Ultrastructural changes in the endocardium and endocrine cardiomyocytes in the wall of the left atrial appendage in patients with atrial fibrillation

OBJECTIVE: To study ultrastructural changes in endocardial tissues and endocrine cardiomyocytes of the left atrial appendage in patients with atrial fibrillation. MATERIAL AND METHODS: Electron microscopy was used to examine the endocardium and endocrine cardiomyocytes of the left atrial appendage in 8 patients with long-standing paroxysmal and persistent atrial fibrillation and in one patient with coronary heart disease without rhythm disturbance (a control group). RESULTS: The investigation revealed that all the patients with atrial fibrillation had similar ultrastructural changes in all endocardial layers and endocrine cardiomyocytes of the left atrial appendage. The endothelium showed massive desquamation of endothelial cells. Predominantly single sharply flattened cells and small cytoplasmic fragments remained on the endocardial surface. The latter devoid of endothelial coating was represented by subendothelial loose connective tissue with noticeable signs of edema. The latter was also observed in the dense fibrous connective tissue of the endocardium. The accumulation of large amounts of edema fluid in the subendothelium led to endothelial cell flattening and desquamation. There was no leukocytic infiltration in the tissue of the endocardium or fibrin and desquamated endothelial cell accumulation on its surface. The endocrine cardiomyocytes exhibited disorders as cytoplasmic swelling, complete or partial lysis (necrosis) of individual myofibrils, and lower levels of endocrine granules and their location near or in direct contact with the sarcolemma. CONCLUSION: The study has shown that long-standing atrial fibrillation deteriorates the main factors that determine normal endothelial function: edema in subendothelial tissue disrupts its interaction with endothelial cells and leads the latter to detach from the endocardium; ultrastructural changes in the endocrine cardiomyocytes that produce hormones can impair systemic blood pressure control and intracardiac hemodynamics.