Changes in left atrial size in patients with lone atrial fibrillation.
ABSTRACT A retrospective analysis was performed on 23 subjects with lone atrial fibrillation who were followed for an average of 6.2 years (1.1-12.8 years). In all patients, underlying organic heart disease was excluded based on history, physical exam, electrocardiogram, echocardiogram, and Doppler ultrasound interrogation. All patients had at least two echocardiographic studies during the period of observation. Atrial fibrillation was chronic in 11 subjects and paroxysmal in 12. All echocardiographic measurements were obtained by averaging the measurements of two blinded investigators. Left atrial size increased an average of 5.6 mm which translates into a 14.7% increase over the baseline measurement. This increase in size was not associated with a change in left ventricular mass or fractional shortening as determined by echocardiography. Subjects with chronic atrial fibrillation had a larger percent increase than subjects with paroxysmal atrial fibrillation (18.9 vs. 10.8%), although this relative change in size failed to reach statistical significance. The only variable which significantly contributed to the change in left atrial size was the duration of follow-up. We conclude that atrial fibrillation occurring in patients with lone atrial fibrillation may cause a slow and progressive increase in left atrial size independent of changes in left ventricular size or function.
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ABSTRACT: Our understanding of the left atrium is growing, although there are many aspects that are still poorly understood. The left atrium size as an imaging biomarker has been consistently shown to be a powerful predictor of outcomes and of different cardiovascular disorders, such as, but not limited to, atrial fibrillation, congestive heart failure, mitral regurgitation and stroke. Left atrial function has been conventionally divided into three integrated phases: reservoir, conduit and booster-pump. The highly dynamic left atrium and its response to the stretch and secretion of atrial neuropeptides leaves the left atrium far from being a simple transport chamber. The aim of this review is to provide an understanding of the left atrial physiology and its relation to disorders within the heart.International Journal of Molecular Sciences 01/2014; 15(9):15146-15160. · 2.46 Impact Factor
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ABSTRACT: Objective: Three-dimensional (3D) speckle tracking echocardiography (3DSTE) is a novel imaging modality for assessing cardiac function. We aimed to analyze left atrial (LA) function using 3DSTE in patients with atrial fibrillation (AF). Methods: 3DSTE was performed in 20 patients prior to their pulmonary vein isolation for AF. Every patient underwent a complete two-dimensional echocardiographic study at the same time. 3DSTE-derived circumferential (CS), longitudinal (LS), radial (RS), 3D (3DS), and area strain (AS) values were measured in the basal (b), mid (m), and superior (s) regions of the LA. 3DSTE-defined maximal (LAmax ) and minimal LA volumes (LAmin ) and LA total emptying fraction were calculated automatically. Eleven randomly selected age- and gender-matched healthy volunteers served as controls. Results: Patients with AF had significantly larger LAmax and LAmin and reduced LS, RS and CS.3DS and AS were significantly lower throughout the LA in cases with AF (3DS-b, -m, -s [AF patients vs. controls]: -18 ± 8% vs. -29 ± 8%, P = 0.001; -14 ± 6% vs. -22 ± 7%, P = 0.002; -10 ± 7% vs. -20 ± 9%, P = 0.002; AS-b, -m, -s [AF patients vs. controls]: 35 ± 15% vs. 52 ± 13%, P = 0.004; 50 ± 21% vs. 72 ± 19%, P = 0.009; 31 ± 21% vs. 65 ± 27%, P < 0.0001, respectively). Conclusions: 3DSTE-derived "uni-dimensional" LS, RS, CS, as well as novel strain parameters (3DS, AS) are significantly reduced in patients with AF compared to matched controls. 3DS and AS might be new strain parameters providing further insights into the alterations of LA function in patients developing AF.Echocardiography 05/2013; · 1.26 Impact Factor
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ABSTRACT: Atrial fibrillation (AF), the most common sustained 42cardiac arrhythmia encountered in clinical practice, is associated with increased morbidity and mortality. Electrophysiologically, it is characterized by a high rate of asynchronous atrial cell depolarization causing a loss of atrial contractile function and irregular ventricular rates. For a long time, AF was considered as a pure functional disorder without any structural background. Only in recent years, have new mapping and imaging techniques identified atrial locations, which are very often involved in the initiation and maintenance of this supraventricular arrhythmia (i.e. the distal portion of the pulmonary veins and the surrounding atrial myocardium). Morphological analysis of these myocardial sites has demonstrated significant structural remodeling as well as paved the way for further knowledge of AF natural history, pathogenesis, and treatment. This architectural myocardial disarrangement is induced by the arrhythmia itself and the very frequently associated cardiovascular disorders. At the same time, the structural remodeling is also capable of sustaining AF, thereby creating a sort of pathogenetic vicious circle. This review focuses on current understanding about the structural and genetic bases of AF with reference to their classification, pathogenesis, and clinical implications. Summary Atrial fibrillation (AF) is associated with significant structural remodeling affecting the atria. This architectural myocardial disarrangement is both the cause and effect of AF in a kind of pathogenetic vicious circle. This review deals with current understanding about the structural and genetic bases of AF with reference to their classification, pathogenesis, and clinical implications.Cardiovascular pathology: the official journal of the Society for Cardiovascular Pathology 01/2013; · 1.63 Impact Factor