Obstruction Of Blood Flow Research Articles

Antithrombotics: backgrounds with haemostasis and antithrombotic therapy

The clinical guidelines on antithrombotics, published by the Dutch Institute of Expertise for Oral Healthcare, give advice on policy to be followed in cases of dental procedures involving bleeding. The guidelines allow room for professional assessment of bleeding risks, for which background knowledge about haemostasis, thrombosis and antithrombotic processes is necessary. Normal haemostasis can be divided in several steps: vasoconstriction, primary haemostasis by aggregation of thrombocytes, and secondary haemostasis by the formation of fibrin out of coagulation factors. In the case of thrombosis, a blood clot forms inside a blood vessel, causing obstruction of blood flow to the underlying tissue. Various antithrombotics are prescribed for the prevention and treatment of thrombosis. Thrombocyte aggregation inhibitors only have an effect on primary haemostasis. Vitamin K antagonists influence secondary haemostasis by lowering the production of several coagulation factors. The direct oral anticoagulants have an immediate effect on an activated coagulation factor, and are currently prescribed in large quantities [in the Netherlands]. Low-molecular-weight heparin also inhibits activated coagulation factors, but is not used for long-term antithrombotic therapy since it is administrated subcutaneously.

Artery dissection as an cause of ischemic stroke in hebiatric patient: a case report

Introduction: The dissection of cervical artery is characterized by laceration in the intima layer that results in a reduction in the lumen of the affected artery causing obstruction of blood flow. This block, partially or totally, is responsible for only a small portion of stroke in adults. However, in patients under 40 years old dissection of the cervical artery is a very common cause of this type of stroke. For this reason, early recognition of this condition in young patients is essential for the adequate clinical intervention. Objective: To report a case of ischemic stroke resulting from cervical artery dissection in a hebiatric patient. Case report: FSM, male, 16 years old, arrived at the neurological center complaining of headache in the occipital region that started eight days ago. He also reported asthenia, photophobia and discrete dysarthria. The physical examination showed bilateral dysdiadocosinesia and positive Romberg. An computed tomography scan of the skull and an MRI were then requested, in which the white and gray substances in the cerebellar hemispheres were hypodensitive, suggestive of ischemic stroke. For the etiological diagnosis, an angioresonance of cervical vessels was performed, which showed dissection of the cervical artery. After diagnostic confirmation, the patient was treated with antithrombotic and anticoagulant, progressing satisfactorily. The incidence of isquemic stroke resulting from dissection of the cervical arteries is a rare condition, affecting about 2.5 / 100,000 people per year. The dissection result in stroke in only 2% of all cases. However, analyzing only cases among young patients the dissection results in stroke in 22.5%. Presentation of multiple intraxial lesions with T2 hypersignal associated with asymmetry of the vertebral arteries with a small narrowed segment are highly suggestive if not specific for ischemic stroke. The early diagnosis of this clinical condition is extremely important for the patient’s satisfactory evolution, since metabolic changes resulting from ischemia result in a decrease in the production of ATP in the infarcted region, which impairs, temporarily or permanently, the main functions of this region. The dissection of cervical arteries, due to its low incidence, is a disorder still under diagnosed. Its late identification results in an increase in the incidence of PICs, especially in young patients. The early recognition of this pathology is essential for an early and effective treatment that reduces the possibility of permanent neurological injuries that would decrease the quality of life of these patients.

Acute DeBakey Type II Dissection Mimics Left Ventricle Outflow Tract Obstruction

A 40-year-old man with hypertension and obesity (body mass index, 50.4 kg/m2) was referred to our institution after an evaluation for symptoms of heart failure (worsening shortness of breath for 2 weeks). Computed tomography with contrast revealed subacute DeBakey type II aortic dissection originating at the sinotubular junction with an enlarged thrombus occupying the false lumen (Figure 1, red arrow) and obstructing blood flow through the stenotic supravalvular aorta.

