RT-28
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New insight on pacing induced
effects
on the myocardium through in ovo pacing
of chick-embryo heart
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Lukas Kappenberger, Michel
Grobéty, Christophe Reymond, David Sedmera, Pavel Kucera.
Division of Cardiology, CHUV and Institute of Physiology of the University of Lausanne,
Switzerland
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Introduction
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When pacemaker treatment was introduced about 40 years
ago into clinical medicine, the primary intention was to avoid syncope due to intermittent
or permanent AV block. For many years pacing for brady-arrhythmias was the only indication
for electrical treatment of arrhythmias. However, it was rapidly realised that the lack of
atrial contribution to systolic contraction led to less than optimal hemodynamic effects
of pacing. In order to adapt cardiac output to the metabolic demand, a rate response to
effort had to be included. The loss of atrioventricular synchronisation however led again
to hemodynamic unsatisfactory results. The stimulation of the ventricle, even on different
sites in comparison with His-Purkinje activation of the ventricle revealed that pacing
reduces ventricular function. The mechanisms underlying this feature are only partially
understood and little is known about long term morphologic, histologic and molecular
changes induced by long-term ectopic activation of the heart. We therefore developed a
model to investigate and understand some mechanisms that might explain the effects of
artificial pacing on the myocardium.
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