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IntroductionPericardiocentesis is a life-saving procedure to remove excess fluid from pericardium in cardiac tamponade, in some circumstances it may be used for diagnostic purposes. Due to invasive nature, it carries potential risks although the use of imaging guidance has reduced risk significantly. We aim to provide an up-to-date analysis of pericardiocentesis complications occurring at a high-volume tertiary cardiac referral centre in UK.MethodThis was a single centre retrospective study of patients who underwent pericardiocentesis between February 2010 and June 2023 at Barts Heart Centre, London. Data was collected from electronic patient record and entered into database. Data extracted included demographics, procedural approach, imaging mode, size of effusion, urgency of procedure, aetiology of pericardium effusion, outcomes and complications of procedure.Result329 patients underwent pericardiocentesis with median age of 57 yrs. Most of the procedures(90.5%) were performed as urgent or emergency for large effusions with evidence of cardiac tamponade or impending tamponade. Majority were drained using subcostal approach(80.8%). All procedures were carried out under transthoracic echocardiogram or fluoroscopic guidance. Malignancy accounted for the cause in half of the study cohort(50.4%). In non-malignant group, idiopathic(10.6%) was most common, followed by parapneumonic aetiology(6.1%). Complications occurred in 19/329 cases(5.8%), with minor complication rate of 3.0%(see table 1) and major of 2.7%(see table 2). Right cardiac chamber puncture occurred in 5/329 cases(1.5%), majority had no significant sequelae. There was one death directly attributable to the procedure as a result of right cardiac chamber puncture. There was one case of injury to adjacent organ, in this case hepatic injury resulting in a liver hematoma. Pericardial decompression occurred in 2/330 cases representing a rate of 1% in patient cohort.Abstract 1-031 Table 1Breakdown of minor complication and procedural complication rateMinor complications10 (3.0%) Bradyarrhythmia2 (0.6%)Atrial fibrillation within 24 hours 4 (1.2%)Vasovagal1 (0.3%) Pleural puncture (no sequelae)3 (0.9%)Peritoneal puncture (no sequelae)1 (0.3%)Abstract 1-031 Table 2Breakdown of major complication and procedural complication rate statistics in both tables displayed as n= and% of cohortMajor complications9 (2.7%) Injury to adjacent organ1 (0.3%) Pericardial Decompression2 (0.6%)Ventricular tachyarrhythmia2 (0.6%)Right cardiac chamber puncture without sequelae4 (1.2%)Right cardiac chamber puncture with sequelae1 (0.3%)ConclusionPericardiocentesis performed in an expert centre under imaging guidance is safe with low complication rate. In our unselected large patient cohort, the rate of major and minor complications was in line with expected complication rate from the literature. Complications whilst rare, can be significant in their nature when they occur, centres should have the necessary expertise and equipment readily available to manage.

Background Glycosuria produced by sodium–glucose co-transporter-2 (SGLT-2) inhibitors is associated with weight loss. SGLT-2 inhibitors reportedly might reduce the occurrence of cardiovascular events. Epicardial adipose tissue (EAT) is a pathogenic fat depot that may be associated with coronary atherosclerosis. The present study evaluated the relationship between an SGLT-2 inhibitor (dapagliflozin) and EAT volume. Methods In 40 diabetes mellitus patients with coronary artery disease (10 women and 30 men; mean age of all 40 patients was 67.2 ± 5.4 years), EAT volume was compared prospectively between the dapagliflozin treatment group (DG; n = 20) and conventional treatment group (CTG; n = 20) during a 6-month period. EAT was defined as any pixel that had computed tomography attenuation of − 150 to − 30 Hounsfield units within the pericardial sac. Metabolic parameters, including HbA1c, tumor necrotic factor-α (TNF-α), and plasminogen activator inhibitor-1 (PAI-1) levels, were measured at both baseline and 6-months thereafter. Results There were no significant differences at baseline of EAT volume and HbA1c, PAI-1, and TNF-α levels between the two treatment groups. After a 6-month follow-up, the change in HbA1c levels in the DG decreased significantly from 7.2 to 6.8%, while body weight decreased significantly in the DG compared with the CTG (− 2.9 ± 3.4 vs. 0.2 ± 2.4 kg, p = 0.01). At the 6-month follow-up, serum PAI-1 levels tended to decline in the DG. In addition, the change in the TNF-α level in the DG was significantly greater than that in the CTG (− 0.5 ± 0.7 vs. 0.03 ± 0.3 pg/ml, p = 0.03). Furthermore, EAT volume significantly decreased in the DG at the 6-month follow-up compared with the CTG (− 16.4 ± 8.3 vs. 4.7 ± 8.8 cm 3 , p = 0.01). Not only the changes in the EAT volume and body weight, but also those in the EAT volume and TNF-α level, showed significantly positive correlation. Conclusion Treatment with dapagliflozin might improve systemic metabolic parameters and decrease the EAT volume in diabetes mellitus patients, possibly contributing to risk reduction in cardiovascular events.

