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The American Journal of Emergency... Aug 2022Pericardial tamponade requires timely diagnosis and management. It carries a high mortality rate. (Review)
Review
INTRODUCTION
Pericardial tamponade requires timely diagnosis and management. It carries a high mortality rate.
OBJECTIVE
This review incorporates available evidence to clarify misconceptions regarding the clinical presentation, while providing an in-depth expert guide on bedside echocardiography. It also details the decision-making strategy for emergency management including pericardiocentesis, along with pre- and peri-procedural pearls and pitfalls.
DISCUSSION
Pericardial effusions causing tamponade arise from diverse etiologies across acute and sub-acute time courses. The most frequently reported symptom is dyspnea. The classically taught Beck's triad (which includes hypotension) does not appear commonly. Echocardiographic findings include: a pericardial effusion (larger size associated with tamponade), diastolic right ventricular collapse (specific), systolic right atrial collapse (sensitive), a plethoric non-collapsible inferior vena cava (sensitive), and sonographic pulsus paradoxus. Emergent pericardiocentesis is warranted by hemodynamic instability, impending deterioration, or cardiac arrest. Emergent surgical indications include type A aortic dissection causing hemopericardium, ventricular free wall rupture after acute myocardial infarction, severe chest trauma, and iatrogenic hemopericardium when bleeding cannot be controlled percutaneously. Pre-procedure management includes blood products for patients with traumatic hemopericardium; gentle intravenous fluids to hypotensive, hypovolemic patients with consideration for vasoactive medications; treatment of anticoagulation, coagulopathies, and anemia. Positive-pressure ventilation and intravenous sedation can lower cardiac output and should be avoided if possible. Optimal location for echocardiography-guided pericardiocentesis is the largest, shallowest fluid pocket with no intervening vital structures. Patient positioning to prevent hypoxia and liberal amounts of local anesthesia can facilitate patients remaining still. Safe needle guidance and confirmation of catheter placement is achieved using low-depth sonographic views, injection of agitated saline, and evaluation of initial aspirate for hemorrhage. Pericardial fluid should be drained slowly to avoid pericardial decompression syndrome.
CONCLUSION
An understanding of the pathophysiology, clinical presentation, echocardiographic findings, and time-sensitive management of pericardial tamponade is essential for emergency physicians.
Topics: Cardiac Tamponade; Echocardiography; Emergency Medicine; Humans; Hypotension; Pericardial Effusion; Pericardiocentesis
PubMed: 35696801
DOI: 10.1016/j.ajem.2022.05.001 -
Circulation Research Jul 2022Establishment of the myocardial wall requires proper growth cues from nonmyocardial tissues. During heart development, the epicardium and epicardium-derived cells...
BACKGROUND
Establishment of the myocardial wall requires proper growth cues from nonmyocardial tissues. During heart development, the epicardium and epicardium-derived cells instruct myocardial growth by secreting essential factors including FGF (fibroblast growth factor) 9 and IGF (insulin-like growth factor) 2. However, it is poorly understood how the epicardial secreted factors are regulated, in particular by chromatin modifications for myocardial formation. The current study is to investigate whether and how HDAC (histone deacetylase) 3 in the developing epicardium regulates myocardial growth.
METHODS
Various cellular and mouse models in conjunction with biochemical and molecular tools were employed to study the role of HDAC3 in the developing epicardium.
RESULTS
We deleted in the developing murine epicardium, and mutant hearts showed ventricular myocardial wall hypoplasia with reduction of epicardium-derived cells. The cultured embryonic cardiomyocytes with supernatants from knockout (KO) mouse epicardial cells also showed decreased proliferation. Genome-wide transcriptomic analysis revealed that and were significantly downregulated in KO mouse epicardial cells. We further found that and expression is dependent on HDAC3 deacetylase activity. The supplementation of FGF9 or IGF2 can rescue the myocardial proliferation defects treated by KO supernatant. Mechanistically, we identified that microRNA (miR)-322 and miR-503 were upregulated in KO mouse epicardial cells and epicardial KO hearts. Overexpression of miR-322 or miR-503 repressed FGF9 and IGF2 expression, while knockdown of miR-322 or miR-503 restored FGF9 and IGF2 expression in KO mouse epicardial cells.
