The Duke University and Johns Hopkins University team, led by Nenad Bursac of Duke's Pratt School of Engineering, reported its findings in the Feb. 1, 2006, Cardiovascular Research. Bursac and study co-author Leslie Tung conducted the experiments at Johns Hopkins before Bursac joined the Duke faculty. The work was supported by the National Institutes of Health and the American Heart Association.
In their experiments, the researchers sought to understand the characteristics of ventricular tachycardia -- a condition characterized by abnormally fast beating of the heart's pumping chambers. In particular, they sought to understand how such arrhythmia may lead to ventricular fibrillation, in which the heart's electrical activity becomes disordered, causing the ventricles to flutter rather than synchronously beat. As a result, pumping of the blood is inefficient, and death can result within minutes.
"Ventricular tachycardia and fibrillation are the leading causes of sudden death in the developed world," Bursac said. "Yet, in humans and animals the anatomy is so complex that mechanisms of such arrhythmias are difficult to dissect systematically."
In their study, Bursac and his colleagues created a simpler version of cardiac tissue using cells from the heart ventricles of neonatal rats. They transferred the cells into culture dishes on which they had stamped precise patterns of proteins known to support heart tissue growth. The proteins caused the cells to orient themselves, interconnect and grow in a manner that mimics normal heart tissue, Bursac explaine
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