A novel approach to terminate roof-dependent atrial flutter with epicardial conduction through septopulmonary bundle.

Atrial flutter, a prevalent cardiac arrhythmia, is primarily characterized by reentrant circuits in the right atrium. However, atypical forms of atrial flutter present distinct challenges in terms of diagnosis and treatment. In this study, we examine three noteworthy clinical cases of atypical atrial flutter, which offer compelling evidence indicating the implication of the lesser-known Septopulmonary Bundle (SPB). This inference is based on the identification of distinct electrocardiographic patterns observed in these patients and their favorable response to catheter ablation, which is a standard treatment for atrial flutter. Remarkably, in each case, targeted ablation at the anterior portion of the left atrial roof effectively terminated the arrhythmia, thus providing further support for the hypothesis of SPB involvement. These insightful observations shed light on the potential significance of the SPB in the etiology of atypical atrial flutter and introduce a promising therapeutic target. We anticipate that this paper will stimulate further exploration into the role of the SPB in atrial flutter and pave the way for the development of targeted ablation strategies.

The dysfunctional adiposity index is a clinical surrogate of pericardial fat in adults without premature CVD: A sub-analysis of the GEA Mexican study control group.

BACKGROUND AND AIM: The Dysfunctional Adiposity Index (DAI) is a clinical surrogate for evaluating adipose tissue functionality and cardiometabolic health. However, its association with Pericardial Fat Volume (PFV) has not been tested. The aim of this study was to evaluate DAI- PFV association, stratified by type 2 diabetes (T2D) status, and identify DAI thresholds for detecting increased PFV among patients without premature CVD. METHODS AND RESULTS: Participants from the GEA-Mexican study underwent a computed tomography scan to measure PFV. Adjusted logistic regression analyses tested the association between DAI and PFV. AUROC curves evaluated DAI's ability to identify elevated PFV (≥57.57 cm³), and the Youden method determined DAI thresholds, along with diagnostic metrics. The study analyzed 997 participants (women: 55%; mean age: 54 ± 9 years; median PFV: 42 cm³ [IQR: 29-58]), with a 13% prevalence of T2D. DAI was positively associated with elevated PFV (OR: 1.33, 95% CI: 1.07-1.70), which was more pronounced among subjects with T2D (OR: 3.01, 95% CI: 1.41-6.40). DAI thresholds were established for all participants (>1.176), individuals without T2D (>1.003), and with T2D (>1.936), yielding sensitivities of 71%, 81%, and 57%, and specificities of 48%, 38%, and 75%, respectively. The adjusted logistic regression tied DAI thresholds to a 1.68-fold elevation in PFV for all, 2.06-fold for those without T2D, and 6.81-fold for those with T2D. CONCLUSION: DAI was positively associated with increased PFV, particularly among participants with T2D. Established DAI thresholds demonstrated good diagnostic values for detecting increased PFV. DAI could serve as an accessible marker to identify PF in clinical settings.

Single-Cell RNA Sequencing Uncovers Paracrine Functions of the Epicardial-Derived Cells in Arrhythmogenic Cardiomyopathy.

