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IDCases 2020A 52-year-old man was evaluated in our outpatient facility because of a thoracic mass for one month. A needle biopsy of the chest mass was performed and microbiological...
A 52-year-old man was evaluated in our outpatient facility because of a thoracic mass for one month. A needle biopsy of the chest mass was performed and microbiological culture showed growth of . Three months after starting antimicrobial therapy, acute phase reactants normalized, and chest CT showed a progressive reduction in the size of the phlegmon. To our knowledge, we report the first case of diaphragmatic and chest wall infection without pulmonary involvement. This supports the theory of hematogenous spread of the germ from oral mucosa to produce thoracic lesions.
PubMed: 32514396
DOI: 10.1016/j.idcr.2020.e00846 -
Biochemical and Biophysical Research... Mar 2016Recent identification of the neonatal 2nd coronary vascular population (2nd CVP) suggests that a subset of these vessels form de novo and mature in the inner myocardial...
Recent identification of the neonatal 2nd coronary vascular population (2nd CVP) suggests that a subset of these vessels form de novo and mature in the inner myocardial wall of the postnatal heart. However, the origin of smooth muscle cells (SMCs) in the postnatal 2nd CVP remains undetermined. Using a tamoxifen-inducible Wt1-CreER driver and a Rosa26-RFP reporter line, we traced the lineage of epicardial cells to determine if they contribute to SMCs of the 2nd CVP. Late embryonic and postnatal induction of Wt1-CreER activity demonstrated that at these stages Wt1-labeled epicardium does not significantly migrate into the myocardium to form SMCs. However, following tamoxifen treatment at an early embryonic stage (E10.5), we detected Wt1 descendants (epicardium-derived cells, or EPDCs) in the outer myocardial wall at E17.5. When the 2nd CVP forms and remodels at postnatal stage, these early labeled EDPCs re-migrate deep into the inner myocardial wall and contribute to 2nd CVP-SMCs in the adult heart. Our findings reveal that SMCs in the postnatal 2nd CVP are pre-specified as EPDCs from the earliest wave of epicardial cell migration. Rather than the re-activation and migration of epicardial cells at later stages, these resident EPDCs mobilize and contribute to smooth muscle of the 2nd CVP during postnatal development.
Topics: Animals; Animals, Newborn; Cell Movement; Coronary Vessels; Mice, Inbred C57BL; Mice, Transgenic; Muscle, Smooth, Vascular; Myocardium; Pericardium; Tamoxifen
PubMed: 26902114
DOI: 10.1016/j.bbrc.2016.02.062 -
European Heart Journal. Cardiovascular... Oct 2022We evaluated independent associations of cardiovascular magnetic resonance (CMR)-measured pericardial adipose tissue (PAT) with cardiovascular structure and function and...
AIMS
We evaluated independent associations of cardiovascular magnetic resonance (CMR)-measured pericardial adipose tissue (PAT) with cardiovascular structure and function and considered underlying mechanism in 42 598 UK Biobank participants.
METHODS AND RESULTS
We extracted PAT and selected CMR metrics using automated pipelines. We estimated associations of PAT with each CMR metric using linear regression adjusting for age, sex, ethnicity, deprivation, smoking, exercise, processed food intake, body mass index, diabetes, hypertension, height cholesterol, waist-to-hip ratio, impedance fat measures, and magnetic resonance imaging abdominal visceral adiposity measures. Higher PAT was independently associated with unhealthy left ventricular (LV) structure (greater wall thickness, higher LV mass, more concentric pattern of LV hypertrophy), poorer LV function (lower LV global function index, lower LV stroke volume), lower left atrial ejection fraction, and lower aortic distensibility. We used multiple mediation analysis to examine the potential mediating effect of cardiometabolic diseases and blood biomarkers (lipid profile, glycaemic control, inflammation) in the PAT-CMR relationships. Higher PAT was associated with cardiometabolic disease (hypertension, diabetes, high cholesterol), adverse serum lipids, poorer glycaemic control, and greater systemic inflammation. We identified potential mediation pathways via hypertension, adverse lipids, and inflammation markers, which overall only partially explained the PAT-CMR relationships.
CONCLUSION
We demonstrate association of PAT with unhealthy cardiovascular structure and function, independent of baseline comorbidities, vascular risk factors, inflammatory markers, and multiple non-invasive and imaging measures of obesity. Our findings support an independent role of PAT in adversely impacting cardiovascular health and highlight CMR-measured PAT as a potential novel imaging biomarker of cardiovascular risk.
