BACKGROUND: Left atrial (LA) appendage closure (LAAC) is effective in patients with atrial fibrillation who are not candidates for long-term anticoagulation. However, the impact of LAAC on LA function is unknown. The aim of this study is to evaluate the impact of LAAC on atrial function.
METHODS: This meta-analysis was conducted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. A search strategy was designed to utilize PubMed/Medline, EMBASE, and Google scholar for studies showing the effect of LAAC on the LA function from inception to November 20, 2021. The standardized mean difference (SMD) was calculated from the means and standard deviations.
RESULTS: Of 247 studies initially identified, 8 studies comprising 260 patients were included in the final analysis. There was a significant increase in LA emptying fraction following LAAC compared with preoperative function (SMD: 0.53; 95% confidence interval [CI]: 0.04-1.01; p = .03; I2  = 75%). In contrast, there were no significant differences in LA volume (SMD: -0.07; 95% CI: -0.82-0.69; p = .86; I2  = 92%) peak atrial longitudinal strain (SMD: 0.50; 95% CI: -0.08-1.08; p = .09; I2  = 89%), peak atrial contraction strain (SMD: 0.38; 95% CI: -0.22-0.99; p = .21; I2  = 81%), strain during atrial contraction (SMD: -0.24; 95% CI: -0.61-0.13; p = .20; I2  = 0%), strain during ventricular systole (SMD: 0.47; 95% CI: -0.32-1.27; p = .24; I2  = 89%), strain during ventricular diastole (SMD: 0.09; 95% CI: -0.32-0.51; p = .66; I2  = 65%).
CONCLUSIONS: LAAC is associated with improvement in the left atrial emptying fraction, but did not significantly influence other parameters.

Atrial dysfunction has been widely considered a marker or consequence of other cardiac conditions rather than the cause itself. Here, we propose the term atrial failure as a clinically relevant entity, defined as any atrial dysfunction causing impaired heart performance, symptoms, and worsening quality of life or life expectancy. Aspects of the etiology, mechanisms, and consequences of atrial failure are discussed. Recent advances in cardiac electrophysiology and imaging have improved our understanding of the highly complex atrial anatomy and function, underlying the paramount importance of the atria in optimal heart performance. It is time to reappraise the concept of the failing atrium as a primary cause or aggravating factor of the symptoms in many of our patients. The concept of atrial failure may foster basic and translational research to gain a better understanding of how to identify and manage atrial dysfunction.

Intra-ventricular flow dynamics has recently emerged as an important evaluation and diagnosis tool in different cardiovascular conditions. The formation of vortex pattern during the cardiac cycle has been suggested to play important epigenetic and energy-modulation roles in cardiac remodelling, adaptations and mal-adaptations. In this new perspective, flow alterations due to different cardiovascular procedures can affect the long-term outcome of those procedures. Especially, repairs and replacements performed on atrioventricular valves are likely to exert direct impact on intra-ventricular flow pattern. In this review, current consensus around the roles of vortex dynamics in cardiac function is discussed. An overview of physiological vortex patterns found in healthy left and right ventricles as well as post-operative ventricular flow phenomenon owing to different atrioventricular valvular procedures are reviewed, followed by the summary of different vortex identification schemes used to characterise intraventricular flow. This paper also emphasises on future research directions towards a comprehensive understanding of intra-cardiac flow and its clinical relevance. The knowledge could encourage more effective pre-operative planning and better outcomes for current clinical practices.

Recent advances in the assessment of myocardial function have facilitated the direct measurement of atrial function using speckle-tracking echocardiography. Currently, normal reference ranges for atrial function using speckle-tracking echocardiography are based on a few initial studies, with variations among modestly sized (n = 100-350) studies.
The authors searched the PubMed, Embase, and Scopus databases for the key terms \"left atrial/atrial/atrium\" and \"strain/function/deformation/stiffness\" and \"speckle tracking/Velocity Vector Imaging/edge tracking.\" Studies of global left atrial function using speckle-tracking were selected if they involved >30 normal or healthy participants without any cardiac risk factors. Normal ranges for reservoir strain, conduit strain, and contractile strain were computed using a random-effects model. Meta-regression and subgroup analysis was performed to explore between-study heterogeneity.
Forty studies (2,542 healthy subjects) satisfied the inclusion criteria. Meta-analysis revealed a normal reference range for reservoir strain of 39% (95% CI, 38%-41%, from 40 articles), for conduit strain of 23% (95% CI, 21%-25%, from 14 articles), and for contractile strain of 17% (95% CI, 16%-19%, from 18 articles). Meta-regression identified heart rate (P = .02) and body surface area (P = .003) as contributors to this heterogeneity. Subgroup analyses revealed heterogeneity due to sample size (n > 100 vs N < 100, P = .02).
The normal reference ranges for the three components of left atrial function are demonstrated. The between-study heterogeneity is explained partly by heart rate, body surface area, and sample size.