Characterization of a novel model of global forebrain ischaemia\u2013reperfusion injury in mice and comparison with focal ischaemic and haemorrhagic stroke

Stroke is caused by obstructed blood flow (ischaemia) or unrestricted bleeding in the brain (haemorrhage). Global brain ischaemia occurs after restricted cerebral blood flow e.g. during cardiac arrest. Following ischaemic injury, restoration of blood flow causes ischaemia–reperfusion (I/R) injury which worsens outcome. Secondary injury mechanisms after any stroke are similar, and encompass inflammation, endothelial dysfunction, blood–brain barrier (BBB) damage and apoptosis. We developed a new model of transient global forebrain I/R injury (dual carotid artery ligation; DCAL) and compared the manifestations of this injury with those in a conventional I/R injury model (middle-cerebral artery occlusion; MCAo) and with intracerebral haemorrhage (ICH; collagenase model). MRI revealed that DCAL produced smaller bilateral lesions predominantly localised to the striatum, whereas MCAo produced larger focal corticostriatal lesions. After global forebrain ischaemia mice had worse overall neurological scores, although quantitative locomotor assessment showed MCAo and ICH had significantly worsened mobility. BBB breakdown was highest in the DCAL model while apoptotic activity was highest after ICH. VCAM-1 upregulation was specific to ischaemic models only. Differential transcriptional upregulation of pro-inflammatory chemokines and cytokines and TLRs was seen in the three models. Our findings offer a unique insight into the similarities and differences in how biological processes are regulated after different types of stroke. They also establish a platform for analysis of therapies such as endothelial protective and anti-inflammatory agents that can be applied to all types of stroke.

Family Perception of Diseases Related to the Reference Time in Stroke Patient: Literature Review

Background: Stroke is a functional brain disorder characterized by neurological deficits or nerve paralysis that occurs suddenly due to obstruction of blood flow to the brain. In 2018 the prevalence of stroke in Indonesia has increased compared to 2013, namely the prevalence of stroke rose from 7 percent to 10.9 percent. South Kalimantan ranks 5th in Indonesia with a stroke prevalence of 12.7%. The duration of stroke is caused by the delays in referring patients to the hospital. Poor perception is one of the factors that causes delay in patients being taken to the hospital for immediate treatment. Purpose: This study aimed to learn about family perceptions of diseases related to patient referral in Empirical studies in the past 5 years. Methods: This study uses the literature review method. a database with the electronic search on Ebsco, ProQuest, Google Scholar, and DOAJ that published in 2016-2019. Results: There is a correlation between the perception of the disease with referral time in stroke patients. Lack of knowledge about the symptoms of stroke symptoms that arise so that the perception of symptoms that arise is an ordinary disease and can disappear by itself. Conclusion: Closely Banjar culture causes families to choose to only bring patients to traditional medicine rather than bringing stroke patients to the hospital. The family has the perception that stroke is a common disease that can be cured by bringing patients to traditional medicine

