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Inherited cardiac arrhythmia syndromes: what have they taught us about arrhythmias and anti-arrhythmic therapy?
| Content Provider | Semantic Scholar |
|---|---|
| Author | Subbiah, R. T. Nishant Campbell, Terence J. Vandenberg, Jamie I. |
| Copyright Year | 2004 |
| Abstract | 1. In recent years, the identification of the gene defects in a vast array of monogenic disorders has revolutionized our understanding of the basic mechanisms underlying numerous disease processes. 2. Mutations in cardiac ion channels have been identified as the basis of a wide range of inherited arrhythmia syndromes, including the congenital long QT syndromes, Brugada syndrome, Lenegre syndrome, Andersen's disease and familial atrial fibrillation. 3. Identification of mutations in the human-ether-a-go-go-related gene (HERG) K(+) channel as the molecular basis of congenital long QT syndrome type 2 also led to the discovery that HERG is the molecular target for the vast majority of drugs (both cardiac and non-cardiac) that cause drug-induced arrhythmias. This has had profound implications not only for the development of anti-arrhythmic agents, but also for drug development in general. 4. The sequencing of the human genome in a sense represents the pinnacle of the reductionist era of molecular medicine. The great challenge now is to re-integrate the information gathered during the 'reductionist era' to provide a better understanding of the intact organism. Computer modelling is likely to be a key component of that re-integration process. |
| File Format | PDF HTM / HTML |
| DOI | 10.1111/j.1440-1681.2004.04132.x |
| Alternate Webpage(s) | http://aups.org.au/Proceedings/34/133-140/133-140.pdf |
| PubMed reference number | 15659058 |
| Alternate Webpage(s) | https://doi.org/10.1111/j.1440-1681.2004.04132.x |
| Volume Number | 31 |
| Issue Number | 12 |
| Journal | Clinical and experimental pharmacology & physiology |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
