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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 -
Radiology May 2013The pericardium represents an important focus of morbidity and mortality in patients with cardiovascular disease. Fortunately, in recent years knowledge regarding this... (Review)
Review
UNLABELLED
The pericardium represents an important focus of morbidity and mortality in patients with cardiovascular disease. Fortunately, in recent years knowledge regarding this enigmatic part of the heart and the diagnosis of related diseases has substantially advanced. To a large extent, this can be attributed to the availability of several noninvasive cardiac imaging modalities. Transthoracic echocardiography, which combines structural and physiologic assessment, is the first-line technique for examination of patients suspected of having or known to have pericardial disease; however, cardiac computed tomography (CT) and magnetic resonance (MR) imaging are becoming increasingly popular for the study of this part of the heart. Modern multidetector CT scanners merge acquisition speed and high spatial and contrast resolution, with volumetric scanning to provide excellent anatomic detail of the pericardium. Multidetector CT is by far the modality of choice for depiction of pericardial calcifications. MR imaging is probably the best imaging modality for the acquisition of a comprehensive view of the pericardial abnormalities. MR imaging combines cardiac and pericardial anatomic assessment with tissue characterization and appraisal of the effects of pericardial abnormalities on cardiac performance. This review aims to elucidate the role of the pericardium and its interaction with the remainder of the heart in normal and pathologic conditions. It focuses on the rapidly evolving insights regarding pericardial disease provided by modern imaging modalities, not infrequently necessitating reconsideration of evidence that has thus far been taken for granted.
SUPPLEMENTAL MATERIAL
http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.13121059/-/DC1.
Topics: Diagnosis, Differential; Heart Diseases; Humans; Magnetic Resonance Imaging; Pericardium; Tomography, X-Ray Computed
PubMed: 23610095
DOI: 10.1148/radiol.13121059 -
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 -
Journal of the American College of... Feb 1986
Topics: Heart; Humans; Methods; Pericardium; Pressure; Surface Properties
PubMed: 3944350
DOI: 10.1016/s0735-1097(86)80497-1 -
BMC Cardiovascular Disorders Jun 2021The primitive neuroectodermal tumors (PNETs) are a family of highly malignant tumors with a multidirectional differential potential. The tumors are characterized by... (Review)
Review
BACKGROUND
The primitive neuroectodermal tumors (PNETs) are a family of highly malignant tumors with a multidirectional differential potential. The tumors are characterized by aggressive small round tumor cells that originate from the spinal cord of the central and sympathetic nervous systems. Cases involving the pericardium are extremely rare. Herein, we present a case of peripheral primitive neuroectodermal tumor (pPNET) that originated in the pericardium.
CASE PRESENTATION
A 23-year-old woman presented with cough and progressive dyspnea for 1 month, followed by eyelid and facial edema for 10 days, without any apparent cause. Significantly elevated tumor markers were detected in her blood. A cardiac ultrasound revealed a 74 mm × 61 mm spherical mass that was attached to the left pericardium, as well as massive pericardial effusion. Positron emission tomography-CT (PET-CT) showed focal hypermetabolism in the left pericardium. Via histopathology and immunohistochemistry, the spherical mass was identified as PNETS. The patient was successfully treated with a combination of surgical resection via thoracotomy and postoperative chemotherapy, and she was disease-free for 7 years at follow-up. Unfortunately, at 7 years after the treatment, the patient's pPNET recurred. Positron emission tomography-MRI (PET-MRI) and 64-slice coronary CTA revealed that the aorta and multiple coronary arteries were involved. Subsequently, the patient refused a heart transplant and voluntarily left the hospital.
CONCLUSIONS
This paper reports on a rare and recurrent case of PNET in the parietal pericardium. With respect to the different biologic characteristics and prognoses of pPNETs (compared to other known pericardium tumors), it is essential to consider this entity as a differential diagnosis in pericardium tumors.
Topics: Cardiac Surgical Procedures; Chemotherapy, Adjuvant; Female; Heart Neoplasms; Humans; Neoplasm Recurrence, Local; Neuroectodermal Tumors, Primitive, Peripheral; Pericardium; Time Factors; Treatment Outcome; Young Adult
PubMed: 34134636
DOI: 10.1186/s12872-021-02113-3 -
JACC. Clinical Electrophysiology Jul 2022Epicardial access is becoming increasingly important for various cardiovascular interventions. Access to dry pericardial space can be challenging and is often associated... (Review)
Review
Epicardial access is becoming increasingly important for various cardiovascular interventions. Access to dry pericardial space can be challenging and is often associated with significant complications. A novel concealed-needle blunt-tip device is designed to capture the parietal pericardium layer and retract it into the distal end of the device, which houses a fixated concealed needle, in a bid to minimize the likelihood of lacerating the visceral layer of the pericardium. This prospective single-arm study evaluated the feasibility of use of this device in 11 human subjects with successful access attained in 91% (10 of 11) of cases without adverse events. (Pericardial Access With ViaOne Device; NCT05006157).