THE MAN WITH THREE ATRIUMS: COR TRIATRIATUM SINISTER

SESSION TITLE: Medical Student/Resident Genetic and Developmental Disorders Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Cor triatriatum sinister (CTS) is a rare congenital cardiac condition characterized by the division of the left atrium by an abnormal fibromuscular membrane potentially causing obstruction of blood flow within the left atrium. The condition is found in less than 0.1% of patients diagnosed with cardiomyopathies and typically diagnosed in childhood. We describe a case of an incidentally diagnosed CTS in an adult. CASE PRESENTATION: A 45-year old male with a past medical history of supraventricular tachycardia and coronary artery disease status post percutaneous stenting was admitted to the hospital for evaluation of shortness of breath, productive cough, fever and chills. On chest x-ray, there was evidence of a left lower lobe pulmonary infiltrate and he was treated for community acquired pneumonia with ceftriaxone and azithromycin. His hospital course was complicated by hypoxemic respiratory failure. Echocardiography was performed, due to persistent tachycardia and shortness of breath and he was found to have CTS (Figure 1). On further questioning he declined a history of dyspnea on exertion, orthopnea or other respiratory complaints since childhood. He was discharged home after resolution of acute community-acquired pneumonia. DISCUSSION: There are three theories on the embryology of CTS; malincorporation, malseptation and entrapment. Among these, malincorporation of the common pulmonary vein into the left atrium creating two chambers separated by a narrowing chamber, is the most accepted theory. Up to 80% of cases are associated with other congenital abnormalities and presentation varies from asymptomatic patients to septic shock with pulmonary edema and respiratory failure. In adults, asymptomatic patients likely have a large foramen (fenestrations) with no intra-atrial pressure gradient unlike symptomatic patients who have no means for compensation and develop elevated left atrial pressure and subsequent pulmonary congestion. On physical exam, no pathognomonic findings are seen, and the absence of an opening snap or loud S1 differentiates the murmur of CTS from mitral stenosis. Echocardiography is a simple, non-invasive tool that can delineate the morphology and diagnose CTS as well as assess severity, describing severe obstruction when the doppler velocity gradient is greater than 2 m/s. Further studies are not needed, but cardiac catheterization, and cardiac magnetic resonance imaging can be useful for diagnosis and management. Management is based on symptoms and ranges from no treatment, to preload reducing agents, to surgical intervention. CONCLUSIONS: Establishing the diagnosis is critical as untreated, hemodynamically-significant CTS can lead to arrhythmias, pulmonary hypertension and right-sided heart failure that can be prevented with favorable outcomes after surgical correction. We present this case due to its rarity and asymptomatic nature in an adult patient. Reference #1: Nassar PN, Hamdan RH. Cor triatriatum sinistrum: classification and imaging modalities. The European journal of cardiovascular medicine. 2011;1(3):84. Reference #2: Ather B, Siddiqui WJ. Cor Triatriatum. In: StatPearls [Internet]. StatPearls Publishing; 2019. Reference #3: Chen Q, Guhathakurta S, Vadalapali G, Nalladaru Z, Easthope RN, Sharma AK. Cor triatriatum in adults: three new cases and a brief review. Tex Heart Inst J. 1999;26(3):206-210. DISCLOSURES: No relevant relationships by Israel Acosta Sanchez, source=Web Response No relevant relationships by Floyd Burke, source=Web Response No relevant relationships by Somshukla Ghosh, source=Web Response No relevant relationships by Hiren Patel, source=Web Response No relevant relationships by Irene Riestra Guiance, source=Web Response

