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Cardiovascular Research 1999 43(4):832-834; doi:10.1016/S0008-6363(99)00189-3
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Role of sympathoadrenergic mechanisms in arrhythmogenesis

Xiao-Jun Du* and Anthony M. Dart

Baker Medical Research Institute, Melbourne, Victoria, Australia

* Corresponding author. Tel.: +61-3-9522-4399; fax: +61-3-9521-1362 xiaojun.du@baker.edu.au

Received 31 May 1999; accepted 31 May 1999

The first 10% of the full text of this article appears below.

See article by Guo et al. ([1], pages 930–938) in this issue.

Ventricular arrhythmias occur frequently following acute myocardial infarction, during reperfusion and in heart failure. They are the likely major cause of sudden cardiac death in the majority of instances and as such represent a continuing and major cardiac health problem. The role of the sympathetic nervous system (SNS) in the genesis of arrhythmias under these conditions has been extensively studied for many years. Nevertheless, the importance of SNS activation in arrhythmogenesis remains controversial. This is again apparent in the current issue of Cardiovascular Research, where the findings from two papers with apparently contradictory interpretations are presented [1,2].

Numerous experimental approaches have been applied to manipulate the activity of the SNS, from dennervation and catecholamine depletion to . . . [Full Text of this Article]


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