BACKGROUND: Arrhythmogenic cardiomyopathy (ACM) manifests with sudden death, arrhythmias, heart failure, apoptosis, and myocardial fibro-adipogenesis. The phenotype typically starts at the epicardium and advances transmurally. Mutations in genes encoding desmosome proteins, including DSP (desmoplakin), are major causes of ACM. METHODS: To delineate contributions of the epicardium to the pathogenesis of ACM, the Dsp allele was conditionally deleted in the epicardial cells in mice upon expression of tamoxifen-inducible Cre from the Wt1 locus. Wild type (WT) and Wt1-CreERT2:DspW/F were crossed to Rosa26mT/mG (R26mT/mG) dual reporter mice to tag the epicardial-derived cells with the EGFP (enhanced green fluorescent protein) reporter protein. Tagged epicardial-derived cells from adult Wt1-CreERT2:R26mT/mG and Wt1-CreERT2: R26mT/mG:DspW/F mouse hearts were isolated by fluorescence-activated cell staining and sequenced by single-cell RNA sequencing. RESULTS: WT1 (Wilms tumor 1) expression was progressively restricted postnatally and was exclusive to the epicardium by postnatal day 21. Expression of Dsp was reduced in the epicardial cells but not in cardiac myocytes in the Wt1-CreERT2:DspW/F mice. The Wt1-CreERT2:DspW/F mice exhibited premature death, cardiac dysfunction, arrhythmias, myocardial fibro-adipogenesis, and apoptosis. Single-cell RNA sequencing of ≈18 000 EGFP-tagged epicardial-derived cells identified genotype-independent clusters of endothelial cells, fibroblasts, epithelial cells, and a very small cluster of cardiac myocytes, which were confirmed on coimmunofluorescence staining of the myocardial sections. Differentially expressed genes between the paired clusters in the 2 genotypes predicted activation of the inflammatory and mitotic pathways-including the TGFß1 (transforming growth factor ß1) and fibroblast growth factors-in the epicardial-derived fibroblast and epithelial clusters, but predicted their suppression in the endothelial cell cluster. The findings were corroborated by analysis of gene expression in the pooled RNA-sequencing data, which identified predominant dysregulation of genes involved in epithelial-mesenchymal transition, and dysregulation of 146 genes encoding the secreted proteins (secretome), including genes in the TGFß1 pathway. Activation of the TGFß1 and its colocalization with fibrosis in the Wt1-CreERT2:R26mT/mG:DspW/F mouse heart was validated by complementary methods. CONCLUSIONS: Epicardial-derived cardiac fibroblasts and epithelial cells express paracrine factors, including TGFß1 and fibroblast growth factors, which mediate epithelial-mesenchymal transition, and contribute to the pathogenesis of myocardial fibrosis, apoptosis, arrhythmias, and cardiac dysfunction in a mouse model of ACM. The findings uncover contributions of the epicardial-derived cells to the pathogenesis of ACM.

Reactivation of the Epicardium at the Origin of Myocardial Fibro-Fatty Infiltration During the Atrial Cardiomyopathy.

RATIONALE: Fibro-fatty infiltration of subepicardial layers of the atrial wall has been shown to contribute to the substrate of atrial fibrillation. OBJECTIVE: Here, we examined if the epicardium that contains multipotent cells is involved in this remodeling process. METHODS AND RESULTS: One hundred nine human surgical right atrial specimens were evaluated. There was a relatively greater extent of epicardial thickening and dense fibro-fatty infiltrates in atrial tissue sections from patients aged over 70 years who had mitral valve disease or atrial fibrillation when compared with patients aged less than 70 years with ischemic cardiomyopathy as indicated using logistic regression adjusted for age and gender. Cells coexpressing markers of epicardial progenitors and fibroblasts were detected in fibro-fatty infiltrates. Such epicardial remodeling was reproduced in an experimental model of atrial cardiomyopathy in rat and in Wilms tumor 1 (WT1)CreERT2/+;ROSA-tdT+/- mice. In the latter, genetic lineage tracing demonstrated the epicardial origin of fibroblasts within fibro-fatty infiltrates. A subpopulation of human adult epicardial-derived cells expressing PDGFR (platelet-derived growth factor receptor)-α were isolated and differentiated into myofibroblasts in the presence of Ang II (angiotensin II). Furthermore, single-cell RNA-sequencing analysis identified several clusters of adult epicardial-derived cells and revealed their specification from adipogenic to fibrogenic cells in the rat model of atrial cardiomyopathy. CONCLUSIONS: Epicardium is reactivated during the formation of the atrial cardiomyopathy. Subsets of adult epicardial-derived cells, preprogrammed towards a specific cell fate, contribute to fibro-fatty infiltration of subepicardium of diseased atria. Our study reveals the biological basis for chronic atrial myocardial remodeling that paves the way of atrial fibrillation.

COVID-19 Vaccine-Related Myocardial and Pericardial Inflammation.