The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Here we found that epicardial cells contain a potent cardiogenic activity identified as follistatin-like 1 (Fstl1). Epicardial Fstl1 declines following myocardial infarction and is replaced by myocardial expression. Myocardial Fstl1 does not promote regeneration, either basally or upon transgenic overexpression. Application of the human Fstl1 protein (FSTL1) via an epicardial patch stimulates cell cycle entry and division of pre-existing cardiomyocytes, improving cardiac function and survival in mouse and swine models of myocardial infarction. The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans. The secreted factor follistatin-like 1 (FSTL1) becomes undetectable in the epicardium of infarcted hearts; when reconstituted using a collagen patch sutured onto an infarcted heart, FSTL1 can induce cell cycle entry and division of pre-existing cardiomyocytes, thus boosting heart function and survival in mouse and pig models of myocardial infarction. FSTL1 boosts cardiac regeneration Human heart tissue has a limited capacity to regenerate but recent studies have suggested that the epicardium might preserve function of the adult myocardium following injury to some extent, possibly by providing myogenic progenitors. This study identifies the secreted factor follistatin-like 1 (FSTL1) as a regenerative factor that is normally present in healthy epicardium, but lost following myocardial infarction, suggesting a mechanism whereby injury diminishes the regenerative potency of the mammalian heart. Reconstitution of FSTL1 by an engineered epicardial biomaterial improved cardiac function in animal models of myocardial infarction, with evidence of cardiomyocyte regeneration amenable to clinical translation.

BackgroundEpicardial adipose tissue represents a metabolically active visceral fat depot that is in direct contact with the left ventricular myocardium. While it is associated with coronary artery disease, little is known regarding its role in aortic stenosis. We sought to investigate the association of epicardial adipose tissue with aortic stenosis severity and progression, myocardial remodelling and function, and mortality in asymptomatic patients with aortic stenosis.MethodsIn a post hoc analysis of 124 patients with asymptomatic mild-to-severe aortic stenosis participating in a prospective clinical trial, baseline epicardial adipose tissue was quantified on CT angiography using fully automated deep learning-enabled software. Aortic stenosis disease severity was assessed at baseline and 1 year. The primary endpoint was all-cause mortality.ResultsNeither epicardial adipose tissue volume nor attenuation correlated with aortic stenosis severity or subsequent disease progression as assessed by echocardiography or CT (p>0.05 for all). Epicardial adipose tissue volume correlated with plasma cardiac troponin concentration (r=0.23, p=0.009), left ventricular mass (r=0.46, p<0.001), ejection fraction (r=−0.28, p=0.002), global longitudinal strain (r=0.28, p=0.017), and left atrial volume (r=0.39, p<0.001). During the median follow-up of 48 (IQR 26–73) months, a total of 23 (18%) patients died. In multivariable analysis, both epicardial adipose tissue volume (HR 1.82, 95% CI 1.10 to 3.03; p=0.021) and plasma cardiac troponin concentration (HR 1.47, 95% CI 1.13 to 1.90; p=0.004) were associated with all-cause mortality, after adjustment for age, body mass index and left ventricular ejection fraction. Patients with epicardial adipose tissue volume >90 mm3 had 3–4 times higher risk of death (adjusted HR 3.74, 95% CI 1.08 to 12.96; p=0.037).ConclusionsEpicardial adipose tissue volume does not associate with aortic stenosis severity or its progression but does correlate with blood and imaging biomarkers of impaired myocardial health. The latter may explain the association of epicardial adipose tissue volume with an increased risk of all-cause mortality in patients with asymptomatic aortic stenosis.Clinicaltrials.gov (NCT02132026).

Background Modulation of the cardiac autonomic nervous system (ANS) is a promising adjuvant therapy in the treatment of atrial fibrillation (AF). In pre-clinical models, pulsed field (PF) energy has the advantage of selectively ablating the epicardial ganglionated plexi (GP) that govern the ANS. This study aims to demonstrate the feasibility and safety of epicardial ablation of the GPs with PF during cardiac surgery with a primary efficacy outcome of prolongation of the atrial effective refractory period (AERP). Methods In a single-arm, prospective analysis, patients with or without a history of AF underwent epicardial GP ablation with PF during coronary artery bypass grafting (CABG). AERP was determined immediately pre- and post- GP ablation to assess cardiac ANS function. Holter monitors were performed to determine rhythm status and heart rate variability (HRV) at baseline and at 1-month post-procedure. Results Of 24 patients, 23 (96%) received the full ablation protocol. No device-related adverse effects were noted. GP ablation resulted in a 20.7 ± 19.9% extension in AERP ( P  < 0.001). Post-operative AF was observed in 7 (29%) patients. Holter monitoring demonstrated an increase in mean heart rate (74.0 ± 8.7 vs. 80.6 ± 12.3, P  = 0.01). There were no significant changes in HRV. There were no study-related complications. Conclusions This study demonstrates the safety and feasibility of epicardial ablation of the GP using PF to modulate the ANS during cardiac surgery. Large, randomized analyses are necessary to determine whether epicardial PF ablation can offer a meaningful impact on the cardiac ANS and reduce AF. Trial registration Clinical trial registration: NCT04775264.