CONCLUSIONS
Our findings reveal a critical signaling pathway in which epicardial HDAC3 promotes compact myocardial growth by stimulating FGF9 and IGF2 through repressing miR-322 or miR-503, providing novel insights in elucidating the etiology of congenital heart defects and conceptual strategies to promote myocardial regeneration.
Topics: Animals; Heart; Mice; MicroRNAs; Myocardium; Myocytes, Cardiac; Pericardium; Signal Transduction
PubMed: 35722872
DOI: 10.1161/CIRCRESAHA.122.320785 -
Radiologic Clinics of North America Jul 2016Lymphoma of the heart and pericardium may develop in up to 25% of patients with disseminated nodal disease, but primary cardiac lymphoma is rare. The majority are... (Review)
Review
Lymphoma of the heart and pericardium may develop in up to 25% of patients with disseminated nodal disease, but primary cardiac lymphoma is rare. The majority are diffuse large B-cell lymphomas, which arise in immunocompetent older individuals, men twice as often as women. Subsets are found in immunocompromised patients, including those with HIV-AIDS or allograft recipients. Cardiac lymphomas tend to arise in the wall of the right heart, especially right atrium, with contiguous infiltration of epicardium and pericardium. Pericardial implants and effusions are common. The disease is often multifocal in the heart, but cardiac valves are usually spared.
Topics: Diagnosis, Differential; Evidence-Based Medicine; Heart Neoplasms; Humans; Lymphoma
PubMed: 27265603
DOI: 10.1016/j.rcl.2016.03.006 -
Heart Asia 2018A 32-year-old woman with no other medical history presented with 1-month history of fever, weight loss and dyspnoea. On examination she had elevated jugular venous...
CASE PRESENTATION
A 32-year-old woman with no other medical history presented with 1-month history of fever, weight loss and dyspnoea. On examination she had elevated jugular venous pressure and tachycardia. Her chest X-ray posterioranterior view (figure 1A) showed a rounded mass in the right cardiophrenic angle obscuring the right atrial margin, producing a 'silhouette' sign. Echocardiography showed a large cystic mass with thickened pericardium, lateral to the right atrium, causing right atrial compression (figure 1B). CT image of the chest showed a cystic lesion compressing the right atrium with thickened pericardium (figure 2A). There were no other lesions found in the lungs or other organs. Laboratory tests showed elevated erythrocyte sedimentation rate (ESR: 96 mm/hour) and C reactive protein (CRP: 32 mg/L). Excision of the mass with partial pericardiectomy was done. Intraoperatively, there was a cyst with thickened pericardial wall and thick yellowish brown fluid. Histopathology of the tissue is shown in figure 2B.Figure 1(A) Chest X-ray posterioranterior view showing a rounded mass in the right cardiophrenic angle. (B) Transthoracic echocardiography apical four-chamber view showing the cystic mass.Figure 2(A) CT of the chest sagittal view showing cystic lesion compressing the right atrium with thickened pericardium. (B) Histopathology specimen of the pericardial tissue.
QUESTION
What is the diagnosis and what should be the management strategy?Congenital pericardial cyst and no further evaluation required.Features are suggestive of tuberculous pericardial cyst and needs treatment with antituberculosis regimen.Features suggestive of pericardial hydatid cyst and requires treatment with albendazole.Features are suggestive of viral pericarditis with encysted effusion.
PubMed: 30116306
DOI: 10.1136/heartasia-2018-011071 -
Nature Biotechnology Dec 2023The epicardium, the mesothelial envelope of the vertebrate heart, is the source of multiple cardiac cell lineages during embryonic development and provides signals that...
