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BMC Medical Imaging May 2021Pericardial hematoma is blood accumulation in the pericardial space. Although rare, it could arise in various conditions, such as after cardiac surgery. Clinical... (Review)
Review
BACKGROUND
Pericardial hematoma is blood accumulation in the pericardial space. Although rare, it could arise in various conditions, such as after cardiac surgery. Clinical diagnosis of pericardial hematoma is implausible; thus, cardiac imaging plays a pivotal role in identifying this condition. We presented a case of multiple pericardial hematomas, which was found as an incidental finding in post-cardiac surgery evaluation. We highlighted the diagnostic challenge and the key features of multi-modality cardiac imaging in pericardial hematoma evaluation.
CASE PRESENTATION
An asymptomatic, 35-years old male, who underwent surgical closure of secundum atrial septal defect (ASD) one month ago, came for routine transthoracic echocardiography evaluation. An intrapericardiac hematoma was visualized at the right ventricle (RV) 's free wall side. Another mass with an indistinct border was visualized near the right atrium (RA). This mass was suspected as pericardial hematoma differential diagnosed with intracardiac thrombus. Cardiac computed tomography (CT) scan showed both masses have an attenuation of 30-40 HU; however, the mass's border at the RA side was still not clearly delineated. Mild superior vena cava (SVC) compression and multiple mediastinal lymphadenopathies were also detected. These findings are not typical for pericardial hematomas nor intracardiac thrombus; hence another additional differential diagnosis of pericardial neoplasm was considered. We pursued further cardiac imaging modalities because the patient refused to undergo an open biopsy. Single-photon emission computer tomography (SPECT)/CT with Technetium-99 m (Tc-99 m) macro-aggregated albumin (MAA) and Sestamibi showed filling defect without increased radioactivity, thus exclude the intracardiac thrombus. Cardiac magnetic resonance imaging (MRI) reveals intrapericardial masses with low intensity of T1 signal and heterogeneously high intensity on T2 signal weighted imaged and no evidence of gadolinium enhancement, which concluded the diagnosis as subacute pericardial hematomas. During follow-up, the patient remains asymptomatic, and after six months, the pericardial hematomas were resolved.
CONCLUSION
Pericardial hematoma should be considered as a cause of pericardial masses after cardiac surgery. When imaging findings are atypical, further multi-modality cardiac imaging must be pursued to establish the diagnosis. Careful and meticulous follow-up should be considered for an asymptomatic patient with stable hemodynamic.
Topics: Adult; Diagnosis, Differential; Heart Atria; Heart Neoplasms; Heart Septal Defects, Atrial; Heart Ventricles; Hematoma; Humans; Incidental Findings; Magnetic Resonance Imaging; Male; Multimodal Imaging; Pericardium; Postoperative Complications; Single Photon Emission Computed Tomography Computed Tomography; Thrombosis; Tomography, X-Ray Computed
PubMed: 34006236
DOI: 10.1186/s12880-021-00617-0 -
CJC Open Jan 2022Mulibrey nanism (MUL) is a rare condition with profound growth delay. Congestive heart failure is a major determinant of prognosis. The aim was to delineate pericardial...
BACKGROUND
Mulibrey nanism (MUL) is a rare condition with profound growth delay. Congestive heart failure is a major determinant of prognosis. The aim was to delineate pericardial constriction and myocardial functional abnormalities in a pediatric MUL sample.
METHODS
A total of 23 MUL patients and 23 individually sex- and age-matched healthy control subjects were prospectively assessed in a cross-sectional study with echocardiography.
RESULTS
Clinical signs of heart failure were present in 7 MUL patients, with severe congestive heart failure in 2. Significant diastolic dysfunction, mainly related to constriction, was found in MUL patients without pericardiectomy (N = 18)-septal bounce, pronounced hepatic vein atrial reversal and right heart inflow-outflow variations, and decreased inferior vena cava collapse during respiration. The appearance of the pericardium was not different from that of control subjects. Longitudinal diastolic myocardial velocities were similar to those in control subjects, suggesting an absence of significant myocardial restriction. Right ventricular free wall longitudinal systolic strain and bilateral longitudinal myocardial systolic velocities were decreased in MUL patients, indicating mild biventricular systolic dysfunction. Myocardial motion abnormalities and persistent congestive heart failure were common (in 3 of 6) in MUL patients with a history of pericardiectomy. Cardiac dimensions were similar between MUL patients and control subjects when adjusting for body size, except for smaller biventricular volumes.
