5965Perimatrial inflammation measured by fluoine-18-fluorodeoxyglucose-positron emission tomography/computed tomography to predict new-onset atrial fibrillation

Relation of Proinflammatory Activity of Epicardial Adipose Tissue to the Occurrence of Atrial Fibrillation

Quantitative Analysis of Quantity and Distribution of Epicardial Adipose Tissue Surrounding the Left Atrium in Patients With Atrial Fibrillation and Effect of Recurrence After Ablation

BackgroundAlthough an increased epicardial adipose tissue (EAT) volume around the left atrium (LA) is related to the atrial fibrillation (AF) burden, the role of EAT inflammation in AF is unclear. We investigated the association between AF and inflammation of the EAT around the LA. MethodsWe retrospectively identified regions of EAT around the LA and measured the density of these areas using computed tomography (CT). ResultsA total of 32 patients who underwent their first catheter ablation for paroxysmal AF (PAF) were enrolled (mean age 62.5±11.1 years). Patients without a history of AF (n=32), but who underwent cardiac CT and were matched by age, sex, and metabolic risk factors, were enrolled in the control group (62.2±12.1 years). The mean EAT density around the LA was significantly higher in the PAF group than in the control group (−108.1±6.7 vs. −111.6±5.5 Hounsfield units; p=0.02), while the densities of subcutaneous adipose tissue (SAT) in the abdomen and thorax did not differ between the two groups. In a multiple logistic regression analysis, a higher EAT density was significantly associated with the presence of PAF after adjusting for other risk factors (odds ratio: 1.25; 95% confidence interval: 1.08–1.45, p=0.003). ConclusionsThis study supports the hypothesis that inflammation of EAT around the LA, but not SAT, is related to the presence of PAF.

Recent Trends in the Incidence, Treatment, and Prognosis of Patients With Heart Failure and Atrial Fibrillation (the Worcester Heart Failure Study)

Drugs That Ameliorate Epicardial Adipose Tissue Inflammation May Have Discordant Effects in Heart Failure With a Preserved Ejection Fraction as Compared With a Reduced Ejection Fraction

the physiological roles of human epicardial adipose tissue (EAT) are not well defined because this strategically located white adipose tissue (WAT) depot is difficult to access and study, and most of the information about it comes from humans with severe cardiac diseases undergoing open heart

Increasing evidence supports a role of inflammation in the development of atrial fibrillation (AF). However, direct evidence of persistent inflammatory activity in the atria of AF patients is scarce. In this study, we used 18-Fluor-Deoxyglucose positron emission tomography computed tomography (18F-FDG PET/CT) to determine atrial inflammation in patients with and without AF. Retrospectively, 18F-FDG PET/CT scans were analyzed. 37 patients with a history of AF were compared to an age and sex matched control group with no history of AF. Standardized uptake values were obtained in the atrial walls, in the left ventricular wall, and in the right ventricular blood pool, respectively. Target to background ratios (TBR) were determined in the atrial and left ventricular walls and compared between the two groups. TBR values of the left atrial wall were slightly but not significantly higher in patients with AF (1.21 ± 0.27) compared to those without AF (1.14 ± 0.29; p = 0.85). Likewise, a weak but not significant difference was observed in signal intensities in the right atrial wall between patients in the AF (1.14 ± 0.45) and the control group (0.96 ± 0.2; p = 0.41). TBR values of the left ventricular myocardium did not differ between the groups; no significant correlation was found between the TBR in the left and right atrial wall and blood glucose levels. 18F-FDG PET/CT performed under routine conditions did not detect a significant difference in inflammatory activity in the left or right atrium between patients with and without AF. Contrary to previous reports, these results therefore do not clearly support a role for ongoing atrial inflammation in patients with AF. Prospective clinical studies using myocardial glucose uptake suppression strategies may be helpful to clarify these issues.

