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Genetic defects hold clues to risk for sudden cardiac death
Date:5/10/2011

that mutations that cause ion channels to open more slowly than they should were strongly associated with increased risk for cardiac events. Patients with these slow activating channels were twice as likely as patients with other mutations to die before the age of 30 or experience serious symptoms.

Even for patients who lacked telltale clinical symptoms, the presence of mutations linked with slow-to-open ion channels was still associated with an increased risk of cardiac events.

"This study creates a paradigm that we not only have to take into account the presence of mutations, but the potential consequences of mutations as well," noted Wojciech Zareba, M.D., Ph.D., director of the Heart Research Follow-up Program and an expert on Long QT. "Some mutations may be more benign and others less so and more research is needed to understand why this is the case."

The team looked at the function of 17 common mutations found in approximately 390 patients drawn from the International Long QT Registry. In the lab, they recreated the mutant proteins and put them in cells to study their effect on ion channels. They used clinical follow-up data from the registry to relate mutant function to cardiac risk.

While this process of testing mutant function is a starting point, Lopes says that in the future new, emerging stem cell technologies may allow physicians to take cells (such as skin cells) directly from patients and turn them into heart cells to more precisely determine mutant function.

"Similar to genetic testing, a simple, standardized way to test mutation function on a large scale is needed in order for this method to be widely adopted in clinical practice," noted Lopes.


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Contact: Emily Boynton
emily_boynton@urmc.rochester.edu
585-273-1757
University of Rochester Medical Center
Source:Eurekalert

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