Arterial Tree Research Articles

Peripheral artery disease affects the function of the legs of claudicating patients in a diffuse manner irrespective of the segment of the arterial tree primarily involved.

Different levels of arterial occlusive disease (aortoiliac, femoropopliteal, multi-level disease) can produce claudication symptoms in different leg muscle groups (buttocks, thighs, calves) in patients with peripheral artery disease (PAD). We tested the hypothesis that different locations of occlusive disease uniquely affect the muscles of PAD legs and produce distinctive patterns in the way claudicating patients walk. Ninety-seven PAD patients and 35 healthy controls were recruited. PAD patients were categorized to aortoiliac, femoropopliteal and multi-level disease groups using computerized tomographic angiography. Subjects performed walking trials both pain-free and during claudication pain and joint kinematics, kinetics, and spatiotemporal parameters were calculated to evaluate the net contribution of the calf, thigh and buttock muscles. PAD patients with occlusive disease affecting different segments of the arterial tree (aortoiliac, femoropopliteal, multi-level disease) presented with symptoms affecting different muscle groups of the lower extremity (calves, thighs and buttocks alone or in combination). However, no significant biomechanical differences were found between PAD groups during the pain-free conditions with minimal differences between PAD groups in the claudicating state. All statistical differences in the pain-free condition occurred between healthy controls and one or more PAD groups. A discriminant analysis function was able to adequately predict if a subject was a control with over 70% accuracy, but the function was unable to differentiate between PAD groups. In-depth gait analyses of claudicating PAD patients indicate that different locations of arterial disease produce claudication symptoms that affect different muscle groups across the lower extremity but impact the function of the leg muscles in a diffuse manner generating similar walking impairments.

Vascular calcification in different arterial beds in ex vivo ring culture and in vivo rat model

Vascular calcification is a risk factor for cardiovascular and kidney diseases. Medial calcification may differently affect the arterial tree depending on vessel location and smooth muscle injury. The aim was to map the anatomical distribution of vascular calcifications on different arteries and artery locations, in cultured artery rings (ex vivo) and in a rat model of elastocalcinosis (in vivo). Vascular calcification was assessed histologically (von Kossa staining of the media) and by calcium content measurement. Arteries of different sizes were harvested from untreated rats for ring culture and from the vitamin D3-nicotine (VDN) rat model for direct observation. When cultured in pro-calcifying conditions, thoracic aorta exhibited similar calcification from the arch to the diaphragm. Calcification increased in abdominal aorta along with the reduction in cross sectional area. Carotid and renal arteries exhibited similar ex vivo calcification. In VDN rats, calcification was greater in carotid artery than in aorta, and was accompanied by fibrosis and apoptosis. Ex vivo, calcification was increased by the induction of lesions on arteries. Along the vascular tree, calcification of the arterial wall increases with the narrowing of vessels in ex vivo ring culture and in vivo. The observed differences represent local susceptibility of the vessels to the calcifying processes.

Laboratory Rat Thrombi Lose One-Third of Their Stiffness When Exposed to Large Oscillating Shear Stress Amplitudes: Contrasting Behavior to Human Clots

Rats impress by their high platelet count resulting in hypercoagulability, which protects the animals from severe bleeding. However, platelets also import numerous stiff junction points into the fibrous system of a clot, also enhancing the pre-stress of the fibrin fibers, which lowers their deformability. Clot deformation is clinically important since large strains are present in the arterial tree (caused by the propagation of pressure and pulse waves), and a clot is considered “safe” when it can deform over a long range of strain amplitudes. We tested clot formation and the behavior of fully formed blood clots of laboratory rats at large sinusoidal shear stress amplitudes by rheometry and compared outcomes to human reference data. We found that fiber density (by scanning electron microscopy) and clot stiffness (by rheometry) was pronounced compared to humans and differed with sexual dimorphism and with rat strain. Using our large amplitude oscillation (LAOS) protocol, we detected that rat clots yielded with a frustrated attempt to stiffen instead of showing the macroscopic stiffening response that is typical for human clots. We attribute this behavior to the appearance of multiple microfractures until, finally, a few leading fibers uptake the load. Rat clots also failed to align fibers in shear direction to initiate affine deformation. The rat clot phenotype differs substantially from the human one, which must be considered in research and toxicological testing. If microfractures in the fiber meshwork are concentrated in vivo, parts of a clot may break off and be washed away. However, homogenously distributed microfractures may open pores and allow the penetration of plasminogen activators. What occurs in the rat vasculature depends on the on-site clot composition.