PURPOSE OF REVIEW: To review myocarditis and pericarditis developing after COVID-19 vaccinations and identify the management strategies. RECENT FINDINGS: COVID-19 mRNA vaccines are safe and effective. Systemic side effects of the vaccines are usually mild and transient. The incidence of acute myocarditis/pericarditis following COVID-19 vaccination is extremely low and ranges 2-20 per 100,000. The absolute number of myocarditis events is 1-10 per million after COVID-19 vaccination as compared to 40 per million after a COVID-19 infection. Higher rates are reported for pericarditis and myocarditis in COVID-19 infection as compared to COVID-19 vaccines. COVID-19 vaccine-related inflammatory heart conditions are transient and self-limiting in most cases. Patients present with chest pain, shortness of breath, and fever. Most patients have elevated cardiac enzymes and diffuse ST-segment elevation on electrocardiogram. Presence of myocardial edema on T2 mapping and evidence of late gadolinium enhancement on cardiac magnetic resonance imaging are also helpful additional findings. Patients were treated with non-steroidal anti-inflammatory drugs and colchicine with corticosteroids reserved for refractory cases. At least 3-6 months of exercise abstinence is recommended in athletes diagnosed with vaccine-related myocarditis. COVID-19 vaccination is recommended in all age groups for the overall benefits of preventing hospitalizations and severe COVID-19 infection sequela.

Epicardial adipose tissue differentiates in patients with and without coronary microvascular dysfunction.

BACKGROUND/OBJECTIVES: Coronary microvascular dysfunction (CMD) is a common disorder, leading to symptoms similar to obstructive coronary artery disease and bears important prognostic implications. Local inflammation is suggested to promote development of CMD. Epicardial adipose tissue (EAT) is a local visceral fat depot surrounding the heart and the coronary arteries, modifying the inflammatory environment of the heart. We compared EAT in patients with and without CMD. METHODS: We retrospectively included consecutive patients undergoing diagnostic coronary angiography as well as transthoracic echocardiography between March and October 2016. EAT thickness was defined as space between the epicardial wall of the myocardium and the visceral layer of the pericardium and EAT index was calculated as EAT thickness/body surface area. Logistic regression analysis was used to determine the association of EAT index with the presence of CMD. RESULTS: Overall, 399 patients (mean age 60.2 ± 14.0 years, 46% male) were included. EAT thickness was significantly higher in patients with CMD compared to patients without CMD (EAT thickness 4.4 ± 1.8 vs. 4.9 ± 2.4 mm, p = 0,048 for patients without and with CMD, respectively). In univariate regression analysis, EAT index was associated with a 30% higher frequency of CMD (odds ratio [95% confidence interval]: 1.30 [1.001-1.69], p = 0.049). Effect sizes remained stable upon adjustment for body mass index (BMI, 1.30 [1.003-1.70], p = 0.048), but were attenuated when ancillary adjusting for age and gender (1.17 [0.90-1.54, p = 0.25). The effect was more pronounced in patients >65 years of age and independent of BMI and sex (1.85 [1.14-3.00], p = 0.013). CONCLUSION: EAT thickness is independently associated with CMD and can differentiate between patients with and without CMD especially in older age groups. Our results support the hypothesis that modulation of local inflammation by epicardial fat is involved in the development of CMD.

Adrenomedullin Induces Cardiac Lymphangiogenesis After Myocardial Infarction and Regulates Cardiac Edema Via Connexin 43.

RATIONALE: Cardiac lymphangiogenesis contributes to the reparative process post-myocardial infarction, but the factors and mechanisms regulating it are not well understood. OBJECTIVE: To determine if epicardial-secreted factor AM (adrenomedullin; Adm=gene) improves cardiac lymphangiogenesis post-myocardial infarction via lateralization of Cx43 (connexin 43) in cardiac lymphatic vasculature. METHODS AND RESULTS: Firstly, we identified sex-dependent differences in cardiac lymphatic numbers in uninjured mice using light-sheet microscopy. Using a mouse model of Adm hi/hi ( Adm overexpression) and permanent left anterior descending ligation to induce myocardial infarction, we investigated cardiac lymphatic structure, growth, and function in injured murine hearts. Overexpression of Adm increased lymphangiogenesis and cardiac function post-myocardial infarction while suppressing cardiac edema and correlated with changes in Cx43 localization. Lymphatic function in response to AM treatment was attenuated in mice with a lymphatic-specific Cx43 deletion. In vitro experiments in cultured human lymphatic endothelial cells identified a novel mechanism to improve gap junction coupling by pharmaceutically targeting Cx43 with verapamil. Finally, we show that connexin protein expression in cardiac lymphatics is conserved between mouse and human. CONCLUSIONS: AM is an endogenous, epicardial-derived factor that drives reparative cardiac lymphangiogenesis and function via Cx43, and this represents a new therapeutic pathway for improving myocardial edema after injury.