ATRIAL FLUTTERS AS AN INITIAL PRESENTATION OF LUNG CANCER CAUSING MALIGNANT PERICARDIAL EFFUSION

SESSION TITLE: Medical Student/Resident Lung Cancer Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pericardial effusion is a devastating cardiac condition, resulting from various etiology. Cardiac arrhythmia is an uncommon presentation of pericardial effusion, while atrial fibrillation is the most common arrhythmia found in this condition. Atrial flutter, as an initial presentation of malignant pericardial effusion, has not yet been reported. We presented a case of an elderly man with atrial flutter from malignant cardiac effusion from a newly diagnosed lung cancer. CASE PRESENTATION: An 81-year-old man, with chronic obstructive pulmonary disease and hypertension, presented with acute onset shortness of breath. He used albuterol MDI but his symptoms were not improved. On evaluation, he had heart rate 179 beats per minute (bpm), blood pressure 172/118 mmHg without pulsus paradoxus, and respiratory rate of 26. He had good mental status and did not have jugular venous distention. Lungs exam was normal. Heart exam revealed tachycardia without murmur. His blood test was unremarkable. His ECG showed atrial flutter with rapid ventricular rate and 2:1 block. He received intravenous Diltiazem 20 mg and his heart rate decreased to 90. Point of care ultrasound (POCUS) showed large pericardial effusion without tamponade physiology and no signs of pulmonary edema. Computed tomography (CT) chest illustrated large pericardial effusion with new left upper lung mass. Cytology from pericardial effusion revealed squamous cell carcinoma. He was diagnosed as malignant pericardial effusion from advance stage squamous cell lung cancer. His hospital course was complicated with septic shock and eventually death. DISCUSSION: Lung cancer is the most common metastasis cancer to the heart and pericardium because of the proximity of the tumor to the heart [1]. There are several possible explanations of malignant pericardial effusion pathogenesis. First, it can be a result of cardiac lymphatic drainage occlusion by the tumor [2]. Second, local or hematogenous spread of the tumor lead to venous blood flow obstruction and an increase in hydrostatic pressure causing pericardial effusion [3]. Third, neoplastic pericardial involvement stimulates an overproduction of pericardial fluid [3]. Pericardial effusion in cancer patients may arise from complications of treatment, including chemotherapy and radiation, and hypoalbuminemia from malignancy-related cachexia. Cytology analysis of pericardial fluid and pericardial biopsy should be performed to confirm the diagnosis. Management includes pericardiocentesis, pericardial window, pericardial sclerosis, and radiation therapy. CONCLUSIONS: We presented a rare case of atrial flutter secondary to malignant pericardial effusion from newly diagnosis of advanced-stage lung cancer. Clinicians should have pericardial effusion as a differential diagnosis of patients with atrial flutter as this is a catastrophic condition, requiring urgent management. Reference #1: DeCamp MM, et al. Malignant effusive disease of the pleura and pericardium. Chest. 1997;112(4 Suppl):2915-2955. Reference #2: Chiles C, et al. Metastatic involvement of the heart and pericardium: CT and MR imaging. Radiographics. 2011;21(2):438-449. Reference #3: Scheinin SA, Sosa-Herrera J. Cardiac tamponade resembling an acute myocardial infarction as the initial manifestation of metastatic pericardial adenocarcinoma. Methodist Debakey Cardiovasc J. 2014; 10:124–128. DISCLOSURES: No relevant relationships by Nehad Shabarek, source=Web Response No relevant relationships by Kulachanya Suwanwongse, source=Web Response

Restoring arteriovenous access: Pilot study using a scoring balloon in 50 patients.

Arteriovenous access failure is most often due to the development of neointimal hyperplastic stenoses. Balloon angioplasty remains standard of care for endovascular treatment of stenoses obstructing blood flow in hemodialysis fistulas and grafts. Scoring balloon technologies have been developed to disrupt the atheromatous plaque and have shown to be safe and effective for treating stenosis in the hemodialysis access circuit. However, improvement in patency has yet to be established. This prospective, single-arm study included 50 patients with stenosed hemodialysis fistula/grafts treated with the AngioSculpt® scoring balloon (Philips) and followed for 6 months. The primary endpoint was target lesion primary patency at 2 and 6 months defined as freedom from re-intervention. Treatment with the scoring balloon resulted in a reduction in stenosis from 78% ± 13.36% to 7.2% ± 7.57% (mean ± standard deviation). Scoring balloon inflation pressures averaged 11.4 atm; no slippage/dissections occurred. After 2 months, 10% of patients required re-intervention. At 6 months, 19% of patients required re-intervention. The 6-month freedom from re-intervention rate was higher for patients with stenosed fistulas (83.3%) compared to patients with stenosed grafts (71.4%). Six-month patency rates were highest for patients with no or one previous intervention (91.6% and 90.0%, respectively); patients with two to five preceding interventions had a 6-month patency rate of 80%, and those with more than five previous interventions had a 50% 6-month patency rate. Results from this pilot study suggest that the AngioSculpt scoring balloon may be a viable treatment option for stenosed arteriovenous fistula/graft access.

