Abstract
Objective: Re-entry ventricular tachycardias (VT) caused by varying conduction velocities of native and lesioned myocardium represent a frequent and potentially lethal complication in myocardial infarction. To modulate this conduction inhomogeneity lentivirus based transduction of resident cells within the lesion with the gap junction protein Connexin 43 (Cx43) was performed.
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