3D reconstruction of coronary arteries using deep networks from synthetic X-ray angiogram data

Cardiovascular disease (CVD) is one of the most common health problems that are responsible for one-third of all deaths around the globe. Although X-Ray angiography has deficiencies such as two-dimensional (2D) representation of three dimensional (3D) structures, vessel overlapping, noisy background, the existence of other tissues/organs in images, etc., it is used as the gold standard technique for the diagnosis and in some cases treatment of CVDs. To overcome the deficiencies, great efforts have been drawn on retrieval of actual 3D representation of coronary arterial tree from 2D X-ray angiograms. However, the proposed algorithms are based on analytical methods and enforce some constraints. With the evolution of deep neural networks, 3D reconstruction from images can be achieved effectively. In this study, we propose a new data structure for the representation of objects in a tubular shape for 3D reconstruction of arteries using deep learning. Moreover, we propose a method to generate synthetic coronaries from data of real subjects. Then, we validate tubular shape representation using 3 typical deep learning architectures with synthetic X-ray data we produced. The input to deep learning architectures is multi-view segmented X-Ray images and the output is the structured tubular representation. We compare results qualitatively in terms of visual appearance and quantitatively in terms of Chamfer Distance and Mean Squared Error. The results demonstrate that tubular representation has promising performance in 3D reconstruction of coronaries. We observe that convolutional neural network (CNN) based architectures yield better 3D reconstruction performance with 9.9e-3 on Chamfer Distance. On the other hand, LSTM-based network fails to learn the coronary tree structure and we conclude that LSTMs are not appropriate for auto-regression problems as depicted in this study.

Evaluation of classifications of the monopodial bronchopulmonary vasculature using clustering methods

Mammalian pulmonary arteries divide multiple times before reaching the vast capillary network of the alveoli. Morphological analyses of the arterial branches can be challenging because more proximal branches are likely biologically distinct from more peripheral parts. Thus, it is useful to group the arterial branches into groups of coherent biology. While the generational approach of dichotomous branching is straightforward, the grouping of arterial branches in the asymmetrically branching monopodial lung is less clear. Several established classification methods return highly dissimilar groupings when employed on the same organ. Here, we established a workflow allowing the quantification of grouping results for the monopodial lung and tested various methods to group the branches of the arterial tree into coherent groups. A mouse lung was imaged by synchrotron x-ray microcomputed tomography, and the arteries were digitally segmented. The arterial tree was divided into its individual segments, morphological properties were assessed from corresponding light microscopic scans, and different grouping methods were employed, such as (fractal) generation or (Strahler) order. The results were ranked by the morphological similarity within and dissimilarity between the resulting groups. Additionally, a method from the mathematical field of cluster analysis was employed for creating a reference classification. In conclusion, there were significant differences in method performance. The Strahler order was significantly superior to the generation system commonly used to classify human lung structure. Furthermore, a clustering approach indicated more precise ways to classify the monopodial lung vasculature exist.

Median Arcuate Ligament Syndrome with Common Hepatic and Splenic Arteries Directly Originating from the Abdominal Aorta: A Case Report

Introduction: Knowledge of the unpaired abdominal vasculature is important for uncomplicated operations. The absent celiac trunk has previously been reported; however, developmental alterations can result in a variety of branching patterns of the downstream arteries from the abdominal aorta. Case Presentation: A 53-year-old female patient with lymphoma underwent abdominopelvic computed tomography (CT) for staging. She had a history of postprandial off-and-on abdominal pain since her youth. CT scan revealed an absent celiac trunk with common hepatic and splenic arteries directly originating from the abdominal aorta. Compression of the median arcuate ligament had narrowed and angulated the 2 branches. Conclusions: When the celiac trunk is absent, its main branches may separately arise from the abdominal aorta. Also, due to the displacement of these branches, their path and diameter can vary from the normal.

The Gut Microbiota and Vascular Aging: A State-of-the-Art and Systematic Review of the Literature.