Association of epicardial fat thickness with left ventricular diastolic function parameters in a community population.

BACKGROUND: We examined the relationship between epicardial fat thickness (EFT) measured by echocardiography and left ventricular diastolic function parameters in a Beijing community population. METHODS: We included 1004 participants in this study. Echocardiographic parameters including E and A peak velocity, the early diastolic velocities (e') of the septal and lateral mitral annulus using tissue doppler imaging, E/e', and EFT were measured. EFT1 was measured perpendicularly on the right ventricular free wall at end diastole in the extension line of the aortic root. EFT2 was the maximum thickness measured perpendicularly on the right ventricular free wall at end diastole. Multivariable linear regression was used to analyze the relationship between EFT and the mean e' and E/e'. RESULTS: The mean age of the participants was 63.91 ± 9.02 years, and 51.4% were men. EFT1 and EFT2 were negatively correlated with lateral e', septal e', and mean e' (p < 0.05), and the correlation coefficient for EFT1 and EFT2 and mean e' was - 0.138 and - 0.180, respectively. EFT1 and EFT2 were positively correlated with lateral E/e', septal E/e', and mean E/e' (p < 0.05), and the correlation coefficient for EFT1 and EFT2 and mean e' was 0.100 and 0.090, respectively. Multivariable egression analysis showed that EFT2 was independently and negatively associated with e' mean (ß = - 0.078 [95% confidence interval = - 0.143, - 0.012, p = 0.020]). There were no interactions between EFT2 and any covariates, including age or heart groups, sex, BMI, or presence of hypertension, diabetes, or coronary heart disease, in relation to left ventricular diastolic dysfunction. CONCLUSIONS: EFT2 was negatively and independently associated with e' mean, which suggests that more attention to this type of adipose fat is required for cardiovascular disease therapy.

Pericardial Adipose Tissue Volume Is Independently Associated With Human Immunodeficiency Virus Status and Prior Use of Stavudine, Didanosine, or Indinavir.

BACKGROUND: Increased pericardial adipose tissue is associated with higher risk of cardiovascular disease. We aimed to determine whether human immunodeficiency virus (HIV) status was independently associated with larger pericardial adipose tissue volume and to explore possible HIV-specific risk factors. METHODS: Persons with HIV (PWH) were recruited from the Copenhagen Comorbidity in HIV Infection (COCOMO) Study and matched 1:1 on age and sex to uninfected controls. Pericardial adipose tissue volume was measured using cardiac computed tomography. RESULTS: A total of 587 PWH and 587 controls were included. Median age was 52 years, and 88% were male. Human immunodeficiency virus status was independently associated with 17 mL (95% confidence interval [CI], 10-23; P < .001) larger pericardial adipose tissue volume. Larger pericardial adipose tissue volume was associated with low CD4+ nadir and prior use of stavudine, didanosine, and indinavir. Among PWH without thymidine analogue or didanosine exposure, time since initiating combination antiretroviral treatment (per 5-year use) was associated with l6 mL (95% CI, -6 to -25; P = .002) lower pericardial adipose tissue volume. CONCLUSIONS: Human immunodeficiency virus status was independently associated with larger pericardial adipose tissue volume. Severe immunodeficiency, stavudine, didanosine, and indinavir were associated with larger pericardial adipose tissue volume. Persons with HIV with prior exposure to these drugs may constitute a distinct cardiovascular risk population.

Acute interaction between human epicardial adipose tissue and human atrial myocardium induces arrhythmic susceptibility.

