. Future work should therefore explore how slowed conduction of the kind investigated by Papadatos et al. (1) allows reentrant circuits to be created.

Comment on

References

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    1. Towbin J A, Schwartz K. In: Foundations of Cardiac Arrhythmias. Spooner P M, Rosen M R, editors. New York: Dekker; 2001. pp. 665–699.
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    1. Noble P J, Noble D. Jpn J Electrocardiol. 2000;20, Suppl. 3:15–19.