Thrombus or tumor? A case report of a rare sarcoma entity: intimal sarcoma of the pulmonary arteries.

BACKGROUND: Tumor embolism is a very rare primary manifestation of cancers and the diagnosis is challenging, especially if located in the pulmonary arteries, where it can mimic nonmalignant pulmonary embolism. Intimal sarcoma is one of the least commonly reported primary tumors of vessels with only a few cases reported worldwide. A typical location of this malignancy is the pulmonary artery. Herein, we present a case report of an intimal sarcoma with primary manifestation in the pulmonary arteries. A 53-year-old male initially presented with dyspnea. On imaging, a pulmonary artery embolism was detected and was followed by thrombectomy of the right ventricular outflow tract, main pulmonary artery trunk, and right pulmonary artery after ineffective lysis therapy. Complementary imaging of the chest and abdomen including a PET-CT scan demonstrated no evidence of a primary tumor. Subsequent pathology assessment suggested an intimal sarcoma further confirmed by DNA methylation based molecular analysis. We initiated adjuvant chemotherapy with doxorubicin. Four months after the completion of adjuvant therapy a follow-up scan revealed a local recurrence without distant metastases. DISCUSSION: Primary pulmonary artery intimal sarcoma (PAS) is an exceedingly rare entity and pathological diagnosis remains challenging. Therefore, the detection of entity-specific molecular alterations is a supporting argument in the diagnostic spectrum. Complete surgical resection is the prognostically most important treatment for intimal cardiac sarcomas. Despite adjuvant chemotherapy, the prognosis of cardiac sarcomas remains very poor. This case of a PAS highlights the difficulty in establishing a diagnosis and the aggressive natural course of the disease. CONCLUSION: In case of atypical presentation of a pulmonary embolism, a tumor originating from the great vessels should be considered. Molecular pathology techniques support in establishing a reliable diagnosis.

Plasma S1P Orchestrates the Reverse Transendothelial Migration of Aortic Intimal Myeloid Cells in Mice.

BACKGROUND: Myeloid cells (MCs) reside in the aortic intima at regions predisposed to atherosclerosis. Systemic inflammation triggers reverse transendothelial migration (RTM) of intimal MCs into the arterial blood, which orchestrates a protective immune response that clears intracellular pathogens from the arterial intima. Molecular pathways that regulate RTM remain poorly understood. S1P (sphingosine-1-phosphate) is a lipid mediator that regulates immune cell trafficking by signaling via 5 G-protein-coupled receptors (S1PRs [S1P receptors]). We investigated the role of S1P in the RTM of aortic intimal MCs. METHODS: Intravenous injection of lipopolysaccharide was used to model a systemic inflammatory stimulus that triggers RTM. CD11c+ intimal MCs in the lesser curvature of the ascending aortic arch were enumerated by en face confocal microscopy. Local gene expression was evaluated by transcriptomic analysis of microdissected intimal cells. RESULTS: In wild-type C57BL/6 mice, lipopolysaccharide induced intimal cell expression of S1pr1, S1pr3, and Sphk1 (a kinase responsible for S1P production). Pharmacological modulation of multiple S1PRs blocked lipopolysaccharide-induced RTM and modulation of S1PR1 and S1PR3 reduced RTM in an additive manner. Cre-mediated deletion of S1pr1 in MCs blocked lipopolysaccharide-induced RTM, confirming a role for myeloid-specific S1PR1 signaling. Global or hematopoietic deficiency of Sphk1 reduced plasma S1P levels, the abundance of CD11c+ MCs in the aortic intima, and blunted lipopolysaccharide-induced RTM. In contrast, plasma S1P levels, the abundance of intimal MCs, and lipopolysaccharide-induced RTM were rescued in Sphk1-/- mice transplanted with Sphk1+/+ or mixed Sphk1+/+ and Sphk1-/- bone marrow. Stimulation with lipopolysaccharide increased endothelial permeability and intimal MC exposure to circulating factors such as S1P. CONCLUSIONS: Functional and expression studies support a novel role for S1P signaling in the regulation of lipopolysaccharide-induced RTM and the homeostatic maintenance of aortic intimal MCs. Our data provide insight into how circulating plasma mediators help orchestrate intimal MC dynamics.

A large post-stenting intramural hematoma in the left anterior descending artery caused by a small intimal calcium spur; should we respect the calcium shape?