CONCLUSIONS
MUL disease presents with significant constriction-related diastolic dysfunction and mild bilateral systolic dysfunction. Constriction-restriction assessments during follow-up could be of benefit in decision-making regarding pericardiectomy in MUL disease. Myocardial abnormalities were prevalent among MUL patients who had undergone pericardiectomy and are consistent with progression of myocardial disease in a significant proportion of patients.
PubMed: 35072025
DOI: 10.1016/j.cjco.2021.08.012 -
Journal of Cardiovascular Imaging Jun 2018Interpretation of cardiac uptake on 18-fluorodeoxyglucose positron emission tomography/computed tomography (F-FDG PET/CT) is often confounded by intense physiological...
BACKGROUND
Interpretation of cardiac uptake on 18-fluorodeoxyglucose positron emission tomography/computed tomography (F-FDG PET/CT) is often confounded by intense physiological FDG uptake and numerous benign conditions. The aim of the study was to describe the echocardiographic features in concordance with cardiac and pericardial F-FDG uptake on whole-body oncology PET/CT.
METHODS
We enrolled 43 consecutive patients (34 solid tumors, 8 lymphomas and 1 leukemia) who were newly diagnosed with non-cardiac malignancy showing incidental cardiac or pericardial F-FDG uptake on PET/CT and underwent transthoracic Doppler echocardiography (TTE) within 1 month of PET/CT. The maximum standardized uptake (SUV) of all lesions was measured.
RESULTS
Fifty-six F-FDG uptake lesions (32 pericardium, 7 myocardium, 9 cardiac chambers and 8 great vessels) were found, and pericardial effusion was the most common echocardiographic finding (22/43, 51.2%) among study population. Pericardial FDG uptake was shown as pericardial effusion (68.8%), intrapericardial echogenic materials (31.3%), pericardial thickening (28.1%), hyperechogenicity of myopericardium (18.8%), and restricted sliding movement or constrictive pericarditis (15.6%) on TTE. Lesions with regional wall motion abnormality ( = 0.004) or constrictive pericarditis ( = 0.021) had significantly higher mean SUV than those without. Myocardial FDG uptake demonstrated pericardial effusion (57.1%), regional wall motion abnormality (57.1%), and increased myocardial wall thickness (42.9%). All cardiac chamber FDG uptakes showed intracardiac mass on TTE.
CONCLUSIONS
Cardiac or pericardial F-FDG uptake on oncology PET/CT shows characteristic echocardiographic features according to which heart sites are involved.
PubMed: 29971271
DOI: 10.4250/jcvi.2018.26.e10 -
The Journal of Physiology Sep 2022Hypertensive heart disease (HHD) increases risk of ventricular tachycardia (VT) and ventricular fibrillation (VF). The roles of structural vs. electrophysiological...
Hypertensive heart disease (HHD) increases risk of ventricular tachycardia (VT) and ventricular fibrillation (VF). The roles of structural vs. electrophysiological remodelling and age vs. disease progression are not fully understood. This cross-sectional study of cardiac alterations through HHD investigates mechanistic contributions to VT/VF risk. Risk was electrically assessed in Langendorff-perfused, spontaneously hypertensive rat hearts at 6, 12 and 18 months, and paced optical membrane voltage maps were acquired from the left ventricular (LV) free wall epicardium. Distributions of LV patchy fibrosis and 3D cellular architecture in representative anterior LV mid-wall regions were quantified from macroscopic and microscopic fluorescence images of optically cleared tissue. Imaging showed increased fibrosis from 6 months, particularly in the inner LV free wall. Myocyte cross-section increased at 12 months, while inter-myocyte connections reduced markedly with fibrosis. Conduction velocity decreased from 12 months, especially transverse to the myofibre direction, with rate-dependent anisotropy at 12 and 18 months, but not earlier. Action potential duration (APD) increased when clustered by age, as did APD dispersion at 12 and 18 months. Among 10 structural, functional and age variables, the most reliably linked were VT/VF risk, general LV fibrosis, a measure quantifying patchy fibrosis, and non-age clustered APD dispersion. VT/VF risk related to a quantified measure of patchy fibrosis, but age did not factor strongly. The findings are consistent with the notion that VT/VF risk is associated with rate-dependent repolarization heterogeneity caused by structural remodelling and reduced lateral electrical coupling between LV myocytes, providing a substrate for heterogeneous intramural activation as HHD progresses. KEY POINTS: There is heightened arrhythmic risk with progression of hypertensive heart disease. Risk is related to increasing left ventricular fibrosis, but the nature of this relationship has not been quantified. This study is a novel systematic characterization of changes in active electrical properties and fibrotic remodelling during progression of hypertensive heart disease in a well-established animal disease model. Arrhythmic risk is predicted by several left ventricular measures, in particular fibrosis quantity and structure, and epicardial action potential duration dispersion. Age alone is not a good predictor of risk. An improved understanding of links between arrhythmic risk and fibrotic architectures in progressive hypertensive heart disease aids better interpretation of late gadolinium-enhanced cardiac magnetic resonance imaging and electrical mapping signals.
