Background: Myocardial infarction can lead to electrical abnormalities and
rhythm disturbances. However, there is limited data on the electrophysiolog
ical basis for these events. Since regional contraction abnormalities featu
re prominently in infarction, we investigated whether stretch of myocardium
from the infarction borderzone can modulate the electrophysiological prope
rties of cardiomyocytes via mechanoelectric feedback providing a mechanism
for post-infarction arrhythmia. Methods: Five weeks after experimental myoc
ardial infarction (MI) in rats due to ligation of the left coronary artery
(n=26) or after sham operation (SO, n=16), action potentials (AP) were meas
ured in left ventricular preparations from the infarction borderzone. Susta
ined stretch was applied via a micrometer. Results: Preparations from MI ge
nerated spontaneous electrical and contractile activity. Cardiomyocytes fro
m MI had a comparable AP amplitude, a more negative resting membrane potent
ial, and a prolonged AP duration (APD) when compared to SO. In SO, stretch
of 150 mu m increased the APD90, This was associated with stretch activated
depolarizations near APD90 (SAD-90). In MI, significantly lower stretch, o
f only 20 mu m, elicited SAD-90s, or SADs near APD50 (SAD-50). Stretch-indu
ced events were suppressed by gadolinium, at a concentration (40 mu M) norm
ally used to inhibit stretch-activated channels. Conclusion: After MI, SADs
are generated in the infarction borderzone at lower degrees of stretch. In
creased sensitivity of the membrane potential of cardiac myocytes to mechan
ical stimuli may contribute to the high risk of arrhythmia after infarction
. These SADs may involve the opening of stretch-activated channels. (C) 200
0 Elsevier Science B.V. All rights reserved.