Epicardial adipose tissue (EAT) deposition has a strong clinical association with atrial arrhythmias; however, whether a direct functional interaction exists between EAT and the myocardium to induce atrial arrhythmias is unknown. Therefore, we aimed to determine whether human EAT can be an acute trigger for arrhythmias in human atrial myocardium. Human trabeculae were obtained from right atrial appendages of patients who have had cardiac surgery (n = 89). The propensity of spontaneous contractions (SCs) in the trabeculae (proxy for arrhythmias) was determined under physiological conditions and during known triggers of SCs (high Ca2+, ß-adrenergic stimulation). To determine whether EAT could trigger SCs, trabeculae were exposed to superfusate of fresh human EAT, and medium of 24 h-cultured human EAT treated with ß1/2 (isoproterenol) or ß3 (BRL37344) adrenergic agonists. Without exposure to EAT, high Ca2+ and ß1/2-adrenergic stimulation acutely triggered SCs in, respectively, 47% and 55% of the trabeculae that previously were not spontaneously active. Acute ß3-adrenergic stimulation did not trigger SCs. Exposure of trabeculae to either superfusate of fresh human EAT or untreated medium of 24 h-cultured human EAT did not induce SCs; however, specific ß3-adrenergic stimulation of EAT did trigger SCs in the trabeculae, either when applied to fresh (31%) or cultured (50%) EAT. Additionally, fresh EAT increased trabecular contraction and relaxation, whereas media of cultured EAT only increased function when treated with the ß3-adrenergic agonist. An acute functional interaction between human EAT and human atrial myocardium exists that increases the propensity for atrial arrhythmias, which depends on ß3-adrenergic rather than ß1/2-adrenergic stimulation of EAT.

Epicardial approach for cardiac electrophysiology procedures.

Since its introduction over two decades ago, percutaneous epicardial procedures have become well-adopted by cardiac electrophysiologists, most commonly for catheter ablation of cardiac arrhythmias as well as left atrial appendage closure. The percutaneous epicardial approach has also been utilized for cardiac pacing and drug delivery. But still, its most common usage is for the treatment of intramural and subepicardial substrates that give rise to ventricular tachycardia, particularly in patients with nonischemic cardiomyopathy. In fact, subxiphoid, percutaneous epicardial mapping and ablation have emerged as an important adjunct and in some cases the preferred strategy for characterizing and treating certain types of ventricular arrhythmias. Herein, we will review the indications and rationale for various epicardial procedures. Additionally, we will explore the anatomy of the pericardium as well as the frequently-used epicardial access techniques. We will further examine the optimal approaches and methodologies for epicardial mapping and ablation and the impact of epicardial fat. We will also discuss the epicardial technique for left atrial appendage closure for the purpose of embolic stroke risk reduction. Finally, we will consider the potential for various complications in the setting of epicardial procedures along with their risk factors and discuss strategies to mitigate such adverse events.

Transvenous management of cardiac implantable electronic device late lead perforation.

INTRODUCTION: Late lead perforation (LLP), defined as perforation ≥30 days from cardiac implantable electronic device implant, is a rare diagnosis and little data exist regarding management practices and outcomes. The purpose of this study was to evaluate the occurrence, safety, and efficacy of transvenous management of clinically significant LLP. METHODS: The electronic medical records of a single-center tertiary hospital were reviewed for all patients who were referred for LLP or its sequelae. RESULTS: Eleven consecutive patients were identified from October 2011 to December 2018 with clinically significant LLP. Patients most often presented with pericardial symptoms with the exception of one asymptomatic patient. The median time from lead implant to intervention for LLP was 246 days. Nine patients were managed with an initial transvenous approach, with one requiring sternotomy (lead 6.3 years old). Two patients had a surgical approach, one performed at an outside hospital with subsequent death and another had a mini-thoracotomy, but the lead was removed percutaneously with no surgical repair. In this small cohort, there was no association between the lead extending beyond the parietal pericardium and surgical repair (P = .99). CONCLUSION: Our single-center experience suggests that LLP can be initially managed with a cautious transvenous approach in most patients, but intraprocedural ultrasound for pericardial monitoring and a rescue plan with immediate surgical back up is mandatory.

