Search

Background Modeling the whole cardiac function involves the solution of several complex multi-physics and multi-scale models that are highly computationally demanding, which call for simpler yet accurate, high-performance computational tools. Despite the efforts made by several research groups, no software for whole-heart fully-coupled cardiac simulations in the scientific community has reached full maturity yet. Results In this work we present $$\texttt {life}^{\texttt {x}}$$ life x -fiber, an innovative tool for the generation of myocardial fibers based on Laplace-Dirichlet Rule-Based Methods, which are the essential building blocks for modeling the electrophysiological, mechanical and electromechanical cardiac function, from single-chamber to whole-heart simulations. $$\texttt {life}^{\texttt {x}}$$ life x -fiber is the first publicly released module for cardiac simulations based on $$\texttt {life}^{\texttt {x}}$$ life x , an open-source, high-performance Finite Element solver for multi-physics, multi-scale and multi-domain problems developed in the framework of the iHEART project, which aims at making in silico experiments easily reproducible and accessible to a wide community of users, including those with a background in medicine or bio-engineering. Conclusions The tool presented in this document is intended to provide the scientific community with a computational tool that incorporates general state of the art models and solvers for simulating the cardiac function within a high-performance framework that exposes a user- and developer-friendly interface. This report comes with an extensive technical and mathematical documentation to welcome new users to the core structure of $$\texttt {life}^{\texttt {x}}$$ life x -fiber and to provide them with a possible approach to include the generated cardiac fibers into more sophisticated computational pipelines. In the near future, more modules will be successively published either as pre-compiled binaries for systems or as open source software.

Backgrounds Alterations in the atrial structure and function associated with aging result in electric remodeling of the left atrium (LA) in patients with persistent atrial fibrillation (AF). We performed this study to evaluate the influence of age on electric remodeling as assessed by the extent of complex fractionated atrial electrograms (CFAEs) in the LA. Methods A total of 122 patients (mean age, 55.9 ± 10.4 years; range, 31‐79; 106 males) who underwent catheter ablation for drug‐refractory persistent AF were included in the study. The extent of CFAE was measured by CFAE area and its index (CFAE area/LA surface area × 100) using three‐dimensional automated software of NavX system. Results The mean value of CFAE extent was significantly different among age groups; the CFAE area decreased significantly with increasing age (30 seconds [43.2 ± 14.5 mm2] vs 40 seconds [28.6 ± 6.0 mm2] vs 50 seconds [22.8 ± 3.4 mm2] vs 60 seconds [15.3 ± 2.6 mm2] vs 70 seconds [10.3 ± 3.2 mm2]; P = .010). A similar significant decrease was observed in the CFAE area index (30 seconds [22.9 ± 7.4] vs 40 seconds [14.9 ± 3.4] vs 50 seconds [10.4 ± 1.6] vs 60 seconds [6.9 ± 1.2] vs 70 seconds [4.6 ± 1.4]; P = .002). Age had a significantly negative correlation with the CFAE area (r = −0.322, P, With increasing age, a significant reduction in complex fractionated atrial electrogram (CFAE) area reflects age‐related electric remodeling, whereas an increase in the LA size and volume reflect anatomic remodeling in patients with persistent AF.

AF is a progressive disease of the atria, involving complex mechanisms related to its initiation, maintenance and progression. Computational modelling provides a framework for integration of experimental and clinical findings, and has emerged as an essential part of mechanistic research in AF. The authors summarise recent advancements in development of multi-scale AF models and focus on the mechanistic links between alternations in atrial structure and electrophysiology with AF. Key AF mechanisms that have been explored using atrial modelling are pulmonary vein ectopy; atrial fibrosis and fibrosis distribution; atrial wall thickness heterogeneity; atrial adipose tissue infiltration; development of repolarisation alternans; cardiac ion channel mutations; and atrial stretch with mechano-electrical feedback. They review modelling approaches that capture variability at the cohort level and provide cohort-specific mechanistic insights. The authors conclude with a summary of future perspectives, as envisioned for the contributions of atrial modelling in the mechanistic understanding of AF.