Coronary heavy calcification (HC) poses a sturdy challenge to percutaneous coronary intervention (PCI). Scores considering calcification length, thickness, or circumferential extent, are widely accepted to dictate upfront calcium modification to improve PCI outcomes. Although often marginalized, calcification shape (morphology) may require consideration during procedure planning in selected cases. This case demonstrates how a focal but spur-shaped calcification led to a massive proximal left anterior descending (LAD) dissecting intramural hematoma.

Prognostic Implications of Initial Focal Contrast Enhancement in Acute Type B Intramural Hematoma.

BACKGROUND: The prognostic implication of initial focal contrast enhancement (FCE), including focal intimal disruption (FID) and intramural blood pool (IBP), in acute type B intramural hematoma (IMH) remain unclear. OBJECTIVES: The purpose of this study was to compare the prognostic implications in IMH with or without FCE. METHODS: A total of 574 patients were enrolled. FID was defined as an intimal disruption with contrast-filled out-pouching from the aorta lumen with a communicating orifice of >3 mm, and IBP was defined as a localized contrast medium-filled pool inside the IMH. RESULTS: A total of 207 (36.1%) patients with initial FCE, including 132 (63.8%) FIDs and 75 (36.2%) IBPs, were identified. Patients with FCE accompanying IMH were more likely to have hypertension (P = 0.001), pleural effusion (P = 0.006), fewer aortic segments involved (P < 0.001), more adverse aortic events (AAEs) (P < 0.001), and fewer freedom from intervention (P = 0.002). Pleural effusion (HR: 1.79; 95% CI: 1.25-2.55; P = 0.001) and FCE (HR: 1.51; 95% CI: 1.12-2.02; P = 0.006) were identified to be the independent risk factors of AAEs. In the subgroup analysis, IMH with initial FID were more likely to progress than those with initial IBP (P < 0.001). FIDs located at the proximal descending aorta (HR: 2.95; 95% CI: 1.65-5.29; P < 0.001) were associated with AAEs. CONCLUSIONS: Patients with FCE accompanying IMH were more likely to progress, especially in those initial FID localized at the proximal descending aorta. (Nature course and predictors of progression of intramural hematoma: A retrospective, multicenter study; ChiCTR2300073829).

Effect of F11 Receptor/Junctional Adhesion Molecule-A-derived Peptide on Neointimal Hyperplasia in a Murine Model.

PURPOSE: To determine whether inhibition of the F11 receptor/JAM-A (F11R) using F11R-specific antagonist peptide 4D results in inhibition of smooth muscle cell (SMC) proliferation and migration in vivo, known as neointimal hyperplasia (NIH), using a mouse focal carotid artery stenosis model (FCASM). MATERIALS AND METHODS: The mouse FCASM was chosen to test the hypothesis because the dominant cell type at the site of stenosis is SMC, similar to that in vascular access stenosis. Fourteen C57BL/6 mice underwent left carotid artery (LCA) partial ligation to induce stenosis, followed by daily injection of peptide 4D in 7 mice and saline in the remaining 7 mice, and these mice were observed for 21 days and then euthanized. Bilateral carotid arteries were excised for histologic analysis of the intima and media areas. RESULTS: The mean intimal area was significantly larger in control mice compared with peptide 4D-treated mice (0.031 mm2 [SD ± 0.024] vs 0.0082 mm2 [SD ± 0.0103]; P = .011). The mean intima-to-intima + media area ratio was significantly larger in control mice compared with peptide 4D-treated mice (0.27 [SD ± 0.13] vs 0.089 [SD ± 0.081]; P = .0079). NIH was not observed in the right carotid arteries in both groups. CONCLUSIONS: Peptide 4D, an F11R antagonist, significantly inhibited NIH in C57BL/6 mice in a FCASM.

Timing of Intervention and Long-Term Outcomes of Type B Aortic Intramural Hematoma with Intimal Disruption at Admission.

BACKGROUND: To compare the 30-day and long-term outcomes between patients with concomitant type B intramural hematoma and intimal disruption upon admission who underwent endovascular repair in the acute or subacute phases. METHODS: Data were extracted from January 1, 2010, to December 31, 2019. Logistic regression and Cox regression were performed to evaluate the impact of timing of intervention on 30-day and long-term outcomes, respectively. RESULTS: The study included 241 patients, among which 159 were in the acute group. No significant difference was observed in 30-day mortality (0.6% vs. 0%, P = 1), 30-day complication rate (2.5% vs. 1.2%, P = 0.664), long-term all-cause mortality (10.7% vs. 7.3%, P = 0.540), and aortic reintervention rate (2.5% vs. 2.4%, P = 1) between the acute and subacute group. In multivariable analysis, the timing of intervention was not associated with 30-day mortality (odds ratio (OR) = 0, 95% confidence interval CI: 0-Inf, P = 0.999), 30-day complication (OR = 0.30, 95% CI: 0.02-3.77, P = 0.348), long-term mortality (hazard ratio = 0.56, 95% CI: 0.20-1.61, P = 0.283), and aortic reintervention (OR = 0.97, 95% CI: 0.15-6.08, P = 0.970). CONCLUSIONS: For patients with concomitant type B intramural hematoma and intimal disruption upon admission, there is no significant difference in 30-day and long-term outcomes between those who undergo endovascular treatment in the acute or subacute phase.