How to get rid of visceral fat: a randomised double-blind clinical trial

Inflammation and oxidative damage are immanent in visceral adiposity that is characterised by excess lipids and lipoproteins, viewed as the core components of arterial plaques, ultimately obstructing blood flow and lymphatic drainage. Accumulated toxicity dysregulates the orexigenic hormone ghrelin and anorexic hormone leptin, which are part of a reciprocal network controlling appetite. Weight gain promotes hormonal imbalance, expressed in disturbances in free T3 and an inverse low testosterone/high cortisol incongruity that provokes stress-eating behaviours. The author explored a number of interventions designed to reduce visceral adipose tissue (VAT), including radiofrequency, lasers and exercise, as well as exercise alone. Short-term gymnastics evidenced a modest advantage in VAT decrease, but there were no changes in body mass index (BMI) or physical appearance. Overtraining appeared to negate the benefits of exercise by increasing inflammation and cortisol, while suppressing testosterone and leptin that inevitably instigated hunger and weight gain. The blood samples of 10 overweight, healthy adults who underwent 12 treatments during the course of 1 month were examined. Results demonstrated a statistically significant decline in very-low-density lipoprotein, triglycerides and VAT, accompanied by a substantial increase in basal metabolic rate and skeletal muscle mass. Importantly, free T3, insulin-like growth factor 1, leptin, and testosterone were elevated towards the top of the normal range, while cortisol and ghrelin gravitated towards the low end of the normal range, without ever spiking outside the limits of hormonal balance.

Mycological and histopathological identification of potential fish pathogens in Nile tilapia

Due to recent rapid progress in the development of freshwater aquaculture in Egypt, many new and precedent fish fungal diseases have emerged. Nile tilapia (Oreochromis niloticus) has been threatened by various diseases that have harmful health consequences and prone to mortalities. The current study was conducted (using 800 randomly collected diseased cultured and wild Nile tilapia) to identify the three most serious fungal pathogens that induced mortalities. The infection can be superficial as Saprolegnia spp. that is characterized by focal dermal cottony growth and is the most common in occurrence. While, systemic infection as Ichthyophonus sp. that invades the highly vascularized organs impairing their functions, Branchiomycosis is a devastating disease that affects gills obstructing blood flow. Saprolegnia spp. was identified through the morphological characters of culture on Sabouraud's dextrose agar media (SDA) and histopathological examination of tissue. Surprisingly, Saprolegnia spp. grew on Eagle's Minimum Essential Medium (MEM) at pH 7.0 only giving zoospores. Ichthyophonus sp. was isolated and is characterized by spherical double-walled multinucleate schizonts that are verified in squash preparations from infected internal organs (liver, spleen, and kidneys) and tissue sections. Additionally, it developed two different forms of growth on MEM depending on culture medium pH. Branchiomyces spp. exhibited different stages of growth in gills and so appeared congested, paled, white-colored or marbled according to the progress of infection. A key diagnostic feature to genus Branchiomyces is the branching of hyphae at their tips with the first report for a description of such branching in compression techniques from gills. Also a microscopic examination of fungal culture aids in the identification. Herein, we report Branchiomyces sanguinis for the first time and Branchiomyces demigrans in Nile tilapia in Egypt. Both species are distinguished based on the shape and diameter of hyphae in compression techniques from infected gills as well as the diameter and location of spores in histological sections. Koch's Postulate confirmed the identity of the investigated pathogens. The current research represents the first comparative mycological and histopathological study for Saprolegnia spp., Ichthyophonus sp., and Branchiomyces spp. as well as their prevalence in wild and cultured Nile tilapia throughout the different seasons in Egypt.

Abstract 547: Hur Dependent Regulation of Inflammatory Remodeling Following Myocardial Ischemia/reperfusion Injury