The gut microbiota is a critical regulator of human physiology, deleterious changes to its composition and function (dysbiosis) have been linked to the development and progression of cardiovascular diseases. Vascular ageing (VA) is a process of progressive stiffening of the arterial tree associated with arterial wall remodeling, which can precede hypertension and organ damage, and is associated with cardiovascular risk. Arterial stiffness has become the preferred marker of VA. In our systematic review, we found an association between gut microbiota composition and arterial stiffness, with two patterns, in most animal and human studies: a direct correlation between arterial stiffness and abundances of bacteria associated with altered gut permeability and inflammation; an inverse relationship between arterial stiffness, microbiota diversity, and abundances of bacteria associated with most fit microbiota composition. Interventional studies were able to show a stable link between microbiota modification and arterial stiffness only in animals. None of the human interventional trials was able to demonstrate this relationship, and very few adjusted the analyses for determinants of arterial stiffness. We observed a lack of large randomized interventional trials in humans that test the role of gut microbiota modifications on arterial stiffness, and take into account BP and hemodynamic alterations.

Patient-specific brain arteries molded as a flexible phantom model using 3D printed water-soluble resin

Visualizing medical images from patients as physical 3D models (phantom models) have many roles in the medical field, from education to preclinical preparation and clinical research. However, current phantom models are generally generic, expensive, and time-consuming to fabricate. Thus, there is a need for a cost- and time-efficient pipeline from medical imaging to patient-specific phantom models. In this work, we present a method for creating complex 3D sacrificial molds using an off-the-shelf water-soluble resin and a low-cost desktop 3D printer. This enables us to recreate parts of the cerebral arterial tree as a full-scale phantom model (10times 6times 4 cm) in transparent silicone rubber (polydimethylsiloxane, PDMS) from computed tomography angiography images (CTA). We analyzed the model with magnetic resonance imaging (MRI) and compared it with the patient data. The results show good agreement and smooth surfaces for the arteries. We also evaluate our method by looking at its capability to reproduce 1 mm channels and sharp corners. We found that round shapes are well reproduced, whereas sharp features show some divergence. Our method can fabricate a patient-specific phantom model with less than 2 h of total labor time and at a low fabrication cost.

Guiding the Prostatic Artery Embolization Procedure With Computational Fluid Dynamics.

Benign prostatic hyperplasia (BPH) is a common disease associated with lower urinary tract symptoms and is the most frequent benign tumor in men. To reduce BPH therapy complications, prostatic artery embolization (PAE) was developed to replace the surgical options. PAE is a minimally invasive technique in which emboli are injected into the prostate arteries (PA), obstructing the blood flow in the hypervascular nodules. In this work, a personalized PAE treatment strategy was proposed using patient-specific computational fluid dynamics (CFD). First, the hemodynamics environment in the iliac arterial tree considering a large network of bifurcations was studied. The results showed complex blood flow patterns in the iliac arterial network. Subsequently, the transport of embolic particulates during PAE for the standard horizontal and hypothetical vertical patient positioning was simulated using Lagrangian particle tracking. Emboli of different sizes were released at various locations across the iliac arterial tree. The emboli entering the PA were mapped back to their initial location to create emboli release maps (ERMs). The obtained ERMs during the standard patient positioning for smaller emboli at certain release locations showed distinct regions in which if the emboli were released within these regions, all of them would reach the PA without nontarget embolization. During the hypothetical vertical patient positioning, the larger emboli formed a larger coherent region in the ERMs. Our patient-specific model can be used to find the best spatial location for emboli injection and perform the embolization procedure with minimal off-target delivery.

The Use of Digital Coronary Phantoms for the Validation of Arterial Geometry Reconstruction and Computation of Virtual FFR

We present computational fluid dynamics (CFD) results of virtual fractional flow reserve (vFFR) calculations, performed on reconstructed arterial geometries derived from a digital phantom (DP). The latter provides a convenient and parsimonious description of the main vessels of the left and right coronary arterial trees, which, crucially, is CFD-compatible. Using our DP, we investigate the reconstruction error in what we deem to be the most relevant way—by evaluating the change in the computed value of vFFR, which results from varying (within representative clinical bounds) the selection of the virtual angiogram pair (defined by their viewing angles) used to segment the artery, the eccentricity and severity of the stenosis, and thereby, the CFD simulation’s luminal boundary. The DP is used to quantify reconstruction and computed haemodynamic error within the VIRTUheartTM software suite. However, our method and the associated digital phantom tool are readily transferable to equivalent, clinically oriented workflows. While we are able to conclude that error within the VIRTUheartTM workflow is suitably controlled, the principal outcomes of the work reported here are the demonstration and provision of a practical tool along with an exemplar methodology for evaluating error in a coronary segmentation process.

