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Association of Epicardial and Pericardial Adipose Tissue Volumes with Coronary Artery Calcification.International Heart Journal Nov 2022Epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) are anatomically close to the myocardium and may influence cardiovascular pathology. Thus, in this...
Epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT) are anatomically close to the myocardium and may influence cardiovascular pathology. Thus, in this study, we aim to assess whether EAT and PAT volumes were associated with coronary artery calcification score (CCS) in patients with suspected coronary artery disease (CAD), especially in overweight and obese individuals.We included consecutive patients with suspected CAD in whom EAT volume, PAT volume, and CCS were measured via computed tomography between September 2015 and June 2017 at the Affiliated Hospital of Chengde Medical University, China. Logistic regression models were applied to analyze the risk factors for CCS ≥ 100 Agatston units (AU) and in different body mass index (BMI) subgroups.EAT and PAT volumes were noted to be higher in people with BMI ≥ 24 kg/m, BMI ≥ 28 kg/m, hyperlipidemia, hypertension, diabetes, stroke, and CCS ≥ 100 AU (P < 0.05). After adjusting for the traditional CAD factors, we found that EAT and PAT volumes were independent risk factors for CCS ≥ 100 AU (odds ratio, 3.001; 95% confidence interval, 1.900-4.740, P < 0.001). In patients with CCS ≥ 100 AU, the EAT and PAT volumes were noted to be greater in the BMI ≥ 24 kg/m and BMI ≥ 28 kg/m subgroups than in the BMI < 24 kg/m and BMI < 28 kg/m subgroups, respectively (P < 0.05).Our results indicate that EAT and PAT volumes may be clinical predictors for a CCS ≥ 100 AU, especially in overweight and obese individuals.
Topics: Humans; Coronary Artery Disease; Vascular Calcification; Overweight; Pericardium; Adipose Tissue; Risk Factors; Obesity; Coronary Angiography
PubMed: 36372406
DOI: 10.1536/ihj.22-006 -
Circulation Research Sep 2014
Topics: Animals; Cell Lineage; Cell Proliferation; Fibroblasts; Pericardium
PubMed: 25214570
DOI: 10.1161/CIRCRESAHA.114.304854 -
Acta Cardiologica Jun 2023Pericardial agenesis is a rarely seen congenital defect characterised by the partial or, more rarely complete, absence of the pericardium. Most often asymptomatic, it is...
Pericardial agenesis is a rarely seen congenital defect characterised by the partial or, more rarely complete, absence of the pericardium. Most often asymptomatic, it is usually incidentally discovered following the demonstration of heart's laevorotation on imaging, in the operating room or at autopsy. In this article, we report the case of an 80-year-old patient with asymptomatic complete pericardial agenesis fortuitous discovered. Pericardial agenesis observations are extremely uncommon reported in the literature, which substantiate its original epidemiological character. In addition, this observation brings some clinical, electrical as well as iconographic elements to better understand the pathology and raises clinical suspicions. Finally, this case report confirms the exceptionally symptomatic nature of the pathology, illustrating the irrelevance of treatment or specific follow-up.
Topics: Humans; Aged, 80 and over; Pericardium; Freedom
PubMed: 34670482
DOI: 10.1080/00015385.2021.1991666 -
Diabetes & Metabolism Journal May 2024Heart failure (HF) management guidelines recommend individualized assessments based on HF phenotypes. Adiposity is a known risk factor for HF. Recently, there has been... (Review)
Review
Heart failure (HF) management guidelines recommend individualized assessments based on HF phenotypes. Adiposity is a known risk factor for HF. Recently, there has been an increased interest in organ-specific adiposity, specifically the role of the epicardial adipose tissue (EAT), in HF risk. EAT is easily assessable through various imaging modalities and is anatomically and functionally connected to the myocardium. In pathological conditions, EAT secretes inflammatory cytokines, releases excessive fatty acids, and increases mechanical load on the myocardium, resulting in myocardial remodeling. EAT plays a pathophysiological role in characterizing both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In HFrEF, EAT volume is reduced, reflecting an impaired metabolic reservoir, whereas in HFpEF, the amount of EAT is associated with worse biomarker and hemodynamic profiles, indicating increased EAT activity. Studies have examined the possibility of therapeutically targeting EAT, and recent studies using sodium glucose cotransporter 2 inhibitors have shown potential in reducing EAT volume. However, further research is required to determine the clinical implications of reducing EAT activity in patients with HF.