Myocardial infarction (MI), resulting from ischemia/reperfusion (I/R) injury due to the obstruction of coronary blood flow, affects an estimated 800,000 Americans annually resulting in a cost of nearly 12 billion dollars to the health care system. Recent medical advances have led to improved survival following acute MI, but unfortunately, the post-MI inflammatory and fibrotic remodeling of the heart is driving an increase in the prevalence of heart failure. Preliminary data from our lab shows that the RNA binding protein Human antigen R (HuR) undergoes nuclear-to-cytoplasmic translocation within 30 minutes and is increased in expression at both 2 hours and 7 days post-I/R. The objective of this work is to determine the mechanistic role of HuR on the regulation of cardiac cytokine/chemokine expression and the functional effect of HuR on macrophage infiltration and polarization post-I/R. Wild-type mice were subjected to 30 minutes of LAD (left anterior descending) coronary artery ligation (ischemia) followed by reperfusion with HuR inhibitor or vehicle control administered at the start of reperfusion. Our results show that inhibition of HuR reduces cardiac mRNA expression of IL-6, TNF-alpha, and ICAM-1 at 2 hours post-reperfusion, but does not affect initial (24 hour) infarct size. In addition, HuR inhibition reduces macrophage infiltration at 7 days post-I/R, as well as cardiac fibrosis and ventricular dilation while preserving cardiac function at 14 days post-I/R. Furthermore, H9c2s treated with HuR inhibitor blunts the mRNA expression of CCL2 after acute stimulation of lipopolysaccharide. In conclusion, we show that HuR inhibition at the time of reperfusion is protective against post-MI inflammatory and fibrotic remodeling through a reduction in inflammatory gene expression and macrophage infiltration. Previous work by the lab has demonstrated a direct role for HuR in cardiac myocytes, but these results also suggest that HuR-mediated gene expression in macrophages may play a role in post-MI inflammatory and fibrotic remodeling.

Emerging Roles for Neuropilin-2 in Cardiovascular Disease.

Cardiovascular disease, the leading cause of death worldwide, is predominantly associated with atherosclerosis. Atherosclerosis is a chronic inflammatory disease characterised by the narrowing of large to medium-sized arteries due to a build-up of plaque. Atherosclerotic plaque is comprised of lipids, extracellular matrix, and several cell types, including endothelial, immune, and vascular smooth muscle cells. Such narrowing of the blood vessels can itself restrict blood flow to vital organs but most severe clinical complications, including heart attacks and strokes, occur when lesions rupture, triggering the blood to clot and obstructing blood flow further down the vascular tree. To circumvent such obstructions, percutaneous coronary intervention or bypass grafts are often required; however, re-occlusion of the treated artery frequently occurs. Neuropilins (NRPs), a multifunctional family of cell surface co-receptors, are expressed by endothelial, immune, and vascular smooth muscle cells and are regulators of numerous signalling pathways within the vasculature. Here, we review recent studies implicating NRP2 in the development of occlusive vascular diseases and discuss how NRP2 could be targeted for therapeutic intervention.

Cardiovascular Biofluid Mechanics

This paper intends to study a real-life application of fluid mechanics in cardiovascular blood flow. The study of blood flow is termed as Hemodynamics. Fluid mechanics can be used to analyze the factors and impact of obstruction in blood flow due to fat, cholesterol, and plaque deposits in the coronary arteries of the human heart. These blockages are the grounds for coronary artery diseases and heart attacks. We will look at varying parameters of flowrate and pressure for different thicknesses of epicardial fat as well as define a relationship between these three.

Aortic Valve Stenosis and Mitochondrial Dysfunctions: Clinical and Molecular Perspectives.

Calcific aortic stenosis is a disorder that impacts the physiology of heart valves. Fibrocalcific events progress in conjunction with thickening of the valve leaflets. Over the years, these events promote stenosis and obstruction of blood flow. Known and common risk factors are congenital defects, aging and metabolic syndromes linked to high plasma levels of lipoproteins. Inflammation and oxidative stress are the main molecular mediators of the evolution of aortic stenosis in patients and these mediators regulate both the degradation and remodeling processes. Mitochondrial dysfunction and dysregulation of autophagy also contribute to the disease. A better understanding of these cellular impairments might help to develop new ways to treat patients since, at the moment, there is no effective medical treatment to diminish neither the advancement of valve stenosis nor the left ventricular function impairments, and the current approaches are surgical treatment or transcatheter aortic valve replacement with prosthesis.

Weighted gene co‑expression network analysis identifies key genes from extracellular vesicles as potential prognostic biomarkers for congenital pulmonary stenosis.

