Remodeling of myocardial sleeve and gap junctions in canine superior vena cava after rapid pacing

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.