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.

Psoriasis strikes back! Epicardial adipose tissue: another contributor to the higher cardiovascular risk in psoriasis.

For many years psoriasis was considered an inflammatory condition restricted to the skin. However, nowadays it is considered an immune-mediated, systemic inflammatory condition associated with numerous medical comorbidities, particularly cardiometabolic diseases, and overall cardiovascular mortality. Several studies have suggested that psoriasis may be an independent risk factor for atherosclerosis, indicating that psoriasis itself poses an intrinsic risk for cardiovascular disease, probably due to the disease's inflammatory burden. However, other causes beyond systemic inflammation and traditional cardiovascular risk factors may be implicated in cardiovascular disease in psoriasis. Recently, epicardial adipose tissue, an emerging cardiovascular risk factor, has been shown to be increased in psoriasis patients and to be associated with subclinical atherosclerosis, providing another possible link between psoriasis and atherosclerosis. The reason for the increase in epicardial adipose tissue in patients with psoriasis is unknown, but it is probably multifactorial, with genetic, immune-mediated and behavioral factors having a role. Thus, along with the increased prevalence of cardiometabolic risk factors and systemic inflammation in psoriasis, epicardial adipose tissue is probably another important contributor to the higher cardiovascular risk observed in psoriasis.

Epicardial adipose tissue thickness and its association with adiponectin in metabolic syndrome patients from Mérida, Venezuela / Associação entre a espessura do tecido adiposo epicárdico e a adiponectina em pacientes com síndrome metabólica em Mérida, Venezuela

Objective: To study the relationship between epicardial adipose tissue (EAT) thickness and plasma levels of adiponectin in Venezuelan patients. Subjects and methods: Thirty-one patients diagnosed with metabolic syndrome (study group) and 27 controls were selected and tested for glycemia, lipids, and adiponectin. EAT thickness, ejection fraction, diastolic function, left ventricular mass (LVM), and left atrial volume (LAV) were determined by transthoracic echocardiography. Results: EAT thickness was greater in metabolic syndrome patients (5.69 ± 1.12 vs. 3.52 ± 0.80 mm; p = 0.0001), correlating positively with body mass index (BMI) (r = 0.661; p = 0.0001); waist circumference (WC) (r = 0.664; p = 0.0001); systolic (SBP) (r = 0.607; p = 0.0001), and diastolic blood pressure (DBP) (r = 0.447; p = 0.0001); insulin (r = 0.505; p = 0.0001); Tg/HDL-C ratio (r = 0.447; p = 0.0001), non-HDL-C (r = 0.353; p = 0.007); LAV (r = 0.432; p = 0.001), and LVM (r = 0.469; p = 0.0001). EAT thickness correlated negatively with adiponectin (r = -0.499; p = 0.0001). Conclusion: A significant association exists between EAT thickness and both metabolic syndrome components and adiponectin concentration, a link that might be used as a biomarker for this disease. .

Objetivo: Estudar a relação entre a espessura do tecido adiposo epicárdico (TAE) e os níveis plasmáticos de adiponectina em pacientes venezuelanos. Sujeitos e métodos: Foram selecionados 31 pacientes com diagnóstico de síndrome metabólica (SM) (grupo de estudo) e 27 controles. Foram medidos a glicose, os lipídios e a adiponectina. Foram determinados a espessura do TAE, a fração de ejeção, a função diastólica, a massa ventricular esquerda (MVE) e o volume atrial esquerdo (VAI) pela ecocardiografia transtorácica. Resultados: A espessura do TAE foi maior em pacientes com SM (5,69 ± 1,12 contra 3,52 ± 0,80 mm; p = 0,0001) com uma correlação positiva com o índice de massa corporal (IMC) (r = 0,661; p = 0,0001), circunferência da cintura (CC) (r = 0,664; p = 0,0001), pressão arterial sistólica (PAS) (r = 0,607; p = 0,0001), diastólica (PAD) (r = 0,447; p = 0,0001), insulina (r = 0,505; p = 0,0001), com a relação TG/HDL-C (r = 0,447; p = 0,0001), com o colesterol HDL (r = 0,353; p = 0,007), VAI (r = 0,432; p = 0,001) e MVI (r = 0,469; p = 0,0001). A espessura do TAE se correlacionou negativamente com a adiponectina (r = -0,499; p = 0,0001). Conclusão: Existe uma relação significativa entre a espessura do TAE, os componentes do SM e a concentração plasmática de adiponectina, o que poderia ser utilizado como um biomarcador para essa doença. .