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El Bloqueo Interauricular (BIA) puede servir como un valioso marcador electrocardiográfico para evaluar el riesgo del desarrollo de arritmias auriculares, y nueva aparición de fibrilación auricular (FA). El BIA se produce por un deterioro en la conducción auricular que implica un retraso en la conducción del estímulo eléctrico desde la aurícula derecha a la aurícula izquierda. Las causas probables de interrupción del haz de Bachmann incluyen isquemia, enfermedad degenerativa del envejecimiento, enfermedades infiltrativas, enfermedad coronaria difusa y afecciones inflamatorias. Los factores de riesgo para el BIA avanzado, la fibrilación auricular (FA) y el accidente cerebrovascular (ACV) parecen ser muy similares, y la patogénesis subyacente probablemente se deba a fibrosis miocárdica y remodelación auricular. El bloqueo interauricular se relaciona clínicamente a la aparición de taquiarritmias supraventriculares y está relacionado al remodelamiento auricular. Aunque el agrandamiento auricular y el BIA comparten un patrón electrocardiográfico similar, son dos entidades separadas. Sin embargo, muchos autores aún asocian una duración de la onda P mayor a 120 ms con agrandamiento de la aurícula izquierda. El remodelamiento auricular modifica la velocidad de conducción, la arquitectura cardiaca, los canales iónicos dependientes de voltaje, y los componentes de resistencia y capacitancia, como son el espacio extracelular y las uniones celulares. La alteración de estas propiedades afecta las propiedades electrofisiológicas de la conducción auricular y favorece el BIA, los trastornos auriculares y la génesis de FA.
Interatrial block (IAB) can serve as a valuable electrocardiographic marker to assess the risk of developing atrial arrhythmias, and new onset of atrial fibrillation (AF). The IAB is produced by a deterioration in atrial conduction that implies a delay in the conduction of the electrical stimulus from the right atrium to the left atrium. Probable causes of Bachmann bundle interruption include ischemia, degenerative disease of aging, infiltrative diseases, diffuse coronary disease, and inflammatory conditions. The risk factors for advanced IAB, atrial fibrillation (AF), and cerebrovascular accident (CVA) appear to be very similar, and the underlying pathogenesis is probably due to myocardial fibrosis, and atrial remodeling. The interatrial block is clinically related to the appearance of supraventricular tachyarrhythmias and is related to atrial remodeling. Although atrial enlargement and IAB share a similar electrocardiographic pattern, they are separate entities. However, many authors still associate P wave duration greater than 120 ms with left atrial enlargement. Atrial remodeling modifies conduction velocity, cardiac architecture, voltage-gated ion channels, and resistance and capacitance components, such as the extracellular space and cell junctions. The alteration of these properties affects the electrophysiological properties of atrial conduction and favors IAB, atrial disorders, and the genesis of AF.
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Abstract Objectives: The aim of the study was to investigate atrial contractile function in patients with paroxysmal atrial fibrillation (AF) in sinus rhythm using transthoracic echocardiography (EchoCG). Methods and results: Thirty-five patients with paroxysmal AF and arterial hypertension (mean age 62 ± 10 years, 43% male) in sinus rhythm were enrolled in the study. The control group was composed of comparable patients with arterial hypertension without heart rhythm disturbances. EchoCG was performed during sinus rhythm according to an extended protocol, which included the ejection fraction (EF) of the left atrium (LA) and tissue Doppler measurements. Myocardial fibrosis was assessed quantitatively by videodensitometry in intraventricular and intraatrial (IAS) septa using an original image post-processing algorithm. We found a significant decrease in the left atrial contraction function during sinus rhythm in patients with AF when compared to controls. LA EF (34 ± 14 vs. 54 ± 17, p = 0.03) and A' velocity (0.17 ± 0.04 vs. 0.22 ± 0.04, p = 0.008) decreased while A/A' ratio (2.7 ± 0.2 vs. 1.9 ± 0.1, p = 0.006) increased. Peak A velocity was not affected. Videodensitometric analysis revealed a 2.3-fold increase in IAS fibrosis fraction in AF patients compared with controls (p = 0.01). Conclusion: Patients with AF in sinus rhythm have markedly depressed atrial contractile function. Videodensitometry of IAS has the potential to be used as inexpensive method of atrial fibrosis assessment in patients with AF.