Contains fulltext : 249141.pdf (Publisher’s version ) (Closed access) Whilst the athlete's heart has been extensively described, less work has focused on the potential for elite athletes to demonstrate further cardiac remodelling upon an increase in training volume. Moreover, little work explored potential side-specific cardiac remodelling. Therefore, we examined the impact of an increase in training volume across 9-months in elite rowers on left- and right-sided cardiac structure, function and mechanics (i. e. longitudinal, radial and circumferential strain, twist and strain-volume loops). As part of the preparations to the 2012 Olympic Games, twenty-seven elite rowers (26.4±3.7years, 19 male) underwent echocardiography prior to and post (9 months) an increase in training volume (24 to 30-35 h weekly). Training increased left ventricular structure, including wall thickness, diameter, volume, mass and LV twist (all p0.05). The 9-month intervention showed no change in right ventricular/atrial structure, function or mechanics (all p>0.05). In conclusion, our data revealed that 9-month increased training volume in elite rowers induced left-sided (but not right-sided) structural remodelling, concomitant with an increase in left ventricular twist, with some changes larger in women. 01 februari 2022

Due to complex 3D human atrial structure, atrial fibrillation (AF) mapping with multielectrode arrays (MEA) mostly represents surface activation. Therefore, MEA may not properly visualize patient specific AF mechanisms, which impairs ablation outcomes. Conversely, near-infrared optical mapping (NIOM) visualizes subsurface intramural activation and can efficiently reveal reentrant drivers responsible for AF maintenance. Delay between surface activation seen by MEA electrograms (EGMs) vs subsurface activation seen by NIOM optical action potentials (OAPs) occurs due to dyssynchrony between myocardium layers, especially during AF. Coronary perfused explanted human atria (n=7) were mapped with NIOM (0.3-0.9mm 2 resolution) and 64-electrode MEA (3mm 2 resolution). Unipolar EGMs were analyzed for the steepest negative deflection. The delay between [-dV/dtmax] of unipolar EGMs and corresponding optical action potentials (OAPs) was compared in 500ms and 300ms pacing and AF. Subsequent structural analysis was done by 9.4T MRI (154-180μm 3 resolution) with gadolinium enhancement and histology. Delay between EGM and OAP local activation times rate-dependently and heterogeneously increased from 6±3 ms and 10±4 ms during 500ms and 300ms pacing to 15±11 ms (with maximum delay 47±18 ms) during pacing induced AF (average cycle length 124±65ms). Large local OAP-EGM delay, seen during AF, correlates with higher fibrosis percentage and fiber twist (p

BACKGROUND On the base of traditional modeling with high-frequency atrial pacing, insertable cardiac monitor is innovatively used to track the incidence of atrial fibrillation (AF), to observe the efficiency and safety of establishment in AF model. MATERIAL AND METHODS Twelve adult beagle dogs were randomly divided into a blank control group and an AF model group. The thinnest available bipolar solid electrode lead-3830 was implanted in AF group, connected to AF pacemaker to establish a high-frequency atrial pacing model by AOO pacing mode, and the occurrence of AF was tracked in real time by an insertable cardiac monitor Reveal LINQ. The areas of the left and the right atrium were measured by echocardiography. In addition, the morphology of left atrial tissues was observed using light and electron microscopes. RESULTS The insertable cardiac monitor Reveal LINQ sensitively, conveniently, accurately, efficiently, and dynamically recorded the AF load in AF group. After the successfully establishment of the AF mode, the area of the left atrium and right atrium were significantly enlarged compared with that before modeling by echocardiography. Furthermore, the area of the left atrium and right atrium in the AF group were larger than that in the control group. The morphological observation of the left atrium tissues in both groups prompted the reconstruction of the atrial structure in dogs in the AF group. CONCLUSIONS The application of insertable cardiac monitor Reveal LINQ improves the efficiency of monitoring the AF load, with high sensitivity, convenience, and accuracy.