Topics: Humans; Adiposity; Biological Specimen Banks; Pericardium; Obesity; Magnetic Resonance Imaging; Biomarkers; Phenotype; Hypertension; Inflammation; United Kingdom; Cholesterol; Lipids
PubMed: 35640889
DOI: 10.1093/ehjci/jeac101 -
Scientific Reports Nov 2021Cardiac morphogenesis relies on intricate intercellular signaling. Altered signaling impacts cardiac function and is detrimental to embryonic survival. Here we report an...
Cardiac morphogenesis relies on intricate intercellular signaling. Altered signaling impacts cardiac function and is detrimental to embryonic survival. Here we report an unexpected regulatory role of the desmosomal cell adhesion molecule desmoglein 2 (Dsg2) on murine heart development. A large percentage of Dsg2-mutant embryos develop pericardial hemorrhage. Lethal myocardial rupture is occasionally observed, which is not associated with loss of cardiomyocyte contact but with expansion of abnormal, non-myocyte cell clusters within the myocardial wall. Two types of abnormal cell clusters can be distinguished: Type A clusters involve endocard-associated, round-shaped CD31 cells, which proliferate and invade the myocardium. They acquire Runx1- and CD44-positivity indicating a shift towards a hematopoietic phenotype. Type B clusters expand subepicardially and next to type A clusters. They consist primarily of Ter119 erythroid cells with interspersed Runx1/CD44 cells suggesting that they originate from type A cell clusters. The observed pericardial hemorrhage is caused by migration of erythrocytes from type B clusters through the epicardium and rupture of the altered cardiac wall. Finally, evidence is presented that structural defects of Dsg2-depleted cardiomyocytes are primary to the observed pathogenesis. We propose that cardiomyocyte-driven paracrine signaling, which likely involves Notch1, directs subsequent trans-differentiation of endo- and epicardial cells. Together, our observations uncover a hitherto unknown regulatory role of Dsg2 in cardiogenesis.
Topics: Animals; Cell Adhesion; Cell Differentiation; Desmoglein 2; Heart; Hematopoiesis; Mice; Myocardium; Myocytes, Cardiac; Organogenesis; Pericardium
PubMed: 34737300
DOI: 10.1038/s41598-021-00996-y -
Journal of Cardiovascular and Thoracic... 2014Epicardial fat volume (EFV) has been reported to correlate with the severity of coronary artery disease (CAD). Pericardial fat volume (PFV) has recently been reported to...
INTRODUCTION
Epicardial fat volume (EFV) has been reported to correlate with the severity of coronary artery disease (CAD). Pericardial fat volume (PFV) has recently been reported to be strongly associated with CAD severity and presence. We aimed to investigate the relationship between EFV and PFV with severity of coronary artery stenosis in patients undergoing 64-slice multi-slice computed tomography (MSCT).
METHODS
One hundred and fifty one patients undergoing MSCT for suspected CAD were enrolled. Non-enhanced images were acquired to assess calcium score. Contrast enhanced images were used to quantify EFV, PFV and severity of luminal stenosis.
RESULTS
Coronary artery stenosis was mild in 25 cases (16.6%), moderate in 58 cases (38.4%) and severe in 68 cases (45%). With increase in severity of coronary artery stenosis, there was significant increase in PFV, EFV as well as epicardial fat thickness in right ventricle free wall in basal view and epicardial fat thickness in left ventricle posterior wall in mid and apical view. There was significant linear correlation between PFV with coronary calcification score (r=0.18, P=0.02), between coronary artery stenosis severity and PFV (r=0.75, P<0.001), EFV (r=0.79, P<0.001), apical epicardial fat thickness in right ventricle free wall (r=0.29, P<0.001), Mid (r=0.28, P<0.001) and basal (r=0.23, P=0.004) epicardial fat thickness in left ventricle posterior wall.
CONCLUSION
PFV, EFV and regional epicardial thickness are correlated with severity of CAD and could be used as a reliable marker in predicting CAD severity.
PubMed: 25610555
DOI: 10.15171/jcvtr.2014.018 -
Medicine Sep 2022Desmoid fibromatosis is a rare benign tumor, but due to its rarity and diverse clinical course, treatment guidelines have not been established. However, since a good... (Review)
Review
RATIONALE
Desmoid fibromatosis is a rare benign tumor, but due to its rarity and diverse clinical course, treatment guidelines have not been established. However, since a good prognosis can be expected, an accurate diagnosis and appropriate treatment are required. We describe a rare case of desmoid fibromatosis on young female that presented as huge abdominal mass.
PATIENTS CONCERNS
A 28-year-old female with left upper abdominal pain 1 month ago was referred.
DIAGNOSES
Abdominal computed tomography and magnetic resonance imaging revealed a heterogeneous soft tissue mass approximately 29 × 17 cm in size in the left abdomen with abdominal wall invasion and pathological fracture in costochondral junction of the left 8th to 10th ribs.