Resumen Objetivo: El objetivo del estudio fue investigar la función contráctil auricular en pacientes con fibrilación auricular paroxística (FA) en ritmo sinusal mediante una ecocardiografía transtorácica (EchoCG). Material y métodos: Treinta y cinco pacientes con FA paroxística e hipertensión arterial (edad media de 62 ± 10 años, el 43% varones) se inscribieron en el estudio en ritmo sinusal. El grupo de control estaba compuesto por pacientes comparables con hipertensión arterial sin alteraciones del ritmo cardíaco. Se realizó una ecocardiografía durante el ritmo sinusal, según el protocolo extendido, incluidas la fracción de eyección (FE) de la aurícula izquierda (AI) y las mediciones Doppler tisulares. La fibrosis miocárdica se evaluó cuantitativamente mediante una videodensitometría de los septos interventricular e interauricular (IAS) utilizando un algoritmo de posprocesamiento de imágenes originales. Resultados: Encontramos una disminución significativa en la función de contracción de la aurícula izquierda durante el ritmo sinusal en pacientes con FA en comparación con el grupo de control. Cabe destacar que la FE de la AI (34 ± 14 vs. 54 ± 17, p = 0.03) y la velocidad A' disminuyeron (0.17 ± 0.04 vs. 0.22 ± 0.04, p = 0,008) mientras que la relación A/A' aumentó (2,7 ± 0,2 vs. 1.9 ± 0.1, p = 0,006). La velocidad pico A no se vio afectada. El análisis videodensitométrico reveló que la fracción de fibrosis IAS en pacientes con FA fue 2.3 veces mayor que en el grupo de control (p = 0.01). Conclusiones: Incluso en ritmo sinusal, los pacientes con FA tienen una función contráctil auricular marcadamente deprimida. La videodensitometría de IAS tiene el potencial de utilizarse como método económico de diagnóstico de la fibrosis auricular en pacientes con FA.
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Background: Rheumatic fever principally influences kids in developing states, particularly where deficiency is common. Atrial fibrosis is a mutual characteristic of clinical atrial fibrillation (AF) and is accompanying with AF in a diversity of experiment sittings, Aim and Objectives: The current work aimed to assess whether there are any clinical or echo-cardiographic parameters that expect the existence of AF among cases with rheumatic mitral valve disorder (RMVD), Subjects and Methods: The current study was a comparative cross-sectional was conducted on 100 RMVD cases at cardio-vascular medicine department Tanta university hospitals within 6-mths starting from September 2019. Cases have been allocated into 2 groups: Group-I: 50 cases with sinus rhythm. Group-II: 50 cases with AF, Results: A significant change was found among study groups regarding Fibrosis characteristics, There is a highly significant difference between the three different types regarding mitral valve area (MVA), LA-diameter, LA volume, LA-diameter/BSA and LA volume index, Age, area of mitral valve, LA-diameter and LA volume were found to be significant predictors for AF, Conclusion: Echo-cardiography factors could recognize cases at higher danger of advancing AF among RMVD cases who may benefit from preventive measures.
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Resumo Fundamento O tecido adiposo epicárdico (TAE) tem sido associado à fibrilação atrial (FA), mas seus mecanismos fisiopatológicos permanecem obscuros. Objetivos Medir a correlação entre TAE e fibrose do átrio esquerdo (AE), e avaliar sua capacidade de prever recidiva após o isolamento da veia pulmonar (IVP). Métodos Pacientes com FA inscritos para um primeiro procedimento de IVP foram submetidos à tomografia computadorizada (TC) cardíaca e ressonância magnética cardíaca (RMC) em menos de 48 horas. Quantificou-se o TAECE em imagens de TC realçadas com contraste no nível do tronco da coronária esquerda. Quantificou-se a fibrose do AE em RMC tridimensional com realce tardio isotrópico de 1,5 mm. Após o isolamento da veia pulmonar (IVP), os pacientes foram submetidos a seguimento para checar a recidiva da FA. A significância estatística foi definida com p<0,05. Resultados A maioria dos 68 pacientes (46 homens, idade 61±12 anos) tinha FA paroxística (71%, n=48). Os pacientes apresentavam volume TAECE mediano de 2,4 cm3/m2 (intervalo interquartil [IIQ] 1,6-3,2 cm3/m2) e um volume médio de fibrose do AE de 8,9 g (IIQ 5-15 g). A correlação entre TAECE e fibrose do AE foi estatisticamente significativa, mas fraca (coeficiente de correlação de postos de Spearman = 0,40, p=0,001). Durante um seguimento médio de 22 meses (IIQ 12-31), 31 pacientes (46%) tiveram recidiva da FA. A análise multivariada produziu dois preditores independentes de recidiva da FA: TAECE (FC 2,05, IC de 95% 1,51-2,79, p<0,001) e FA não paroxística (FC 2,36, IC de 95% 1,08-5,16, p=0,031). Conclusão A correlação fraca entre TAE e AE sugere que a fibrose do AE não é o principal mecanismo que liga o TAE e a FA. O TAE mostrou-se mais fortemente associado à recidiva da FA do que à fibrose do AE, corroborando a existência de outros mediadores mais importantes do TAE e da FA.
