Structural remodelling of atrial myocardium in patients with cardiac valve disease and atrial fibrillation

L. Wouters, G. S. Liu, W. Flameng, V. Thijssen, F. Thone, M. Borgers*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Objectives: To assess both qualitatively and quantitatively the structural alterations in atrial myocardium associated with cardiac valve disease with or without atrial fibrillation (AF). Patients and methods: Of 62 consecutive patients from two hospital centres who underwent surgery for mitral, tricuspid or aortic valve repair, a biopsy was obtained from the right atrial appendage. Light microscopic morphometry was carried out, and the percentage of myocytes with either myolytic or degenerative changes, the amount of connective tissue and the average cell surface area were scored. Results: Irrespective of AF, a high degree of myolysis was present in the atrial cardiomyocytes. Atrial myocytes in patients with AF were significantly larger than in patients without AF. There was a significant positive correlation between cardiomyocyte size and structural changes. Electron microscopy showed that the majority of altered cardiomyocytes displayed the structural characteristics of fetal heart cells such as a decreased amount of myofibrils, large increase in glycogen, unorganized sarcoplasmic reticulum, mitochondria of varying size and shape, and nuclei with dispersed heterochromatin. Conclusions: Atrial myocytes of patients with valvular heart disease and AF show structural changes similar to those seen in ventricular myocytes from chronic hibernating myocardium and atrial myocytes in a goat model of sustained chronic AF. These structural changes may explain the depressed contractile behaviour of the atrial myocardium during AF and the delay in recovery of contractility after cardioversion.

Original languageEnglish
Pages (from-to)158-163
Number of pages6
JournalExperimental and Clinical Cardiology
Volume5
Issue number3
Publication statusPublished - 2000

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