Assessment of the aortic tunica media histological changes in relation with the cause of death.

AIM: The authors set out to evaluate the correlations between three of the main morphological aortic parameters (elastic fibers - FE, collagen fibers - FCOL, and smooth muscle fibers - FM) and the cause of death. MATERIALS AND METHODS: Study groups included 25 cases died of a vascular disease (V_P), 37 cases died of a non-vascular disease (NV_P) and 28 cases died of a violent/suspect non-pathological cause of death (V_Dth), the latter group representing also the control group. Four aortic cross-sections (base, arch, thoracic, and abdominal regions) were collected during autopsy from the selected cases, fixed in 10% buffered formalin and first of all photographed together with a calibrating ruler. Then, they were embedded in paraffin, sectioned off at 4 µm and stained with Hematoxylin-Eosin (HE) and Orcein. The obtained histological slides were transformed into virtual slides. Fibrillary components amounts were using a custom-made software, developed in MATLAB (MathWorks, USA). Statistical tools used were Pearson's correlation test, t-test (two-sample assuming equal variances) and one-way analysis of variance (ANOVA) test. RESULTS AND DISCUSSIONS: The amounts of the three fibrillary components of the aortic tunica media had a synchronous variation in all aortic regions in each of the three groups, excepting FCOL in the group of patients died from vascular pathology, which presented only a trend of synchronous variation along the aorta. FE had their lowest values and FCOL had their highest values in patients died from vascular pathology. FCOL had always higher levels than FE in people died from any pathological condition, vascular or non-vascular. FM had always at least two times lower level than that of the other types of fibers, regardless of whether the person died due to a pathological condition or not. CONCLUSIONS: The different pathological conditions causing death are influencing the fibrillary composition of aortic tunica media. Further studies are required to reveal other changes in the morphology of aortic wall in particular and vascular wall in general that could be related with different pathological conditions affecting the entire organism.

Unveiling the Hidden Landscape of Arterial Diseases at Single-Cell Resolution.

High-resolution single-cell technologies have shed light on the pathogenesis of cardiovascular diseases by enabling the discovery of novel cellular and transcriptomic signatures associated with various conditions, and uncovering new contributions of inflammatory processes, immunity, metabolic stress, and risk factors. We review the information obtained from studies using single-cell technologies in tissues with atherosclerosis and aortic aneurysms. Insights are provided on the biology of endothelial, smooth muscle, and immune cells in the arterial intima and media. In addition to cellular diversity, numerous examples of plasticity and phenotype switching are highlighted and presented in the context of normal cell functions.

A review on the treatment of intimal hyperplasia with perivascular medical devices: role of mechanical factors and drug release kinetics.

INTRODUCTION: Intimal hyperplasia (IH) is a significant factor limiting the success of revascularization surgery for blood flow restoration. IH results from a foreign body response and mechanical disparity that involves complex biochemical reactions resulting in graft failure. The available treatment option utilizes either different pharmacological interventions or mechanical support to the vascular grafts with limited success. AREAS COVERED: This review explains the pathophysiology of IH, responsible mechanical and biological factors, and treatment options, emphasizing perivascular devices. They are designed to provide mechanical support and pharmacology actions. The perivascular drug delivery concept has successfully demonstrated efficacy in various animal studies. Accurate projections of drug release mechanisms using mathematical modeling could be used to formulate prolonged drug elution devices. Numerical modeling aspects for the prediction of design outcomes have been given due importance that fulfills the unmet clinical need for better patient care. EXPERT OPINION: IH could be effectively prevented by simultaneous mechanical scaffolding and sustained local drug delivery. Future perivascular medical devices could be designed to integrate these essential features. Numerical modeling for device performance prediction should be utilized in the development of next-generation perivascular devices.

