Cultured Heart cells that were induced to imitate characters of the heart have led researchers to discern possible reasons for irregular heart rhythms. Studies of this engineered tissue have unraveled that while electric shocks akin to those produced by defibrillators normally stopped errant waves, in few cases caused them to advance and proliferate.
These findings have been reported on Feb 1, 2006, by the teams in The Duke University and Johns Hopkins University, headed by Nenad Bursac of Duke's Pratt School of Engineering and Cardiovascular Research. The experiments were conducted by Bursac and study co-author Leslie Tung at Johns Hopkins prior to Bursac joining the Duke faculty. National Institutes of Health and the American Heart Association have provided adequate support for this work. The experiments hovered around understanding Ventricular Tachycardia threadbare. Ventricular Tachycardia results when the heart's pumping chambers produce abnormally fast paced beats, arrhythmias, especially when this condition gives rise to ventricular fibrillation. Ventricular fibrillation is a condition when the heart's electrical activity becomes unsettled and disarranged, causing a ventricular flutter rather than concurrent beats. This can lead to ineffective pumping of blood that may result in sudden death.
Bursac and his team used cells from the heart ventricles of neonatal rats to create an easier version of the heart tissue. These cells were then transferred into a culture dishes that contained requisite arrangement of proteins intended to support the growth of heart tissue. The proteins fuel the cells to multiply in a manner the imitates normal heart tissue. These simulated tissues were charged with electrical activity and attempts were made to curb it with pace-setting pulses. The team found that the pulses managed to arrest the wave in 80% of cases, while in the remaining cases a single wave multiplied into many waves that continued to catalyze the cardiac cells at a fast rate. In 20% of the cases, the purpose of actually ceasing the wave did not happen; in contrast it actually worsened the condition. This estimation almost matches the frequency of similar occurrences in patients with implanted defibrillators.
ICD devices render a potent shock when fast pulses mobilize tachycardia. Continued study of the engineered tissues could reveal further regarding better methods to arrest arrhythmias. The results have amply suggested the efficacy of using engineered tissue in studying the complex electrophysiological characteristics of the heart, according to Bursac. This would certainly hold the key to progressive drug and gene therapies purported to stabilize heart rhythms.
Source: Eureka Alert