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Cardiovascular Research 1999 44(1):13-16; doi:10.1016/S0008-6363(99)00214-X
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Altered expression of cardiac K+ channel genes during sub-acute and healing phases of myocardial infarction

Tatsuto Kiyosue* and Makoto Arita

Department of Physiology, Oita Medical University, Hasama, Oita 879-5593, Japan

* Corresponding author. Tel.: +81-97-586-5652; fax: +81-97-549-6046 kiyosue@oita-med.ac.jp

Received 24 June 1999; accepted 1 July 1999

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

See article by Yao et al. [2] (pages 132–145) in this issue.


   1 Remodeling of the heart after myocardial infarction
 
In animal models of myocardial infarction (MI), in which the coronary artery is occluded permanently, the incidence of ventricular arrhythmias is classified into three categories according to when they occur after the onset of MI: acute, sub-acute and chronic phase arrhythmias [1]. In men who suffered from MI, ventricular tachyarrhythmias frequently occur in essentially the same manner as that encountered in the animal models. In the acute phase (within several hours from the onset of MI), the occurrence of life-threatening arrhythmias (ventricular tachycardia and ventricular fibrillation) is common. Reentry and triggered activities are the major causes of such fatal arrhythmias seen during the early phase of MI [1].

The hearts that survive acute MI undergo dynamic remodeling to cope with metabolic and mechanical derangements caused by the MI. Most of the myocytes in the ischaemic region . . . [Full Text of this Article]


   2 Inward rectifier K+ channels after MI
 

   3 Delayed rectifier K+ channels after MI
 

   4 Transient outward current after MI
 

   5 Conclusion
 

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