Abstract
Objective: Atrial fibrillation (AF) is a progressive disease and associated with electrical remodeling in the atria. Because of positive clinical effects of ACE-inhibitors we wanted to elucidate, whether angiotensin and AT-receptors may be involved in the gap junction remodelling of the gap junction proteins (connexins) Cx43 and Cx40 in AF in the human left and right atria.
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