Aortic Intima-Media Thickness is Increased in Neonates of Mothers with Gestational Diabetes Mellitus: The Role of Thioredoxin-Interacting Protein as a Marker of Oxidative Stress.

BACKGROUND: Offspring exposed in foetal life to gestational diabetes mellitus (GDM) are at increased risk for future metabolic diseases. OBJECTIVE: To explore the prognostic role of abdominal aorta intima-media thickness (aIMT) in neonates exposed to GDM as a possible biomarker for later atherogenesis and its possible correlation with thioredoxin- interacting protein (TXNIP), a protein involved in oxidative stress. METHODS: In this prospective, observational study, mother-infant pairs were studied in 2 groups (57 patients with GDM and 51 controls without GDM). TXNIP levels were measured in the placenta, as well as in the umbilical and neonatal blood. The data were correlated with aIMT in neonates. RESULTS: aIMT was increased in GDM offspring (patients: median [range]=0.39 mm [0.31-0.46] vs controls: median=0.28 mm [0.23-0.33]; p=0.001) and remained significant after adjusting for possible confounders (e.g., triglycerides, blood pressure, vitamin D, birth weight and gender; ß coefficient=0.131 p=0.049). TXNIP levels were increased in trophoblasts (p=0.001) and syncytiotrophoblasts (p=0.001) and were decreased in endothelial cells (p=0.022) in GDM offspring vs controls. Moreover, TXNIP levels in trophoblasts positively correlated with aIMT (r=0.369; p=0.001). TXNIP levels in umbilical/ neonatal blood were not associated with GDM. CONCLUSION: Increased aIMT was demonstrated in the offspring of mothers with GDM. Non-invasive measurement of aIMT could be used as a biomarker to identify children at increased risk for atherogenesis later in life. This information may encourage early preventive measures. TXNIP may be associated with GDM and/or aIMT.

The Role of TGF-ß Signaling in Saphenous Vein Graft Failure after Peripheral Arterial Disease Bypass Surgery.

Saphenous vein bypass grafting is an effective technique used to treat peripheral arterial disease (PAD). However, restenosis is the major clinical challenge for the graft vessel among people with PAD postoperation. We hypothesize that there is a common culprit behind arterial occlusion and graft restenosis. To investigate this hypothesis, we found TGF-ß, a gene specifically upregulated in PAD arteries, by bioinformatics analysis. TGF-ß has a wide range of biological activities and plays an important role in vascular remodeling. We discuss the molecular pathway of TGF-ß and elucidate its mechanism in vascular remodeling and intimal hyperplasia, including EMT, extracellular matrix deposition, and fibrosis, which are the important pathways contributing to stenosis. Additionally, we present a case report of a patient with graft restenosis linked to the TGF-ß pathway. Finally, we discuss the potential applications of targeting the TGF-ß pathway in the clinic to improve the long-term patency of vein grafts.

A nonobstructive condition: Medial arterial calcification. / ä¸å¼•èµ·ç®¡è ”ç‹­çª„çš„è¡€ç®¡ä¸­è†œé’™åŒ–.

Vascular calcification, including intimal and medial calcification, is closely associated with a significant increase in cardiovascular diseases. Although increased understandings were achieved, people still know much more about intimal calcification than medial calcification because the latter doesn't obstruct the arterial lumen, commonly considered as a non-significant finding. We clarified the pathologic characteristic of medial calcification, its difference from intimal calcification, principally focused on its clinical relevance, such as diagnosis, nosogenesis, and hemodynamics. We underline the importance of identifying and distinguishing medial calcification, understanding its effect to local/systematic arterial compliance, and relationship to diabetic neuropathy. Recent studies emphasize do not ignore its predictive role in cardiovascular mortality. It is of great clinical significance to summarize the mechanisms of occurrence, lesion characteristics, diagnostic methods, pathogenic mechanisms, hemodynamic changes, and the distinction as well as association of intimal calcification with intimal calcification.

Multilineage commitment of Sca-1+ cells in reshaping vein grafts.