Epicardial Fat in Atrial Fibrillation: The Effect of Cardioautonomic Nervous System Function

Epicardial adipose tissue (EAT) is linked to both Atrial fibrillation (AF) and metabolic syndrome (MetS). Whether EAT inflammation relates to AF type, recurrence after ablation, or MetS, is incompletely known, likewise if it can be measured by CT angiography. To establish the link between (1) atrial EAT inflammatory composition and AF type, AF recurrence, and metabolic comorbidities. (2) EAT inflammation and EAT-volume or density. Patients undergoing thoracoscopic ablation for advanced AF (that is, usually persistent, with enlarged left atria and previous failed ablations) with a cardiac CT-scan before and 6months after surgery were enrolled. CT-EAT atrial volume and attenuation (density), were used for analyses. Patients' left atrial appendages (LAA + EAT) were excised during ablation and stained for adipocytes and different inflammatory cells. Among the 134 included patients, 113 had a LAA available for (immuno)histo-chemistry. Patients with persistent versus paroxysmal AF had more EAT neutrophils: 155[257] versus 63[106] cells/mm2, (p = 0.003), and less anti-inflammatory CD163 + macrophages: 126[134] versus 224[179], (p = 0.03). The AUC curve for differentiating persistent from paroxysmal AF through neutrophil-count was 0.75 (p value < 0.001, CI 0.63-0.87). EAT neutrophil-count related to CT-EAT-attenuation (multivariable analysis: expB 1.01, CI 1.00-1.02, (p = 0.04)). CT-EAT-attenuation distinguished persistent from paroxysmal AF: - 73.0 ± 4.6 versus - 75.3 ± 5.3HU, (p = 0.03). Patients with versus without recurrence had similar inflammatory cell counts, but larger adipocytes, multivariable analysis: ExpB 1.002, CI 1.00-1.003, (p = 0.02). Hypertensive and diabetic patients also had an increased adipocyte size. Patients with persistent versus paroxysmal AF exhibited increased EAT neutrophils, which is reflected by CT-EAT-attenuation. Those with AF recurrence, hypertension and diabetes had adipocyte hypertrophy which may imply a common mechanism underlying these conditions.

Atrial Epicardial Adipose Tissue (EAT) is presumably involved in the pathogenesis of atrial fibrillation (AF). The transient nature of postoperative AF (POAF) suggests that surgery-induced triggers provoke an unmasking of a pre-existent AF substrate. The aim is to investigate the association between the volume of EAT and the occurrence of POAF. We hypothesise that the likelihood of developing POAF is higher in patients with high compared to low left atrial (LA) EAT volumes. Quantification of LA EAT based on the Hounsfield Units using custom made software was performed on pre-operative coronary computed tomography angiography scans of patients who underwent cardiac surgery between 2009 and 2019. Patients with mitral valve disease were excluded. A total of 83 patients were included in this study (CABG=34, aortic valve=33, aorta ascendens n=7, combination n=9), of which 43 patients developed POAF. The EAT percentage in the LA wall nor indexed EAT volumes differed between patients with POAF and with sinus rhythm (all P>0.05). In multivariable analysis, age and LA volume index (LAVI) were the only independent predictors for early POAF (OR: 1.076 and 1.056, respectively). As expected, advanced age and LAVI were independent predictors of POAF. However, the amount of local EAT was not associated with the occurrence of AF after cardiac surgery. This suggests that the role of EAT in POAF is rather limited, or that the association of EAT in the early phase of POAF is obscured by the dominance of surgical-induced triggers.

Epicardial adipose tissue (EAT), the visceral fat of the heart, is highly inflammatory fat depot with pro-inflammatory transcriptome and proteosome. EAT contributes to the development and progression of coronary artery disease (CAD) and atrial fibrillation (AF) through multifactorial inflammatory pathways. However, the paradigm linking EAT inflammation and cardiovascular risk was recently reevaluated. EAT inflammation may be also necessary process for adipose tissue remodeling and expansion to accommodate excess lipids. EAT inflammation may be also considered an adaptive response of adipose tissue to the effects of glucagon-like peptide-1 receptor (GLP-1Rs) and glucose-dependent insulinotropic polypeptide (GIP) analogs. The presence of GLP-1 (GLP-1R) and GIP receptors (GIP-R) suggest direct interaction of these agents with EAT. EAT GLP-1R and GIP-R activation can induce a beneficial balance between increased adipogenesis and reduced ectopic fat accumulation. Cardiovascular effects of liraglutide, semaglutide and tirzepatide can be mediated by EAT inflammation.