Background Structural remodeling of human atria plays a key role in sustaining atrial fibrillation ( AF ), but insufficient quantitative analysis of human atrial structure impedes the treatment of AF . We aimed to develop a novel 3‐dimensional (3D) structural and computational simulation analysis tool that could reveal the structural contributors to human reentrant AF drivers. Methods and Results High‐resolution panoramic epicardial optical mapping of the coronary‐perfused explanted intact human atria (63‐year‐old woman, chronic hypertension, heart weight 608 g) was conducted during sinus rhythm and sustained AF maintained by spatially stable reentrant AF drivers in the left and right atrium. The whole atria (107×61×85 mm 3 ) were then imaged with contrast‐enhancement MRI (9.4 T, 180×180×360‐μm 3 resolution). The entire 3D human atria were analyzed for wall thickness (0.4–11.7 mm), myofiber orientations, and transmural fibrosis (36.9% subendocardium; 14.2% midwall; 3.4% subepicardium). The 3D computational analysis revealed that a specific combination of wall thickness and fibrosis ranges were primarily present in the optically defined AF driver regions versus nondriver tissue. Finally, a 3D human heart–specific atrial computer model was developed by integrating 3D structural and functional mapping data to test AF induction, maintenance, and ablation strategies. This 3D model reproduced the optically defined reentrant AF drivers, which were uninducible when fibrosis and myofiber anisotropy were removed from the model. Conclusions Our novel 3D computational high‐resolution framework may be used to quantitatively analyze structural substrates, such as wall thickness, myofiber orientation, and fibrosis, underlying localized AF drivers, and aid the development of new patient‐specific treatments.

Atrial fibrillation (AF) is prevalent in aging populations; however not all individuals age at the same rate. Instead, individuals of the same chronological age can vary in health status from fit to frail. Our objective was to determine the impacts of age and frailty on atrial function and arrhythmogenesis in mice using a frailty index (FI). Aged mice were more frail and demonstrated longer lasting AF compared to young mice. Consistent with this, aged mice showed longer P wave duration and PR intervals; however, both parameters showed substantial variability suggesting differences in health status among mice of similar chronological age. In agreement with this, P wave duration and PR interval were highly correlated with FI score. High resolution optical mapping of the atria demonstrated reduced conduction velocity and action potential duration in aged hearts that were also graded by FI score. Furthermore, aged mice had increased interstitial fibrosis along with changes in regulators of extracellular matrix remodelling, which also correlated with frailty. These experiments demonstrate that aging results in changes in atrial structure and function that create a substrate for atrial arrhythmias. Importantly, these changes were heterogeneous due to differences in health status, which could be identified using an FI.

Atrial structure plays an important role in the mechanisms of atrial disease. However, detailed imaging of human atria remains limited due to many imaging modalities lacking sufficient resolution. We propose the use of optical coherence tomography (OCT), which has micrometer resolution and millimeter-scale imaging depth well-suited for the atria, combined with image stitching algorithms, to develop large, detailed atria image maps. Human atria samples (n = 7) were obtained under approved protocols from the National Disease Research Interchange (NDRI). One right atria sample was imaged using an ultrahigh-resolution spectral domain OCT system, with 5.52 and 2.72 μm lateral and axial resolution in air, respectively, and 1.78 mm imaging depth. Six left atria and five pulmonary vein samples were imaged using the spectral domain OCT system, Telesto I (Thorlabs GmbH, Germany) with 15 and 6.5 μm lateral and axial resolution in air, respectively, and 2.51 mm imaging depth. Overlapping image volumes were obtained from areas of the human left and right atria and the pulmonary veins. Regions of collagen, adipose, and myocardium could be identified within the OCT images. Image stitching was applied to generate fields of view with side dimensions up to about 3 cm. This study established steps towards mapping large regions of the human atria and pulmonary veins in high resolution using OCT.

Atrial Function After Persistent AF AblationIntroduction The atrial outcome after extensive ablation is unknown. We sought to quantify atrial structure and function years after successful ablation for persistent atrial fibrillation (PsAF). Methods and Results We studied after 80 ± 15 months 26 patients (54 ± 8 years, 1 woman) with PsAF successfully treated by ablation (2.2 ± 0.7 stepwise approach procedures, cumulative RF duration 126 ± 37 minutes). At follow-up atrial scar burden and atrial outflows were quantified using delayed–enhanced and velocity-encoded MRI, respectively. Cine imaging was used to quantify atrial conduit function (CF), active emptying fraction (AEF), expansion index (EI), and the inter-appendage mechanical activation delay. Patients underwent exercise testing at baseline and follow-up. LA and RA scar extent were 29 ± 6 and 4.3 ± 2.8%, respectively. LA and RA AEF were 10.0 ± 5.3 and 30 ± 8%. Mean inter-appendage delay was 83 ± 47 ms [42–217]. Complete LAA isolation was found in 3 patients. A wave was absent in 9/26 patients. LA scar extent related to the number of procedures (R = 0.58, P = 0.002) and total RF duration (R = 0.56, P = 0.003). Among follow-up characteristics, LA scar extent related to LAAEF (R = −0.73, P < 0.0001), LAEI (R = −0.64, P = 0.0003), A-wave peak (R = −0.72, P < 0.0001), and inter-appendage mechanical delay (R = 0.47, P = 0.02). At multivariable analysis, LA scar extent was independently related to LAAEF and LAEI. LAAEF and LA scar extent correlated with exercise capacity at follow-up (R = 0.44, P = 0.02, and R = −0.40; P = 0.04). Conclusion LA contractility and compliance are markedly impaired years after successful PsAF ablation. LA dysfunction is closely related to scar burden.