Topics: Humans; Heart Failure; Pericardium; Adipose Tissue; Stroke Volume; Adiposity; Sodium-Glucose Transporter 2 Inhibitors; Risk Factors; Epicardial Adipose Tissue
PubMed: 38310880
DOI: 10.4093/dmj.2023.0190 -
International Journal of Molecular... Apr 2023Epicardial adipose tissue (EAT) is an endocrine and paracrine organ constituted by a layer of adipose tissue directly located between the myocardium and visceral... (Review)
Review
Epicardial adipose tissue (EAT) is an endocrine and paracrine organ constituted by a layer of adipose tissue directly located between the myocardium and visceral pericardium. Under physiological conditions, EAT exerts protective effects of brown-like fat characteristics, metabolizing excess fatty acids, and secreting anti-inflammatory and anti-fibrotic cytokines. In certain pathological conditions, EAT acquires a proatherogenic transcriptional profile resulting in increased synthesis of biologically active adipocytokines with proinflammatory properties, promoting oxidative stress, and finally causing endothelial damage. The role of EAT in heart failure (HF) has been mainly limited to HF with preserved ejection fraction (HFpEF) and related to the HFpEF obese phenotype. In HFpEF, EAT seems to acquire a proinflammatory profile and higher EAT values have been related to worse outcomes. Less data are available about the role of EAT in HF with reduced ejection fraction (HFrEF). Conversely, in HFrEF, EAT seems to play a nutritive role and lower values may correspond to the expression of a catabolic, adverse phenotype. As of now, there is evidence that the beneficial systemic cardiovascular effects of sodium-glucose cotransporter-2 receptors-inhibitors (SGLT2-i) might be partially mediated by inducing favorable modifications on EAT. As such, EAT may represent a promising target organ for the development of new drugs to improve cardiovascular prognosis. Thus, an approach based on detailed phenotyping of cardiac structural alterations and distinctive biomolecular pathways may change the current scenario, leading towards a precision medicine model with specific therapeutic targets considering different individual profiles. The aim of this review is to summarize the current knowledge about the biomolecular pathway of EAT in HF across the whole spectrum of ejection fraction, and to describe the potential of EAT as a therapeutic target in HF.
Topics: Humans; Heart Failure; Stroke Volume; Adipose Tissue; Pericardium; Phenotype
PubMed: 37047810
DOI: 10.3390/ijms24076838 -
The Journal of Invasive Cardiology Aug 2021Pericardial constriction can be present without pericardial calcium and often without pericardial thickening. This epicardial coronary artery motion abnormality due to...
Pericardial constriction can be present without pericardial calcium and often without pericardial thickening. This epicardial coronary artery motion abnormality due to entrapment in a thickened, fibrotic pericardium, is characteristic of constrictive pericarditis, and differentiates this entity from other close differential diagnoses, such as restrictive and dilated cardiomyopathy.
Topics: Coronary Vessels; Diagnosis, Differential; Humans; Pericarditis, Constrictive; Pericardium
PubMed: 34338662
DOI: No ID Found -
Heart Rhythm Mar 2017
Review
Topics: Brugada Syndrome; Catheter Ablation; Electrocardiography; Heart Conduction System; Humans; Pericardium
PubMed: 27979714
DOI: 10.1016/j.hrthm.2016.12.001 -
Circulation. Arrhythmia and... Jun 2015
Topics: Animals; Body Surface Potential Mapping; Electrocardiography; Epicardial Mapping; Heart Conduction System; Pericardium
PubMed: 26082525
DOI: 10.1161/CIRCEP.115.003056 -
JACC. Cardiovascular Interventions Jun 2023
Topics: Humans; Treatment Outcome; Pericardial Effusion; Cardiac Tamponade; Pericardium
PubMed: 37204396
DOI: 10.1016/j.jcin.2023.03.053 -
Experimental Physiology Aug 2020What is the central question of this study? Are the mechanisms that cause ventricular interdependence different when due to primary right to left ventricular pressure...
NEW FINDINGS
What is the central question of this study? Are the mechanisms that cause ventricular interdependence different when due to primary right to left ventricular pressure loading? What is the main finding and its importance? An instantaneous selective increase in aortic pressure causes an immediate increase in right ventricular end-systolic pressure independent of the pericardium, whereas a selective increase in pulmonary artery pressure decreases left ventricular diastolic compliance owing to a subsequent increasing right ventricular end-diastolic volume as a function of an intact pericardium limiting biventricular volume. Changes in contraction synchrony of either ventricle do not appear to be causing these effects.
ABSTRACT
I characterized the dynamic factors determining ventricular interdependence with and without the pericardium. I measured right (RV) and left ventricular (LV) pressures and volumes simultaneously using conductance catheters in seven pentobarbitone-anaesthetized open-chested 5- to 7-week-old piglets. I studied these effects during apnoea, inferior vena caval occlusion and rapid partial aortic and pulmonary arterial occlusions. Conductance catheter-defined long-axis regional volumes were assessed to define regional contractile synchrony. Closed-pericardium measures were made from an initial (baseline) volume, then after two 20 ml kg fluid loads followed by an open-pericardium step. Baseline RV and LV volumes were similar. Aortic occlusion increased LV pressures and volumes and RV end-systolic pressure such that RV end-systolic elastance increased without changes in RV contraction synchrony, not affected by the pericardium. Pulmonary artery occlusion increased RV end-systolic pressure but not end-systolic volume. On the subsequent beat, RV end-diastolic pressure increased, whereas LV end-diastolic volume and diastolic compliance decreased. These effects were attenuated by opening the pericardium. Contraction synchrony across longitudinal segments was unaltered by either aortic or pulmonary artery occlusion. I conclude that the determinants of systolic and diastolic ventricular interdependence are different. Increasing RV pressures causes diastolic RV-to-LV interdependence, decreasing LV diastolic compliance and dependent on an intact pericardium. An increase in LV end-systolic pressure increases RV end-systolic elastance independent of the pericardium and has a minimal effect on RV diastolic function or contraction synchrony.
Topics: Animals; Arterial Pressure; Diastole; Heart Ventricles; Pericardium; Swine; Systole; Ventricular Function
PubMed: 32436594
DOI: 10.1113/EP088550