Topics: Action Potentials; Animals; Arrhythmias, Cardiac; Cross-Sectional Studies; Fibrosis; Multimodal Imaging; Pericardium; Rats; Rats, Inbred SHR; Tachycardia, Ventricular; Ventricular Fibrillation
PubMed: 35984854
DOI: 10.1113/JP282526 -
Circulation. Arrhythmia and... Jun 2024Endocardial catheter-based pulsed field ablation (PFA) of the ventricular myocardium is promising. However, little is known about PFA's ability to target intracavitary...
BACKGROUND
Endocardial catheter-based pulsed field ablation (PFA) of the ventricular myocardium is promising. However, little is known about PFA's ability to target intracavitary structures, epicardium, and ways to achieve transmural lesions across thick ventricular tissue.
METHODS
A lattice-tip catheter was used to deliver biphasic monopolar PFA to swine ventricles under general anesthesia, with electroanatomical mapping, fluoroscopy and intracardiac echocardiography guidance. We conducted experiments to assess the feasibility and safety of repetitive monopolar PFA applications to ablate (1) intracavitary papillary muscles and moderator bands, (2) epicardial targets, and (3) bipolar PFA for midmyocardial targets in the interventricular septum and left ventricular free wall.
RESULTS
(1) Papillary muscles (n=13) were successfully ablated and then evaluated at 2, 7, and 21 days. Nine lesions with stable contact measured 18.3±2.4 mm long, 15.3±1.5 mm wide, and 5.8±1.0 mm deep at 2 days. Chronic lesions demonstrated preserved chordae without mitral regurgitation. Two targeted moderator bands were transmurally ablated without structural disruption. (2) Transatrial saline/carbon dioxide assisted epicardial access was obtained successfully and epicardial monopolar lesions had a mean length, width, and depth of 30.4±4.2, 23.5±4.1, and 9.1±1.9 mm, respectively. (3) Bipolar PFA lesions were delivered across the septum (n=11) and the left ventricular free wall (n=7). Twelve completed bipolar lesions had a mean length, width, and depth of 29.6±5.5, 21.0±7.3, and 14.3±4.7 mm, respectively. Chronically, these lesions demonstrated uniform fibrotic changes without tissue disruption. Bipolar lesions were significantly deeper than the monopolar epicardial lesions.
CONCLUSIONS
This in vivo evaluation demonstrates that PFA can successfully ablate intracavitary structures and create deep epicardial lesions and transmural left ventricular lesions.
Topics: Animals; Ventricular Septum; Catheter Ablation; Swine; Heart Ventricles; Feasibility Studies; Papillary Muscles; Time Factors; Pericardium; Cardiac Catheters; Ultrasonography, Interventional; Electrophysiologic Techniques, Cardiac; Equipment Design; Female
PubMed: 38753535
DOI: 10.1161/CIRCEP.124.012734 -
International Journal of Nanomedicine 2012Myocardial infarction (MI) is characterized by heart-wall thinning, myocyte slippage, and ventricular dilation. The injury to the heart-wall muscle after MI is... (Review)
Review
Myocardial infarction (MI) is characterized by heart-wall thinning, myocyte slippage, and ventricular dilation. The injury to the heart-wall muscle after MI is permanent, as after an abundant cell loss the myocardial tissue lacks the intrinsic capability to regenerate. New therapeutics are required for functional improvement and regeneration of the infarcted myocardium, to overcome harmful diagnosis of patients with heart failure, and to overcome the shortage of heart donors. In the past few years, myocardial tissue engineering has emerged as a new and ambitious approach for treating MI. Several left ventricular assist devices and epicardial patches have been developed for MI. These devices and acellular/cellular cardiac patches are employed surgically and sutured to the epicardial surface of the heart, limiting the region of therapeutic benefit. An injectable system offers the potential benefit of minimally invasive release into the myocardium either to restore the injured extracellular matrix or to act as a scaffold for cell delivery. Furthermore, intramyocardial injection of biomaterials and cells has opened new opportunities to explore and also to augment the potentials of this technique to ease morbidity and mortality rates owing to heart failure. This review summarizes the growing body of literature in the field of myocardial tissue engineering, where biomaterial injection, with or without simultaneous cellular delivery, has been pursued to enhance functional and structural outcomes following MI. Additionally, this review also provides a complete outlook on the tissue-engineering therapies presently being used for myocardial regeneration, as well as some perceptivity into the possible issues that may hinder its progress in the future.