The initiation and perpetuation of atrial fibrillation (AF) can be regarded as a complication of a progressive transformation of atrial structure and function. This transformation is the result of complex changes at the molecular, cellular and organ levels, leading to the profibrillation arrhythmic mechanisms in AF. Numerous individual and environmental factors are probably involved in this process. Therefore, progress in the diagnosis, prevention and treatment of AF requires highly integrative research from the benchtop to bedside and from specific signaling pathways and electrophysiological mechanisms to population-based studies. The European Network for Translational Research in Atrial Fibrillation was formed to provide this variety of expertise and has identified central research objectives for improvements in AF prevention and therapy.

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. (Cardiol J 2011; 18, 6: 625-631)

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. It can occur at any age, however, it becomes extremely common in the elderly, with a prevalence approaching more than 20% in patients older than 85 years. AF is associated with a wide range of cardiac and extra-cardiac complications and thereby contributes significantly to morbidity and mortality. Present therapeutic approaches to AF have major limitations, which have inspired substantial efforts to improve our understanding of the mechanisms underlying AF, with the premise that improved knowledge will lead to innovative and improved therapeutic approaches. Our understanding of AF pathophysiology has advanced significantly over the past 10 to 15 years through an increased awareness of the role of "atrial remodeling". Any persistent change in atrial structure or function constitutes atrial remodeling. Both rapid ectopic firing and reentry can maintain AF. Atrial remodeling has the potential to increase the likelihood of ectopic or reentrant activity through a multitude of potential mechanisms. The present paper reviews the main novel results on atrial tachycardia-induced electrical, structural and contractile remodeling focusing on the underlying pathophysiological and molecular basis of their occurrence. Special attention is paid to novel strategies and targets with therapeutic significance for atrial fibrillation.

Atrial structures are important in the current era of cardiac interventions using percutaneous transcatheter procedures. Understanding their locations and component parts helps to reduce risks of procedural-related damage. The general arrangement of the myofibers that make up the atrial walls is reviewed to provide a morphologic basis for atrial conduction and potential substrates of arrhythmias. The right atrium, dominated by its appendage, is characterized by having an extensive array of pectinate muscles. These extend almost perpendicularly from the terminal crest. The left atrium has relatively smooth walls and a small tubular-shaped appendage. The myofibers show changes in orientations when traced through the thickness of the walls. Extensions of atrial myocardium onto the pulmonary veins and the superior caval vein are common. Apart from Bachmann's bundle, there are other muscular bridges of variable numbers and sizes that provide interatrial connections, connections between the left atrium and the coronary sinus, and connections between the muscular sleeves of the right pulmonary veins and the right atrium. The purpose of this review is to summarize the three-dimensional arrangement of gross atrial structures, the myoarchitecture and variations in muscular interatrial connections. These are important features in intra- and interatrial conduction.

