Key result
Age- and pathology-driven histologic atrial conduction changes linked to atrial arrhythmias and varying thrombus risk.
Histologic abnormalities from aging and diverse pathologic causes play a key role in the onset of atrial fibrillation and its associated thromboembolic risk.
Aging- and disease-driven atrial remodeling may stratify AF thromboembolic risk; extends histopathologic knowledge but leaves open prospective clinical validation.
Atrial fibrillation (AF) is an arrhythmia associated with a wide variety of cardiac conditions, and it carries a risk of thromboembolism which varies with the underlying disease. The prevalence of AF increases markedly with age, and a review of histopathologic studies reveals that normal aging produces histologic changes in atrial conduction that may lead to the development of atrial arrhythmias. The diverse pathologic causes of AF also result in histologic abnormalities, and an examination of the relation of the etiology of the arrhythmia to pathologic changes suggests a possible reason for the varying risk of thrombus formation. The interaction between the histologic abnormalities and the presence of triggers of AF may also play an important role in the onset and maintenance of this common condition.
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Rodney H. Falk (1998) conducted a review in Atrial fibrillation. Histopathologic changes and aging was evaluated. Histologic changes in atrial conduction driven by normal aging and diverse pathologic causes may lead to the development of atrial arrhythmias and varying risks of thrombus formation.
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