Disparities between determinants of impaired vascular structure and function in young people with primary hypertension: a systematic review.

Early effects of primary hypertension on arterial structure and function in children and young people (CYP) and their determinants remain elusive. We aimed to review independent determinants of carotid intima-media thickness (cIMT), carotid wall cross-sectional area (WCSA) and carotid-femoral pulse wave velocity (cfPWV) in CYP with primary hypertension. We performed a systematic review of studies reporting multivariable analysis of cfPWV, cIMT and WCSA in CYP (up to 25 years of age) with primary hypertension. Literature search was performed in PubMed database and 13, 12 and two articles including 3860 (age range 4-25 years, 50% male individuals), 2038 children (5-25 years, 55% male individuals) and 136 children (5-17 years, 85% male individuals) were selected for final analysis of cfPWV, cIMT and WCSA, respectively. Ninety and 86% of the studies reported higher cfPWV and cIMT in CYP with elevated blood pressure (BP) compared with normotensive controls. Different indices of BP were positively associated with cfPWV in 92% of studies, whereas BMI showed association in 31%. Carotid IMT associated with BP indices in 50% and with BMI in 25% of the studies. WCSA was studied longitudinally and its improvement associated with decrease in measures of central obesity. We found a disparity between the determinants of structural and functional impairment of arterial tree in CYP with primary hypertension. In contrast to cIMT and WCSA, increase of cfPWV is almost exclusively determined by BP.

An Anatomic Assessment of the Intercavernous Sinuses and Review of the Literature.

Introduction As expanded endoscopic endonasal approaches are gaining popularity, a thorough understanding of the anatomy of the intercavernous sinuses is pertinent to avoid bleeding complications. There have been few studies reporting the presence and dimensions of the anterior intercavernous sinus (AIS), posterior intercavernous sinus (PIS), and inferior intercavernous sinus (IIS). We performed a cadaveric study to better understand these structures. Methods Colored latex was injected into the arterial and venous trees of 17 cadaveric heads. Dissections assessed the presence and dimensions of the AIS, PIS, and IIS. In an additional three specimens, the sellar contents were subjected to histological analysis. Results Of the 20 total specimens, 13 (65%) demonstrated the gross presence of all three sinuses. In six specimens (30%), only the AIS and PIS could be identified, and in one specimen, only an AIS and IIS were identified. An AIS was identified in all 20 (100%) specimens, PIS in 18 (88%), and an IIS in 14 (70%). In two specimens (10%), the AIS covered the entire face of the sella. Dimensions of the AIS averaged 1.7 × 11.7 × 2.8 mm, PIS averaged 1.5 × 10.8 × 1.7 mm, and IIS averaged 8.7 × 11.8 × 1.0 mm when present. Conclusion All examined specimens demonstrated the presence of an AIS, and most had a PIS. The presence of an IIS was more variable. Preoperative awareness of these sinuses is helpful in planning transsphenoidal surgery to minimize the risk of bleeding.

ASSESSMENT OF STIFFNESS OF LARGE TO SMALL ARTERIES IN MULTI-STAGE RENAL DISEASE: A NUMERICAL STUDY

Objective: Arterial stiffness, as assessed via pulse wave velocity (PWV), is a major biomarker for risk assessment in patients with chronic kidney disease. However, the mechanisms responsible for the changes in PWV in the presence of kidney disease are not yet fully elucidated. In the present study, we aimed to investigate the direct effects attributable to biomechanical alterations to the arterial tree caused by renal disease progression on arterial stiffness, independent of any biochemical or compensatory effects. Design and method: Particularly, we used a previously validated one-dimensional (1-D) model of the cardiovascular system to simulate arterial pressure and flow at control with two kidneys (2KDN) and in arterial tree configurations representative of different stages of kidney disease, namely subject with a single functional kidney (1KDN), without any functional kidney (0KDN) and a transplant recipient (TX) with a single functional kidney re-attached to the external iliac artery. We evaluated the respective variations in blood pressure (BP), as well as arterial stiffness of large, medium, and small-sized vessels via carotid-femoral PWV (cfPWV), carotid-radial PWV (crPWV), and radial-digital PWV (rdPWV), respectively. Results: Our results showed that BP was increased in 1KDN and 0KDN, and that systolic BP values were restored in the TX configuration. Furthermore, a rise was reported in all PWVs for all tested configurations. The relative difference in stiffness from control to 0KDN was higher in the case of crPWV (+20 %); approximately twice the difference observed for cfPWV and rdPWV (+11 %). In TX, we observed a restoration of the PWVs to values close to 1KDN. Globally, it was demonstrated that alterations of the outflow boundaries to the renal arteries as occurring in different stages of renal disease lead to changes in blood pressure and central and peripheral PWV in line with previously reported clinical data. Conclusions: Our findings suggest that the PWV variations observed in clinical practice with renal disease progression may be partially attributed to biomechanical alterations of the arterial tree, and their effect on blood pressure.

