WEDNESDAY, Nov. 22, 2006 (HealthDay News) -- The altered function of sodium channels in cells could help spur sudden death in heart failure patients, German researchers report.
The study, conducted using mice and muscle cells from rabbits, offers a potential molecular explanation for abnormally rapid heartbeats (ventricular tachyarrhythmias - VTs) that can cause sudden death associated with heart failure, said the team from Georg-August-University in Gottingen.
The noted that people with inherited mutations in genes that regulate the influx of sodium ions (Na+) into the muscle cells of the heart through special Na+ channels are predisposed to VTs.
It was already known that a protein called calmodulin regulates Na+ function and that expression and activity of the calmodulin effector CaMKII is upregulated in heart failure patients. So, the German scientists decided to study the effect of CaMKII on Na+ channel function.
They found that overexpression of CaMKII altered Na+ channel function in mice and in cultured heart muscle cells from rabbits. Mice bred to overexpress CaMKII were more likely to suffer VTs than normal mice.
The team concluded that CaMKII regulation of Na+ channel function may play a role in the onset of potentially deadly VTs.
The study was published online Nov. 22 by the Journal of Clinical Investigation and will appear in the December print issue of the journal.
The American Heart Association has more about heart failure.