Pathology of atrial fibrillation in man.

Abstract

Quantitative studies on the sinoatrial (SA) node and internodal tracts in IOO heartsfrom patients coming to necropsy with atrialfibrillation have been carried out. In patients with atrialfibrillation developing only in the last two weeks of life, pulmonary emboli and acute pericarditis were common precipitating factors. Atrial dilatation was common but the SA node and internodal tracts were within normal limits. In contrast patients with long-term atrial fibrillation showed combinations of nodal artery stenosis, muscle loss in the SA node or internodal tracts, and atrial dilatation. The pathological conditions found most commonly were chronic rheumatic valve disease, ischaemic heart disease, hypertension, and cor pulmonale. Atrialfibrillation in some aged patients was associated with loss of muscle fibres in the SA node without any clear pathological cause.The sinoatrial (SA) node is now universally accepted as the site of initiation of the impulse for cardiac contraction; it is also well established that specialized myogenic fibres are responsible for its inherent rhythm (HofEman and Cranefield, I960). The impulse passes to the atrioventricular node via internodaltracts within the atria (James, i96i, I963) and, while in man these tracts do not have specific histological features, there is ample physiological proof of their existence (Vassalle et al., I964).Great emphasis has always been placed on the pathophysiological basis of atrial fibrillation, both in man and animals. The morphological changes which may predispose to or accompany this arrhythmia have received considerably less attention. Clinical studies in man have shown conditions such as rheumatic valve disease to be strongly associated with atrial fibrillation (Stock, I970). Old age seems both to predispose to atrial fibrillation (Taran and Szilagyi, I958) and to mitigate against DC conversion (Waris, Kreus, and Salokannel, 197I).Though our knowledge of the pathology of atrial fibrillation is far from complete, valuable work has been carried out by Hudson (I965) who suggested that damage to the SA node was one factor. Other features described in this arrhythmia include damage to internodal pathways (James, i962), atrial dilatation (Laas, i962), and occlusion of the nodal artery Received 28 July 1971.(Lippestad and Marton, I967). It is uncertain, however, whether each of these lesions can cause arrhythmia acting singly, or in combination or, indeed, if they are invariably present in atrial fibrillation. It is also probable that in some transitory episodes of atrial fibrillation, as in digitalis therapy, purely physiological mechanisms are acting without structural damage. Materials and methodsHearts were taken from I00 patients with atrial fibrillation coming to necropsy at St. George's Hospital and The Central Middlesex Hospital, London. These patients represent a consecutive series over a one-year period. All the patients had an electrocardiogram recording atrial fibrillation during the last two weeks of life, and cases were only included when clin...

The role of arrhythmias in the progression of heart failure

“…In addition to this 'tachycardiomyopathy' occurring at ventricular level, long-standing atrial fibrillation leads to a sort of atrial cardiomyopathy. This includes ultrastructural changes [24], an increase in atrial size [25], and a decrease in atrial contractility [26] that represent the anatomical and mechanical counterparts of the remodelling process, as well as a progressive depletion of atrial natriuretic peptide leading to an 'endocrinological silence' [27] It would appear logical to apply these general concepts suggesting a potentially detrimental role of atrial fibrillation to patients with heart failure, who have already a limited cardiac reserve and a reduced exercise tolerance. In contrast with these considerations, the impact of atrial fibrillation on mortality in patients with heart failure is controversial and, actually, most recent studies suggest that atrial fibrillation carries no independent risk.…”

Atrial Amyloidosis

“…2 Increased amounts of atrial fibrosis were found in patients with AF, who also showed an activated angiotensin system. 3,4 In addition to angiotensin II-related changes, the amount of atrial fibrosis increases with patient age. 4 Another structural change commonly observed with increasing age in the heart is amyloidosis, which, like atrial fibrosis, may disturb atrial conduction.…”

“…3,4 In addition to angiotensin II-related changes, the amount of atrial fibrosis increases with patient age. 4 Another structural change commonly observed with increasing age in the heart is amyloidosis, which, like atrial fibrosis, may disturb atrial conduction. Amyloidosis represents a diverse group of diseases characterized by the presence of extracellular proteinaceous deposits showing characteristic structural and tinctorial properties.…”

The effects of aging on atrial endocardial electrograms in patients with paroxysmal atrial fibrillation

“…2 patients AF was associated with loss of muscle fibers in the sinoatrial node and its approaches without any clear pathological cause. 1 Erickson and Lev have shown degenerative changes in the conduction system with age. 10 With this histologic background in mind, changes in the electrophysiologic properties of the atrial muscle with advancing age can be expected.…”

“…Davies and Pomerance reported that AF in some aged patients was associated with loss of muscle fibers in the sinoatrial node and its approaches without any clear pathological cause. 1 Muscle loss with advancing age was found to be accompanied by an increase in fibrous tissue in both the sinoatrial node and the internodal tracts. [2][3][4] It was strongly suggested that muscle loss and increase of fibrosis in the atria is a slow but continuous process starting at about 60 years of age.…”