Journal
BASIC RESEARCH IN CARDIOLOGY
Volume 101, Issue 4, Pages 269-280Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00395-006-0588-1
Keywords
superior vena cava; atrial fibrillation; gap junctions
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We studied the response of the superior vena cava (SVC) myocardial sleeve to atrial fibrillation (AF). We examined adult male dogs without pacing (N=6) and after rapid atrial pacing (600 bpm) for 2 weeks (P2w; N=5) and 6-8 weeks (P6-8w; N=5). After pacing, the sleeve was increased in thickness (non-paced vs. either paced group, both P < 0.05). This was associated with an increase in proliferative activity, which was higher in the P2w than the P6-8w animals (P < 0.05). In addition, collagen content increased, and the component cardiomyocytes become more unevenly oriented and shorter and narrower in shape (non-paced vs. either paced group, both P < 0.05). Pacing had different effects on connexin40 (Cx40) and Cx43 gap junctions. There was a 98% increase in Cx43 signal in P2w, and a 74% increase in P6-8w animals (non-paced vs. each paced group, both P < 0.05). In contrast, Cx40 signal decreased 47% in P2w but increased 44% in P6-8w animals (non-paced vs. each paced group, both P < 0.05). Rapid atrial pacing results in a specific pattern of remodeling of the canine SVC sleeve, including changes in size and shape, spatial orientation, and gap junction expression profile of the component cardiomyocytes. These changes may co-operatively affect the electrical properties and contribute to the formation and maintenance of the arrhythmogenic substrate of AF.
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