Histopathological substrate of the atrial myocardium in the progression of obstructive sleep apnoea-related atrial fibrillation.

Abstract

Obstructive sleep apnoea (OSA) is closely related to atrial fibrillation (AF), and OSA-induced atrial structural remodelling is the basis of AF maintenance. However, the process of atrial structural remodelling during the progression of acute OSA to chronic OSA is still unclear. To investigate changes in the atrial myocardium in acute sleep apnoea (6h) and chronic sleep apnoea (12weeks) by echocardiography, atrial myocardium morphology analysis, PAS staining, TUNEL staining, Masson's trichrome staining and analyses of ultrastructural changes. Eighteen adult beagle dogs under general anaesthesia were used to establish an OSA model. The animals were divided into the control group, acute OSA group and chronic OSA group, and there were six animals in each group. Cardiac ultrasounds of dogs from the three groups were examined. Left and right atrial muscle tissues were taken for HE staining, PAS staining, TUNEL staining, Masson's trichrome staining and transmission electron microscopy. In the acute OSA model, the left atrial diameter of the dogs began to increase 3h after ventilation, and this difference was more obvious at 6h. The morphology of the myocardial cells did not change significantly, but mitochondrial swelling was observed in some atrial myocytes at 3h. In the chronic OSA model, the left atrial diameter gradually increased, the volume of the right and left atria increased, the glycogen and collagen volume fractions and apoptosis ratio were significantly increased in atrial myocytes, mitochondria swelling and lengthening occurred in some atrial myocytes, the matrix became lighter, the mitochondrial ridge density decreased and the myofilament arrangement was disordered. The disc was distorted and not continuous, and there was some cardiomyocyte necrosis. With the prolongation of apnoea, the atrium gradually enlarges, myocardial cells become disordered, glycogen aggregates, the number of necrotic cells increases, fibrosis worsens, mitochondrial abnormalities occur and the arrangement of the discs are disordered, providing a basis for the maintenance of AF.