Introduction Obesity is a chronic disease, which has significant health consequences and is a staggering burden to health care systems. Obesity can have harmful effects on the cardiovascular system, including heart failure, hypertension, coronary heart disease, and atrial fibrillation (AF). One of the possible substrates might be epicardial adipose tissue (EAT), which can be the link between AF and obesity. EAT is a fat deposit located between the myocardium and the visceral pericardium. Numerous studies have demonstrated that EAT plays a pivotal role in this relationship regarding atrial fibrillation. Areas covered This review will focus on the role of obesity and the occurrence of atrial fibrillation (AF) and examine the connection between these and epicardial adipose tissue (EAT). The first part of this review will explain the pathophysiology of EAT and its association with the occurrence of AF. Secondly, we will review bariatric and metabolic surgery and its effects on EAT and AF. Expert commentary In this review, the epidemiology, pathophysiology, and treatment methods of AF are explained. Secondly, the effects on EAT were elucidated. Due to the complex pathophysiological link between EAT, AF, and obesity, it is still uncertain which treatment strategy is superior.

Vitamins K2 and D3 may improve cardiovascular health by modulating inflammation and vascular calcification. Inflammation contributes to atherosclerosis and can be assessed through imaging and systemic biomarkers. This study investigated whether vitamin K2 and D3 supplementation reduces inflammation in epicardial adipose tissue (EAT), including pericoronary adipose tissue (PCAT), and systemic inflammation in elderly men at cardiovascular risk. In the Aortic Valve DECalcification (AVADEC) trial, 388 men aged 65-74 received daily vitamin K2 (720μg) and D3 (25μg) or placebo for 24 months. EAT inflammation was assessed using non-contrast CT [EAT volume and attenuation] and contrast-enhanced CT [PCAT attenuation]. Systemic inflammation was evaluated via hs-CRP, IL-6, TNF-α, Fetuin-A, and osteopontin (OPN). Dephosphorylated uncarboxylated matrix Gla protein (dp-ucMGP), the inactive form of MGP, served as a proxy for vitamin K2 status. After 24 months, EAT volume increased in the placebo group (Δ5.66cm3,95% CI 1.35; 9.98) and non-significantly in the vitamin group (Δ3.44cm3, 95% CI -0.44; 7.33), with an intergroup difference of -2.22cm3 (95% CI -8.01; 3.57). EAT attenuation declined similarly (intergroup difference: 0.32 HU, 95% CI -0.23; 0.87). PCAT attenuation remained unchanged. No significant changes were seen in systemic markers, though OPN increased modestly in the vitamin group (Δ25.72pg/mL, 95% CI 2.40; 49.05). dp-ucMGP decreased significantly with supplementation (intergroup difference: 255.31pmol/L, 95% CI -289.56; -221.05). Despite reduction in dp-ucMGP, high-dose vitamin K2 and D3 supplementation did not affect EAT, PCAT or systemic inflammation over 24 months. Alternative strategies may be needed to target inflammatory pathways in cardiovascular disease prevention.

