Abstract
Background:
Atrial remodeling is a complex process involving tissue, cellular mechanical and electrical function, and coherence. There is a lack of information about atrial cells remodeling in 2 most represented diseases in canines: myxomatoses mitral valve disease and dilated cardiomyopathy. Moreover, there is little data about intercalated disc (ICD) proteins expression in diseases associated with atrial arrhythmias such as atrial extrasystoles and atrial fibrillation.

Aim:
To estimate remodeling of several proteins associated with ICD: connexin 40 & 43, desmin, plakoglobin, N-cadherin.

Methods:
Fourteen dogs’ specimens for histomorphological and immunohistochemical study of the atrium myocardium at 6 zones: right anterior pulmonary vein (PV), right and left atrium at anterior and posterior portions, interatrial septum (IAS).

Results:
DCMAFib(n=3) has decreased expression of the all proteins; DCMFAT(n=5) has decreased plakoglobin in both atria, pulmonary vein (PV); N-cad - in atria, IAS; connexin 43 & 40 in atria; desmin maladaptive accumulation in PV, left atrium. MMVDAFib(n=3) had plakoglobin decreased in PV, atria; N-cad - in PV, IAS, atria; Cx 43 & 40 - in PV, right atrium and had dispersion in other zones; desmin maladaptive accumulation in PV, atria. MMVDFAT(n=2) - N-cad in atria; adaptive desmin accumulation.

Conclusion:
Differences between atrial remodeling in dogs with MMVD and DCM were described, presenting complicated interactions between ICD proteins within arrhythmia. Possibly, the paradigm of AFib can be reconsidered as a simple consequence of DCM. In the MMVD we suspect that AFib is a logical consequence of the structural atrial remodeling. Additionally, we found signs of cardiomyocytes disruption and loss of cell-to-cell contacts

Key words: Atrial fibrillation; Connexin; Dilated cardiomyopathy; Myxomatous mitral valve disease; Plakoglobin.