Pulmonary stenosis (PS) is a congenital heart disease characterized by a dynamic or fixed anatomic obstruction of blood flow from the right ventricle to the pulmonary arterial vasculature. In the present study, extracellular vesicle long RNAs (EVLRs) from pregnant females who had healthy infants or PS infants were analyzed by RNA sequencing, and their diagnostic potential for PS during pregnancy was evaluated. A method for the selection of genes that could be considered as informative for the prediction PS based on extracellular vesicles (EVs) from pregnant females using long‑read RNA sequencing was developed. Blood samples were collected from females carrying fetuses with PS and females carrying unaffected fetuses (n=6 in each group). Physical characterization of EVs was performed using nanoparticle tracking analysis, transmission electron microscopy and western blotting. EVLRs from plasma were profiled by RNA sequencing and mRNA co‑expression modules were constructed by weighted gene co‑expression network analysis (WGCNA). Gene Ontology (GO) enrichment analysis was used to predict the function of the genes in each module. Hub genes were filtered out based on WGCNA and visualized using Cytoscape. EVLRs consisted of mRNAs, microRNAs and long non‑coding RNA. Overall, 26modules were identified containing 16,394genes. All modules were independent of each other. One particular module, referred to as the blue module, was markedly different between the two groups. A total of 735hub genes in the blue module were identified, of which 33were visualized, demonstrating the connection between these hub genes. GO enrichment analysis demonstrated that the analyzed hub genes were enriched in 'glucose transport', 'ATP‑dependent chromatin remodeling', 'histone deacetylation', 'histone H3‑K4 methylation', 'DNA methylation', 'apoptotic signaling pathway' and 'glucocorticoid receptor signaling pathway'. The hub genes identified in this module may provide a genetic framework for prenatal PS diagnosis. Furthermore, functional analysis of these associated genes may provide a theoretical basis for further research on PS pathogenesis.

Surgical treatment of a giant right atrial myxoma

BackgroundRight atrial myxoma is a rare anomaly. When present, it can rarely cause blood flow obstruction in the right cardiac chamber depending on its size and location. We herein report a rare case of a giant right atrial myxoma, which caused right heart failure due to tricuspid valve obstruction, along with our treatment experience.Case presentationA 59-year-old woman was admitted to our hospital for palpitations and edema of the lower extremity. Computed tomography image and transthoracic echocardiography showed a 57 mm × 63 mm giant tumor obstructing the tricuspid valve inflow. The tumor was excised surgically and the residual septal defect was repaired with a Dacron patch. Tricuspid valve annuloplasty was performed additionally. The postoperative course was uneventful and the patient was discharged on postoperative day 5.ConclusionGiant right atrial myxoma is a rare cause of tricuspid valve stenosis and right heart failure. Surgical resection is the most appropriate treatment option and should be performed as soon as possible after diagnosis.

Fibrinolytic therapy in newborns with superior vena cava syndrome. Case report

Introduction: Superior vena cava syndrome is described as the obstruction of blood flow through the superior vena cava. The literature reports that the incidence of this pathology varies from 1 case in every 650 inhabitants and 1 case in every 3 100 inhabitants. Since this condition is very rare in the pediatric population, no clear figure has been reported regarding its incidence in children. The use of a central venous catheter in newborns is a risk factor for this condition, as it may cause a thrombus due to the inflammatory reaction against the device. Therefore, it is necessary to initiate anticoagulation management and remove the catheter.Case presentation: Premature male newborn, (31.4 weeks gestation), with acute respiratory distress syndrome, early neonatal sepsis, pneumonia, necrotizing enterocolitis on 2 occasions, intestinal obstruction due to adhesions and intestinal volvulus. At 90 days of age, he presented thrombosis of the superior vena cava without involvement of the jugular and subclavian vein junction in the right atrium. Anticoagulant management was started, but given his unfavorable evolution, a multidisciplinary medical board was held to assess the risks, benefits, and treatment options in this age group. It was decided to start intracavitary tissue plasminogen activator treatment associated with mechanical thrombectomy and angioplasty of the superior vena cava. Due to the difficulty of conducting clinical trials in this population and the rates of major bleeding complications obtained with thrombolytic therapies, there is very little information available on the use of tissue plasminogen activator in newborns. For this reason, alteplase is seldom considered as the therapy of choice. However, in patients with life-threatening thrombosis, such as the present case, the results obtained in adults could be extrapolated in search of a favorable outcome.Conclusions: Fibrinolytic therapy is a way to reduce the size of the thrombus, but it dramatically increases the risk of bleeding; consequently, these patients must be strictly monitored. In pediatric populations, due to the diameter of the blood vessels, thrombectomy is difficult to perform; additionally, recurrent thrombosis and the need for transfusion of blood products are frequent.

