Giuseppina Belotti, Antonella Fedele, Cinzia Gatti, Claudio Poluzzi, Giuseppe Penati, Alessandro Locatelli, Antonino Piti.
Cardiology Department, Ospedale Treviglio-Caravaggio, Treviglio, Italy
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Atrial fibrillation (AF) causes by itself
electrophysiological changes1-3 resulting in atrial electrical remodeling; this
remodeling increases the propensity for AF relapse3,4 and disappears within one
week of sinus rhythm restoration5. AF-related changes are mediated by
rate-induced intracellular calcium overload6 and are
attenuated3,7 and shortened in duration4 by
verapamil. Furthermore, pretreatment with calcium blocking agents might maintain the
sinus rhythm for longer period of time after cardioversion8. On the other hand,
intracellular calcium plays a crucial role also in ventricular relaxation. Intracellular
calcium movements regulate relaxation and the cytosol must be cleared of calcium for
complete myocyte relaxation to occur; the increase of intracellular calcium is
associated to LV impaired relaxation9. Ventricular relaxation occurs at the onset of the
diastole, during isovolumic relaxation phase and during early rapid filling of the
ventricle; when myocardia relaxation is impaired, isovolumic relaxation phase takes
more time and early diastolic filling is reduced in rate and amount10. Doppler
ecocardiography allows the evaluation of all these parameters.
The aim of the study was to evaluate whether left ventricular relaxation impairment,
that shares pathophysiological mechanism of calcium overload with atrial electrical
remodeling, is associated to AF recurrences.
There will be investigated the relation of early recurrences of AF, after external
electrical cardioversion (EC), to LV relaxation parameters, evaluated on transmitral
flow velocity profile at Doppler echocardiography.
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