Topics: Clinical Studies as Topic; Feasibility Studies; Humans; Pericardium; Prospective Studies
PubMed: 35750622
DOI: 10.1016/j.jacep.2022.04.016 -
Anatomical Record (Hoboken, N.J. : 2007) Jun 2019The proepicardium (PE) is a transitory extracardiac embryonic structure which plays a crucial role in cardiac morphogenesis and delivers various cell lineages to the... (Review)
Review
The proepicardium (PE) is a transitory extracardiac embryonic structure which plays a crucial role in cardiac morphogenesis and delivers various cell lineages to the developing heart. The PE arises from the lateral plate mesoderm (LPM) and is present in all vertebrate species. During development, mesothelial cells of the PE reach the naked myocardium either as free-floating aggregates in the form of vesicles or via a tissue bridge; subsequently, they attach to the myocardium and, finally, form the third layer of a mature heart-the epicardium. After undergoing epithelial-to-mesenchymal transition (EMT) some of the epicardial cells migrate into the myocardial wall and differentiate into fibroblasts, smooth muscle cells, and possibly other cell types. Despite many recent findings, the molecular pathways that control not only proepicardial induction and differentiation but also epicardial formation and epicardial cell fate are poorly understood. Knowledge about these events is essential because molecular mechanisms that occur during embryonic development have been shown to be reactivated in pathological conditions, for example, after myocardial infarction, during hypertensive heart disease or other cardiovascular diseases. Therefore, in this review we intended to summarize the current knowledge about PE formation and structure, as well as proepicardial cell fate in animals commonly used as models for studies on heart development. Anat Rec, 302:893-903, 2019. © 2018 Wiley Periodicals, Inc.
Topics: Animals; Cell Differentiation; Cell Movement; Epithelial Cells; Epithelial-Mesenchymal Transition; Fibroblasts; Humans; Mesoderm; Myocytes, Smooth Muscle; Pericardium; Pluripotent Stem Cells; Species Specificity
PubMed: 30421563
DOI: 10.1002/ar.24028 -
Frontiers in Endocrinology 2023In recent decades, the epicardial adipose tissue (EAT) has been at the forefront of scientific research because of its diverse role in the pathogenesis of cardiovascular... (Review)
Review
In recent decades, the epicardial adipose tissue (EAT) has been at the forefront of scientific research because of its diverse role in the pathogenesis of cardiovascular diseases (CVDs). EAT lies between the myocardium and the visceral pericardium. The same microcirculation exists both in the epicardial fat and the myocardium. Under physiological circumstances, EAT serves as cushion and protects coronary arteries and myocardium from violent distortion and impact. In addition, EAT acts as an energy lipid source, thermoregulator, and endocrine organ. Under pathological conditions, EAT dysfunction promotes various CVDs progression in several ways. It seems that various secretions of the epicardial fat are responsible for myocardial metabolic disturbances and, finally, leads to CVDs. Therefore, EAT might be an early predictor of CVDs. Furthermore, different non-invasive imaging techniques have been proposed to identify and assess EAT as an important parameter to stratify the CVD risk. We also present the potential therapeutic possibilities aiming at modifying the function of EAT. This paper aims to provide overview of the potential role of EAT in CVDs, discuss different imaging techniques to assess EAT, and provide potential therapeutic options for EAT. Hence, EAT may represent as a potential predictor and a novel therapeutic target for management of CVDs in the future.
Topics: Humans; Cardiovascular Diseases; Pericardium; Myocardium; Coronary Vessels; Adipose Tissue
PubMed: 37260440
DOI: 10.3389/fendo.2023.1167952 -
Circulation Research Jun 2012Epithelial to mesenchymal transition (EMT) converts epithelial cells to mobile and developmentally plastic mesenchymal cells. All cells in the heart arise from one or... (Review)
Review
Epithelial to mesenchymal transition (EMT) converts epithelial cells to mobile and developmentally plastic mesenchymal cells. All cells in the heart arise from one or more EMTs. Endocardial and epicardial EMTs produce most of the noncardiomyocyte lineages of the mature heart. Endocardial EMT generates valve progenitor cells and is necessary for formation of the cardiac valves and for complete cardiac septation. Epicardial EMT is required for myocardial growth and coronary vessel formation, and it generates cardiac fibroblasts, vascular smooth muscle cells, a subset of coronary endothelial cells, and possibly a subset of cardiomyocytes. Emerging studies suggest that these developmental mechanisms are redeployed in adult heart valve disease, in cardiac fibrosis, and in myocardial responses to ischemic injury. Redirection and amplification of disease-related EMTs offer potential new therapeutic strategies and approaches for treatment of heart disease. Here, we review the role and molecular regulation of endocardial and epicardial EMT in fetal heart development, and we summarize key literature implicating reactivation of endocardial and epicardial EMT in adult heart disease.
Topics: Animals; Endocardium; Epithelial Cells; Epithelial-Mesenchymal Transition; Heart; Heart Diseases; Humans; Pericardium
PubMed: 22679138
DOI: 10.1161/CIRCRESAHA.111.259960