Berardo Sarubbi*°, Giuseppe Pacileo*, Valentino Ducceschi*°, Maria Giovanna Russo*, Carlo Pisacane*, Raimondo Calvanese*, Giuseppe Santoro*, Maurizio Cotrufo°, Raffaele Calabro*°.
*Division of Paediatric Cardiology, Second University of Naples, Monaldi Hospital, °Second University of Naples, Italy, Research Doctorate in “Cardiological and Cardiosurgical Sciences”
|
|
Ventricular arrhythmias and sudden arrhythmic death are a common
feature in patients with dilated cardiomyopathies, left ventricular hypertrophy and regional wall motion
abnormalities. The leading cause of ventricular tachyarrhythmias in these patients is supposed to be the
mechanical dysfunction itself through the “mechanoelectrical feedback”, defined as the development of
electrophysiological changes during or after changes in mechanical loading1-2.
Basic research and animal experiments have shown that diastolic stretch, following a sudden increase in
ventricular volume and pressure, decreases monophasic action potential (MAP)
duration3 and amplitude4
and the ventricular effective refractory periods3 for as long as stretch is
applied and can generate spontaneous depolarisations5, whose velocity
of generation has been supposed to trigger the volume pulse-related ectopic
ventricular excitations6. Electrical instability, following mechanical
stretch, has been experimentally observed
both in terms of development of afterdepolarization and in terms of increased dispersion of refractoriness and
repolarization.
The aim of the present study was to assess the presence of mechano-electrical feedback in humans, evaluating
ventricular repolarization time indexes following acute changes in left ventricular pressure.
|