Artificial sweeteners sucralose and acesulfame potassium: A bittersweet story for the cardiovascular system?

Artificial sweeteners (AS) are well known to activate two categories of receptors; sweet taste receptor with high affinity and bitter taste receptors with low affinity. Interestingly, recent data from our and other groups suggested that these two receptors families are expressed throughout the arterial tree. Therefore, it could be interesting to explore if AS may have an impact on vascular function, and to decipher the role of these taste receptors. The aims of this ongoing work is to investigate whether AS, like sucralose and acesulfame potassium (AceK) (1) exhibit vasomotor effect and (2) in that case determine the underlying mechanisms. Biomolecular and functional investigations have been performed on isolated rodent aortas, human dermal micro-arteries and omental arteries. Ex vivo vasomotor function was assessed using isometric tension measurements in organ bath systems. We first confirmed that both endothelial and smooth muscle cells from rodent and human arteries express the transcripts encoding for TAS1R2 and TAS1R3; the heterodimer receptor known to be responsible for the sweet taste. Our ex vivo data showed that only high concentrations (about 10 mM) of AceK and sucralose induce vasomotor responses. While AceK exhibited a vasoconstrictive effect, sucralose induced vasorelaxation. Both responses were found to be independent of the endothelium. Pharmacological inhibition (gurmarin and lactisol) and the use of a TAS1R3 KO mice model demonstrated that AS vasomotor effects do not rely on the sweet taste receptors. In contrast, inhibition of TAS2Rs abolished all responses suggesting that bitter taste receptors are more likely responsible for the AS-induced vascular effects. Additionally, our last observations show that the vasoconstrictive effect of AceK is mediated by RhoA/ROCK pathway. These evidences support the idea that AS can alter vasomotor signaling in the smooth muscle cells. These acute effects are probably mediated by the bitter taste receptor family. Their activation at the vascular level as well as the underlying pathways remains poorly understood, and the physiopathological consequences need to be further investigated.

HEART-TO-ANKLE PULSE WAVE VELOCITY AS USED IN CARDIO-ANKLE VASCULAR INDEX (CAVI) AND CAVI_0 IS A NEARLY DIASTOLIC WAVE SPEED METRIC

Objective: Cardio-ankle vascular index (CAVI) and CAVI_0 are arterial stiffness indices based on the heart-to-ankle pulse wave velocity (haPWV). haPWV is derived from the heart-to-ankle transit time (haTT = tb+tba) as haPWV = L/haTT, with L an estimated transit distance. tb is the time difference between aortic valve closure (causing the aortic dicrotic notch) and the dicrotic notch in the brachial pressure waveform; tba is the time difference between the diastolic feet in the brachial and ankle pressure waveforms. CAVI and CAVI_0 aim to normalise haPWV for blood pressure at the time of measurement. As tb and tba are determined at different pressures — tb at dicrotic notch pressure (P_notch); tba at diastolic blood pressure (DBP; Fig. C) — determining the pressure that governs haPWV (P_haPWV) and hence should ideally be used for normalisation of haPWV is not trivial. CAVI uses P_m = (SBP+DBP)/2 to normalise haPWV, whereas CAVI_0 uses DBP (SBP: brachial systolic blood pressure). We aim to analytically estimate P_haPWV and compare this to the normalisation pressures used in CAVI and CAVI_0. Design and method: Consistent with CAVI/CAVI_0 assumptions, the arterial tree was assumed to consist of tubes with exponential pressure-diameter relationship and uniform stiffness index beta_0, allowing us to calculate PWV at P_notch (PWV_notch) and at DBP (PWV_DBP; Fig. A). P_notch was calculated as 0.55DBP+0.45SBP [Adji et al.,J Hypertens 2012;30:1540–1551]. The resulting PWVs, together with heart-to-ankle (L_ha=170 cm) and heart-to-brachial (L_hb=38 cm) path lengths [Alastruey et al.,11th Int Conf Press Surges 2012;401–442] (Fig. B), allowed analytically estimating tb and tba: tb=L_hb/PWV_notch and tba=(L_ha-L_hb)/PWV_DBP. P_haPWV was finally estimated as the weighted average of P_notch and DBP using tb and tba as weights. Results: Choosing SBP/DBP=120/80 mmHg (and hence P_m=100 mmHg) and beta_0 = 10 yielded tb = 0.048 s and tba = 0.187 s, giving P_haPWV = 84 mmHg. This implies that P_haPWV was much closer to DBP (as used in CAVI_0) than to P_m (as used in CAVI). This result was only marginally influenced by blood pressure: e.g., SBP/DBP = 160/90 mmHg (P_m = 125 mmHg) yielded P_haPWV = 96 mmHg. Conclusions: DBP offers a more accurate estimate of P_haPWV than Pm, supporting the utility of CAVI_0 as an enhancement of CAVI.