INTERVENTIONS
Surgical resection was performed.
OUTCOMES
33 × 23 × 6 cm sized tumorous mass showed proliferation of bland fibromatosis and myofibroblast with nuclear β-catenin expression on pathological examination. Desmoid fibromatosis arising from intra-abdominal soft tissue with ribs and pericardium invasion was diagnosed.
LESSONS
The mainstay of treatment of symptomatic desmoid fibromatosis is surgical resection, and in the case of abdominal tumor, it can be more dangerous when it invades adjacent organ. We report a case that required additionally multidisciplinary approach for surgery and postoperative treatment of huge abdominal desmoid tumor which infiltrate bone and pericardium beyond abdominal cavity.
Topics: Adult; Female; Fibroma; Fibromatosis, Aggressive; Humans; Pericardium; Ribs; beta Catenin
PubMed: 36107577
DOI: 10.1097/MD.0000000000030371 -
American Journal of Physiology. Heart... Jan 2010A safe, easy, and quick access into the pericardial space may provide a window for diagnostics and therapeutics to the heart. The objective of this study was to provide...
A safe, easy, and quick access into the pericardial space may provide a window for diagnostics and therapeutics to the heart. The objective of this study was to provide proof of concept for an engagement and access catheter that allows access to the pericardial space percutaneously. A multilumen catheter was developed to allow navigation and suction fixation to the right atrial appendage/wall in a normal swine model. Advancement through the multilumen catheter using a second catheter with a distal needle tip allows access to the pericardial space without pericardial puncture and advancement of a standard guide wire into the space. Navigation into the pericardial space was undertaken by fluoroscopy alone and was accomplished in 10 swine (5 acute and 5 chronic). As a specific application of this pericardial access method, a pacing lead was implanted on the epicardial surface. Five chronic swine experiments were conducted with successful pacing engagement verified by lead impedance and pacing threshold and sensing. Lead impedance exceeded 1,000 Omega preengagement and dropped by an average of 200 Omega upon implant (769 +/- 498 Omega). Pacing thresholds at 0.4 ms ranged from approximately 0.5 to 2.1 V acutely (1.03 +/- 0.92 V). No cardiac effusion or tamponade was observed in any of the acute or chronic studies. The ability to engage, maintain, and retract the right atrial appendage/wall and to engage an epicardial lead was successfully demonstrated. These findings support the feasibility of safe access into the pericardial space in a normal swine model and warrant further investigations for clinical translation.
Topics: Animals; Cardiac Catheterization; Cardiac Pacing, Artificial; Catheterization; Electric Impedance; Electrocardiography; Electrodes, Implanted; Feasibility Studies; Female; Fluoroscopy; Heart Ventricles; Male; Pericardium; Swine
PubMed: 19855061
DOI: 10.1152/ajpheart.00575.2009 -
Scientific Reports Aug 2021Previously, genetic lineage tracing based on the mesothelial marker Wt1, appeared to show that peritoneal mesothelial cells have a range of differentiative capacities...
Previously, genetic lineage tracing based on the mesothelial marker Wt1, appeared to show that peritoneal mesothelial cells have a range of differentiative capacities and are the direct progenitors of vascular smooth muscle in the intestine. However, it was not clear whether this was a temporally limited process or continued throughout postnatal life. Here, using a conditional Wt1-based genetic lineage tracing approach, we demonstrate that the postnatal and adult peritoneum covering intestine, mesentery and body wall only maintained itself and failed to contribute to other visceral tissues. Pulse-chase experiments of up to 6 months revealed that Wt1-expressing cells remained confined to the peritoneum and failed to differentiate into cellular components of blood vessels or other tissues underlying the peritoneum. Our data confirmed that the Wt1-lineage system also labelled submesothelial cells. Ablation of Wt1 in adult mice did not result in changes to the intestinal wall architecture. In the heart, we observed that Wt1-expressing cells maintained the epicardium and contributed to coronary vessels in newborn and adult mice. Our results demonstrate that Wt1-expressing cells in the peritoneum have limited differentiation capacities, and that contribution of Wt1-expressing cells to cardiac vasculature is based on organ-specific mechanisms.
Topics: Animals; Cell Differentiation; Cell Lineage; Coronary Vessels; Epithelial Cells; Epithelium; Female; Gene Expression; Gene Expression Profiling; Gene Expression Regulation, Developmental; Intestines; Male; Mice; Muscle, Smooth, Vascular; Pericardium; Peritoneum; Transcriptome; WT1 Proteins
PubMed: 34354169
DOI: 10.1038/s41598-021-95380-1 -
Diabetes & Vascular Disease Research 2022Epicardial adipose tissue is an emerging cardiovascular risk factor. The aim of this study was to evaluate right ventricular function and investigate its association...