Adjunctive percutaneous ablation targeting epicardial arrhythmogenic structures in patients of atrial fibrillation with recurrence after multiple procedures.

INTRODUCTION: Repeat ablation strategy for atrial fibrillation (AF) recurrence after multiple ablation procedures is known to be challenging. This study evaluated the insights of adjunctive ablation for epicardial arrhythmogenic substrates in those patients via a percutaneous epicardial approach. METHODS AND RESULTS: Thirty-five consecutive patients with AF/atrial tachycardia (AT) recurrence, who had two or more prior ablation procedures, were enrolled from September 2016 to December 2018. In addition to a standard endocardial approach, epicardial mapping and ablation were performed via a percutaneous subxiphoid access in the electrophysiology lab. Adjunctive epicardial ablations for left lateral ridge (LLR) were performed in 31 of 35 patients (88.6%) for efficient transmural lesions with pacing capture loss. Marshall Bundle (MB) potentials were documented on epicardial LLR in three patients and abolished by direct epicardial ablation. Bachmann's bundle (BB) was ablated as an epicardial conduction gap in four patients with a refractory anterior wall line. Two epicardial AT/AF triggers were detected followed by successful termination with epicardial ablation. No periprocedural complications occurred. About 23 of 35 patients (65.7%) remained free from AF/AT after 23.2 ± 9 months of the procedure. CONCLUSIONS: Patients with multiple failed prior AF procedures refractory to antiarrhythmic therapy might warrant a percutaneous epicardial mapping and ablation strategy, with adjunctive therapy for targeting LLR/MB, BB, and underlying epicardial triggers in addition to a standard endocardial approach.

Targeting perivascular and epicardial adipose tissue inflammation: therapeutic opportunities for cardiovascular disease.

Major shifts in human lifestyle and dietary habits toward sedentary behavior and refined food intake triggered steep increase in the incidence of metabolic disorders including obesity and Type 2 diabetes. Patients with metabolic disease are at a high risk of cardiovascular complications ranging from microvascular dysfunction to cardiometabolic syndromes including heart failure. Despite significant advances in the standards of care for obese and diabetic patients, current therapeutic approaches are not always successful in averting the accompanying cardiovascular deterioration. There is a strong relationship between adipose inflammation seen in metabolic disorders and detrimental changes in cardiovascular structure and function. The particular importance of epicardial and perivascular adipose pools emerged as main modulators of the physiology or pathology of heart and blood vessels. Here, we review the peculiarities of these two fat depots in terms of their origin, function, and pathological changes during metabolic deterioration. We highlight the rationale for pharmacological targeting of the perivascular and epicardial adipose tissue or associated signaling pathways as potential disease modifying approaches in cardiometabolic syndromes.

Association of Local Epicardial Adipose Tissue Depots and Left Ventricular Diastolic Performance in Patients With Preserved Left Ventricular Ejection Fraction.

BACKGROUND: Although full-volume quantification of epicardial adipose tissue (EAT) is a predictor of LV diastolic dysfunction (LVDD), how localized EAT depots are linked to LVDD remains unclear. We evaluated the effect of local EAT depots on LV diastolic function parameters in patients with preserved LV ejection fraction (LVEF).Methods and Results:From 423 consecutive patients who underwent cardiac CT angiography, we recruited 252 with sinus rhythm and normal LVEF. The EAT volume index (EATV/body surface area) and the localized EAT thickness around the right coronary artery (EATRCA), left anterior descending artery (EATLAD), left circumflex artery (EATLCX), right ventricle (EATRV), left ventricle (EATLV), right atrium (EATRA), and left atrium (EATLA) were measured using cardiac CT. In the LVDD group (n=71), the EATV index (75±30 vs. 64±28 mL/m2, P=0.010), EATLCX(10.7±3.8 vs. 9.4±3.4 mm, P=0.008), and EATLV(2.6±1.6 vs. 2.1±1.4 mm, P=0.024) were greater than in the non-LVDD group (n=181). In contrast, EATLCXand EATLVwere markedly associated with decreased lateral e' and increased lateral E/e'. Multiple regression analysis indicated that EATLCXand EATLVwere strongly associated with LV diastolic function parameters. CONCLUSIONS: Localized EAT depots are linked to altered mitral annular motion. Further study is warranted to clarify whether localized EAT depots are functionally linked to the clinical manifestations of LVDD.