A Hybrid Particle-Flow CFD Modeling Approach in Truncated Hepatic Arterial Trees for Liver Radioembolization: A Patient-specific Case Study.

Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer. At its intermediate, unresectable stage, HCC is typically treated by local injection of embolizing microspheres in the hepatic arteries to selectively damage tumor tissue. Interestingly, computational fluid dynamics (CFD) has been applied increasingly to elucidate the impact of clinically variable parameters, such as injection location, on the downstream particle distribution. This study aims to reduce the computational cost of such CFD approaches by introducing a novel truncation algorithm to simplify hepatic arterial trees, and a hybrid particle-flow modeling approach which only models particles in the first few bifurcations. A patient-specific hepatic arterial geometry was pruned at three different levels, resulting in three trees: Geometry 1 (48 outlets), Geometry 2 (38 outlets), and Geometry 3 (17 outlets). In each geometry, 1 planar injection and 3 catheter injections (each with different tip locations) were performed. For the truncated geometries, it was assumed that, downstream of the truncated outlets, particles distributed themselves proportional to the blood flow. This allowed to compare the particle distribution in all 48 “outlets” for each geometry. For the planar injections, the median difference in outlet-specific particle distribution between Geometry 1 and 3 was 0.21%; while the median difference between outlet-specific flow and particle distribution in Geometry 1 was 0.40%. Comparing catheter injections, the maximum median difference in particle distribution between Geometry 1 and 3 was 0.24%, while the maximum median difference between particle and flow distribution was 0.62%. The results suggest that the hepatic arterial tree might be reliably truncated to estimate the particle distribution in the full-complexity tree. In the resulting hybrid particle-flow model, explicit particle modeling was only deemed necessary in the first few bifurcations of the arterial tree. Interestingly, using flow distribution as a surrogate for particle distribution in the entire tree was considerably less accurate than using the hybrid model, although the difference was much higher for catheter injections than for planar injections. Future work should focus on replicating and experimentally validating these results in more patient-specific geometries.

Loss of CD226 protects apolipoprotein E-deficient mice from diet-induced atherosclerosis

CD226 is a costimulatory molecule that regulates immune cell functions in T cells, natural killer cells, and macrophages. Because macrophage-derived foam cell formation is a crucial factor contributing to the development of atherosclerosis, we aimed to evaluate the potential roles of CD226 in the pathogenesis of atherosclerosis. The effects of CD226 on atherosclerosis were investigated in CD226 and apolipoprotein E double-knockout (CD226−/− ApoE−/−) mice fed with a high-cholesterol atherogenic diet. CD226 expression in macrophages was evaluated using flow cytometry. Histopathological analysis was performed to evaluate the atherosclerotic lesions. Inflammatory cell infiltration was detected using immunofluorescence staining. Bone marrow-derived macrophages (BMDMs) and peritoneal macrophages (PEMs) were isolated from the mice and used to explore the mechanism in vitro. The in vivo results indicated that CD226 knockdown protected against atherosclerosis in ApoE−/− mice, evidenced by reduced plaque accumulation in the brachiocephalic artery, aortic roots, and main aortic tree. CD226 gene-deficient macrophages showed reduced foam cell formation under ox-low density lipoprotein stimulation compared with wild-type (WT) cells. CD226 deficiency also decreased the expression of CD36 and scavenger receptor (SR)-A (responsible for lipoprotein uptake) but increased the expression of ATP-binding cassette transporter A1 and G1 (two transporters for cholesterol efflux). Therefore, loss of CD226 hinders foam cell formation and atherosclerosis progression, suggesting that CD226 is a promising new therapeutic target for atherosclerosis.

