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[Pathology of atrial fibrillation]
1Department of Internal Medicine, Juntendo University School of Medicine, Tokyo.
Insights
Atrial fibrillation may stem from reentry within residual atrial muscle bundles, not sinoatrial node cell loss. Pathological changes like fibrosis and fatty metamorphosis in myocytes suggest this mechanism.
Area of Science:
- Cardiology
- Pathology
- Electrophysiology
Context:
- Atrial fibrillation (AF) is a common arrhythmia linked to heart disease and systemic disorders.
- The precise pathological basis of AF remains unclear, though anatomical substrates are increasingly recognized.
- Age-related myocardial changes are common, necessitating differentiation from disease-specific alterations.
Purpose:
- To investigate the pathological myocardial changes associated with long-term atrial fibrillation.
- To compare sinoatrial node cellularity in AF patients versus age-matched controls.
- To identify potential anatomical substrates for AF reentry mechanisms.
Summary:
- Quantitative histological analysis showed no significant difference in sinoatrial node cell reduction between AF patients and controls.
- Pathological findings in AF patients included depletion of muscular bundles, fibrosis, and fatty metamorphosis of atrial myocytes.
- These changes suggest that AF may be caused by reentry within remaining atrial muscular bundles, particularly circumferential ones in the right atrium.
Impact:
- Provides insights into the pathophysiology of atrial fibrillation, moving beyond sinoatrial node dysfunction.
- Highlights the role of atrial myocardial structural changes in AF development.
- Suggests potential targets for therapeutic interventions aimed at disrupting reentry pathways in AF.
Abstract:
Atrial fibrillation is one of the most common arrhythmias which is associated with various organic heart diseases or systemic disorders. Although a pathological basis for atrial fibrillation has not been clarified, an anatomical substrate corresponding to long-term atrial fibrillation has been recently demonstrated. Age-related changes of the atrial myocardium were frequently observed in healthy people. Quantitative histological study of the sinoatrial node revealed no difference in the reduction of the nodal cells between 12 patients with atrial fibrillation and 21 age-matched controls. The pathological findings of the myocardium including atrial preferential pathways in patients with long-term atrial fibrillation showed depletion of the muscular bundles, fibrosis and fatty metamorphosis of the atrial myocytes. These findings suggest that atrial fibrillation might be related to reentry in the residual muscular bundles including circumferential muscular bundles in the right atrium.