Vein graft failure remains a significant clinical problem. Similar to other vascular diseases, stenosis of vein grafts is caused by several cell lines; however, the sources of these cells remain unclear. The objective of this study was to investigate the cellular sources that reshape vein grafts. By analyzing transcriptomics data and constructing inducible lineage-tracing mouse models, we investigated the cellular components of vein grafts and their fates. The sc-RNAseq data suggested that Sca-1+ cells were vital players in vein grafts and might serve as progenitors for multilineage commitment. By generating a vein graft model in which the venae cavae from C57BL/6J wild-type mice were transplanted adjacent to the carotid arteries of Sca-1(Ly6a)-CreERT2; Rosa26-tdTomato mice, we demonstrated that the recipient Sca-1+ cells dominated reendothelialization and the formation of adventitial microvessels, especially at the perianastomotic regions. In turn, using chimeric mouse models, we confirmed that the Sca-1+ cells that participated in reendothelialization and the formation of adventitial microvessels all had a non-bone-marrow origin, whereas bone-marrow-derived Sca-1+ cells differentiated into inflammatory cells in vein grafts. Furthermore, using a parabiosis mouse model, we confirmed that non-bone-marrow-derived circulatory Sca-1+ cells were vital for the formation of adventitial microvessels, whereas Sca-1+ cells derived from local carotid arteries were the source of endothelium restoration. Using another mouse model in which venae cavae from Sca-1 (Ly6a)-CreERT2; Rosa26-tdTomato mice were transplanted adjacent to the carotid arteries of C57BL/6J wild-type mice, we confirmed that the donor Sca-1+ cells were mainly responsible for smooth muscle cells commitment in the neointima, particularly at the middle bodies of vein grafts. In addition, we provided evidence that knockdown/knockout of Pdgfrα in Sca-1+ cells decreased the cell potential to generate SMCs in vitro and decreased number of intimal SMCs in vein grafts. Our findings provided cell atlases of vein grafts, which demonstrated that recipient carotid arteries, donor veins, non-bone-marrow circulation, and the bone marrow provided diverse Sca-1+ cells/progenitors that participated in the reshaping of vein grafts.

A rare presentation of Sintilimab-induced swelling along the vessels: Case report.

RATIONALE: Immune-related adverse events are occasionally reported in Sintilimab treatment. This study reports a forward and reverse swelling case along the vein after infusion of Sintilimab. At present, swelling along the vascular direction during peripheral infusion are limitedly reported at home and abroad, especially when choosing a vein with thick, elastic, and good blood return. PATIENT CONCERNS: A 56-year-old male who suffered from esophageal cancer and liver cancer and received albumin-bound paclitaxel and nedaplatin chemotherapy in combination with Sintilimab immunotherapy appeared swelling along the vessel after infusion of Sintilimab. The patient was punctured 3 times. DIAGNOSES: Sintilimab-induced vascular edema may be a side effect resulted from a combination of variables such as relatively poor vascular function of the patient, chemical extravasation, allergic skin reactions, venous valves, vascular intima, and diameter stenosis. Sintilimab rarely causes vascular edema only when drug allergic reaction is the underlying factor. As only a few cases of vascular edema caused by Sintilimab have been reported, causes to such a drug-induced vascular edema remained unclear. INTERVENTIONS: The swelling was controlled by an intravenous specialist nurse according to delayed extravasation treatment and the doctor anti-allergy treatment, but the uncertainty of repeated puncture and symptom diagnosis caused pain and anxiety to the patient and his family. OUTCOMES: The symptom of swelling was gradually relieved after the anti-allergic treatment. The patient completed the following drug infusion without discomfort after the third puncture. When the patient was discharged the next day, swelling in his both hands disappeared, and the patient had no anxiety or discomfort. LESSONS: The side effects of immunotherapy may accumulate over time. Early identification and appropriate nursing management are the keys to minimizing patients' pain and anxiety. To effectively treat symptoms, nurses could benefit from quickly identifying the source of swelling.

In silico experiments of intimal hyperplasia development: disendothelization in an axisymmetric idealized artery.

We use in silico experiments to study the role of the hemodynamics and of the type of disendothelization on the physiopathology of intimal hyperplasia. We apply a multiscale bio-chemo-mechanical model of intimal hyperplasia on an idealized axisymmetric artery that suffers two kinds of disendothelizations. The model predicts the spatio-temporal evolution of the lesions development, initially localized at the site of damages, and after few days displaced downstream of the damaged zones, these two stages being observed whatever the kind of damage. Considering macroscopic quantities, the model sensitivity to pathology-protective and pathology-promoting zones is qualitatively consistent with experimental findings. The simulated pathological evolutions demonstrate the central role of two parameters: (a) the initial damage shape on the morphology of the incipient stenosis, and (b) the local wall shear stresses on the overall spatio-temporal dynamics of the lesion.

NAG-Net: Nested attention-guided learning for segmentation of carotid lumen-intima interface and media-adventitia interface.