Funding Acknowledgements Type of funding sources: None. BACKGROUND In systemic amyloidosis cardiac infiltration by amyloid fibrils leads to increased stiffness of the myocardium and of the atrial walls. There is a reduction in left atrial mechanical function and a high risk of thrombi formation. Atrial deformation by speckle tracking echocardiography peak atrial longitudinal strain (PALS) can predict the incidence of atrial fibrillation (AF) and ischaemic stroke in the general population and in patients (pts) with cryptogenic stroke. The predictive value of PALS seems to differ in different pts populations according to the prevalence of ventricular versus atrial myopathy (1). PURPOSE to compare parameters of atrial function in cardiac amyloidosis pts in sinus rhythm (SR) and AF and to observe if they are associated with the occurrence of new onset AF at follow-up (FUP). METHODS between 2016-2021 all pts with diagnosis of cardiac aTTR amyloidosis referred to the Clinic underwent an echocardiographic study including 2D-speckle tracking evaluation of left ventricular and left and right atrial strain. All pts received a regular FUP (clinical, echo, ECG and 24 hours Holter monitoring). Atrial function was evaluated by PALS in all pts and by PALS and PACS (peak atrial longitudinal strain during atrial contraction phase) in pts in SR. RESULTS 47 pts with aTTR cardiac amyloid (39/47 wild-tipe) were studied. Mean age = 82 ± 5 years, LV mass = 190 ± 46 g/m2; LV EF= 53%±9, GLS= -10%±4, EF/GLS ratio=-5,5 ± 2, left atrial (LA) volume = 49 ± 9 ml/m2, LA PALS 9,7%±6,6, right atrial (RA) PALS 15,9 ± 9,6. At the time of diagnosis 29 pts were in SR and 18 pts were in AF. Pts in AF had lower PALS (5,1%±3,7 in AF pts vs 11,9%±6,9 in SR pts, p = 0,001) and lower (less negative) GLS (-9,1%±3,1 in AF pts vs -11,8%± 4,2 in SR pts, p = 0,02). LA volume was not significantly different in AF pts compare to SR pts (51,4 ml/m2 ± 7,65 vs 47,6 ml/m2 ± 10,9; p = 0,19). During a median FUP of 21 months 8 pts had a new onset AF. There was no significant difference in atrial size and atrial deformation parameters between pts who had new onset AF at FUP compared to pts who did not (Tab 1). The only parameter associated with new onset AF at FUP was GLS (-8.21%± 2,8 vs -13.01%±4,02, CI -10.8—5.6 vs -14.8—11.18, respectively, in pts who developed new onset AF compared to pts who did not, p = 0.007). 5 pts had a cardioembolic stroke at FUP: at the time of the admission for stroke they were all in AF. CONCLUSIONS Our data show that in this group of pts with aTTR cardiac amyloidosis all echo parameters of LA size and function were overall impaired. In this setting of advanced disease LA volume was not significantly different in pts in AF compared to pts in SR and was not associated with new-onset AF at FUP. Deformation parameters were significantly more impaired in pts in AF compared to pts in SR, however PALS was not associated with the occurrence of new onset AF at follow-up. The only parameter associated with the occurrence of new onset AF at follow-up was GLS. Abstract Table 1

Epicardial adipose tissue (EAT) is a contributing factor of metabolic syndrome (MS) and coronary artery disease (CAD). However, it is still unclear which measurement location of EAT area best reflects its cardiometabolic risk. The purpose of our study was to investigate the distribution of EAT and its relationship to the total EAT volume and MS. To assess volume and cross-sectional areas of EAT, coronary CT angiography were obtained in 256 asymptomatic subjects. The EAT areas within the threshold range of -190 to -30 Hounsfield units were measured at six representative slices. Correlations between single slice EAT areas and total EAT volumes were high across all measurement locations (correlation coefficient r > 0.80). The receiver-operator characteristic curves demonstrated EAT area at left main coronary artery (LMCA) was well discriminative for MS (AUC 0.82, p < 0.001) and CAD (AUC 0.76, p < 0.001). EAT areas across all measurement locations were significantly increased linearly with increasing number of MS components. EAT areas were significantly associated with MS at all measurement locations; the highest odds ratio (OR) between EAT area and MS was at the LMCA level (OR 5.86, p < 0.001). The OR between EAT area and coronary artery calcium was also significant in LMCA locations (OR 1.56, p = 0.042). We demonstrated that the single-slice EAT area measurement is a simple and reliable method compared with time-consuming volumetric measurements. The EAT area at LMCA level was the best single slice representing the risk of metabolic syndrome and coronary atherosclerosis.