Atrial fibrillation (AF) is the most common arrhythmia in the world. Despite the large number of studies focused on the causes and mechanisms of AF, it remains a clinical challenge. Atrial electrical and structural remodelling caused by AF is responsible for the perpetuation of the arrhythmia. However, a validated noninvasive method for assessment of atrial fibrosis in clinical practice is lacking. In this review, we aim to present an update about the origins and mechanisms of atrial remodelling, particularly focusing on atrial fibrosis, and compare imaging techniques that can detect atrial changes and greatly contribute to the clinical management of patients with AF.

Atrial remodeling is a term introduced in 1995 to describe alterations in atrial structure or function. Atrial electrical remodeling is characterized by a reduction of refractory period and action potential duration, dispersion in refractoriness, and a reduction in conduction velocity of impulse propagation. Numerous animal and human studies have demonstrated that atrial electrical remodeling impairs normal atrial conduction and provides an environment for ectopic and re-entrant activity, thus creating a substrate for the initiation or maintenance of atrial fibrillation. Interestingly, atrial electrical remodeling has been shown to be reversible. In this systematic review, we examine the occurrence of reverse atrial electrical remodeling in various clinical settings.

We report the case of a 47-year-old white man who presented with 1-year history of palpitations while swallowing. Event monitor confirmed the episodes were atrial tachycardia. Medical management with a calcium channel blocker did not alleviate the patient\'s symptoms. Gastrointestinal endoscopy did not reveal any abnormality. Electrophysiologic study was performed to identify and map the tachycardia. Swallowing during the procedure was used to repeatedly induce the tachycardia. A focal right atrial tachycardia that was mapped to the lower posterior right atrium was successfully ablated. Follow-up at 6 months and 1 year showed complete resolution of symptoms. An in-depth review of the literature and all published case reports of swallowing-induced atrial tachycardia is presented, and possible mechanisms of this rare form of tachycardia are discussed.

1. There has been considerable debate whether responses mediated via beta1- and beta2-adrenoceptors (beta1ARs and beta2ARs) display the same degree of desensitization after prolonged or repeated exposure to agonists. 2. Examples are provided for selective desensitization of functional responses and loss of binding sites for beta1ARs. Equally, examples are given of selective desensitization and down-regulation involving beta2ARs. 3. This review examines whether receptor subtype-selective desensitization of betaAR-mediated responses can occur and whether even within the same subtype, there may be tissue-selective desensitization. Possible reasons why apparent selectivity of desensitization of functional responses may occur are considered and are divided into methodological and non-methodological factors. 4. Methodological factors discussed are: the concentration of agonist used for inducing desensitization and the washout times before construction of the post-incubation concentration-response curve (CRC), the need for correction of CRCs from time-matched controls, and the methods adopted for plotting CRCs. 5. Four non-methodological factors are considered. Firstly, the roles of different receptor reserves for the responses of each tissue can have an important effect on whether desensitization is apparent; a large reserve will make desensitization less likely to be apparent. Secondly, there is more than one site at which desensitization occurs; receptors are uncoupled from adenylyl cyclase activation, there is an additional site at the level of stimulation of cyclic AMP-dependent protein kinase and betaARs may ultimately be down-regulated. These processes may differ depending on the tissue and conditions and this may influence whether differential desensitization occurs between tissues. Thirdly, the apparent degree of desensitization after washout of an agonist can depend upon the rate of resensitization. Experiments to overcome this problem are described which demonstrate betaAR desensitization in the continued presence of agonist. Finally, the role of up-regulation of PDE in desensitization is discussed.

This review discusses the latest developments in the hemodynamics of mitral stenosis. English-language journal articles, reviews, and textbooks from the clinical, physiology, and engineering literature related to mitral valve stenosis were identified and reviewed. The main conclusions are: (1) the hemodynamics of mitral stenosis are determined by the complex anatomical and pathophysiologic features of the valve apparatus, (2) the properties of the left ventricle, atrium, and pulmonary vasculature also have a major impact on the hemodynamic significance and the clinical syndrome of mitral stenosis, (3) the valve and the cardiac chambers have a functional reserve that become exhausted as the stenosis worsens and/or the compensatory mechanisms of the chambers fail, and (4) a careful approach to data acquisition and analysis will lead to an accurate assessment of the hemodynamics of mitral stenosis before and after therapeutic interventions.

暂无摘要。