These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Vulnerable substrate and multiple ion channel disorder in a diseased heart will be new targets for antiarrhythmic therapy.
    Author: Dai DZ.
    Journal: Acta Pharmacol Sin; 2000 Apr; 21(4):289-95. PubMed ID: 11324452.
    Abstract:
    Life-threatening arrhythmia remains a problem contributing to major death in cardiovascular diseases. Till date the antiarrhythmic drugs (AAD) including the Class I and the pure Class III agents have not been recommended for controlling malignant ventricular arrhythmias in a diseased heart, not because of low efficacy but because of an increase in mortality due to their toxic effects. A vulnerable substrate (VS) possessing some properties such as reduced NE and SOD activity, hypertrophied myocardium, and an increase in QT dispersion, is reported to develop in non-infarcted zone of an infarcted heart. Hypertrophied ventricle and exaggerated cardiac arrhythmia can be produced on chronic medication with levothyroxin and this model shares some properties of VS. There is a significant difference in the pattern of disordered ion channels between the congenital long QT syndrome(LQTS) and the acquired heart disease. The affected ion channel in congenital LQTS is single. A novel mutation causing an early appearance of stop codon was discovered in HERG gene resultant with a single disarranged IKr channel leading to a prolonged QT interval. In contrast it is characterised with multi-channels and non-specific disorder in the hypertrophied myocardium in the acquired heart disease. The disordered ion channel is the consequence of the VS lesion influencing the lipid membrane in a diseased heart. The VS and multiple ion channel disorder are provided as new targets to treat cardiac arrhythmias in a diseased heart.
    [Abstract] [Full Text] [Related] [New Search]