Topics: Animals; Cells, Cultured; Guided Tissue Regeneration; Humans; Injections, Intralesional; Minimally Invasive Surgical Procedures; Myocardial Ischemia; Myocytes, Cardiac; Pericardium; Tissue Engineering; Tissue Scaffolds
PubMed: 23271906
DOI: 10.2147/IJN.S37575 -
Frontiers in Endocrinology 2021In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity... (Review)
Review
In March 2020, the WHO declared coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a global pandemic. Obesity was soon identified as a risk factor for poor prognosis, with an increased risk of intensive care admissions and mechanical ventilation, but also of adverse cardiovascular events. Obesity is associated with adipose tissue, chronic low-grade inflammation, and immune dysregulation with hypertrophy and hyperplasia of adipocytes and overexpression of pro-inflammatory cytokines. However, to implement appropriate therapeutic strategies, exact mechanisms must be clarified. The role of white visceral adipose tissue, increased in individuals with obesity, seems important, as a viral reservoir for SARS-CoV-2 angiotensin-converting enzyme 2 (ACE2) receptors. After infection of host cells, the activation of pro-inflammatory cytokines creates a setting conducive to the "cytokine storm" and macrophage activation syndrome associated with progression to acute respiratory distress syndrome. In obesity, systemic viral spread, entry, and prolonged viral shedding in already inflamed adipose tissue may spur immune responses and subsequent amplification of a cytokine cascade, causing worse outcomes. More precisely, visceral adipose tissue, more than subcutaneous fat, could predict intensive care admission; and lower density of epicardial adipose tissue (EAT) could be associated with worse outcome. EAT, an ectopic adipose tissue that surrounds the myocardium, could fuel COVID-19-induced cardiac injury and myocarditis, and extensive pneumopathy, by strong expression of inflammatory mediators that could diffuse paracrinally through the vascular wall. The purpose of this review is to ascertain what mechanisms may be involved in unfavorable prognosis among COVID-19 patients with obesity, especially cardiovascular events, emphasizing the harmful role of excess ectopic adipose tissue, particularly EAT.
Topics: Adipose Tissue; Angiotensin-Converting Enzyme 2; COVID-19; Cardiomyopathies; Heart Diseases; Humans; Inflammation; Intra-Abdominal Fat; Obesity; Pericardium; Prognosis; SARS-CoV-2; Serine Endopeptidases
PubMed: 34484128
DOI: 10.3389/fendo.2021.726967 -
Stem Cell Research & Therapy May 2015Engineered bioimplants for cardiac repair require functional vascularization and innervation for proper integration with the surrounding myocardium. The aim of this work...
Engineered bioimplants for cardiac repair require functional vascularization and innervation for proper integration with the surrounding myocardium. The aim of this work was to study nerve sprouting and neovascularization in an acellular pericardial-derived scaffold used as a myocardial bioimplant. To this end, 17 swine were submitted to a myocardial infarction followed by implantation of a decellularized human pericardial-derived scaffold. After 30 days, animals were sacrificed and hearts were analyzed with hematoxylin/eosin and Masson's and Gallego's modified trichrome staining. Immunohistochemistry was carried out to detect nerve fibers within the cardiac bioimplant by using βIII tubulin and S100 labeling. Isolectin B4, smooth muscle actin, CD31, von Willebrand factor, cardiac troponin I, and elastin antibodies were used to study scaffold vascularization. Transmission electron microscopy was performed to confirm the presence of vascular and nervous ultrastructures. Left ventricular ejection fraction (LVEF), cardiac output (CO), stroke volume, end-diastolic volume, end-systolic volume, end-diastolic wall mass, and infarct size were assessed by using magnetic resonance imaging (MRI). Newly formed nerve fibers composed of several amyelinated axons as the afferent nerve endings of the heart were identified by immunohistochemistry. Additionally, neovessel formation occurred spontaneously as small and large isolectin B4-positive blood vessels within the scaffold. In summary, this study demonstrates for the first time the neoformation of vessels and nerves in cell-free cardiac scaffolds applied over infarcted tissue. Moreover, MRI analysis showed a significant improvement in LVEF (P = 0.03) and CO (P = 0.01) and a 43 % decrease in infarct size (P = 0.007).