Xenogeneic pericardium-based substitutes are employed for several surgical indications after chemical shielding, limiting their biocompatibility and therapeutic durability. Adverse responses to these replacements might be prevented by tissue decellularization, ideally removing cells and preserving the original extracellular matrix (ECM). The aim of this study was to compare the mostly applied pericardia in clinics, i.e., bovine and porcine tissues, after their decellularization, and obtain new insights for their possible surgical use. Bovine and porcine pericardia were submitted to TRICOL decellularization, based on osmotic shock, detergents and nuclease treatment. TRICOL procedure resulted in being effective in cell removal and preservation of ECM architecture of both species’ scaffolds. Collagen and elastin were retained but glycosaminoglycans were reduced, significantly for bovine scaffolds. Tissue hydration was varied by decellularization, with a rise for bovine pericardia and a decrease for porcine ones. TRICOL significantly increased porcine pericardial thickness, while a non-significant reduction was observed for the bovine counterpart. The protein secondary structure and thermal denaturation profile of both species’ scaffolds were unaltered. Both pericardial tissues showed augmented biomechanical compliance after decellularization. The ECM bioactivity of bovine and porcine pericardia was unaffected by decellularization, sustaining viability and proliferation of human mesenchymal stem cells and endothelial cells. In conclusion, decellularized bovine and porcine pericardia demonstrate possessing the characteristics that are suitable for the creation of novel scaffolds for reconstruction or replacement: differences in water content, thickness and glycosaminoglycans might influence some of their biomechanical properties and, hence, their indication for surgical use.

Epicardial adipose tissue (EAT) is associated with cardiovascular risk. The longitudinal change in EAT volume (EATv) and density (EATd), and potential modulators of these parameters, has not been described. We prospectively recruited 90 patients with non-obstructive coronary atherosclerosis on baseline computed tomography coronary angiography (CTCA) performed for suspected coronary artery disease to undergo a repeat research CTCA. EATv in millilitres (mL) and EATd in Hounsfield units (HU) were analysed and multivariable regression analysis controlling for traditional cardiovascular risk factors (CVRF) performed to assess for any predictors of change. Secondary analysis was performed based on statin therapy. The median duration between CTCA was 4.3years. Mean EATv increased at follow-up (72 ± 33 mL to 89 ± 43 mL, p < 0.001) and mean EATd decreased (baseline −76 ± 6 HU vs. −86 ± 5 HU, p < 0.001). There were no associations between baseline variables of body mass index, age, sex, hypertension, hyperlipidaemia, diabetes or smoking on change in EATv or EATd. No difference in baseline, follow-up or delta EATv or EATd was seen in patients with (60%) or without baseline statin therapy. In this select group of patients, EATv consistently increased and EATd consistently decreased at long-term follow-up and these changes were independent of CVRF, age and statin use. Together with the knowledge of strong associations between EAT and cardiac disease, these findings may suggest that EAT is an independent parameter rather than a surrogate for cardiovascular risk.

Animal-derived xenogeneic biomaterials utilized in different surgeries are promising for various applications in tissue engineering. However, tissue decellularization is necessary to attain a bioactive extracellular matrix (ECM) that can be safely transplanted. The main objective of the present study is to assess the structural integrity, biocompatibility, and potential use of various acellular biomaterials for tissue engineering applications. Hence, a bovine pericardium (BP), porcine pericardium (PP), and porcine tunica vaginalis (PTV) were decellularized using a Trypsin, Triton X (TX), and sodium dodecyl sulfate (SDS) (Trypsin + TX + SDS) protocol. The results reveal effective elimination of the cellular antigens with preservation of the ECM integrity confirmed via staining and electron microscopy. The elasticity of the decellularized PP (DPP) was markedly (p < 0.0001) increased. The tensile strength of DBP, and DPP was not affected after decellularization. All decellularized tissues were biocompatible with persistent growth of the adipose stem cells over 30 days. The staining confirmed cell adherence either to the peripheries of the materials or within their matrices. Moreover, the in vivo investigation confirmed the biocompatibility and degradability of the decellularized scaffolds. Conclusively, Trypsin + TX + SDS is a successful new protocol for tissue decellularization. Moreover, decellularized pericardia and tunica vaginalis are promising scaffolds for the engineering of different tissues with higher potential for the use of DPP in cardiovascular applications and DBP and DPTV in the reconstruction of higher-stress-bearing abdominal walls.