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. It can occur at any age but is very rare in children and becomes extremely common in the elderly, with a prevalence approaching 20% in patients >85 years of age.1 AF is associated with a wide range of potential complications and contributes significantly to population morbidity and mortality. Present therapeutic approaches to AF have major limitations, including limited efficacy and significant adverse effect liability. These limitations have inspired substantial efforts to improve our understanding of the mechanisms underlying AF, with the premise that improved mechanistic insights will lead to innovative and improved therapeutic approaches.2 Our understanding of AF pathophysiology has advanced significantly over the past 10 to 15 years through an increased awareness of the role of “atrial remodeling.” Any persistent change in atrial structure or function constitutes atrial remodeling. Many forms of atrial remodeling promote the occurrence or maintenance of AF by acting on the fundamental arrhythmia mechanisms illustrated in Figure 1. Both rapid ectopic firing and reentry can maintain AF. Reentry requires a suitable vulnerable substrate, as well as a trigger that acts on the substrate to initiate reentry. Ectopic firing contributes to reentry by providing triggers for reentry induction. Atrial remodeling has the potential to increase the likelihood of ectopic or reentrant activity through a multitude of potential mechanisms. This article reviews the types of atrial remodeling, their underlying pathophysiology, the molecular basis of their occurrence, and finally, their potential therapeutic significance. Figure 1. General schema representing AF mechanisms and the role of remodeling. The mechanisms underlying AF are portrayed schematically in Figure 2. AF can be maintained by rapid focal firing, which may itself be regular but result in fibrillatory activity because of wave breakup in portions of the atrium that …

Studies from our laboratory and others indicate that, in addition to its purported atherothrombotic effects, hyperhomocysteinaemia (Hhe) is a powerful stimulus for ventricular remodelling, dysfunction and clinical heart failure. Because changes in atrial structure and function can impact on cardiac function in progressive ventricular remodelling and dysfunction, we conducted experiments to examine structural and functional remodelling of the atria in the hyperhomocysteinaemic hypertensive rat, a previously described model of ventricular diastolic dysfunction. Atrial muscle preparations were isolated from hearts of spontaneously hypertensive rats that were fed control, intermediate Hhe-inducing or severe Hhe-inducing diet for 10 weeks. Atrial developed tension, +dT/dt(max) and -dT/dt(max) were found to increase in parallel with levels of Hhe and ventricular diastolic dysfunction. Post-rest developed tension and the maximum developed tension observed in the presence of isoproterenol were also increased significantly in both Hhe groups compared with control. These results indicate that Hhe increases both basal and maximal contractile function in atrial muscle. Atrial structural remodelling was characterized by increased interstitial fibrosis in both Hhe groups. These data suggest that Hhe-associated changes in atrial structure and function may act to maintain ventricular filling in Hhe-induced diastolic dysfunction.

Aims The aim of this study was to establish the degree of structural and functional adaptations in the left (LA) and right atria (RA) in elite male athletes engaged in ‘high dynamic : high static’ (HDHS) and ‘low dynamic : high static’ (LDHS) sporting disciplines compared with sedentary controls.\ud Methods and results Eighteen male, elite HDHS athletes (13 boxers and 7 triathletes), 18 male, elite LDHS athletes (8 weightlifters and 10 Akido), and 20 male, age-matched sedentary controls were assessed using conventional 2D and myocardial speckle tracking (MST) echocardiography. Absolute LA and RA volumes [end systole (VOLes), pre A (VOLpreA), and end diastole (VOLed)] as well as the functional indices of reservoir (RESvol), conduit (CONvol), and booster volumes (BOOvol) were defined. MST allowed the assessment of atrial strain (ε) during the reservoir (RESε), conduit (CONε), and booster (BOOε) phases of the cardiac cycle. Both LA and RA sizes were significantly larger in HDHS compared with LDHS and controls (P < 0.05) across all structural and functional volume parameters with no significant difference between LDHS and controls (LAVOLes 35 ± 8, 26 ± 10, and 23 ± 5 mL/m2; RAVOLes 37 ± 10, 26 ± 9, and 23 ± 5 mL/m2, LARESvol 35 ± 9, 25 ± 11, and 23 ± 7 mL; RARESvol 41 ± 11, 34 ± 11, and 28 ± 7 mL for HDHS, LDHS, and controls, respectively). RA : LA ratios were >1 in all groups due to a comparatively larger RA volume (RAVOLes : LAVOLes 1.05 ± 0.26, 1.12 ± 0.55, and 1.04 ± 0.28 for HDHS, LDHS, and controls, respectively, P > 0.05). There was no significant between group differences for any ε parameter.\ud Conclusion Bi-atrial hypertrophy is demonstrated in HDHS athletes and not in LDHS athletes, suggesting that the dynamic component to training is the primary driver for both LA and RA adaptation. Although functional data derived from volume shifts suggest augmented function in HDHS athletes, MST imaging demonstrated no difference in intrinsic atrial ε in any of the groups.