Topics: Animals; Coronary Vessels; Immunohistochemistry; Magnetic Resonance Imaging; Myocardial Infarction; Myocardium; Neovascularization, Pathologic; Pericardium; S100 Proteins; Swine; Tissue Scaffolds; Tubulin; Ventricular Function, Left
PubMed: 26205795
DOI: 10.1186/s13287-015-0101-6 -
TheScientificWorldJournal Nov 2007During heart development, cells of the primary and secondary heart field give rise to the myocardial component of the heart. The neural crest and epicardium provide the... (Review)
Review
During heart development, cells of the primary and secondary heart field give rise to the myocardial component of the heart. The neural crest and epicardium provide the heart with a considerable amount of nonmyocardial cells that are indispensable for correct heart development. During the past 2 decades, the importance of epicardium-derived cells (EPDCs) in heart formation became increasingly clear. The epicardium is embryologically formed by the outgrowth of proepicardial cells over the naked heart tube. Following epithelial-mesenchymal transformation, EPDCs form the subepicardial mesenchyme and subsequently migrate into the myocardium, and differentiate into smooth muscle cells and fibroblasts. They contribute to the media of the coronary arteries, to the atrioventricular valves, and the fibrous heart skeleton. Furthermore, they are important for the myocardial architecture of the ventricular walls and for the induction of Purkinje fiber formation. Whereas the exact signaling cascades in EPDC migration and function still need to be elucidated, recent research has revealed several factors that are involved in EPDC migration and specialization, and in the cross-talk between EPDCs and other cells during heart development. Among these factors are the Ets transcription factors Ets-1 and Ets-2. New data obtained with lentiviral antisense constructs targeting Ets-1 and Ets-2 specifically in the epicardium indicate that both factors are independently involved in the migratory behavior of EPDCs. Ets-2 seems to be especially important for the migration of EPDCs into the myocardial wall, and to subendocardial positions in the atrioventricular cushions and the trabeculae. With respect to the clinical importance of correct EPDC development, the relation with coronary arteriogenesis has been noted well before. In this review, we also propose a role for EPDCs in cardiac looping, and emphasize their contribution to the development of the valves and myocardial architecture. Lastly, we focus on the congenital heart anomalies that might be caused primarily by an epicardial developmental defect.
Topics: Animals; Heart Defects, Congenital; Humans; Morphogenesis; Myocytes, Cardiac; Pericardium; Proto-Oncogene Protein c-ets-1; Proto-Oncogene Protein c-ets-2
PubMed: 18040540
DOI: 10.1100/tsw.2007.294 -
Heart Rhythm Feb 2021The absence of strategies to consistently and effectively address nonparoxysmal atrial fibrillation by nonpharmacological interventions has represented a long-standing... (Review)
Review
The absence of strategies to consistently and effectively address nonparoxysmal atrial fibrillation by nonpharmacological interventions has represented a long-standing treatment gap. A combined epicardial/endocardial ablation strategy, the hybrid Convergent procedure, was developed in response to this clinical need. A subxiphoid incision is used to access the pericardial space facilitating an epicardial ablation directed at isolation of the posterior wall of the left atrium. This is followed by an endocardial ablation to complete isolation of the pulmonary veins and for additional ablation as needed. Experience gained with the hybrid Convergent procedure during the last decade has led to the development and adoption of strategies to optimize the technique and mitigate risks. Additionally, a surgical and electrophysiology "team" approach including comprehensive training is believed critical to successfully develop the hybrid Convergent program. A recently completed randomized clinical trial indicated that this ablation strategy is superior to an endocardial-only approach for patients with persistent atrial fibrillation. In this review, we propose and describe best practice guidelines for hybrid Convergent ablation on the basis of a combination of published data, author consensus, and expert opinion. A summary of clinical outcomes, emerging evidence, and future perspectives is also given.
Topics: Atrial Fibrillation; Catheter Ablation; Endocardium; Heart Conduction System; Heart Rate; Humans; Pericardium; Practice Guidelines as Topic; Recurrence
PubMed: 33045430
DOI: 10.1016/j.hrthm.2020.10.004