Abstract Background Epicardial adipose tissue (EAT) has been associated with atrial fibrillation (AF), but its pathophysiological mechanisms remain unclear. Objectives To measure the correlation between EAT and left atrium (LA) fibrosis, and to assess their ability to predict relapse after pulmonary vein isolation (PVI). Methods Patients with AF enrolled for a first PVI procedure underwent both cardiac computerized tomography (CT) and cardiac magnetic resonance (CMR) imaging within less than 48 hours. EATLMwas quantified on contrast-enhanced CT images at the level of the left main. LA fibrosis was quantified on isotropic 1.5 mm 3D delayed enhancement CMR. After pulmonary vein isolation (PVI), patients were followed up for AF relapse. Statistical significance was set at p<0.05. Results Most of the 68 patients (46 men, age 61±12 years) had paroxysmal AF (71%, n=48). Patients had a median EATLMvolume of 2.4 cm3/m2(interquartile range [IQR] 1.6-3.2 cm3/m2), and a median amount of LA fibrosis of 8.9 g (IQR 5-15 g). The correlation between EATLMand LA fibrosis was statistically significant but weak (Spearman's R=0.40, p=0.001). During a median follow-up of 22 months (IQR 12-31), 31 patients (46%) had AF relapse. Multivariate analysis yielded two independent predictors of AF relapse: EATLM(HR 2.05, 95% CI 1.51-2.79, p<0.001), and non-paroxysmal AF (HR 2.36, 95% CI 1.08-5.16, p=0.031). Conclusion The weak correlation between EAT and LA suggests that LA fibrosis is not the main mechanism linking EAT and AF. EAT was more strongly associated with AF relapse than LA fibrosis, supporting the existence of other more important mediators of EAT and AF.
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Atrial fibrillation (AF) is one of the most common arrhythmias, associated with high morbidity, mortality, and healthcare costs, and it places a significant burden on both individuals and society. Anti-arrhythmic drugs are the most commonly used strategy for treating AF. However, drug therapy faces challenges because of its limited efficacy and potential side effects. Catheter ablation is widely used as an alternative treatment for AF. Nevertheless, because the mechanism of AF is not fully understood, the recurrence rate after ablation remains high. In addition, the outcomes of ablation can vary significantly between medical institutions and patients, especially for persistent AF. Therefore, the issue of which ablation strategy is optimal is still far from settled. Computational modeling has the advantages of repeatable operation, low cost, freedom from risk, and complete control, and is a useful tool for not only predicting the results of different ablation strategies on the same model but also finding optimal personalized ablation targets for clinical reference and even guidance. This review summarizes three-dimensional computational modeling simulations of catheter ablation for AF, from the early-stage attempts such as Maze III or circumferential pulmonary vein isolation to the latest advances based on personalized substrate-guided ablation. Finally, we summarize current developments and challenges and provide our perspectives and suggestions for future directions.
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Atrial fibrillation is a common cardiac arrhythmia encountered closely related to structural remodeling such as atrial fibrosis. Galectin-as a biomarker of fibrosis; therefore, it may be involved in atrial remodeling association of Gal-3 with atrial fibrillation.
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@#Objective To explore the changes of focal adhesion kinase (FAK) in the fibrotic atrium of patients with valvular atrial fibrillation and explore its downstream signaling pathways. Methods A total of 45 patients with mitral valve disease were included in this study and were divided into a valvular atrial fibrillation group (VAF, ≥6 months, 25 patients) and a sinus rhythm group (SR, 20 patients) based on having atrial fibrillation or not. The atrial appendage tissue was obtained during the operation , histopathological examination and Western blotting were performed. The degree of atrial fibrosis and changes in FAK and its downstream pathways in fibrotic myocardium were observed. Results This study revealed a higher degree of atrial fibrosis in valvular atrial fibrillation and disordered cell arrangement. Expression of fibroblast differentiation marker alpha smooth muscle actin (α-SMA) was significantly increased in atrial fibrillation, and the expression of FAK and downstream AKT/S6K pathway proteins was up-regulated, while the other signal was observed, there was no significant change in ERK1/2 signaling pathway. Conclusion Atrial fibrosis in valvular atrial fibrillation is an important feature of atrial structural remodeling. We found overproduction of collagen fibers disrupted the continuity of atrial myocytes, leading to abnormal conduction and providing a matrix environment for the development of atrial fibrillation. The expression of focal adhesion kinase and downstream AKT/S6K signaling pathway in fibrotic myocardium may be involved in the process of atrial fibrosis, providing a basis for the study of its mechanism.
