The Left Atrium Is a Window to the Outcomes of Patients With Atrial Fibrillation

The prevalence of atrial fibrillation (AF) is increasing, notably in elderly populations,¹ and its onset is troublesome because it can induce heart failure and stroke unless medical or interventional therapies are promptly started. Some patients with AF who remain asymptomatic can be incidentally found to have AF or unfortunately confirmed to have AF after an episode of heart failure or stroke.

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AF begets left atrial (LA) remodeling and vice versa. The prevention of ongoing remodeling is important, especially in the LA, because it is normally a compliant chamber and can operate as a ‘buffer’ for maintaining LA pressure within the normal range. When the LA becomes stiff because of advanced remodeling, the LA pressure rapidly increases during atrial filling (reservoir phase). In patients with longstanding AF, the LA enlarges and stiffens, resulting in refractory heart failure. Thus, the early recognition of AF burden on the LA is very important to improve outcomes in AF patients.

Echocardiography is the first-line imaging modality for assessing the LA structure and function. The size of the LA can be quantitatively assessed on apical 4- and 2-chamber views by the biplane Simpson method. Because the optimal plane of the LA for estimating the volume of the chamber is different from the optimal plane of the left ventricle (LV) for estimating its volume, it is necessary to obtain non-foreshortened images of both chambers. According to the ASE and EACVI guidelines for estimating the volumes of cardiac chambers by echocardiography,² the cutoff value for the maximal LA volume (LAVmax) index (i.e., LAVi) for LA dilatation is the following: LAVi >34 mL/m². the minimal LA volume (LAVmin) can also be estimated, thus enabling assessment of LA function during the reservoir phase. The LA emptying fraction (LAEF), which is a parameter of LA function during the reservoir phase, is calculated as: ([LAVmax − LAVmin] / LAVmax) × 100%.³

In this issue of the Journal, Hiasa et al present their subanalysis of data from the prospective ANFIE Registry to investigate the relationships of LA structure and function to the clinical outcomes at 2 years of 1,474 patients with AF aged ≥75 years.^4,5 They demonstrate that patients with LAEF ≤45% vs. >45% were at higher risk of cardiovascular events and hospitalization for heart failure, while the risk of all-cause death was higher in patients with LAVi >48 mL/m² vs. patients with LAVi ≤48 mL/m². It is generally accepted that the LAVi can be used as a biomarker of the chronicity of LV diastolic dysfunction. On the other hand, the occurrence of AF can promote LA dilatation irrespective of LV dysfunction. Thus, the LAVi mirrors the functional abnormalities of both the LA and LV. This current study indicates an additional value of LAEF to LAVi in predicting cardiovascular events and heart failure in elderly patients with AF.⁵ The accurate evaluation of LA function by echocardiography during AF remains challenging.⁶ In patients with irregular heartbeats due to AF, the LAEF varies for each cardiac cycle in accordance with the preceding R-R interval. Furthermore, the value of the LAEF is needed to calculate both the maximal and minimal volumes of the LA. The LA strain might be an alternative to LAEF, and it can be generated from an apical 4-chamber view.^7,8

The LA reservoir function appears to be of increasing diagnostic and prognostic utilities for the assessment of patients with heart failure.^8,9 Historically, Barbier et al demonstrated that LA reservoir function was determined by LA pump function, LV long-axis shortening and LA stiffness.¹⁰ Suga elegantly clarified using a circulatory analog model that cardiac output was determined by atrial compliance.¹¹ These findings remind us that LA reservoir function is adversely affected by LA pump failure, LV longitudinal dysfunction and LA stiffening.

After the occurrence of AF, the patient immediately loses LA pump function. In cases of an underlying LV diastolic dysfunction, the occurrence of AF could lead to the signs and symptoms of heart failure. Furthermore, AF promotes LA dilatation and stiffening, and the patient ultimately loses LA pump and reservoir functions.

Catheter ablation can successfully eliminate the burden of AF, enabling structural reverse remodeling of the LA.¹² However, in a recent study of 140 patients with AF who underwent successful catheter ablation, it was concluded that abnormal LA pump and reservoir function persisted despite normalization of the LAVi to 34 mL/m².¹² The results of this study suggested that patients with AF in whom sinus rhythm is successfully restored still have underlying substrate in the LA, and physicians should remain aware of the patient’s risk for heart failure.

Chronic AF is also problematic because it induces annular dilatation of both the mitral and tricuspid valves, which lead to mitral and tricuspid regurgitation. Echocardiographic findings of bilateral atrial dilatation are frequently observed in patients with irreversible AF. Diuretics can temporarily relieve fluid retention in these patients; however, they gradually develop bilateral heart failure that is refractory to pharmacological and interventional therapies. Despite current developments in interventional therapies such as transcather mitral or tricuspid repair, their efficacy is limited in patients with AF and advanced atrial remodeling.

The prevalence of AF undoubtedly increases with aging, leading to the development of impaired cardiac performance, and triggering cardiovascular events and heart failure (Figure). This report by Hiasa et al adds important evidence regarding the importance of structural and functional assessments of the LA for risk stratification of the outcomes in elderly patients with AF.⁵

Figure.

Possible clinical scenarios in the development of atrial fibrillation, which induces left atrial (LA) pump failure, dilatation and stiffening, as well as bilateral dilatation of the atrial annuli. Both LA and annular remodeling are associated with an increased incidence of cardiovascular events and heart failure.

References

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