The epicardium, the mesothelial envelope of the vertebrate heart, is the source of multiple cardiac cell lineages during embryonic development and provides signals that are essential to myocardial growth and repair. Here we generate self-organizing human pluripotent stem cell-derived epicardioids that display retinoic acid-dependent morphological, molecular and functional patterning of the epicardium and myocardium typical of the left ventricular wall. By combining lineage tracing, single-cell transcriptomics and chromatin accessibility profiling, we describe the specification and differentiation process of different cell lineages in epicardioids and draw comparisons to human fetal development at the transcriptional and morphological levels. We then use epicardioids to investigate the functional cross-talk between cardiac cell types, gaining new insights into the role of IGF2/IGF1R and NRP2 signaling in human cardiogenesis. Finally, we show that epicardioids mimic the multicellular pathogenesis of congenital or stress-induced hypertrophy and fibrotic remodeling. As such, epicardioids offer a unique testing ground of epicardial activity in heart development, disease and regeneration.
Topics: Humans; Pericardium; Heart; Myocardium; Cell Differentiation; Cell Lineage; Biology
PubMed: 37012447
DOI: 10.1038/s41587-023-01718-7 -
Cell Reports Mar 2020Cardiac ischemia leads to the loss of myocardial tissue and the activation of a repair process that culminates in the formation of a scar whose structural...
Cardiac ischemia leads to the loss of myocardial tissue and the activation of a repair process that culminates in the formation of a scar whose structural characteristics dictate propensity to favorable healing or detrimental cardiac wall rupture. To elucidate the cellular processes underlying scar formation, here we perform unbiased single-cell mRNA sequencing of interstitial cells isolated from infarcted mouse hearts carrying a genetic tracer that labels epicardial-derived cells. Sixteen interstitial cell clusters are revealed, five of which were of epicardial origin. Focusing on stromal cells, we define 11 sub-clusters, including diverse cell states of epicardial- and endocardial-derived fibroblasts. Comparing transcript profiles from post-infarction hearts in C57BL/6J and 129S1/SvImJ inbred mice, which displays a marked divergence in the frequency of cardiac rupture, uncovers an early increase in activated myofibroblasts, enhanced collagen deposition, and persistent acute phase response in 129S1/SvImJ mouse hearts, defining a crucial time window of pathological remodeling that predicts disease outcome.
Topics: Animals; Cicatrix; Homeostasis; Mice; Mice, Inbred Strains; Myocardial Infarction; Myocardium; Myofibroblasts; Pericardium; Phenotype; RNA-Seq; Rupture; Single-Cell Analysis; Stromal Cells
PubMed: 32130914
DOI: 10.1016/j.celrep.2020.02.008 -
Advances in Experimental Medicine and... 2019Cardiovascular disease (CVD) is the main cause of morbidity and mortality in industrialized countries, despite the evolution of treatments and revascularization... (Review)
Review
Cardiovascular disease (CVD) is the main cause of morbidity and mortality in industrialized countries, despite the evolution of treatments and revascularization strategies. Obesity, also accompanied by a chronic inflammatory process, is an independent risk factor for CVD. Abdominal adipose tissue is a complex, metabolically very active organ capable of producing different adipokines and hormones, responsible for endocrine-metabolic comorbidities. The epicardial adipose tissue (EAT) has not been as extensively studied as the abdominal or subcutaneous adipose tissue. However, recent evidence associates it with an increased cardiometabolic risk due to its apposition with the heart. EAT stores triglycerides to provide energy to the myocardium and is characterized by its greater ability to release and capture free fatty acids. EAT strategic localization allows a singular cross talk with cardiomyocytes and vascular wall cells. The fact that EAT produces pro-inflammatory adipokines as well as metalloproteinases and pro-oxidant substances, highlights its possible direct impact on plaque vulnerability and heart failure, being still necessary further studies of EAT behavior in CVD.
Topics: Adipokines; Adipose Tissue; Cardiovascular Diseases; Humans; Metalloproteases; Myocardium; Pericardium; Reactive Oxygen Species; Risk Factors; Triglycerides
PubMed: 31140176
DOI: 10.1007/978-3-030-11488-6_9