Epicardial adipose tissue thickness as a potential predictor of gestational diabetes mellitus: a prospective cohort study.

BACKGROUND: Gestational diabetes mellitus (GDM) is the most common metabolic disorder that can occur during pregnancy and is associated with a long-term risk of both maternal and neonatal comorbidities. This study aimed to investigate the association between echocardiographic epicardial adipose tissue (EAT) and the risk for GDM during the early second trimester of pregnancy. METHOD: We recruited all singleton pregnancies between January 2014 and December 2018 at 16 weeks + 0 days to 19 weeks + 6 days. We then used generalized linear models to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for EAT as a potential predictor for GDM. Receiver-operating-characteristic (ROC) analysis was then conducted to investigate the discriminative capacity of any individual maternal factor for the prediction of GDM. RESULTS: In total, our study involved 314 pregnant women with GDM and 1832 pregnant women without GDM. Multivariate regression analysis revealed that EAT thickness (OR = 2.87; 95% CI: 2.49-3.31) was significantly associated with the presence of GDM (P < 0.001). Furthermore, EAT thickness was also significantly associated with a range of adverse outcomes in the GDM group, including large size for gestational age, neonatal hypoglycemia, admission to the neonatal intensive care unit, preterm delivery, and hyperbilirubinemia (P < 0.001). ROC analysis revealed that the area under the curve was 0.790 (95% CI: 0.768-0.812). When the cutoff value for EAT thickness was set to 5.49 mm, the sensitivity was 95.2% and the specificity was 50.5%. CONCLUSIONS: Echocardiographic EAT thickness is positively and significantly associated with both the risk of GDM and adverse outcomes related to GDM. Echocardiographic EAT has the potential to predict GDM prior to actual clinical diagnosis.

Association of epicardial adipose tissues with obstructive sleep apnea and its severity: A meta-analysis study.

BACKGROUND AND AIMS: Obstructive sleep apnea (OSA) is a global disease that is a manifestation of metabolic syndrome. Epicardial adipose tissue (EAT), a special type of visceral adipose tissue, has been proposed to be an independent predictor of visceral adiposity. Both OSA and EAT have a close association with diabetes and coronary artery disease. Whether EAT thickness is associated with OSA is controversial. METHODS AND RESULTS: Several databases were searched from their inception to October 13, 2019. We estimated the summarized weighted mean difference (WMD) with 95% confidence intervals (CIs) for EAT thickness in the OSA and non-OSA groups. Then, we conducted a meta-analysis to evaluate the association between EAT thickness and OSA. The relationship between EAT thickness and OSA severity was also assessed. Nine studies with a total of 1178 participants were included. Globally, patients with OSA had a higher EAT thickness than patients without OSA (WMD = 0.95, 95% CI: 0.73-1.16, P < 0.001). Compared to the non-OSA patients, those with mild, moderate, and severe OSA had a progressively higher EAT thickness (WMD = 0.62, 95% CI: 0.41-0.83; WMD = 0.83, 95% CI: 0.50-1.15; and WMD = 1.06, 95% CI: 0.70-1.43, respectively; all P < 0.001). CONCLUSION: EAT thickness was shown to be higher in patients with OSA than in patients with non-OSA measured by echocardiography. The increase in the EAT thickness was associated with OSA severity.

Difference in epicardial adipose tissue distribution between paroxysmal atrial fibrillation and coronary artery disease.

