Objective: Rapid electrical activity in pulmonary veins (PVs) has been proposed as a mechanism for focal atrial fibrillation. The way in which the myocardial sleeve inside PVs can form a substrate for focal activity is not well understood. Therefore, we have studied tissue structure and connexin distribution at the veno-atrial transition in the dog.
Methods: In adult mongrel dogs, the anatomy of the PV area was studied. Tissue structure in individual veins was assessed in formalin fixed sections using Masson's Trichrome staining. Gap junction protein distribution was examined using antibodies against connexin40 (Cx40) and connexin43 (Cx43). The ultrastructure of myocytes in myocardial sleeves was studied using electron microscopy.
Results: Individual PVs in the dog had a gross morphology similar to that observed in the human, with myocardial sleeves extending into the veins for 4-20 mm. In all veins examined, myocytes in myocardial sleeves had a normal atrial morphology and anti-desmin staining pattern. Cx43 was expressed throughout the sleeve at levels comparable to normal atrial myocardium. By contrast, Cx40 expression was lower in myocardial sleeves than in the rest of the left atrium. Myocytes in the sleeve, which were ultrastructurally similar to normal atrial myocytes, were predominantly organized in a circumferential pattern.
Conclusions: PVs in the dog and various canine models of heart disease will be a suitable model for (patho)physiology of the veno-atrial transition. Myocytes in myocardial sleeves are similar to normal atrial myocytes. The circumferential orientation of these myocytes may provide a substrate for rapid circular reentry.