Mechanical stretch has been shown to provoke arrhythmia. We wanted to analyze 
ventricular arrhythmia induced by local left ventricular stretch in order to 
find out, where arrhythmias originate and whether they can be prevented 
pharmacologically. Isolated rabbit hearts (Langendorff technique) were submitted 
to increased left ventricular stretch at the left wall by insertion of an 
additional intraventricular balloon and adjusting the end-diastolic pressure 
(EDP) to 25 mmHg for 10 min followed by 20 min recovery at normal EDP of 5-8 
mmHg. Activation and repolarization processes were investigated by ventricular 
256 electrode epicardial mapping. The hearts were treated during the whole 
procedure either with vehicle, 0.5 μM flecainide (sodium channel blocker) or 100 
μM streptomycin (here used as stretch-activated ion-channel blocker). In 
addition, we performed a series of experiments, in which we enhanced EDP to 30 
mmHg (global stretch instead of local stretch) by inflating the left ventricular 
pressure balloon (strain, 0.148 ± 0.034). Each series was performed with n = 6. 
Stretch resulted in local strain of 25% at the left wall together with a local 
slowing of the activation process at the left wall, in a change in the 
activation pattern, and in ventricular arrhythmia. Coronary flow was not 
affected. Ventricular arrhythmias originated from the border between the 
stretched area and the non-stretched region. Flecainide and streptomycin reduced 
the prolongation of the activation process at the stretched left wall and 
mitigated the difference in total activation time between left and front wall 
but only partially prevented arrhythmia. In the additional global stretch 
experiments relative coronary flow and the other parameters remained unchanged, 
in particular TAT. Thus, in contrast to the local stretch series, there was no 
difference in the change in TAT between left and front wall. Only rare single 
ventricular extrasystoles (<1/min; originating from LV (front and left wall) 
i.e. from within the stretched region) were seen during stretch (but not at the 
beginning) and during recovery. Local left ventricular stretch can elicit 
ventricular arrhythmias. Local slowing of electrical activation seems involved 
so that the difference in total activation time of the stretched free left wall 
and the non-stretched increased.