Epicardial adipose tissue volume (EAT) has been linked to coronary artery disease and the risk of major adverse cardiac events. As manual quantification of EAT is time-consuming, requires specialized training, and is prone to human error, we developed a deep learning method (DeepFat) for the automatic assessment of EAT on non-contrast low-dose CT calcium score images. Our DeepFat intuitively segmented the tissue enclosed by the pericardial sac on axial slices, using two preprocessing steps. First, we applied a HU-attention-window with a window/level 350/40-HU to draw attention to the sac and reduce numerical errors. Second, we applied a novel look ahead slab-of-slices with bisection (“ bisect ”) in which we split the heart into halves and sequenced the lower half from bottom-to-middle and the upper half from top-to-middle, thereby presenting an always increasing curvature of the sac to the network. EAT volume was obtained by thresholding voxels within the sac in the fat window (− 190/− 30-HU). Compared to manual segmentation, our algorithm gave excellent results with volume Dice = 88.52% ± 3.3, slice Dice = 87.70% ± 7.5, EAT error = 0.5% ± 8.1, and R = 98.52% (p < 0.001). HU-attention-window and bisect improved Dice volume scores by 0.49% and 3.2% absolute, respectively. Variability between analysts was comparable to variability with DeepFat. Results compared favorably to those of previous publications.

Background Heart failure (HF) with preserved ejection fraction (HFpEF) is increasingly prevalent worldwide due to aging and comorbidities. Epicardial adipose tissue (EAT), favored by diabetes and obesity, was shown to contribute to HFpEF pathophysiology and is an emerging therapeutic target. This study explored the relationship between ventricular EAT measured by cardiovascular magnetic resonance (CMR), metabolic factors, and imaging characteristics in controls, pre-HF patients, and HFpEF patients. Methods Patients from a Belgian cohort enrolled from December 2015 to June 2017 were categorized by HF stage: pre-HF (n = 16), HFpEF (n = 104) and compared to matched controls (n = 26) and to pre-HF (n = 191) from the Beta3-LVH cohort. Biventricular EAT volume was measured in end-diastolic short-axis cine stacks. In the Belgian cohort, associations between EAT, HF stage, and various biological and imaging markers were explored. The clinical endpoint was a composite of mortality or first HF hospitalization in the HFpEF group. Results EAT significantly differed between groups, with higher values in HFpEF patients compared to pre-HF and controls (72.4 ± 20.8ml/m 2 vs. 55.0 ± 11.8ml/m 2 and 48 ± 8.9ml/m 2 , p < 0.001) from the Belgian cohort and to pre-HF (52.0 ± 15.0 ml/m 2 , p < 0.001) from the Beta3-LVH cohort. Subsequent analyses focused on the Belgian cohort. In contrast to atrial fibrillation, diabetes prevalence and body mass index (BMI) did not differ between pre-HF and HFpEF patients. Multivariable logistic regression and random forest classification identified EAT, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and H 2 FPEF score as strong markers of HFpEF status. EAT was significantly correlated with H 2 FPEF score (r = 0.41, p = 0.003), BMI (r = 0.30, p < 0.001), high‐sensitive troponin T (r = 0.41, p < 0.001), NT-proBNP (r = 0.37, p < 0.001), soluble suppression of tumorigenicity-2 (sST2) (r = 0.30, p < 0.001), E/e’ ratio (r = 0.33, p < 0.001), and left ventricular global longitudinal strain (r = 0.35, p < 0.001). In HFpEF patients, diabetes, ischemic cardiomyopathy, and elevated sST2 were independently associated with elevated EAT. In contrast with diabetes and BMI, increased EAT was not associated with prognosis. Conclusions EAT assessed by CMR was significantly higher in HFpEF patients compared to controls and pre-HF patients, irrespective of diabetes and BMI. EAT was moderately associated with HFpEF status. HFpEF patients with elevated EAT exhibited a marked diabetic, ischemic, and inflammatory profile, highlighting the potential role of drugs targeting EAT. Trial registration Characterization of Heart Failure With Preserved Ejection Fraction; Assessment of Efficacy of Mirabegron, a New beta3-adrenergic Receptor in the Prevention of Heart Failure (Beta3_LVH). Trial registration number ClinicalTrials.gov. Identifier: NCT03197350; NCT02599480. Graphical abstract