BACKGROUND: An increase in epicardial adipose tissue (EAT) volume is associated with the development of atrial fibrillation (AF) and coronary artery disease (CAD), but little is known about differences in its distribution. METHODS AND RESULTS: We included 50 patients with paroxysmal AF (PAF), 50 patients with CAD, and 50 control patients. Using multidetector computed tomography, EAT volumes surrounding the whole heart (total EAT), the atrium (atrial-EAT), and the ventricle (ventricular-EAT) were measured. EAT atrial/ventricular (A/V) ratio was calculated by dividing atrial- by ventricular-EAT volume. The total EAT volume indexes in the PAF and CAD groups were significantly larger than those in the control group. The atrial-EAT volume index in the PAF group was significantly larger than that in the CAD and control groups, whereas the ventricular-EAT volume index in the CAD group was significantly larger than that in the PAF and control groups. Thus, EAT A/V ratio was smaller in the CAD and control group than that in the PAF group (0.28 ± 0.12 vs. 0.38 ± 0.13 vs. 0.54 ± 0.33, P < .001). Univariate and multivariate linear regression analysis showed EAT A/V ratio to be independently associated with cardiovascular disease type (PAF vs. CAD; P < .001, ß = .463). CONCLUSIONS: Atrial- and ventricular-dominant distribution of EAT was observed in the PAF and CAD groups, respectively. Uneven distribution of EAT may imply the direct contribution of EAT-related inflammation to the pathogenesis of AF or CAD.

Relationship Between Epicardial Adipose Tissue and Body Composition as Determined by Multi-Frequency Bioelectrical Impedance Analysis in Patients with Stage 5 Chronic Kidney Disease.

BACKGROUND The main cause of mortality among chronic kidney disease (CKD) patients is cardiovascular disease (CVD). Epicardial adipose tissue (EAT) is considered to be novel cardiovascular risk factor. We assessed EAT in non-dialyzed stage 5 CKD patients and explored the association of EAT with body composition as determined by multi-frequency BIA. MATERIAL AND METHODS The present included 70 stage 5 CKD patients who had not undergone dialysis and 40 healthy control subjects. EAT thickness was assessed by echocardiography. Hydration status and body composition were evaluated by multi-frequency bioelectrical impedance analysis. RESULTS Stage 5 CKD patients had significantly higher EAT thickness than healthy subjects (6.56±1.18 vs. 4.05±1.45, p<0.001). Fat tissue mass, systolic blood pressure (SBP), age, fat tissue index, and body mass index were positively correlated with EAT thickness in the CKD patient group (p<0.05). Lean tissue mass, lean tissue index (LTI), and high-density lipoprotein (HDL) were negatively correlated with EAT thickness in the CKD patient group (p<0.05). Stepwise multiple regression analysis showed that age, SBP, and LTI were independently associated with EAT thickness in CKD patients. CONCLUSIONS We found significantly higher EAT thickness in stage 5 CKD patients who were not on dialysis compared to healthy controls. EAT was significantly associated with age, SBP, and LTI in CKD patients. Interventions to reduce the risk factors associated with EAT thickness might protect against CVD disease in CKD patients.

Epicardial Adipose Thickness and Neutrophil Lymphocyte Ratio in Acute Occlusive Cerebrovascular Diseases.

OBJECTIVES: We investigate the relationship between the severity of vascular disease and epicardial adipose tissue thickness(EAT-t) and the neutrophil/lymphocyte (NEU/LY) ratio in acute stroke patients. METHODS: Seventy-six patients and 38 healthy controls were included in the study. Strokes were divided into three groups: lacunar infarction, middle cerebral artery infarction (MCA), and other arterial infarcts. Patients were assessed using the GCS (Glasgow coma scale) and NIHSS (National Institutes of Health Stroke Scale) scales. In addition to laboratory measurements, EAT-t was evaluated in all patients by using echocardiography. RESULTS: The EAT-t value and NEU/LY ratio were higher in the patient group than in the control group. The MCA group was found to have a significantly higher NEU/LY ratio than the lacuna group (p = 0.017) as well as the other patient (p = 0.025) group. There was a positive correlation of NIHSS score with EAT-t (r = 0.291; p = 0.013), and NEU/LY ratio (r = 0.289; p = 0.014). CONCLUSION: The EAT-t and NEU/LY ratio were high in patients with acute ischemic stroke patients. The higher ratio of NEU/LY compared to other infarcts in the MCA group. These findings support the relationship between acute ischemic stroke severity and inflammation .