Objectives: Atrial arrhythmias are prevalent during clinically abnorma
l myocardial loading, e.g. when the atrium is dilated or stretched. Th
e initiating cause of the first premature beat that leads to this arrh
ythmia is unclear, as are the reasons for sustaining it. One possibili
ty is that abnormal mechanical factors induce electrophysiological cha
nges conducive to arrhythmia via 'mechanoelectric feedback'. The aim o
f this study is to investigate the concept that atrial stretch modulat
es the electrophysiological properties of the atrium via mechanoelectr
ic feedback, and that mechanoelectric feedback can produce atrial arrh
ythmias. Methods: Guinea-pigs were humanely killed by cervical disloca
tion and the hearts removed and perfused with oxygenated Krebs-Hensele
it solution by the Langendorff method. The heart was paced at an atria
l site near the sinus node. Monophasic action potentials and electroca
rdiograms were recorded from the left atrium and left ventricle with s
uction electrodes. Transient stretch was induced by inflating a fluid-
filled intra-atrial latex balloon catheter. Results: Increase in atria
l volume produced several significant changes in the epicardial monoph
asic action potentials. It produced (i) decreases in the amplitude; (i
i) a decrease in duration from 62.55 to 51.95 ms measured at 50% repol
arisation (10.6 +/- 3.6 ms, P < 0.05, n = 6); (iii) an increase in dur
ation from 122.45 to 140 ms measured at 90% repolarisation (17.55 +/-
4.5 ms, P < 0.05, n = 6) -- due to the presence of early afterdepolari
sations. (iv) These load-induced electrophysiological changes coincide
d with the occurrence of arrhythmia or premature atrial beats. Conclus
ions: Load changes in the atrium can produce electrophysiological chan
ges of a kind that may be relevant to clinical atrial arrhythmia.