Adjunctive low-voltage area ablation for patients with atrial fibrillation: An updated meta-analysis of randomized controlled trials.

BACKGROUND: The efficacy and safety of adjunctive low-voltage area (LVA) ablation on outcomes of catheter ablation (CA) for atrial fibrillation (AF) remains uncertain. METHODS: PubMed, Embase, Cochrane Library, and ClinicalTrials.gov were searched for randomized controlled trials (RCTs) comparing CA with versus without LVA ablation for patients with AF. Risk ratios (RR) with 95% confidence intervals (CI) were pooled with a random-effects model. Our primary endpoint was recurrence of atrial tachyarrhythmia (ATA), including AF, atrial flutter, or atrial tachycardia. We used R version 4.3.1 for all statistical analyses. RESULTS: Our meta-analysis included 10 RCTs encompassing 1780 patients, of whom 890 (50%) were randomized to LVA ablation. Adjunctive LVA ablation significantly reduced recurrence of ATA (RR 0.76; 95% CI 0.67-0.88; p < .01) and reduced the number of redo ablation procedures (RR 0.54; 95% CI 0.35-0.85; p < .01), as compared with conventional ablation. Among 691 (43%) patients with documented LVAs on baseline substrate mapping, adjunctive LVA ablation substantially reduced ATA recurrences (RR 0.57; 95% CI 0.38-0.86; p < .01). There was no significant difference between groups in terms of periprocedural adverse events (RR 0.78; 95% CI 0.39-1.56; p = .49). CONCLUSIONS: Adjunctive LVA ablation is an effective and safe strategy for reducing recurrences of ATA among patients who undergo CA for AF.

The role of galectin-3 in patients with permanent and paroxysmal Atrial Fibrillation and echocardiographic parameters of left atrial fibrosis.

BACKGROUND: Biochemical markers and imaging tests have been used with the aim of stratifying the risk and detecting atrial fibrosis. Speckle-tracking echocardiography (STE) is used for the detection of atrial fibrosis and Gal-3 provides an important prognostic value. The objective of the study was to assess the association between atrial fibrosis markers and serum levels, genetic polymorphisms and genic expression of galectin-3. METHODS: 206 patients with permanent AF and 70 patients with paroxysmal AF were included in the study. Real time PCR (TaqMan) system was used to study SNPs rs4652 and 4644 of the gene LGALS3. Serum levels of Gal-3 were determined by ELISA and STE was performed to assess fibrosis. RESULTS: Mean age of individuals with permanent AF was 66.56 ± 12 years. As for the echocardiography results, those patients showed an decrease in the following parameters peak atrial longitudinal strain (PALS) (p = 0.002) when compared to the same parameters from the paroxysmal AF group of patients. There was a correlation between serum levels of Gal-3 and PALS in the group of patients with permanent AF; the lower the levels of gal-3, the lower the LA strain (r = 0.24; p = 0.01). CONCLUSIONS: Echocardiographic findings showed association with the groups, and with serum levels of Gal-3 in patients with permanent AF. The distribution of allelic and genotypic frequencies, and of the haplotypes of polymorphism LGALS3 rs4652 and rs4644 did not present statistical variation, which suggests that those SNPs are not associated with the AF clinical forms (permanent and paroxysmal).

Fisiopatología del bloqueo interauricular y su rol como predictor de arritmias supraventriculares

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.

Atrial contractile function and fibrosis in patients with paroxysmal atrial fibrillation in sinus rhythm / Función contráctil auricular y fibrosis en pacientes con fibrilación auricular paroxística en ritmo sinusal

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.

Relação entre Gordura Epicárdica e Fibrilação Atrial Não Pode Ser Totalmente Explicada pela Fibrose Atrial Esquerda / The Relationship between Epicardial Fat and Atrial Fibrillation Cannot Be Fully Explained by Left Atrial Fibrosis

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.

How Can Galectin-3 as a Biomarker of Fibrosis Improve Atrial Fibrillation Diagnosis and Prognosis?

Galectin-3 (Gal-3) is a biomarker of fibrosis that has been associated with atrial remodeling. Acknowledging the presence of a biomarker in patients with atrial fibrillation (AF) can allow for a better clinical treatment. The aim of this study was to assess the association of Gal-3 with atrial fibrosis in patients with AF. This is a systematic review study. From the total number of studies analyzed, 12 demonstrated a relation between atrial fibrosis and Gal-3 in patients with AF and presented statistically significant association values. We conclude that Gal-3 is associated with atrial fibrosis in patients with AF in all types, as well as after the arrhythmia treatment by ablation.

Atrial fibrillation promotion in a rat model of heart failure induced by left ventricle radiofrequency ablation.

BACKGROUND: Atrial fibrillation (AF) frequently coexists with congestive heart failure (CHF). The increased susceptibility to AF in CHF has been attributed to a variety of structural and electrophysiological changes in the atria, particularly dilation and interstitial fibrosis. We evaluated atrial remodeling and AF vulnerability in a rat model of CHF induced by left ventricle (LV) radiofrequency (RF) ablation. METHODS: Wistar rats were divided into 3 groups: RF-induced CHF (Ab, n = 36), CHF animals treated with spironolactone (AbSpi, n = 20) and sham controls (Sham, n = 29). After 12 weeks, animals underwent echocardiographic and electrophysiological evaluation and were sacrificed for histological (atrial fibrosis) and Western blotting (TGF-ß1, collagen I/III, connexin 43 and CaV1.2) analysis. RESULTS: Mild LV dysfunction and marked atrial enlargement were noted in both ablated groups. AF inducibility (episodes ≥2 s) increased in the Ab group compared to sham animals (31/36, 86%; vs. 15/29, 52%; p = 0.005), but did not differ from the AbSpi group (16/20, 80%; p = NS). Sustained AF (>30 s) was also more frequent in the Ab group compared to shams (56% vs. 28%; p = 0.04). Spironolactone reduced atrial fibrosis (p < 0.01) as well as TGF-ß1 (p < 0.01) and collagen I/III (p < 0.01) expression but did not affect connexin 43 and CaV1.2 expression. CONCLUSIONS: Rats with RF-induced CHF exhibit pronounced atrial structural remodeling and enhanced AF vulnerability. This model may be useful for studying AF substrate in CHF.