BACKGROUND
Epicardial adipose tissue is an emerging cardiovascular risk factor. The aim of this study was to evaluate right ventricular function and investigate its association with EAT in T2DM patients.
METHODS
154 T2DM patients were divided into two groups according to EAT thickness: T2DM with EAT <5 mm and T2DM with EAT ≥5 mm. Seventy non-T2DM patients were enrolled as control group. RV function was evaluated using both conventional echocardiography as well as two-dimensional speckle tracking echocardiography. EAT thickness was measured as the echo-free space between the free wall of the right ventricle and the visceral layer of pericardium at end-systole.
RESULTS
Compared to control group, EAT thickness was significantly higher and RV systolic function and early diastolic function are all impaired in all T2DM patients. In T2DM with EAT ≥5 mm group, RV systolic function and early diastolic function suffered more severe impairment when compared with T2DM with EAT <5 mm group. Multivariate linear regression analysis revealed that EAT was associated with RV systolic and early diastolic dysfunction independent of traditional cardiovascular risk factors.
CONCLUSIONS
Our research suggest that in T2DM patients RV systolic function and early diastolic function are all impaired which are associated with the thickened EAT.
Topics: Adipose Tissue; Diabetes Mellitus, Type 2; Echocardiography; Humans; Pericardium; Ventricular Function, Right
PubMed: 35999047
DOI: 10.1177/14791641221118622 -
Journal of Cardiovascular Magnetic... Oct 2015The aim of the current study was to examine whether the use of highly active antiretroviral therapy (HAART) in patients with HIV is associated with changes in...
Increased pericardial fat accumulation is associated with increased intramyocardial lipid content and duration of highly active antiretroviral therapy exposure in patients infected with human immunodeficiency virus: a 3T cardiovascular magnetic resonance feasibility study.
BACKGROUND
The aim of the current study was to examine whether the use of highly active antiretroviral therapy (HAART) in patients with HIV is associated with changes in pericardial fat and myocardial lipid content measured by cardiovascular magnetic resonance (CMR).
METHODS
In this prospective case-control study, we compared 27 HIV seropositive (+) male subjects receiving HAART to 22 control male subjects without HIV matched for age, ethnicity and body mass index. All participants underwent CMR imaging for determination of pericardial fat [as volume at the level of the origin of the left main coronary artery (LM) and at the right ventricular free wall] and magnetic resonance spectroscopy (MRS) for evaluation of intramyocardial lipid content (% of fat to water in a single voxel at the interventricular septum). All measurements were made by two experienced readers blinded to the clinical history of the study participants. Two-sample t-test, Spearman's correlation coefficient or Pearson's correlation coefficient and multivariable logistic regression were used for statistical analysis.
RESULTS
Pericardial fat volume at the level of LM origin was higher in HIV (+) subjects (33.4 cm(3) vs. 27.4 cm(3), p = 0.03). On multivariable analysis adjusted for age, Framingham risk score (FRS) and waist/hip ratio, pericardial fat remained significantly associated to HIV-status (OR 1.09, p = 0.047). For both HIV (+) and HIV (-) subjects, pericardial fat volume showed strong correlation with intramyocardial lipid content (r = 0.58, p < 0.0001) and FRS (r = 0.53, p = 0.0002). Among HIV (+) subjects, pericardial fat was significantly higher in patients with lipo-accumulation (37 cm(3) vs. 27.1 cm(3), p = 0.03) and showed significant correlation with duration of both HIV infection (r = 0.5, p = 0.01) and HAART (r = 0.46, p = 0.02).
CONCLUSIONS
Pericardial fat content is increased in HIV (+) subjects on chronic HAART (>5 years), who demonstrate HAART-related lipo-accumulation and prolonged HIV duration of infection. Further investigation is warranted to determine whether increased pericardial fat is associated with higher cardiovascular risk leading to premature cardiovascular events in this patient population.
Topics: Adipose Tissue; Adiposity; Adult; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Case-Control Studies; Drug Administration Schedule; Feasibility Studies; HIV Infections; Humans; Lipid Metabolism; Logistic Models; Magnetic Resonance Imaging; Magnetic Resonance Spectroscopy; Male; Middle Aged; Multivariate Analysis; Myocardium; Odds Ratio; Pericardium; Predictive Value of Tests; Prospective Studies; Reproducibility of Results; Risk Factors; Time Factors; Treatment Outcome
PubMed: 26520571
DOI: 10.1186/s12968-015-0193-2