[Possibility of gene-specific treatment for hereditary arrhythmic diseases].
Recent genetic and molecular technology have shown that genetic abnormalities related to the cardiac ion channels can be a cause of some hereditary arrhythmic diseases. Until now, advanced analysis has proceeded especially in congenital long QT syndrome, and six different subtypes have been identified in Romano-Ward syndrome and 2 subtypes in Jervell & Lange-Nielsen syndrome. Since the mechanism of QT interval prolongation in each subtype is based on the malfunction of different cardiac ion channels, the same pharmacological treatment may show different antiarrhythmic effects for each subtype. In this paper, we review some of the hereditary arrhythmic diseases and discuss the possibility of gene-specific treatment in such diseases.
Chinushi
Masaomi
M
School of Health Science, Niigata University School of Medicine.
Washizuka
Takashi
T
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D002304:Cardiac Pacing, Artificial; D006801:Humans; D007473:Ion Channels / Q000235:genetics; D008133:Long QT Syndrome / Q000235:genetics / Q000628:therapy*; D008801:Mexiletine / Q000627:therapeutic use; D062553:NAV1.4 Voltage-Gated Sodium Channel; D020108:Nicorandil / Q000627:therapeutic use; D026941:Sodium Channel Blockers / Q000627:therapeutic use; D015222:Sodium Channels / Q000235:genetics; D014693:Ventricular Fibrillation / Q000235:genetics / Q000628:therapy*
D000319:Adrenergic beta-Antagonists; D000889:Anti-Arrhythmia Agents; D007473:Ion Channels; D062553:NAV1.4 Voltage-Gated Sodium Channel; C106251:SCN4A protein, human; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D008801:Mexiletine; D020108:Nicorandil