[Morphological features of the myocardium of the atrial appendages in patients with different forms of atrial fibrillation].

Aim: to analyze the morphological features of the myocardium of the atrial appendages in patients with different forms of atrial fibrillation (AF) and to compare the findings with the clinical parameters of patients.

Material And Methods: Light and electron microscopies were used to examine the myocardium of the atrial appendages in adult patients with paroxysmal (PAF), persistent (PrAF), or long-standing persistent atrial fibrillation (LPAF) and in comparison group patients with sinus rhythm without history of AF. A morphometric method was employed to evaluate myocardial fibrosis and to measure the diameter of cardiomyocytes (CMCs); the degree of lipomatosis and amyloidosis was semiquantitatively determined; and the content of CMC myofibrils was estimated. Atrial natriuretic peptide content in the myocytes was measured by immunoconfocal microscopy.

Results: In all groups, the patients with AF were found to have signs of atrial structural remodeling: fibrosis, lipomatosis, isolated atrial amyloidosis, CMC hypertrophy with the phenomena of a partial loss of myofibrils without significant differences between these parameters in different groups. In PAF patients, atrial remodeling was accompanied by hypertrophy of a number of CMCs with their higher myofibrilar mass; the increased CMC size in the left atrial appendage prevented left atrial enlargement; the degree of amyloidosis negatively correlated with the CMC myofibrillar loss that was recorded in the minor CMCs; the degree of CMC myolysis positively correlated with mitral valve insufficiency and left atrial enlargement. In contrast to the clinical and morphological changes that are typical of PAF, in LPAF the increase in CMC sizes was positively correlated with left atrial enlargement and mitral annular dilatation; while the myofibrillar loss phenomenon was noted in the most hypertrophied CMCs; the degree of amyloidosis was positively correlated with CMC myofibrillar loss. In the patients with PrAF, the size of CMCs did not correlate with their myofibril content.

Conclusion: The patients with PAF were ascertained to have opposite changes in the ratio of CMC hypertrophy to left atrial enlargement, amyloidosis, and CMC myofibrillar loss, hypertrophy of CMCs and their myofibril content in comparison with these indicators in LPAF.