Cardiovascular diseases (CVD), as the leading cause of death in the world, poses a serious threat to human health. The segmentation of carotid Lumen-intima interface (LII) and Media-adventitia interface (MAI) is a prerequisite for measuring intima-media thickness (IMT), which is of great significance for early screening and prevention of CVD. Despite recent advances, existing methods still fail to incorporate task-related clinical domain knowledge and require complex post-processing steps to obtain fine contours of LII and MAI. In this paper, a nested attention-guided deep learning model (named NAG-Net) is proposed for accurate segmentation of LII and MAI. The NAG-Net consists of two nested sub-networks, the Intima-Media Region Segmentation Network (IMRSN) and the LII and MAI Segmentation Network (LII-MAISN). It innovatively incorporates task-related clinical domain knowledge through the visual attention map generated by IMRSN, enabling LII-MAISN to focus more on the clinician's visual focus region under the same task during segmentation. Moreover, the segmentation results can directly obtain fine contours of LII and MAI through simple refinement without complicated post-processing steps. To further improve the feature extraction ability of the model and reduce the impact of data scarcity, the strategy of transfer learning is also adopted to apply the pretrained weights of VGG-16. In addition, a channel attention-based encoder feature fusion block (EFFB-ATT) is specially designed to achieve efficient representation of useful features extracted by two parallel encoders in LII-MAISN. Extensive experimental results have demonstrated that our proposed NAG-Net outperformed other state-of-the-art methods and achieved the highest performance on all evaluation metrics.

Differences between inflammatory cells infiltrated into tunica intima, media, and adventitia of ascending aortic aneurysms within diabetic and hypertensive patients.

The risk factors that are the most significant for the development of most cardiovascular diseases are arterial hypertension (AH), type 2 diabetes (DM), and inflammation. However, for the development of aortic aneurysms, DM is not one of them. Our study aimed to evaluate the difference between inflammatory infiltration in three individual layers of the ascending aortic aneurysm within diabetic and hypertensive patients. Forty-five patients aged 36 to 80 were divided into a group with diabetic patients without AH (group DM, N=8) and hypertensive patients without DM (group AH, N=37). For the histological analysis, aortic aneurysms were stained with hematoxylin eosin and Movat. We used immunochemical methods to detect pro- (M1), anti-inflammatory (M2) macrophages, T-helper, T-killer cells, B cells, and plasma cells. Statistical analysis was done by independent-samples Kruskal-Wallis test adjusted by Bonferroni correction for multiple tests (P<0.05). We found no difference in the volume density of collagen, elastin, vascular smooth muscle cells (VSMC), and ground substance between groups. In the DM group, there were significantly fewer M2, T-helpers, and T-killers in the media than in the intima and the adventitia (P<0.05). There were no significant differences in the number of M1, B, and plasma cells between all three vascular layers (P<0.05). In the AH group, there were significantly fewer B and plasma cells, T-helper, T-killer cells, M1, and M2 in the media than in the intima and adventitia (P<0.05). Our results conclude that the tunica media in the aneurismal wall of the AH group retained immune privilege. In contrast, in the DM group, all three layers were immune-privileged.

Intimal growth on the luminal surface of arteriovenous grafts in rats.

BACKGROUND: Endothelial cells are known to grow on the luminal surface of arteriovenous grafts (AVGs) used in hemodialysis. Although endothelial cells are important for preventing infection, a detailed growth of endothelial cells in AVGs is unknown. This study sought to create a simpler animal model of AVGs and to investigate how endothelial cells form on the luminal surface. METHODS: Polyethylene grafts were placed between the cervical artery and vein of Wistar rats. The grafts were removed at 6 h, 24 h, 3 days, or 7 days after placement. The luminal surface was observed under optical and polarizing microscopy and stained with endothelial cell markers (LEL, CD31), the progenitor cell marker CD34, and the macrophage marker ED-1. RESULTS: Microscopy demonstrated many diffuse vascular endothelial cells on the luminal surface of AVGs after placement. While there was no difference in the number of LEL-positive cells between the arterial side (AS) and venous side (VS) at 6 h or 7 days, there were significantly more of these cells on the VS at both 24 h and 3 days (p < 0.05). Analysis at 24 h showed some CD31-positive cells and few CD34-positive cells. CONCLUSIONS: This was the first study to use a simple rat model of AVG placement. Endothelial cell formation was initially more active on the VS than on the AS, but these cells subsequently increased in number across the luminal surface. Future clinical studies might contribute clinically by confirming whether AS versus VS puncture results in different infection rates.