Analysis of the Variations in the Colic Branching Pattern of the Superior Mesenteric Artery: A Cadaveric Study With Proposal to Modify Its Current Anatomical Classification

Background: Vascular anatomy of the ascending colon is more complex and variable as compared to the left. Variations range from the mode of origin, branching to territorial supply. The present study was undertaken to learn the anatomical variations of the superior mesenteric artery (SMA) and its colic branches in detail.Materials and methods: The study included 50 formalin fixed cadavers aged between 40 and 65 years. The colic branches arising from SMA were dissected to trace their mode of origin, branching pattern, and territorial supply. Based on the mode of origin of the colic branches, the SMA anatomy was classified into four patterns: I; II a, b, c; III; and IV.Results: SMA itself showed variations in its origin (as celiacomesenteric and hepatomesenteric trunk), so the colic branches arising from it. In most of the cases, middle (MCA), right (RCA), and ileocolic artery (ICA) originated independently from SMA (I). A common stem (CS) was reported between MCA and RCA (IIa) in seven cases; RCA and ICA in one (IIb); MCA and LCA in one. MCA originated from the coeliac trunk (CT) in one case. In one case, each of absent RCA (III) and accessory artery arising from SMA (IV) was also noticed. In one case, the right branch of MCA gave origin to RCA. Additionally, close association was observed between pattern IIa and incomplete inter-colic anastomosis.Conclusion: Variations in the origin of SMA may potentially influence branching patterns of colic arteries. MCA is the most variant and ICA is the most consistent branch of SMA. Distinctive variations like MCA arising from CT or arising as CS with LCA and incomplete inter-colic anastomosis in pattern IIa are of outrageous importance for operating surgeons during surgical procedures of colon. Based on study results, we propose a modification in the classification of SMA anatomy to include the CS of MCA and LCA as type IId; however, its success relies upon universal acceptance.

Variations in origin of inferior pancreaticoduodenal artery

Coeliac trunk and Superior Mesenteric arteries are very much susceptible to variations and were described by Tandler in 1904. Abdominal aorta branches are classified as single double or visceral parietal. Double visceral branches are middle suprarenal, renal and testicular arteries and single visceral branches are coeliac trunk, superior mesenteric and inferior mesenteric arteries. Materials and Methods: After obtaining ethical committee approval, we observed the origin, course and branching pattern of pancreatico duodenal arteries in 50 cadavers kept for dissection from 2019-2022 in Rohilkand Medical College and Hospital and Ayaan Institute of Medical Sciences. Results: In a male cadaver aged approximately 60 years, we observed that inferior pancreatico duodenal artery is absent. In another male cadaver aged about 70 years, we observed an additional inferior pancreatico duodenal artery. In remaining specimens, we observed the branching pattern very much normal.

Probing the possibility of lesion formation/progression in vicinity of a primary atherosclerotic plaque: A fluid-solid interaction study and angiographic evidences.

It is shown that certain locations in the arterial tree, such as coronary and cerebral arteries, are more prevalent to plaque formation. Endothelial activation and consequent plaque development are attributed to local hemodynamic parameters such as wall shear stress (WSS), oscillatory shear index (OSI), relative residence time (RRT), and stress phase angle. After a certain level of plaque progression, these hemodynamic parameters are disturbed before and after the plaque. In the current study, it is hypothesized that the vicinity of a primary lesion is susceptible for further degeneration and second plaque formation. A fluid-solid interaction (FSI) model of the coronary artery with different levels of asymmetric constriction, is simulated and the trend of hemodynamic parameters were studied in both of the plaque side (PS) and the opposite wall (facing the plaque [PF]). Also, a novel factor is introduced that can identify the high-risk regions associated with WSS oscillations to negative values. Our results indicate that when more than half of the artery is constricted, the downstream of the plaque is highly exposed to endothelial pathogenesis the PS, such that negative WSS, and as well, critical values of OSI and RRT, that is, -1.2 Pa, 0.42 and 6.5s, respectively arise in this region. PS endothelial cells in this region exposed to the highest risk of atherosclerosis based on the proposed index (3 out of 3). As well, three cases of angiographic images are provided that confirms existence of secondary lesion close to the primary one as predicted by our computational simulations.