Background— It is unknown how atrial fibrillation (AF) is actually initiated by triggers. Based on consistencies in atrial structure and function in individual patients between episodes of AF, we hypothesized that human AF initiates when triggers interact with deterministic properties of the atria and may engage organized mechanisms. Methods and Results— In 31 patients with AF, we mapped AF initiation after spontaneous triggers or programmed stimulation. We used 64-pole basket catheters to measure regional dynamic conduction slowing and to create biatrial activation maps during transitions to AF. Sixty-two AF initiations were recorded (spontaneous, n=28; induced, n=34). Notably, AF did not initiate by disorganized mechanisms, but by either a dominant reentrant spiral wave (76%) or a repetitive focal driver. Both mechanisms were located 21±17 mm from their triggers. AF-initiating spirals formed at the site showing the greatest rate-dependent slowing in each patient. Accordingly, in 10 of 12 patients with multiple observed AF episodes, AF initiated using spatially conserved mechanisms despite diverse triggers. Conclusions— Human AF initiates from triggers by organized rather than disorganized mechanisms, either via spiral wave re-entry at sites of dynamic conduction slowing or via repetitive focal drivers. The finding that diverse triggers initiate AF at predictable, spatially conserved functional sites in each individual provides a novel deterministic paradigm for AF with therapeutic implications.