Sex differences in renal ischemia-reperfusion injury.

Ischemia-reperfusion injury of the kidney is caused by the sudden and temporary obstruction of blood flow to the organ. Renal ischemia-reperfusion injury is associated with high morbidity and mortality, but effective therapies are lacking. Sexual dimorphism in renal injury has been acknowledged since the 1940s, and the possible role of sex hormones has been intensively investigated in the past decades. Clinical and experimental data demonstrate sexual differences in renal anatomy, physiology, and susceptibility to renal diseases including but not limited to ischemia-reperfusion injury. Some data suggest the protective role of female sex hormones, whereas others highlight the detrimental effect of male hormones in renal ischemia-reperfusion injury. Although the important role of sex hormones is evident, the exact underlying mechanisms remain to be elucidated. This review focuses on collecting the current knowledge about sexual dimorphism of renal ischemia-reperfusion injury, with emphasis on molecular mechanisms and potential novel therapeutic strategies.

Polyphenolic Compounds and Gut Microbiome in Cardiovascular Diseases.

The onset of Cardiovascular Disease (CVD) is known to be associated with multiple risk factors related to exogenous exposures on predisposed genetic makeup. Diet and lifestyle have a cascade effect on microbiota biodiversity, thus impacting inflammation and heart health. Atherosclerosis is a type of CVD where chronic inflammation contributes to plaque buildup in the arteries resulting in narrowed blood vessels, which obstruct blood flow. Polyphenolic compounds, including flavonoids, most commonly consumed in the form of plants, have been identified to have various mechanisms of action to reduce the inflammatory response in the body. Flavonoids provide a variety of nutraceutical functions including antioxidant, antimicrobial, anti-inflammatory, antiangiogenic, antitumor, and improved pharmacokinetic properties. Therefore, the medicinal use of polyphenolic compounds as an intervention for the inflammatory response, especially relating to the gut microbiome, may significantly reduce the risk of atherosclerotic plaque development and disease onset. This review addresses the role of polyphenolic compounds and gut microbiome in cardiovascular disease. Research studies conducted in cells and animals were reviewed. These studies clearly illustrate that dietary polyphenolic compounds influence resident gut microbiota thus they are associated with the prevention of atherosclerosis progression. Further research in this field is warranted to identify potential gut microbiome mediated therapeutic approaches for CVD.

Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors.

Cardiovascular disease (CD) is the leading cause of death in the developed world, with major atherothrombotic events, being mainly attributed to the rupture of unstable, vulnerable atherosclerotic lesions, leading to blood flow obstruction. Since unstable atherosclerotic plaques frequently do not cause hemodynamically significant blood flow restriction, conventional stress imaging tests cannot depict the vulnerable, high-risk for rupture atherosclerotic lesions. Therefore, molecular imaging techniques targeting specific pathophysiologic features related to atherosclerotic plaque rupture mechanism, hold promise for precise and individualized treatment strategies of CD. In the current report, we describe in a patient diagnosed with pancreatic neuroendocrine tumor, the selective uptake of 68Ga-DOATATE by an atherosclerotic lesion in the thoracic aorta. This data indicates that 68Ga-DOTATATE, which is a positron emitting tomography tracer, targeting the recruitment of macrophages taking place in the vulnerable plaque, could potentially serve as an imaging probe for the detection of high-risk, prone to rupture plaques.