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Objective:To investigate the expression of fibrillin-1 (FBN-1) in the atrium tissue of the patients with rheumatic heart valve disease complicated with atrial fibrillation(AF), and to explore its relationship with atrial fibrosis in the patients with valvular atrial fibrillation.Methods:Eighty-four consecutive patients with rheumatic heart valve disease underwent cardiac surgery were enrolled in this study.The patients were divided into AF group(n=39) and sinus rhythm group(SR group, n=45).The clinical data of patients were collected before operation.The right atrium tissue (0.3-0.5 mm3) was disserted during operation.The degrees of right atrial fibrosis of the patients in two groups were observed by Masson staining.Western blotting method was used to measure the protein expressions of FBN-1 in atrium tissue of the patients in two groups.Results:There were no significant differences in the gender ratio, age, blood pressure, blood biochemical indicators and other aspects of medical history between two groups(P>0.05);the diameters of left and right atrium of the patients in AF group were significantly larger than those in SR group(P<0.05).The Masson staining results showed that there was obvious fibrosis in AF group, and the collagen volume fraction and collagen level in AF group were significantly higher than those in SR group (P<0.05).The expression level of FBN-1 in right atrium tissue in AF group was obviously higher than that in SR group(P<0.05).The expression level of FBN-1 protein in right atrium tissue of the patients with valvular atrial fibrillation was positively correlated with the collagen level(r=0.544,P=0.021).Conclusion:There is obvious atrium fibrosis in the patients with valvular atrial fibrillation;it is closely related to the up-regulation of the expression of FBN-1 gene.
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Objective To investigate the expression of α-smooth muscle actin (α-SMA)in patients with valvular atrial fibrillation and study the relationship betweenα-SMA and atrial fibrosis in patients with valvular atrial fibrillation (AF).Methods For this study we enrolled 84 consecutive patients with rheumatic heart disease who were to receive cardiac surgery.The patients were divided into AF group (AF,n=39)and sinus rhythm group (SR, n=45).Their clinical data including baseline demographics,routine laboratory test and echocardiographics were collected before surgery.The right atrial tissue (0 .3-0 .5 cm3 )was disserted during the surgery.Right atrial fibrosis was observed by Masson staining.The mRNA expression ofα-SMA in atrial tissue were determined by Real-time quantitative PCR.Western blot was used to measure the protein expression ofα-SMA in atrial tissue.Results The two groups did not significantly differ in sex ratio,age,blood pressure,blood biochemical indicators or other aspects of medical history (P>0.05).However,left and right atrium diameters in AF group were significantly larger than those in SR group (P<0 .05 ).Masson staining suggested that collagen volume fraction and collagen content were significantly higher in AF group than in SR group (P<0 .05 ).The mRNA and protein expressions ofα-SMA in right atrial tissue were obviously higher in AF group than in SR group (coefficients P<0 .05 ).The mRNA and protein expressions ofα-SMA from right atrial tissue in the 84 patients were positively correlated with collagen content (coefficients of 0.587 and 0.607;P=0.029,0.014,respectively).Conclusion There is significant atrial fibrosis in patients with valvular atrial fibrillation,which is closely related to up-regulated expression ofα-SMA gene.
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Influenced by a variety of pathologic factors, cardiac fibroblasts can transdifferentiate into myofibroblasts and pro-liferate excessively, followed by an overdue secretion of extracellular matrix ( ECM) .This process involves complicated signaling path-ways and electrophysiological mechanisms and may result in atrial fibrosis and contribute to atrial remodeling in structure, function and electrophysiological signaling, which is considered as a most important phase of atrial fibrillation.This review focuses on the role of fi-broblasts in atrial fibrosis, atrial remodeling, and the development of atrial fibrillation.
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Objective To investigate the effect of microRNA-101 (miRNA-101) on atrial fibrosis in human chronic atrial fibrillation (AF). Methods Right atrial appendages were obtained from 59 patients (30 with AF) undergoing cardiac surgery, including 47 patients with valve heart disease and 12 patients with congenital heart disease. The expression of miRNA-101 was determined by quantitative real-time PCR in the right atrial appendages of patients with and without AF. The cell-specific localization of miRNA-101 was detected by in situ hybridization assay. The mRNA and protein expression levels of transforming growth factor β typeⅠreceptor (TGFβRⅠ) and collagen type I (COL1) were determined by quantitative real-time PCR and Western-blot assay, respectively. Collagen in the right atrial appendages was observed by Masson staining assay. Results The expression of miRNA-101 was found to be significantly down-regulated in AF patients compared with patients with sinus rhythm (SR) (P 0.05). But the protein expression of TGFβRI in patients with AF was significantly higher than that of patients with SR (P < 0.05). The mRNA and protein expressionsl of COL1 were significantly higher in patients with AF than thoset of patients with SR (P < 0.05). The collagen was significantly increased in patients with AF than that of patients with SR (P < 0.05). Conclusions Downregulation of miRNA-101 may contribute to atrial fibrosis in human atrial fibrillation by targeting TGFβRⅠ.