Mestrado em Tecnologia de Diagnóstico e Intervenção Cardiovascular - Área de especialização: Intervenção Cardiovascular. Introdução - Os resultados favoráveis da oclusão percutânea do apêndice auricular esquerdo (AAE) na prevenção de fenómenos tromboembólicos em doentes com fibrilhação auricular não-valvular, conduziram a um aumento da utilização desta técnica. Contudo, desconhecem-se os efeitos a longo prazo da oclusão do AAE na estrutura, função mecânica e função endócrina da aurícula esquerda (AE). Objetivo - Descrever e caracterizar o efeito da oclusão percutânea do AAE na estrutura, função mecânica e função endócrina auricular esquerda, avaliada por técnicas ecocardiográficas e doseamento sanguíneo, em modelo experimental animal, até aos 90 dias de seguimento após procedimento de oclusão, comparativamente com grupo de controlo. Metodologia – Estudo verdadeiro experimental com grupo experimental (Ge) e grupo de controlo (Gc). Dez modelos (suíno comum) foram divididos aleatoriamente em Ge (n=5) e Gc (n=5). No Ge foi realizada oclusão percutânea do AAE com dispositivo Watchman® Foi realizada avaliação da função auricular por ecocardiografia transtorácica (ETT) no momento basal (MB), e seguimento a 90 dias (S90d) e colhidas amostras biológicas de sangue e urina no MB, e seguimento a 10, 45 e 90 dias. A estrutura e função mecânica da AE foram avaliadas através das dimensões da AE, Doppler pulsado do fluxo transmitral e das veias pulmonares, Doppler tecidular do anel mitral e deformação auricular por speckle tracking. Nas amostras biológicas foram avaliadas as concentrações de PNA, marcadores da função renal, sódio e lípidos. A análise estatística foi realizada através de testes de comparação de valores médios em cada momento de contacto e da variação basal-S90d (Δb-S90). Resultados – Foi excluído 1 dos modelos do Gc e 4 modelos do Ge sobreviveram até S90d. Verificou-se um aumento do volume auricular máximo e mínimo no Ge com diferença estatisticamente significativa na Δb-S90d, p=0,035 e p=0,05, mas sem diferenças nos volumes de ejeção e fração de ejeção auricular. A velocidade de pico da onda a` do Doppler tecidular do anel mitral mostrou-se diminuída no Ge, com tendência para diferença estatisticamente significativa na comparação Δb-S90d (p=0,134). No Doppler pulsado das veias pulmonares, verificou-se diminuição da velocidade da onda Sp no Ge com diferença estatisticamente significativa na Δb-S90d (p=0,029). No entanto as diferenças encontradas não tiveram reflexo na função ventricular esquerda, com manutenção das pressões de enchimento e sem sinais de disfunção sistólica ou diastólica. A deformação miocárdica auricular não mostrou diferenças entre os grupos. A concentração de PNA no sangue periférico no Ge foi tendencialmente superior no S90d não tendo a Δb-S90d apresentado diferença estatisticamente significativa entre os grupos. A função renal não sofreu alterações com a oclusão do AAE, com manutenção do valor de creatinina e cistatina-C. Não se verificou natriurese associada a oclusão do AAE em condições basais ou após expansão de volume e saturação com cloreto de sódio hipertónico. Conclusão – Este estudo parece fornecer evidência inicial que a oclusão percutânea do AAE pode não causar efeito negativo na estrutura auricular, tendo-se verificado ligeiro aumento do volume sem impacto clinico. A oclusão do AAE também não causou prejuízo na função renal, sugerindo que a oclusão do AAE não conduz a remodelling auricular adverso, nem a alterações na função mecânica e endócrina. ABSTRACT - Introduction - Favorable results with the occlusion of the left atrial appendage (LAA) using percutaneous devices for the prevention of thromboembolic events in patients with non-valvular atrial fibrillation, has lead to a widespread use of this technique. However, the long-term effects on left atrial (LA) structure, mechanical and endocrine function are unclear. Objective – Describe and characterize the effect of percutaneous closure of the LAA in structure, and left atrial mechanical function endocrine function, evaluated by echocardiographic techniques and blood samples evaluation, in experimental animal model, up to 90 days follow-up procedure after occlusion compared with control group. Methodology - True experimental study with experimental group (Ge) and control group (Gc). Ten models (common pig) were randomly assigned to Ge (n=5) and Gc (n=5). In Ge was performed percutaneous closure of the LAA with Watchman® device Evaluation of atrial function was performed by transthoracic echocardiography (TTE) at baseline (MB), and follow-up at 90 days (S90d) and biological samples of blood and urine collected in MB, 10, 45 and 90 days. The structure and mechanical function of AE were evaluated through the dimensions of AE, pulsed Doppler of transmitral flow and pulmonary veins, tissue Doppler imaging of mitral annular motion LA deformation by speckle tracking. In biological samples were evaluated concentrations of ANP, renal function parameters, sodium and lipids. Statistical analysis was performed using comparison tests of mean values at each point of contact and variation of baseline-S90d (Δb-S90). Results - One model of Gc was excluded and 4 models of the Ge survived 4 until S90d. There was an increase in the maximum and minimum atrial volume in Ge with a statistically significant difference in Δb-S90d, p=0.035 and p=0.05, but with no differences in ejection volumes and ejection fraction. The peak velocity of tissue Doppler a` wave was decreased in Ge, with a trend toward statistically significant difference in comparison S90d-Δb (p=0.134). In pulsed Doppler of pulmonary veins, the Sp wave velocity decreased in Ge with statistically significant difference Δb-S90d (p=0.029). However the differences were not reflected in left ventricular function, with maintenance of filling pressures and no signs of systolic or diastolic dysfunction. The atrial myocardial deformation showed no differences between groups. The concentration of ANP in peripheral blood in Ge was tendentiously higher in S90d with no Δb-S90d statistically significant difference between groups. Renal function did not change with occlusion of the LAA, with maintenance of creatinine and cystatin-C. There was no natriuresis associated with occlusion of the LAA in basal conditions or after volume expansion and saturation with hypertonic sodium chloride. Conclusion - This study provids initial evidence that the percutaneous LAA occlusion may cause no negative effect on atrial structure Was found a slight increase in atrial volume without clinical impact. The occlusion of the LAA did also not impair renal function, suggesting that the LAA occlusion does not lead to adverse atrial remodeling, or changes in mechanical or endocrine function.

Objective:Several allometric methods for indexing cardiac structures to body size have been proposed but the optimal way for normalization of cardiac structures is still controversial. We aimed to estimate the allometric exponents that best describe the relationships between cardiac dimensions and b

Atrial fibrillation is the most common arrhythmia syndrome in the U.S., affecting over 3 million people ([1,2][1]). Most cases are sporadic, and risk factors include increasing age, hypertension, cardiomyopathies of ischemic or nonischemic origin, and valve diseases that alter atrial structure and

We read with great interest the imaging vignette by Gurudevan et al. ([1][1]), presenting 3 patients in whom a thrombus was seen adherent to the septal left atrium (LA), potentially attributed to a recently described novel atrial structure, the left atrial septal pouch (LASP). Krishnan et al. ([2][2